ADRENOCORTICAL CARCINOMA - February 1996 1 UI - 96069311 AU - Mendonca BB; Lucon AM; Menezes CA; Saldanha LB; Latronico AC; Zerbini C; Madureira G; Domenice S; Albergaria MA; Camargo MH; et al TI - Clinical, hormonal and pathological findings in a comparative study of adrenocortical neoplasms in childhood and adulthood. AB - PURPOSE: We reviewed clinical and laboratory findings in 6 male and 32 female patients with functional adrenocortical neoplasms, and compared pediatric and adult data. RESULTS: Children had a higher incidence of virilization (72%), whereas in adults the predominant feature was Cushing's syndrome (60%). CONCLUSIONS: No statistically significant relation was noted between tumor weight and prognosis but there was a negative correlation between patient age and prognosis since children had a more favorable followup than adults. A Weiss criteria grade IV or greater correlated well with a poor prognosis in adults but not children, while staging was more reliable in children. None of the following predicted a poor prognosis in patients who underwent complete resection: (1) need for extended resection, (2) presence of renal vein or inferior vena cava tumor thrombus, or (3) tumor aneuploidy (14 of 14 tumors were aneuploid).

ADRENOCORTICAL CARCINOMA - June 1995 1 UI - 95216572 AU - Gotoh A; Sugita Y; Maeda H; Umezu K TI - [Bilateral testicular Leydig cell tumor with adrenocortical adenoma: a case report] SO - Hinyokika Kiyo 1995;41(2):149-52 AD - Department of Urology, Kobe National Hospital. AB - BACKGROUND AND OBJECTIVE: Reduced serum levels of dehydroepiandroste- rone sulphate (DHEAS) have been shown in patients with Cushing's syndrome resulting from adrenocortical adenoma, in contrast with normal DHEAS levels in patients with Cushing's disease. PATIENTS: Thirty-two patients with adrenal incidentaloma and, as controls, 17 patients with overt Cushing's syndrome, were studied. RESULTS: Serum DHEAS levels lower than normal were found in 21/24 (87.5%) patients with adrenocortical incidentaloma, but in only 1/8 patients with a mass of non-adrenocortical origin. Patients with endogenous hypercortisolism are thought to be at high risk for adrenalectomy and may experience significant postoperative surgical mortality/morbidity. Comparative mean length of hospitalization for patients undergoing unilateral anterior versus posterior approach was 8 versus 6 days, and bilateral anterior versus posterior was 11 versus 6 days.

(50) Histiocytic Sarcoma 1 (2%) Leukemia Mononuclear 26 (52%) 10 (20%) 13 (26%) Lymphoma Malignant Mixed 1 (2%) * Number of animals with any tissue examined microscopically Page 5 NTP Experiment-Test: 05007-06 INCIDENCE RATES OF NEOPLASMS BY ANATOMIC SITE (SYSTEMIC LESIONS ABRIDGED) (a) Report: PEIRPT05 Study Type: CHRONIC POLYSORBATE 80 Date: 09/03/94 Route: DOSED FEED Time: 12:48:09 FISCHER 344 RATS FEMALE UNTREATD 2.5% 5.0% CONTROL TUMOR SUMMARY Total Animals with Primary Neoplasms (b) 49 48 48 Total Primary Neoplasms 138 118 124 Total Animals with Benign Neoplasms 47 44 46 Total Benign Neoplasms 91 87 93 Total Animals with Malignant Neoplasms 35 21 20 Total Malignant Neoplasms 41 25 24 Total Animals with Metastatic Neoplasms 2 1 Total Metastatic Neoplasm 2 2 Total Animals with Malignant Neoplasms Uncertain Primary Site Total Animals with Neoplasms Uncertain- Benign or Malignant 6 6 7 Total Uncertain Neoplasms 6 6 7

Adrenal 1-8 CTTR 24652 Adrenal Cortical Adenoma Adrenal 9-14 CTTR 24438 Adrenal Cortical Carcinoma Adrenal 16-23 CTTR 23069 Pheochromocytoma Cart 1-8 Cttr 24873 Condroma Cart 9-13 Cttr 25062 Mixoid Condrosarcoma Bone 1-7 Cttr 24771 Fiberous Dysplasia Bone 8-15 Cttr 17696 Metastatic Carcinoma Bone 16-23 Cttr 22168 Low grade Condrosarcoma Ovary 1-9 Cttr 24778 thecoma Ovary 10-17 CTTR 24239 carcinoid Ovary 18-29 Cttr 24744 Brenner Tumor Ovary 30-37 cttr 24983 Maligant Mixed Mesodermal Tumor Ovary 38-45 cttr 24252 Granulosa Cell tumor Ovary 46-53 cttr 24220 Dysgerminoma Ovary 54-62 cttr 25028 Immature Teratoma Ovary 63-70 cttr 24559 Krukenberg Tumor Ovary 71-78 Cttr 25186 Clear cell Ca Ovary 79-84 Cttr 23710 Endomerroid Carcinoma Ovary 85-92 cttr 23827 Papillary cystadencarcinoma Ovary 93-100 cttr 23913 Sertoli Leydig cell tumor Ovary 101-107 cttr 18401 Struma Ovarii

(Addams)Monday Morning 11:33 AME11 1 1/2 hours Adrenal Cysts: CT Features and Differentiation from Nonhyperfunctioning Adenoma A. Rozenblit, MD, Bronx, NY * E.S. Amis, Jr, MD PURPOSE: To define the CT features of cystic adrenal lesions (CALs) and differentiate CALs from nonhyperfunctioning adenomas of similar density. MATERIALS AND METHODS: CT scans of 12 patients with CALs were analyzed retrospectively. RESULTS: The mean CAL diameter was 6.3 cm, with 9 lesions smaller than 5 cm. Wall thickness was 3 mm or less in 9 and exceeded 6 mm in 3 lesions; 1 CAL in the latter group was cystic carcinoma. CONCLUSION: Although CALs and adenomas can be similar in size, attenuation and nodule-like adrenal involvement, a nonenhancing lesion with wall calcification suggests a CAL.

ADRENOCORTICAL CARCINOMA - February 1996 1 UI - 96069311 AU - Mendonca BB; Lucon AM; Menezes CA; Saldanha LB; Latronico AC; Zerbini C; Madureira G; Domenice S; Albergaria MA; Camargo MH; et al TI - Clinical, hormonal and pathological findings in a comparative study of adrenocortical neoplasms in childhood and adulthood. AB - PURPOSE: We reviewed clinical and laboratory findings in 6 male and 32 female patients with functional adrenocortical neoplasms, and compared pediatric and adult data. RESULTS: Children had a higher incidence of virilization (72%), whereas in adults the predominant feature was Cushing's syndrome (60%). CONCLUSIONS: No statistically significant relation was noted between tumor weight and prognosis but there was a negative correlation between patient age and prognosis since children had a more favorable followup than adults. A Weiss criteria grade IV or greater correlated well with a poor prognosis in adults but not children, while staging was more reliable in children. None of the following predicted a poor prognosis in patients who underwent complete resection: (1) need for extended resection, (2) presence of renal vein or inferior vena cava tumor thrombus, or (3) tumor aneuploidy (14 of 14 tumors were aneuploid).

JUXTAGLOMERULAR CELL TUMOR (JGCT) (Robertson-Kihara Syndrome) Juxtaglomerular cell tumors of the kidney are uncommon neoplasms that were first described in 1967 by Robertson and three months later a second report appeared by Kihara et al who independently had described an almost identical case. The typical presentation of a patient with renin secreting tumor includes the triad of hypertension, hypokalemia, and elevated plasma renin. One mechanism that was considered to explain this phenomenon was based on the fact that continuous secretion of renin from the tumor with a relatively long biological half life of renin would allow renin production by the tumor to exceed renin decay, plasma renin activity reaches an equilibrium level, these levels may be so high throughout the vascular tree that the renin ratio may not indicate laterality. However, arteriography remains important to rule out renal artery stenosis as the cause of excess renin production, to determine degree of vascularity of the tumor since renal cell carcinoma, another rennin secreting tumor is usually quite vascular. The third method of tumor localization is surgical exploration; however, because of the small size of the tumor, even careful palpation of the surface of both kidneys may not reveal the tumor location. The differential diagnosis for a patient with hypertension, hyperreninism and secondary hyperaldosteronism include renal artery stenosis that can be ruled out by arteriography, malignant hypertension that can be ruled out if hyperaldosteronism persists after adequate hypotensive medical treatment and other renin secreting tumor like renal cell carcinoma and Wilm's tumor that on rare occasions secrete renin.

ADRENOCORTICAL CARCINOMA - February 1996 1 UI - 96069311 AU - Mendonca BB; Lucon AM; Menezes CA; Saldanha LB; Latronico AC; Zerbini C; Madureira G; Domenice S; Albergaria MA; Camargo MH; et al TI - Clinical, hormonal and pathological findings in a comparative study of adrenocortical neoplasms in childhood and adulthood. AB - PURPOSE: We reviewed clinical and laboratory findings in 6 male and 32 female patients with functional adrenocortical neoplasms, and compared pediatric and adult data. RESULTS: Children had a higher incidence of virilization (72%), whereas in adults the predominant feature was Cushing's syndrome (60%). CONCLUSIONS: No statistically significant relation was noted between tumor weight and prognosis but there was a negative correlation between patient age and prognosis since children had a more favorable followup than adults. A Weiss criteria grade IV or greater correlated well with a poor prognosis in adults but not children, while staging was more reliable in children. None of the following predicted a poor prognosis in patients who underwent complete resection: (1) need for extended resection, (2) presence of renal vein or inferior vena cava tumor thrombus, or (3) tumor aneuploidy (14 of 14 tumors were aneuploid).

Maira I. New has conducted pioneering research in the area of congenital adrenal hyperplasia (CAH), a term describing a family of mongenic autosomal recessive disorders of steroidogenesis in which enzymatic defects result in impaired synthesis of cortisol by the adrenal cortex. The most common type of CAH is 21-hydroxylase deficiency (21-OHD), which occurs in a classical (simple virilizing and salt wasting, in which aldosterone synthesis also is deficient) and nonclassical form. The classical form of 21-OHD occurs in approximately 1:14,000 live births, while the nonclassical form, which is associated with a milder enzyme defect, occurs with a frequency of 1:100 in a heterogeneous population and more frequently in specific ethnic groups. Nonclassical 21-OHD is the most frequent autosomal genetic defect in man. For example, some patients with exon 1 (P30L)/intron 2 (A or C to G) mutations have the salt wasting form of 21-OHD, while others have the nonclassical form. New's group also is seeking the mechanism by which genotype does not predict phenotype, as well as searching for new mutations in patients with CAH.

Patients and laypersons looking for guidance among the target sources of this collection of links are strongly advised to review the information retrieved with their professional health care provider. Endocrine Pathology [jpeg archive + comments] - WebPath, University of Utah (US) Endocrine Sites on the Web - Am Assoc of Clin Endocrinologists (US) Pathology of Diabetes Mellitus - WebPath, University of Utah (US) About Diabetic Eye Disease [for people at-risk] - National Eye Institute (US) Seaweed Fight Diabetes and Thicken Cat Food [A. Kjaervik] - (NO) Tracking the Genes to Conquer Diabetes [E Colimore] - Franklin Institute Sci Museum (US) About Diabetes Self-Management [magazine] Diabetic Ketoacidosis About Diabetic Ketoacidosis and Nonketotic Hyperosmolarity [RR Hemphill] - EMBBS (US) Hyperglycemic Hyperosmolar Nonketotic Coma About Hyperglycemic Hyperosmolar Nonketotic Syndrome [T O'Hanlon-Nichlos] - Am. Graves' Disease The Graves' Disease Home Page [S Lim Hoon Chin] - (SG) About Graves' Disease - Am Thyroid Assoc. /Stanford & UCSF (US) The Hypothyroid Page [K Millering] Hypothyroidism - Thyroid Int'l 3-1996 Primary and Secondary Hypothyroid - Missouri U. (US) Thyroid Neoplasms About Thyroid Tumors - Dr Quinn's Textbook via Otology Online (US) Thyroid Nodule Clinical Guidelines for Diagnosis & Management of Thyroid Nodules - Am Assoc of Clin Endocrinologists Thyroid Nodule [D Gordon] - LUMEN (US)

Matched controls consisted of groups of 10 untreated mice of each sex; pooled controls, used for statistical evaluation, consisted of the matched controls combined with 40 untreated male and 40 untreated female mice from similar bioassays of four other test chemicals. In rats, C-cell adenoma of the thyroid showed a significant dose-related trend in the females, using pooled controls (controls 1/46, low-dose 2/50, high-dose 7/46, P=0.013), and by direct comparison, an increased incidence in the high-dose group (P=0.027). Cortical adenoma of the adrenal also showed a significant dose-related trend in the females, using pooled controls (controls 0/50, low-dose 2/49, high-dose 5/50,P=0.017), and by direct comparison, an increased incidence in the high-dose group (P=0.022). Hemangioma of the spleen occurred in male rats at a significantly higher incidence in the low-dose group than in the pooled controls (controls 0/52, low-dose 4/48, P=0.049); however, neither the incidence in the high-dose group (0/47) nor the test result for dose-related trend was statistically significant. In mice, hepatocellular carcinoma in males showed a highly significant dose-related trend, using either matched controls (controls 0/9, low-dose 36/50, high-dose 40/50, P<0.001) or pooled controls (controls 5/49, P<0.001). In females, the incidence of hepatocellular carcinoma was not significant; however, the incidence of neoplastic nodule was significantly higher in both the low- and high-dose groups than in the pooled controls (controls 1/48, low-dose 14/49, P<0.001; high-dose 9/47, P=0.007), using pooled controls for tests for both doses.

DESIGN: Prospective study evaluating the prevalence of unilateral IMC uptake (tumour uptake with no visualization of the contralateral adrenal gland) and bilateral uptake (uptake in both the tumoral and the contralateral adrenal glands) in patients with unilateral incidentaloma. PATIENTS: Thirty-five patients with a unilateral mass highly suggestive of benign adrenocortical adenoma on CT scan. RESULTS: The baseline scan showed 16 patients (46%) with unilateral uptake (group A) and 19 (54%) with bilateral uptake (group B). Patients in group A exhibited lower ACTH values at 0800h (P = 0.05) and higher cortisol values after an overnight DXM suppression test (P = 0.02), than did patients in group B. In addition, 3 patients in group A failed the overnight and the low-dose DXM suppression tests. On the suppression scan performed in 14 patients (7 in each group), patients in group A continued to exhibit unilateral tumour uptake and bilateral uptake was suppressed in 72% of patients in group B. An adrenal mass was removed in 3 patients of group A with confirmed benign adrenocortical adenomas. SUBJECTS: 20 patients with primary non-functioning adrenal tumours that were diagnosed incidentally during the eight years 1986-93 and who were treated in our departmen- t. INTERVENTIONS: All patients underwent detailed endocrine studies followed by unilateral adrenalectomy.

This should be given 1 day prior to the procedure and continued each day for 7 days following the procedure. BLOOD SAMPLING On the day of injection, serum lipids should be ordered, under the Doctor's Orders, to determine if the patient has high serum cholesterol which would cause a falsely low 131 I iodocholesterol adrenal uptake. on a 128x128 matrix day 3: -posterior for 20 min or at least 50,000 cts -anterior for 10-20 min depending on count rate day 5: -same as day 3 but add a Rt lateral 10 min image (Hirsutism) Image ovaries as well on anterior views. If colonic activity is excessive, order a different laxative and soap suds enema and repeat the scan either the next day or on day 7. If the adrenal glands are poorly visualized at day 5, repeat on day 7. This should be given 1 day prior to the procedure and continued each day for 7 days following the procedure.

[NO DESCRIPTION: Not enough sentences on document]

Obviously, I cannot be your doctor, cannot substitute for a physician of your own, and cannot diagnose or treat over the 'web. Whether you are a medical student seeking a study guide, or a sick person seeking answers, you must understand that these notes, and any correspondence we may have, are provided for informational purposes only, and with the understanding that I am not engaged in rendering medical or professional services. Exam 2, 1994-1995 "Suppose the media reports that fingerpainting in kindergarten causes cancer. Exam 3, 1994-1995 "Should I pay $5000 to radon-proof my home? Exam 4, 1994-1995 "You have just been appointed surgeon-general. Exam 1, 1995-1996 "What killed the second twin?

In the kidney, aldosterone causes transfer of Na from the lumen of the distal tubule into the tubular cells in exchange for K and hydrogen. In the kidney, aldosterone causes transfer of Na from the lumen of the distal tubule into the tubular cells in exchange for K and hydrogen. Summary: Decreased CH20/GFR; decreased maximal urine osmolality. Summary: RESULTS: Children had a higher incidence of virilization (72%), whereas in adults the predominant feature was Cushing's syndrome (60%). URL: http://anaes.sickkids.on.ca/AnaesWeb/Green_Book/synd_files/synd28 Summary: Possibly renin released from ischemic kidney stimulating adrenal cortex toexcrete excessive aldosterone; renin, angiotensin potent stimuli foraldosterone excretion; adrenocortical hyperplasia and juxtaglomerularhyperplasia possibly due to common cause; possibly renal lesion causing adrenaldefect.

Excess aldosterone causes the kidneys to absorb too much sodium and water and eliminate too much potassium. SEX OR AGE MOST AFFECTED Both sexes, but more common in females. High blood pressure or kidney disease, causing increased production in the kidneys of a hormone (renin) that controls aldosterone levels. HOW TO PREVENT--If you have kidney disease or high blood pressure, remain under a doctor's care and adhere strictly to your treatment program--even if you have no symptoms. If it is caused by kidney disease or high blood pressure, medical treatment for these disorders will control symptoms of hyperaldosteronism. DIET--Eat a diet that is low in sodium and high in potassium.

Excess aldosterone causes the kidneys to absorb too much sodium and water and to eliminate too much potassium. The adrenal glands (which are attached at the upper part of the kidneys), the kidneys, the fluids and electrolytes in the bloodstream, and other body cells are involved. High blood pressure or kidney disease, causing increased production in the kidneys of a hormone (renin) that controls aldosterone levels. A child who has kidney disease or high blood pressure should remain under a doctor's care and adhere strictly to the treatment program -- even if there are no symptoms. If it is caused by kidney disease or high blood pressure, medical treatment for these disorders will control symptoms of hyperaldosteronism. Encourage your child to eat a diet that is low in sodium (see Appendix 29) and high in potassium.

Liver Transplantation/us [Ultrasonography] Postoperative Care Postoperative Complications/ra [Radiography] Postoperative Complications/us [Ultrasonography] Preoperative Care Abstract Thoughtfully planned and skillfully executed diagnostic and interventional imaging is indispensible in preoperative assessment of the pediatric liver transplant candidate and for the detection and management of the myriad postoperative complications that may affect the liver recipient. Gov't Support, U.S. Gov't, P.H.S. Abstract Endothelium-derived nitric oxide is a potent endogenous vasodilator that is derived from the metabolism of L-arginine. Anticholinergic therapy should be added to beta 2 agonist therapy in severe and life-threatening cases and may be considered in cases of mild to moderate asthma (grade A). Inhaled corticosteroids are an integral component of therapy and should be prescribed for all patients receiving oral corticosteroid therapy at discharge (grade A). Spinal Cord Injuries/co [Complications] Spinal Cord Injuries/pp [Physiopathology] Abstract The term "spinal shock" applies to all phenomena surrounding physiologic or anatomic transection of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity below the level of the injury. Wounds, Gunshot/co [Complications] Abstract Three weeks after a shotgun wound to the chest and abdomen, a patient developed acute ureteral colic caused by a migrating shotgun pellet.

Association with variety of diseases; excessive secretion of aldosterone asphysiologic response to stimuli originating outside of gland; increasedstimulation of renin-angiotensin system; associated with most edematousdisorders; extreme sensitivity to sodium-retaining properties ofmineralocorticoids; arterial hypovolemia; decreased flow to kidneys; nephroticsyndrome; unilateral renal disease, stenosis of renal artery, malignantnephrosclerosis, accelerated essential hypertension. SG:Physical signs, including mental status findings, observed on examination or during history taking LB:Laboratory data, including special test and examinations such as EEG, ECG, ophthalmoscopy, and endoscopy Blood: elevation of levels of renin and angiotensin II; hypokalemic alkalosis;sodium decrease common finding. CR:Disease course and prognosis , including complications and results of treatment when known Adrenals apparently normal or hyperplastic; in presence of constricting lesionin renal artery, stenosed wall of artery embedded with ganglionic cells, nervefibers.

Possibly renin released from ischemic kidney stimulating adrenal cortex toexcrete excessive aldosterone; renin, angiotensin potent stimuli foraldosterone excretion; adrenocortical hyperplasia and juxtaglomerularhyperplasia possibly due to common cause; possibly renal lesion causing adrenaldefect. SG:Physical signs, including mental status findings, observed on examination or during history taking Rare; in children, adults; slow growth, possibly dwarfing; blood pressure lowor normal. Possibly spasms of carpopedal, quadrate muscles of thigh; tetany; possiblyenuresis; possibly features of acidosis; slight mental retardation. Features of defective tubular function; hypokalemic, hypochloremic alkalosis;potassium in muscle depleted; blood containing increased quantities of pressoragent resembling angiotensin; elevation of aldosterone excretion; normalhydrocortisone, 17-ketosteroid excretion; sp g of urine 1.010 or less; urinaryconcentrating ability impaired. CR:Disease course and prognosis , including complications and results of treatment when known

ADRENOCORTICAL CARCINOMA - February 1996 1 UI - 96069311 AU - Mendonca BB; Lucon AM; Menezes CA; Saldanha LB; Latronico AC; Zerbini C; Madureira G; Domenice S; Albergaria MA; Camargo MH; et al TI - Clinical, hormonal and pathological findings in a comparative study of adrenocortical neoplasms in childhood and adulthood. AB - PURPOSE: We reviewed clinical and laboratory findings in 6 male and 32 female patients with functional adrenocortical neoplasms, and compared pediatric and adult data. RESULTS: Children had a higher incidence of virilization (72%), whereas in adults the predominant feature was Cushing's syndrome (60%). CONCLUSIONS: No statistically significant relation was noted between tumor weight and prognosis but there was a negative correlation between patient age and prognosis since children had a more favorable followup than adults. A Weiss criteria grade IV or greater correlated well with a poor prognosis in adults but not children, while staging was more reliable in children. None of the following predicted a poor prognosis in patients who underwent complete resection: (1) need for extended resection, (2) presence of renal vein or inferior vena cava tumor thrombus, or (3) tumor aneuploidy (14 of 14 tumors were aneuploid).

ADRENAL CORTICAL HYPERFUNCTION HYPERALDOSTERONISM Aldosterone is the most potent mineralocorticoid produced by the adrenals. In the kidney, aldosterone causes transfer of Na from the lumen of the distal tubule into the tubular cells in exchange for K and hydrogen. A helpful test is to give spironolactone 200 to 400 mg/day orally, which reverses the manifestations of the disease, including hypertension, within 5 to 8 wk (this may also occur in patients with hypertension not due to increased aldosterone). This is usually carried out by determining the plasma renin value in the morning with the patient recumbent, giving furosemide 80 mg orally, and then repeating the renin determination after the patient has remained upright for 3 h. Normal individuals will have a marked increase in renin in the upright position, while the patient with hyperaldosteronism will not. Diagnosis is thus dependent upon demonstrating elevated secretion of aldosterone in urine or blood, expansion of the extracellular space as demonstrated by lack of increase in plasma renin in the upright posture, and the K abnormalities noted. Secondary aldosteronism,an increased production of aldosterone by the adrenal cortex caused by stimuli originating outside the adrenal, mimics the primary condition and is related to hypertension and edematous disorders (eg, cardiac failure, cirrhosis with ascites, the nephrotic syndrome).

ADRENAL CORTICAL HYPERFUNCTION HYPERALDOSTERONISM Aldosterone is the most potent mineralocorticoid produced by the adrenals. In the kidney, aldosterone causes transfer of Na from the lumen of the distal tubule into the tubular cells in exchange for K and hydrogen. A helpful test is to give spironolactone 200 to 400 mg/day orally, which reverses the manifestations of the disease, including hypertension, within 5 to 8 wk (this may also occur in patients with hypertension not due to increased aldosterone). This is usually carried out by determining the plasma renin value in the morning with the patient recumbent, giving furosemide 80 mg orally, and then repeating the renin determination after the patient has remained upright for 3 h. Normal individuals will have a marked increase in renin in the upright position, while the patient with hyperaldosteronism will not. Diagnosis is thus dependent upon demonstrating elevated secretion of aldosterone in urine or blood, expansion of the extracellular space as demonstrated by lack of increase in plasma renin in the upright posture, and the K abnormalities noted. Secondary aldosteronism,an increased production of aldosterone by the adrenal cortex caused by stimuli originating outside the adrenal, mimics the primary condition and is related to hypertension and edematous disorders (eg, cardiac failure, cirrhosis with ascites, the nephrotic syndrome).

[NO DESCRIPTION: Not enough sentences on document]

Variable; abnormal albumin metabolism; imbalance of estrogens, progesteronehormones; excessive secretion of antidiuretic hormone; orthostatic capillaryleak with secondary hyperaldosteronism; capillary changes due tomicroangiopathy; defect in venomotor tone with intravascular 'sequestration' ofplasma and extracellular fluid. SG:Physical signs, including mental status findings, observed on examination or during history taking Young or middle-aged women, somewhat overweight; general nonpitting edemaworsening during day; excessive diurnal weight gain; exacerbation, resolutionof edema usually related to menstrual cycle; aggravation of edema with uprightposture; usually history of menstrual dysfunction or gynecologic surgery,personal or family history for diabetes as big babies, glycosuria, functionalhypoglycemia or repeated abortions. LB:Laboratory data, including special test and examinations such as EEG, ECG, ophthalmoscopy, and endoscopy Decrease in plasma volume in upright posture. CR:Disease course and prognosis , including complications and results of treatment when known

The patient was treated symptomatically with bismuth subsalicylate (PeptoBismol®), Paregoric®, and luperamide and his symptoms resolved. Laboratory studies showed a potassium of 2.2 mEq/L. On th e day of admission, the patient had an episode of blood streaked emesis and abdominal pain. 0.73 mg/m l/hr; (normal range for upright patient with normal salt intake 0.4-6.7 mg/ml/hr; overnight supine values approximately half). Serum Aldosterone (patient upright): 36.8 ng/dl; (normal equals 4-31 ng/dl in upright position with normal salt intake ; supine values are less than 16 ng/dl). The hypertensive patients requiring further evaluation are those who develop spontaneous hypokalemia (K 3.5 meq/L), those who have difficulty maintaining normal serum potassium values despite potassium supplementation, those with serum values that fail to normalize within 4 weeks of diuretics abstinence, and those with refractory hypertension with no evidence of secondary cause. The criteria for diagnosis of primary aldosteronism often can be established with relative ease in hypertens ive patients receiving no treatment who demonstrate the following: significant hypokalemia (3 meq/l), inappropriate kaliuresis (24 hour urinary potassium > 30mEq), elevated plasma aldosterone, plasma renin activity below 1 ng/ml, and an abdominal CT sh owing an adenoma.

Bilateral, symmetric visualization of the adrenals on the NP-59 exam in a patient with biochemically confirmed glucocorticoid (ACTH) excess is invariably due to adrenal hyperplasia (In the setting of excess ACTH the NP-59 scan typically demonstrates bilateral, symmetric increased accumulation of the tracer). Clinically, patients with adrenal hyperplasia as the etiology may demonstrate increased serum aldosterone levels during upright posturing after prolonged recumbence, while levels decline or are unchanged in patients with an adenoma. Additionally, bilateral nodularity is not synonymous with hyperplasia, and adrenal venous sampling is required to detect the presence of a surgically correctable adrenal adenoma in these patients. Non-hyperfunctioning adrenal adenomas (i.e.: there is no biochemical evidence of adrenal hyperfunction) are detected in about 8% of patients at autopsy, and in approximately 2% of patients undergoing abdominal CT scanning. Even in patients with lung cancer, an adrenal mass is more likely to be an adenoma than a metastasis [Radiology, 1992,Vol.184, p.1-13]. CT features of a benign adenoma include a smooth contour, smaller than 5 cm in size, and an attenuation value of zero or less (values between 0 and 10 indicate a high probability of a benign lesion, but values over 10 may be benign or malignant and further evaluation is warranted).

Here is a 1.3 cm left adrenal adenoma found in a patient with hypertension. She had hypokalemia on a routine chemistry panel. Further workup revealed a high serum aldosterone and a low serum renin, findings consistent with an aldosterone secreting adrenal adenoma (Conn's syndrome). This lesion accounts for about two-thirds of cases of primary hyperaldosteronism (PHA), while bilateral adrenal hyperplasia accounts for about 30% of PHA. Such adenomas are typically less than 2 cm in size and yellow on cut surface. Forward to the next image Back to the previous image Return to the index

Causes, incidence, and risk factors Most of the cases result from a benign tumor of the adrenal gland, which occurs more frequently in women, and is highest in those between 30 and 50 years old. Symptoms: headache muscular weakness fatigue intermittent paralysis numbness increased urination increased thirst visual changes blood pressure, high increased urine output (polyuria) Signs and tests: serum potassium level, low abdominal CT scan that shows adrenal mass plasma aldosterone level, elevated urinary aldosterone, elevated plasma renin activity, low ECG that shows abnormalities associated with low potassium levels This disease may also alter the results of the following tests: sodium, urine serum sodium potassium; urine osmolality, urine serum magnesium - test CO2 Dietary sodium restriction and administration of a diuretic that blocks aldosterone action (spironolactone) may control the symptoms without surgery. [Alternative names] [Definition] [Causes, incidence, and risk factors] [Prevention] [Symptoms] [Signs and tests] [Treatment] [Expectations (prognosis)] [Complications] [Calling your health care provider]

Causes, incidence, and risk factors Most of the cases result from a benign tumor of the adrenal gland, which occurs more frequently in women, and is highest in those between 30 and 50 years old. Symptoms: headache muscular weakness fatigue intermittent paralysis numbness increased urination increased thirst visual changes blood pressure, high increased urine output (polyuria) Signs and tests: serum potassium level, low abdominal CT scan that shows adrenal mass plasma aldosterone level, elevated urinary aldosterone, elevated plasma renin activity, low ECG that shows abnormalities associated with low potassium levels This disease may also alter the results of the following tests: sodium, urine serum sodium potassium; urine osmolality, urine serum magnesium - test CO2 Dietary sodium restriction and administration of a diuretic that blocks aldosterone action (spironolactone) may control the symptoms without surgery. [Alternative names] [Definition] [Causes, incidence, and risk factors] [Prevention] [Symptoms] [Signs and tests] [Treatment] [Expectations (prognosis)] [Complications] [Calling your health care provider]

Causes, incidence, and risk factors Most of the cases result from a benign tumor of the adrenal gland, which occurs more frequently in women, and is highest in those between 30 and 50 years old. Symptoms: headache muscular weakness fatigue intermittent paralysis numbness increased urination increased thirst visual changes blood pressure, high increased urine output (polyuria) Signs and tests: serum potassium level, low abdominal CT scan that shows adrenal mass plasma aldosterone level, elevated urinary aldosterone, elevated plasma renin activity, low ECG that shows abnormalities associated with low potassium levels This disease may also alter the results of the following tests: sodium, urine serum sodium potassium; urine osmolality, urine serum magnesium - test CO2 Dietary sodium restriction and administration of a diuretic that blocks aldosterone action (spironolactone) may control the symptoms without surgery. [Alternative names] [Definition] [Causes, incidence, and risk factors] [Prevention] [Symptoms] [Signs and tests] [Treatment] [Expectations (prognosis)] [Complications] [Calling your health care provider]

ADRENOCORTICAL CARCINOMA - February 1996 1 UI - 96069311 AU - Mendonca BB; Lucon AM; Menezes CA; Saldanha LB; Latronico AC; Zerbini C; Madureira G; Domenice S; Albergaria MA; Camargo MH; et al TI - Clinical, hormonal and pathological findings in a comparative study of adrenocortical neoplasms in childhood and adulthood. AB - PURPOSE: We reviewed clinical and laboratory findings in 6 male and 32 female patients with functional adrenocortical neoplasms, and compared pediatric and adult data. RESULTS: Children had a higher incidence of virilization (72%), whereas in adults the predominant feature was Cushing's syndrome (60%). CONCLUSIONS: No statistically significant relation was noted between tumor weight and prognosis but there was a negative correlation between patient age and prognosis since children had a more favorable followup than adults. A Weiss criteria grade IV or greater correlated well with a poor prognosis in adults but not children, while staging was more reliable in children. None of the following predicted a poor prognosis in patients who underwent complete resection: (1) need for extended resection, (2) presence of renal vein or inferior vena cava tumor thrombus, or (3) tumor aneuploidy (14 of 14 tumors were aneuploid).

Causes, incidence, and risk factors Most of the cases result from a benign tumor of the adrenal gland, which occurs more frequently in women, and is highest in those between 30 and 50 years old. Symptoms: headache muscular weakness fatigue intermittent paralysis numbness increased urination increased thirst visual changes blood pressure, high increased urine output (polyuria) Signs and tests: serum potassium level, low abdominal CT scan that shows adrenal mass plasma aldosterone level, elevated urinary aldosterone, elevated plasma renin activity, low ECG that shows abnormalities associated with low potassium levels This disease may also alter the results of the following tests: sodium, urine serum sodium potassium; urine osmolality, urine serum magnesium - test CO2 Dietary sodium restriction and administration of a diuretic that blocks aldosterone action (spironolactone) may control the symptoms without surgery. [Alternative names] [Definition] [Causes, incidence, and risk factors] [Prevention] [Symptoms] [Signs and tests] [Treatment] [Expectations (prognosis)] [Complications] [Calling your health care provider]

List of technical and popular medical terms: English(h) List of technical and popular medical terms: English(h)

Department : Internal Medicine Responsible Staff : N. Tsaparas Duration : 10th Semester / 15 Hours / 1 Credit / ECTS Credits : 0.5 Goals : Assessment and management of wafer and electrolyte disorders on the basis of the underlying pathophysiological mechanisms. Contents : Disorders of ECF volume and osmolality (hypovolemic hypo- and hypernartemia, edema, polyuria, inappropriate ADH secretion, hyperaldosteronism), Hypokalemia, Hyperkalemia, Metabolic disorders of acid-base balance, Hypocalcemia, hypercalcemia.

Cushing's & Conn's Syndromes    48%    [find similar] NP-59 Adrenal Scintigraphy     48%    [find similar] Episodic Muscle     46%    [find similar] Genitourinary Scintigraphy -- Table of C...    46%    [find similar] Ed's Pathology Notes    36%    [find similar] C.G. Brilla, publications    11%    [find similar]

Glucose-induced vascular smooth muscle dysfunction: The role of protein kinase C 495 The importance of adrenaline, insulin and insulin sensitivity as determinants for blood pressure in young Danes 499 Alterations in beta-adrenoceptors and polyploidy in cultured aortic smooth muscle cells from different age groups of spontaneously hypertensive rats and Wistar-Kyoto rats 517 The regulation of pH in resistance arteries from spontaneously hypertensive and Wistar-Kyoto rats: The effect of bicarbonate 529 Effect of one-kidney, one clip hypertension on the structure and function of porcine intramyocardial small arteries 535 Effect of intravenous calcium antagonists on left ventricular diastolic function in hypertension: Assessed by pulsed-Doppler echocardiogram

Which hormones might cause hypertension? Malignant Hypertension The high creatinine and urea and low haemoglobin suggest chronic renal failure. The commonest causes are : Chronic glomerulonephritis Chronic pyelonephritis Obstructive Uropathy Malignant Hypertension Polycystic Kidneys fThe Collagenoses Amyloid Disease Malignant Hypertension is suggested here by the race (it is relatively common in West Indians), the history of headaches and blindness due to encephalopathy and retinopathy, and the low potassium. The potassium is low because of secondary hyperaldosteronism resulting in the excretion of potassium in exchange for retained sodium. Malignant hypertension causes narrowing of arterioles, particularly those supplying the juxtaglomerular apparatus. Other hormones which can cause hypertension include the catecholamines adrenaline and noradrenaline which can be secreted by adrenal medullary tumours.

[NO DESCRIPTION: Not enough sentences on document]

[NO DESCRIPTION: Not enough sentences on document]

The pair of adrenals in the center are normal. Those at the top come from a patient with adrenal atrophy (with either Addison's disease or long-term corticosteroid therapy). The adrenals at the bottom represent bilateral cortical hyperplasia. Forward to the next image Back to the previous image Return to the index

[NO DESCRIPTION: Not enough sentences on document]

(50) Lymphoma Malignant Histiocytic 1 (2%) 2 (4%) Lymphoma Malignant Lymphocytic 6 (12%) 2 (4%) 4 (8%) Lymphoma Malignant Mixed 9 (18%) 4 (8%) 3 (6%)

[NO DESCRIPTION: Not enough sentences on document]

Lab Name: Ligand Assay Days Test is Set Up: Tuesday Times of Anaysis: 48 hours Normal Vol: 3 ml whole blood Pediatric Volume: 3 ml whole blood Container: Lavender top tube Collection Intructions: Whole blood. Cause for Rejection: Date and time not specified, specimen greater than 30 minutes in transit to the laboratory, stored specimen not frozen. Reference Range: 9-52 pg/ml Usage: Knowledge of ACTH levels in addition to serum cortisol and urinary free cortisol is useful in the differential diagnosis of Cushing's syndrome, ectopic ACTH syndrome (e.g., carcinoma of lung, islet cell tumors, carcinoid tumors, medullary carcinoma of thyroid), Addison's disease by hypopituitarism and ACTH-producing pituitary tumors (e.g., Nelson's syndrome). In normal individuals with a daytime pattern of activities, ACTH levels reach a peak between 6:00AM - 8:00AM. ACTH levels in pituitary dependent Cushing's disease may be elevated or high normal (inappropriately elevated for the time of the day). Pituitary dependent Cushing's disease (i.e., pituitary ACTH hypersecretion) usually demonstrates reduced or lack of ACTH suppression by low-dose dexamethasone (2 mg q 6 hours for 24 hours) and reduced or normal suppression of ACTH by high dose dexamethasone (8 mg q 6 hours for 24 hours).

- Discussion: - for primary hyperaldosteronism, HTN, CHF, Cirrhosis; - also used for diuretic induced hypokalemia when oral supplements or other potassium sparing agents are inappropriate; - diruetic of choice for cirrhotic edema and ascites; - Adult: Edema: - 25-200 mg/day administered in single or divided doses; - if diuresis remains inadequate, add 2nd diuretic agent w/ action more proximal in the renal tubule; - HTN: - 50-100mg/day initially; adjust dose after 2 weeks; - add 2nd diuretic agent w/ action on proximal renal tubule if HTN persists; - or. 25-100mg/24hr PO in divided doses; - max dose: 400mg/day for primary hyperaldosteronism; - may take upto 3-4 days for diuretic effect; - Contraindicated with anuria, hyperkalemia, renal impairment;

821 Primary Chemotherapy for Clinical Stage II Nonseminomatous Germ Cell Testicular Tumors: Selection Criteria and Long-Term Results Seth E. Lerner, Bhupinder S. Mann, Michael L. Blute, Ronald L. Richardson, and Horst Zincke Excellent long-term survival rates can be achieved with primary chemotherapy in patients with stage II nonseminomatous germ cell testicular tumors. 829 Utilization and Outcomes of Surgical Gastrostomies and Jejunostomies in an Era of Percutaneous Endoscopic Gastrostomy: A Population-Based Study Larry R. Bergstrom, David E. Larson, Alan R. Zinsmeister, Michael G. Sarr, and Marc D. Silverstein In 77 adult patients with surgical gastrostomy or jejunostomy for placement of a feeding tube, the associated complications and outcome were similar to those in patients with percutaneous endoscopic gastrostomy. 837 Incidence of Sudden Infant Death Syndrome in Olmsted County, Minnesota: 1945 Through 1992 Steven A. McLaughlin, Maria G. Valdes, Robert M. Jacobson, Peter C. Wollan, C. Mary Beard, Lynn Weissman, and Steven J. Jacobsen In a study of cases of sudden infant death syndrome in Olmsted County, Minnesota, the incidence rates showed an increasing trend from 1945 through 1992. 847 Stroke Epidemiology in Novosibirsk, Russia: A Population-Based Study Valery L. Feigin, David O. Wiebers, Yury P. Nikitin, W. Michael O'Fallon, and Jack P. Whisnant The incidence rate of first-ever stroke in Novosibirsk, Russia, is one of the highest in the world, but the 30-day case-fatality rates are similar to those reported elsewhere. 853 Human Babesiosis Rajiv K. Pruthi, William F. Marshall, John C. Wiltsie, and David H. Persing This article describes a 62-year-old man with babesiosis, reviews the literature, and briefly discusses this increasingly important infection. 885 26-Year-Old Man With HIV Infection and Abdominal Pain William S. MacMorran, Andrew D. Badley, and Walter R. Wilson Right upper quadrant abdominal pain in a young man with acquired immunodeficiency syndrome was attributable to biliary tract disease.

Frank Vogel and Gudrun Lutsch Golgi and ER structure of yeast cells Structure and location of small heat shock proteins Localization of cytochrome P450 enzymes related to hyperaldosteronism and hypertension and of components of the renin-angiotensin system Selected Publications Structure of the Group The electron microscopy group is organized as core facility operating in close collaboration with other research groups of the MDC. Main tasks are localization of intracellular antigens on the electron and light microscopic level, analysis of the structure of isolated macromolecules and improvement of preparation procedures for biological specimens. Golgi and ER structure of yeast cells F. Vogel in collaboration with W.-H. Schunck Based on Tokuyasu´s cryosectioning technique a new preparation strategy for yeast cells has been created. Using the advantage of this new morphological approach, at the first time the stacked nature and an archaic organization of separated Golgi elements in wild type yeast cells could be determined (Figure 22 A, B). The results obtained reveal: - individual P450 forms induce morphological different ER structures (membrane stacks and tubular ER) - the ER morphology seems to be determined by the composition of the membrane spanning domain of ER resident proteins (see also the report by W.-H. Schunck). G. Lutsch, M. Wieske in collaboration with R. Benndorf, M. Gaestel, J. Stahl, R. Vetter, J. Behlke, and M. van Heel (Berlin) Small heat shock proteins are known to build high molecular mass complexes, the structure of which we have analyzed by electron microscopy (Figure 22 C).

Please check the synonyms listed below to find other names for this specific disorder. If you order the full text version of this report from NORD, you can contact the agencies listed in the Resources section for more detailed information and avenues to support. Conn Syndrome is characterized by an increased level of the hormone aldosterone in the blood causing increased sodium levels in the blood. An increase in blood volume (hypervolemia), and a low potassium level (hypokalemic alkalosis) also occur. An increase in blood pressure (hypertension), excessive urination (polyuria), and excessive thirst (polydipsia) can also occur. To READ organizational information, click on the Name.

ED'S PATHOLOGY MELTDOWN Part I -- General Pathology [These notes are intended for students who have already learned the material in a course in general and systemic pathology and who are now preparing for an exam. The causes of hypoxia: Ischemia ("ischemic hypoxia"; "stagnant hypoxia"): Loss of arterial blood flow (literally, "holding back the blood") Local causes -- Occlusion of the arteries that bring in fresh blood -- Occlusion of the veins which allow blood to leave, so that fresh blood can flow in -- Shunting of arterial blood elsewhere ("steal syndromes"; "Robin Hood" syndromes) Systemic causes -- Failure of the heart to pump enough blood Hypoxemia: Too little oxygen in the blood Oxygen problems ("hypoxic hypoxia") -- Too little oxygen in the air -- Failure to properly ventilate the lungs -- Failure of the lungs to properly oxygenate the blood -- Failure of the heart to pump enough blood through the lungs -- Tremendously increased dead space (i.e., pulmonary thromboembolus) Hemoglobin problems ("anemic hypoxia") -- Inadequate circulating red cell mass ("anemia") -- Inability of hemoglobin to carry the oxygen (carbon monoxide poisoning, methemoglobinemia) -- "High affinity" hemoglobins that will not give up their oxygen to the tissues Failure of the cytochromes ("histotoxic hypoxia") Cyanide poisoning Rotenone poisoning Dinitrophenol poisoning Other curious poisons I wish I had time to review blood gases here. Embryogenesis, skin-cell and gut-epithelium shedding, a woman's monthly cycle, elimination of autoreactive or no-longer-useful immune cells, all forms of atrophy, suicide on a T-cell's instructions (hepatitis, graft-vs.-host, many others), suicide of a cell with an injured genome (p53-mediated), hypoxia or cell injury insufficient to produce frank necrosis of a large group of cells. The genes that mutate are the proto-oncogenes (mutated="activated" into oncogenes, one copy being sufficient to turn a cell bad), and the antioncogenes = "tumor suppressor genes", both copies of which must be destroyed="inactivated" to turn a cell bad. Metastatic calcification results from disease remote from the site of calcification that has caused elevated blood calcium or phosphate; calcium deposits in the lung alveoli, on the far-side of gastric parietal cell, around the renal tubules, and perhaps in the elastica of blood vessels. Mitochondrial abnormalities: All very swollen: Reye's Parking-lot crystals Mitochondrial myopathy (AZT, genetic) Too many Hurthle cell (oncocyte) Giant alcoholic's liver Hereditary cytoskeleton problems: Spherocytosis fragile red blood cells; lack spectrin, ankyrin, or protein 4.1 Chediak-Higashi phagocytes show poor chemotaxis, giant lysosomes Storage diseases which will produce huge cells.

The Chemical Pathology section of the Laboratory Medicine Course aims to teach students the physiological and pathological principles regarding biochemical investigations, the interpretation of results and the clinical applications of such testing to the diagnosis, management and screening of diseases. (i) the major clinical causes renal disease endocrine diseases renin-angiotensin-aldosterone glucocorticoids phaeochromocytoma co-arctation of the aorta (ii) investigation for secondary hypertension when to look for it - general clues age severity historical clues examination (iii) hypertension due to renal disease renovascular disease renal parenchymal disease end stage renal disease assessment of the kidney in hypertension function radiology (iv) investigation of the renin-angiotensin system the underlying physiology the plasma potassium -differential diagnosis of hypokalaemic hypertension suppression and stimulation radiology (v) diagnosis of phaeochromocytoma clinical clues simple biochemical clues blood pressure responses biochemical testing radiology Primary - congenital absence/failure of development; destruction; decreased function Secondary - hypothalamic/pituitary disease Clinical features - Weight gain, tiredness, constipation, cold intolerance, hypothermia, menorrhagia, muscle cramps, myopathy; typical facies, thickened and cool skin, slow heart rate, cardiac failure, pericardial effusion, goitre, prolonged relaxation phase of tendon reflexes Biochemistry - Primary hypothyroidism: raised TSH, low T4, T3, exaggerated response to TRH Secondary: low TSH, low hormones; test pituitary function to exclude hypoadrenalism Monitoring treatment (replacement thyroxine, occasionally T3): keep TSH in reference range. Primary - Thyroid adenomas, autoimmune (Graves' disease), thyroiditis Secondary - Pituitary-dependent: rare, but should be suspected if the patient is clinically toxic with high TSH and thyroid hormone levels Clinical features - Loss of weight, irritability, altered sleep pattern, diarrhoea, heat intolerance, palpitations, weakness, fatigue; Goitre/thyroid nodules, skin warm, excessive sweating, tachycardia, arrhythmias, proximal muscle weakness Biochemistry Primary hyperthyroidism: suppressed TSH, raised T4, T3; no response to TRH, reduced T3 suppression Secondary: non-suppressed TSH in presence of raised T4, T3 Monitoring of treatment (anti-thyroid drugs alone or with thyroxine replacement, radioiodine): TSH becomes normal and thyroid hormone levels fall with successful treatment; if not on block-replace regimen, may become hypothyroid with raised TSH, low hormones Associated autoimmune abnormalities Eye disease, skin changes (pretibial myxoedema), thyroid acropachy Hypothalamic disease Disease States: Symptoms and signs Pituitary disease Anterior Pituitary Disease: over-production or underproduction hormones, damage to the optic chiasma and possible associated hypothalamic disease Tests of Pituitary Function: Basal hormone levels, Dynamic tests (expensive and may be dangerous) Specific disorders of the Pituitary Acromegaly - overproduction of growth hormone (hGH) or rarely abnormal GHRH prodn: IGF1 Pituitary Dwarfism - (there are many other causes of short stature) Hyperprolactinaemia - "stress". Hysterical polydipsia (HPD), patients who drink excess hypotonic fluids Adrenal disorders Cortex: Cushing's disease (pit), Cushing's syndrome (adr) Diagnosis: Diurnal variation of cortisol, Dexamethasone-(DX) Suppression Test (DST): Urinary Free Cortisol Site of Lesion: Plasma ACTH levels, Abdominal CT scan, Corticotropin Release Hormone tests Addison's Disease: Synacthen tests, Plasma ACTH levels Congenital Adrenal Hyperplasia (CAH): Conn's Syndrome: Medulla: Phaeochromocytoma Reproductive chemical pathology in the female Oral contraception Amen/Oligomenorrhoea: Primary or Secondary amen/oligomenorrhoea Infertility - diagnosis, monitoring therapy: in vitrofertilisation Ectopic pregnancy Hirsutism: Polycystic Ovary Syndrome (PCO), Hormone secreting tumours, Drugs Chemical pathology of pregnancy Physiological changes - Haemodilution, Glycosuria, Bindin globulins, beta HCG Testing for pregnany Screening: Neural tube defects, Down's syndrome (chromosome analysis), Chorionic Villus biopsy Placental tumours, Hydatidiform mole, Chorion Carcinoma Toxaemia of pregnancy Foeto-placental monitoring Reproductive chemical pathology in the male Hypogonadism, Primary, Secondary Gynaecomastia Infertility in the male Carcinoma of the prostate: Prostatic specific antigen

(50) Histiocytic Sarcoma 1 (2%) 3 (6%) Lymphoma Malignant Histiocytic 7 (14%) 3 (6%) Lymphoma Malignant Lymphocytic 13 (26%) 14 (28%) 6 (12%) Lymphoma Malignant Mixed 2 (4%) 5 (10%) 3 (6%) Lymphoma Malignant Undifferentiated Cell 1 (2%) *Number of animals with any tissue examined microscopically Page 5 NTP Experiment-Test: 05097-02 INCIDENCE RATES OF NEOPLASMS BY ANATOMIC SITE (SYSTEMIC LESIONS ABRIDGED) (a) Report: PEIRPT05

Note: In children and adolescents, mood can be irritable and duration must be at least 1 year. Presence, while depressed, of two (or more) of the following: poor appetite or overeating insomnia or hypersomnia low energy or fatigue low self-esteem poor concentration or difficulty making decisions feelings of hopelessness During the 2-year period (1 year for children or adolescents) of the disturbance, the person has never been without the symptoms in Criteria A and B for more than 2 months at a time. insomnia or hypersomnia nearly every day psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down) fatigue or loss of energy nearly every day feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick) diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others) recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide The symptoms do not meet criteria for a Mixed Episode The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. During the period of mood disturbance, three (or more) of the following symptoms have persisted (four if the mood is only irritable) and have been present to a significant degree: inflated self-esteem or grandiosity decreased need for sleep (e.g., feels rested after only 3 hours of sleep) more talkative than usual or pressure to keep talking flight of ideas or subjective experience that thoughts are racing distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli) increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments) The symptoms do not meet criteria for a Mixed Episode The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning or in usual social activities or relationships with others, or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features. During the period of mood disturbance, three (or more) of the following symptoms have persisted (four if the mood is only irritable) and have been present to a significant degree: inflated self-esteem or grandiosity decreased need for sleep (e.g., feels rested after only 3 hours of sleep) more talkative than usual or pressure to keep talking flight of ideas or subjective experience that thoughts are racing distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli) increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., the person engages in unrestrained buying sprees, sexual indiscretions, or foolish business investments) The episode is associated with an unequivocal change in functioning that is uncharacteristic of the person when not symptomatic. Acetazolamine, Alphamethyldopa, Amantadine, Amphetamines, Ampicillin, Azathioprine (AZT), 6-Azauridine, Baclofen, Beta Blockers, Bethanidine, Bleomycin, Bromocriptine, C-Asparaginase, Carbamazepine, Choline, Cimetidine, Clonidine, Clycloserin, Cocaine, Corticosteroids (including ACTH), Cyproheptadine, Danazol, Digitalis, Diphenoxylate, Disulfiram, Ethionamide, Fenfluramine, Griseofulvin, Guanethidine, Hydralazine, Ibuprofen, Indomethacin, Lidocaine, Levodopa, Methoserpidine, Methysergide, Metronidazole, Nalidixic Acid, Neuroleptics (butyrophenones, phenothiazines, oxyindoles), Nitrofurantoin, Opiates, Oral Contraceptives, Phenacetin, Phenytoin, Prazosin, Prednisone, Procainamide, Procyclidine, Quanabenzacetate, Rescinnamine, Reserpine, Sedative/Hypnotics (barbiturates, benzodiazepines, chloral hydrate), Streptomycin, Sulfamethoxazole, Sulfonamides, Tetrabenazine, Tetracycline, Triamcinolone, Trimethoprim, Veratrum, Vincristine.

ADRENOCORTICAL CARCINOMA - April 1996 1 UI - 96089477 AU - Toraya S; Nomura K; Kono A; Aiba M; Ogasawara M; Kikuchi C; Demura H TI - Characteristics of aldosterone-producing adenoma responsive to upright posture. AB - A small subgroup of primary aldosteronism due to aldosteronoma, named aldosterone-producing renin-responsive adenoma (AP-RA), has been reported to masquerade as idiopathic hyperaldosteronism (IHA) because of the responsiveness of the plasma aldosterone concentration (PAC) to upright posture (UP). We found two patients with AP-RA in 19 patients with aldosteronoma who were examined by UP stimulation and were treated surgically. In 17 patients with typical aldosterone- producing adenoma (APA), PAC decreased or increased only slightly (less than 200% of the basal level); in contrast, it increased to over 300% of the basal level in two patients with AP-RA. Adenomas typically had a maximal mitotic rate of fewer than 2 mitotic figures per 10 high-power fields (all cases), a prominent small nest growth pattern (7 cases), predominantly clear or foamy cytoplasm (6 cases), and no tumor necrosis (all cases), whereas carcinomas were character- ized by at least 4 mitotic figures (often many more) per 10 high-power fields in the most active area (all cases), lack of a significant small nest growth pattern component (45 cases--solid or trabecular growth most common), at least a considerable proportion of cells with eosinophilic cytoplasm (all cases), and tumor necrosis (45 cases). Carcinomas were almost always larger than adenomas, but two adenomas (5.9 cm and 7 cm) overlapped in size with the four smallest carcinomas (5.5 cm, 6 cm, 7 cm, and 7 cm, respectively).

PATIENTS: Thirty-five patients with a unilateral mass highly suggestive of benign adrenocortical adenoma on CT scan. RESULTS: The baseline scan showed 16 patients (46%) with unilateral uptake (group A) and 19 (54%) with bilateral uptake (group B). Patients in group A exhibited lower ACTH values at 0800h (P = 0.05) and higher cortisol values after an overnight DXM suppression test (P = 0.02), than did patients in group B. In addition, 3 patients in group A failed the overnight and the low-dose DXM suppression tests. On the suppression scan performed in 14 patients (7 in each group), patients in group A continued to exhibit unilateral tumour uptake and bilateral uptake was suppressed in 72% of patients in group B. An adrenal mass was removed in 3 patients of group A with confirmed benign adrenocortical adenomas. SUBJECTS: 20 patients with primary non-functioning adrenal tumours that were diagnosed incidentally during the eight years 1986-93 and who were treated in our departmen- t. INTERVENTIONS: All patients underwent detailed endocrine studies followed by unilateral adrenalectomy. RESULTS: Nineteen patients were cured of their hypertension postoperatively, whereas 13 patients had persistent diastolic hypertension.

They are responsible for the balance of water and electrolytes, for the overall regulation of the metabolism of proteins, carbohydrates and lipids and for the secondary sex characteristics. Different enzymes participate in the synthesis of these hormones, among them various cytochrome P450-dependent steroid hydroxylases, catalyzing the following reaction: RH + O2 + NADPH + H+ --> Mitochondrial cytochromes P450 accept the necessary electrons for oxygen activation and following substrate hydroxylation from NADPH via ferredodoxin reductase and ferredoxin (adrenodoxin). The function of adrenodoxin as electron donor to mitochondrial cytochromes P450 CYP11A1 and CYP11B1 Interestingly, various P450 systems differ by a factor of 100-1000 in their electron transfer rate and thus substrate conversion efficiency, the reason of which is unclear at present. Site-directed mutagenesis of the single tyrosine residue of adrenodoxin, Y82, which has been supposed by others on the basis of chemical modification studies as being involved in the electron transfer from the reductase to CYP11A1, revealed that this aromatic residue does not participate in the electron transfer, but is localized close to the interaction site of this protein with CYP11A1 and CYP11B1. Interestingly, the effects of mutation are less pronounced when studying the interaction with CYP11A1 instead of CYP11B1 suggesting that electron donation from adrenodoxin to these proteins is determined at least in part by different features of the cytochromes.

PATIENTS: Thirty-five patients with a unilateral mass highly suggestive of benign adrenocortical adenoma on CT scan. RESULTS: The baseline scan showed 16 patients (46%) with unilateral uptake (group A) and 19 (54%) with bilateral uptake (group B). Patients in group A exhibited lower ACTH values at 0800h (P = 0.05) and higher cortisol values after an overnight DXM suppression test (P = 0.02), than did patients in group B. In addition, 3 patients in group A failed the overnight and the low-dose DXM suppression tests. On the suppression scan performed in 14 patients (7 in each group), patients in group A continued to exhibit unilateral tumour uptake and bilateral uptake was suppressed in 72% of patients in group B. An adrenal mass was removed in 3 patients of group A with confirmed benign adrenocortical adenomas. SUBJECTS: 20 patients with primary non-functioning adrenal tumours that were diagnosed incidentally during the eight years 1986-93 and who were treated in our departmen- t. INTERVENTIONS: All patients underwent detailed endocrine studies followed by unilateral adrenalectomy. RESULTS: Nineteen patients were cured of their hypertension postoperatively, whereas 13 patients had persistent diastolic hypertension.

This adrenal gland removed surgically in a patient with Cushing's syndrome has been sectioned in half to reveal an adenoma. Some remaining atrophic adrenal is seen at the right. The adenoma is composed of yellow firm tissue just like adrenal cortex. This neoplasm is well-circumscribed. It is benign. Forward to the next image Back to the previous image Return to the index

Return to the organ system pathology menu.

Diagnostic Ultrastructural Pathology presents individual problem-based cases in a well-illustrated format, using numerous electron micrographs to convey appropriate and necessary visual information for the diagnosis of human disease. The format facilitates the teaching of the case approach for diagnostic ultrastructural pathology using clinical - ultrastructural - pathologic correlation. The material is useful to a wide variety of physicians and students of medicine, structure, and disease at various levels of training, as well as in the training of and operational use by technical support staff. The cases were selected using four principal criteria: Classic cases, which are diagnosed readily by light microscopy to facilitate the electron microscopic diagnosis of less classic cases Diagnostic cases, for which ultrastructural analysis is essential for diagnosis Supportive cases, where either the light or the electron microscopic diagnosis is supportive, and thus confirmatory, of the other; and New facts cases, which establish new knowledge regarding the pathogenesis of disease using electron microscopy as the investigative modality. Volume III presents the cases dealing with the endocrine and hematopoietic systems. 50 case studies demonstrating the diagnostic use of the electron microscope More than 400 technically excellent electron micrographs of human tissues Mini-literature reviews with each case presentation Cases indexed separately by presenting symptom or problem, differential diagnostic group, ultrastructural pathologic diagnostic criteria, and final diagnostic Go to Top

Return to the organ system pathology menu.

Hypernatremia can develop from excess water loss, frequently accompanied by an impaired thirst mechanism, inadequate volume replacement, inappropiate volume management after surgery, excessive use of diuretics, Diabetes Mellitus, insensible losses from the skin and respiratory tract ( those losses are hypoosmolar to plasma and average 800 to 1,000 ml per day in adults ), Acute Renal Failure and excessive enteral feeding. Less commonly, hypernatremia is due to hypertonic salt administration ( eg, accidental intravascular injection of hypertonic saline used for induction of abortion or use of large doses of sodium bicarbonate therapy during cardiac arrest). Typically, hypernatremia develops in adults as result from a chronic process and symptoms are usually associated with other conditions of other diseases. Unless polyuria is present, Central Nervous System (CNS) and tissue signs characterize acute symptomatic hypernatremia, which include : Thirst (unless hypothalamic lesions are the cause), restlessness, weakness, seizures, delirium, maniacal behaviour and coma. Symptoms are more likely to occur with acute rises in plasma sodium concentration, whereas chronic hypertonicity generally produces fewer CNS manifestations, since brain cells accumulate ideogenic osmoles, which minimize the tendency for brain shrikage that results from increases in effective ECF osmolality. Mild hypernatremia can be seen with primary hyperaldosteronism ( increased and inappropriate production of aldosterone from the adrenal leading sodium retention with hypertension , suppression of plasma renin, and hypokalemia and its manifestations) and Cushing

AB - Radioiodinated metaiodobenzylguanidine (MIBG) scintigraphy is known for its high specificity in detecting pheochromocytoma and other tumors of neural crest origin. (27 Refs) 2 UI - 97073837 AU - Caldarella A; Comin CE; Palomba A; Tamburini A; Tintori V TI - [Adrenal cortex neoplasms in children: diagnostic and therapeutic difficulties] SO - Pathologica 1996;88(3):175-80 AD - Istituto di Anatomia e Istologia Patologica, Universita di Firenze. 3 UI - 97113778 AU - Giunta C; Youil R; Venter D; Chow CW; Somers G; Lafferty A; Kemper B; Cotton RG TI - Rapid diagnosis of germline p53 mutation using the enzyme mismatch cleavage method. 5 UI - 97124773 AU - Cobb VJ; Williams BC; Mason JI; Walker SW TI - Forskolin treatment directs steroid production towards the androgen pathway in the NCI-H295R adrenocortical tumour cell line. 6 UI - 97124795 AU - Fallo F; Pilon C; Barzon L; Pistorello M; Pagotto U; Altavilla G; Boscaro M; Sonino N TI - Effects of taxol on the human NCI-H295 adrenocortical carcinoma cell line. Apoptosis was investigated by measuring DNA fragmentation with ELISA assay after cell exposure to taxol at IC50 for 24 h. For secretion studies, aldosterone, cortisol, testosterone and dehydroepiandrosterone-sulphate (DHEA-S) were measured by RIA in the conditioned medium after 96 h exposure to taxol 10(-10)-10(-6) M, and expressed as percentage of steroid production by control cells.

When normal cultured cells are exposed to carcinogens in vitro, they acquire many altered characteristics of morphology, growth, and metabolism, and the cells may exhibit tumor formation in vivo. Transformation is usually not a sudden, all at once, change but rather is a stepwise process involving successive generations of cells which become increasingly deviant until final irreversible transformation is achieved. The paramount criterion that cells are fully transformed to the neoplastic state is that they can produce tumors in animals when transplanted to the appropriate host. The hybridization of tumor cells with normal cells usually results in benign hybrid cells, indicating that the tumor genotype is recessive. - Angiogenesis factors- Tumor cells like fetal and some other normal cells produce a number of substances which stimulate the proliferation of capillary endothelial cells, providing vascularization for the proliferating tumor. Growth factors have a number of characteristics in common: they are all polypeptides which bind to specific high affinity membrane receptors; they are produced and act on cells at "short range", unlike endocrine action; each cell has receptors for multiple factors; some factors, such as interleukin 2 (IL2) act on very few cell types, while others, for example, epidermal growth factor (EGF), act on many; factors vary in the point of the cell cycle in which they act; factors may, according to cell type, inhibit cell division and cause differentiation.

Interpretation: ACTH is elevated in Addison's disease (>1000 pg/mL), congenital adrenal hyperplasia, pituitary-dependent Cushing's disease, ectopic ACTH-producing tumors, pseudo-Cushing's states and Nelson's syndrome. Plasma ACTH normally undergoes a diurnal variation with lowest level in late pm. In Cushing's disease (pituitary-dependent adrenal hyperplasia) and ectopic ACTH -producing tumors, ACTH may be with the normal range, but plasma cortisol is increased. In Cushing's syndrome caused by adrenal adenoma or carcinoma or nodular hyperplasia, plasma cortisol is increased but ACTH is low. Functional tests may be used to distinguish ACTH secretion. Interfering Substances: Hypoglycemia, insulin, levodopa, metyrapone, vasopressin may increase production of ACTH; whereas dexamethasone and other corticosteroids decrease ACTH.

Here should be listed all the research projects in which our laboratorium participates. However, due to the starting of new research lines and reorganisations at both the university and the hospital, this menu is not available. For a link to all the research being done at our University, please check the OZIS system. We apologize for any inonvenience this may cause. Click here to go back to the AZN homepage. Click here to go back to the LEV homepage.

AB - Previous studies have shown a significant association between allelic frequencies at the ANP gene locus and aldosterone responsiveness to angiotensin in aldosterone-producing adenoma (APA). We searched for any gross insertions or deletions in the ANP gene in APA and any associations between allelic frequencies at the Hpa II and Sca I RFLP sites within the ANP gene and angiotensin-responsive and unresponsive APA and normal subjects. We also searched for possible point mutations in the promoter region of the ANP gene (-595 to transcript- ion start site) in peripheral blood and tumor DNA from 59 patients with APA and in peripheral blood DNA from 39 normal subjects by polymerase chain reaction and single strand conformation polymorphism (PCR-SSCP) analysis. No large alterations in the ANP gene were observed, and no difference in allelic frequencies at the RFLP sites were seen between the two tumor subtypes, angiotensin-responsive and angiotensin-unresponsive APA, or between the APA group and normal subjects. SSCP analysis, however, did reveal mutations in the promoter region of the ANP gene (-375 to -595) in both peripheral blood and tumor DNA from 8 of 59 (14%) patients with APA, compared with only one of 39 normal controls (2.6%). This study suggests that alterations in the proximal promoter region of the ANP gene in APA may be important in the regulation of ANP transcription and may be involved in the underlying pathophysiology of aldosterone-producing adenoma in at least some patients.

i. Hypokalemia associated with triamterene (Dyrenium). Hypokalemia associated with hydrochlorothiazide (Hydrodiuril). A i) is greater than ii) B ii) is greater than i) C i) and ii) are equal or very nearly equal Return to Question Menu. Go back to previous question. Go back to previous question. Go back to previous question.

[NO DESCRIPTION: Not enough sentences on document]

[NO DESCRIPTION: Not enough sentences on document]

Microabscess^ Involved^ Heart disease, NOS^ Lung, NOS^ Kidney, NOS^ Splenic disorder, NOS^ Disease of liver, NOS^ Disease of pericardium, NOS^ Skin pH, NOS^ Lymph, NOS^ Lymph node, NOS^ . ###21504^31^W^F^1982^2^^ Infiltration, NOS^ Infiltrating duct carcinoma^ Right^ Right breast, NOS^ Right^ Altered^ Modified radical mastectomy, NOS^ Posterior axillary line^ Lymph, NOS^ Lymph node, NOS^ Positive^ Neoplasm, uncertain whether benign or malignant^ . Peritoneum, NOS^ Surface^ Soft^ Soft tissues, NOS^ Soft tissues of pelvis, NOS^ Retroperitoneum, NOS^ Inferior^ Kidney disease, NOS^ Aortic lymph node^ Mesentery, NOS^ Mesenteric lymph node, NOS^ Diaphragm, NOS^ Diaphragmatic pleura^ Disease of lung, NOS^ Disease of bone, NOS^ Bone marrow, NOS^ Rib syndrome^ Vertebra, NOS^ . Heart, NOS^ Cardiac catheterization, NOS^ Initial^ With^ Lung, NOS^ Stenosis, NOS^ Patent^ Right^ Shunt, NOS^ Increased size, NOS^ Left^ Atrium, NOS^ Following^ Atrium, NOS^ Common ventricle^ Regurgitation^ . Multiple^ Intermittent^ Including^ Right^ Right bundle branch block^ Immature^ Ventricle, NOS^ Contraction, NOS^ Complete^ Heart disease, NOS^ Heart block, NOS^ Pacing the floor^ . Autopsy examination, NOS^ Lung, NOS^ Splenic disorder, NOS^ Disease of liver, NOS^ Kidney disease, NOS^ Positive^ Candidiasis, NOS^ Candidiasis, NOS^ .

h Salt sensitivity in essential hypertensive is associated with insulin sensitivity h Comparison of fourth and fifth Korotkoff diastolic blood pressures in 6-32 year old individuals. h Hypertension promotes coronary calcium deposition in asymptomatic men h Evidence suggesting that urinary kallikrein excretion is heritable in African American families with essential hypertension h Left ventricular mass and diastolic function in primary aldosteronism and primary hypertension h Endothelium-dependent vasodilatation may be impaired by normal range cholesterol levels

Plasma cortisol at 8 am was 57 mg/dL (reference range 5-25 mg/dL); cortisol drawn at 4 pm was and cortisol at 11 pm was mg/dL (reference range 2-10 mg/dL). Plasma was drawn for ACTH and a two day, low dose dexamathasone suppression test was begun, administering 0.5 mg dexamethasone every 6 hours for two days; urine free cortisol collected during the second day was 6,130 mg (reference In normal individuals, cortisol is highest on rising and falls progressively during the day to reach a nadir between midnight and 2 am; normal 8 am values are 5-25 mg/dL, while values at bedtime should be In the usual overnight test, a 1 mg dose (slightly (1.5x) above the equivalent physiologic amount of cortisol produced in one day) is administered at bedtime to prevent the majority of ACTH production occurring during sleep. In equivocal cases, a somewhat larger dose of dexamethasone (0.5 mg q 6 hours for two days, about 3 times physiologic equivalent of cortisol) will suppress ACTH and cortisol production to below normal in almost all normal and mildly ill individuals; urine free cortisol or plasma cortisol at 8 am should fall to below normal in patients without Cushing's syndrome. A sizable minority of patients with Cushing's disease have only mild overproduction of cortisol, and this level of dexamethasone may suppress cortisol production to normal; for this reason, Orth (3) suggests discontinuing use of this test.

(57 Refs) 2 UI - 96063767 AU - Sato N; Watanabe Y; Saga T; Mitsudo K; Dohke M; Minami K TI - Adrenocortical adenoma containing a fat component: CT and MR image evaluation. 4 UI - 96065991 AU - Takeda R; Matsubara T; Miyamori I; Hatakeyama H; Morise T TI - Vascular complications in patients with aldosterone producing adenoma in Japan: comparative study with essential hypertension. AB - The incidence of vascular complications in 224 patients with aldosterone-producing adenoma (APA) which was proven on adrenal surgery, was compared to that in 224 sex- and age-matched patients with essential hypertension (EHT). Lesions less than or equal to 0 H were classified as benign, lesions greater than 20 H were regarded as malignant, and lesions between 0 and 20 H were regarded as indeterminate. Of 11 CT-indeterminate lesions, four of five adenomas had an ASR less than 70, and four of six metastases had an ASR greater than 80. An algorithm was developed for diagnosis of adrenal lesions that uses the density reading on noncontrast CT as the first step, with chemical-shift MR imaging for CT-indeterminate lesions.

(57 Refs) 2 UI - 96063767 AU - Sato N; Watanabe Y; Saga T; Mitsudo K; Dohke M; Minami K TI - Adrenocortical adenoma containing a fat component: CT and MR image evaluation. 4 UI - 96065991 AU - Takeda R; Matsubara T; Miyamori I; Hatakeyama H; Morise T TI - Vascular complications in patients with aldosterone producing adenoma in Japan: comparative study with essential hypertension. AB - The incidence of vascular complications in 224 patients with aldosterone-producing adenoma (APA) which was proven on adrenal surgery, was compared to that in 224 sex- and age-matched patients with essential hypertension (EHT). Lesions less than or equal to 0 H were classified as benign, lesions greater than 20 H were regarded as malignant, and lesions between 0 and 20 H were regarded as indeterminate. Of 11 CT-indeterminate lesions, four of five adenomas had an ASR less than 70, and four of six metastases had an ASR greater than 80. An algorithm was developed for diagnosis of adrenal lesions that uses the density reading on noncontrast CT as the first step, with chemical-shift MR imaging for CT-indeterminate lesions.

(57 Refs) 2 UI - 96063767 AU - Sato N; Watanabe Y; Saga T; Mitsudo K; Dohke M; Minami K TI - Adrenocortical adenoma containing a fat component: CT and MR image evaluation. 4 UI - 96065991 AU - Takeda R; Matsubara T; Miyamori I; Hatakeyama H; Morise T TI - Vascular complications in patients with aldosterone producing adenoma in Japan: comparative study with essential hypertension. AB - The incidence of vascular complications in 224 patients with aldosterone-producing adenoma (APA) which was proven on adrenal surgery, was compared to that in 224 sex- and age-matched patients with essential hypertension (EHT). Lesions less than or equal to 0 H were classified as benign, lesions greater than 20 H were regarded as malignant, and lesions between 0 and 20 H were regarded as indeterminate. Of 11 CT-indeterminate lesions, four of five adenomas had an ASR less than 70, and four of six metastases had an ASR greater than 80. An algorithm was developed for diagnosis of adrenal lesions that uses the density reading on noncontrast CT as the first step, with chemical-shift MR imaging for CT-indeterminate lesions.

The primary goal of my work is to determine the nature of the interactions between the hormone systems that govern pressure and volume homeostasis. To date, this work has focused on the renin-angiotensin-aldosterone system. Ongoing projects include: 1) An assessment of the genes encoding 11-beta-hydroxylase and 18-hydroxylase in functioning adrenal adenomas producing elevated levels of 18-methyl oxidation metabolites of cortisol in patients with primary hyperaldosteronism. One issue is whether a related mutation might also account for their overproduction in primary hyperaldosteronism. The primary focus of this work will be to test the hypothesis that aldosterone, rather than angiotensin, is an independent stimulus for ventricular hypertrophy. Blumenfeld, J.D. (1993) Hypertension and adrenal disorders.

A new monochromosomal somatic cell hybrid panel from BIOS Laboratories consists of 24 distinct hybrids, of which 21 contain one and 3 contain two chromosomes. Most of the hybrids, developed and characterized by Raghbir Athwal (Temple University Medical School) in collaboration with BIOS, are constructed in the A9 mouse cell line, with four remaining in a Chinese hamster ovary background. The human donor genome is derived from the normal human fibroblast cell line GM0634. In collaboration with researchers led by Melvin Simon (California Institute of Technology), Research Genetics has constructed mouse and human genomic BAC libraries from which DNA pools, high-density membranes, and individual clones are now available. Library clones are arrayed in 384-well microtiter plates. For each library, large genomic DNA is prepared from cultured mouse 129/sv or human 978SK cell lines.

ADRENOCORTICAL CARCINOMA - October 1995 1 UI - 95612356 AU - Boscaro M; Fallo F; Barzon L; Daniele O; Sonino N TI - Adrenocortical carcinoma: epidemiology and natural history (Meeting abstract). SO - Congresso Internazionale, I Tumore del Surrene [International Congress, Tumors of the Adrenal Glands], March 25-26, 1994, Turin, Italy, p. 37, 1994 AD - Division of Endocrinology-Institute of Semeiotica Medica, University of Padova, Padova, Italy AB - Adrenocortical carcinoma is a rare and very aggressive tumor. The results of tumor staging were stage I (tumor size less than 5 cm) 1 patient (3%); stage II (local disease) 10 patients (28%); stage III-IV (locoregional disease/metastases) 24 patients (69%). Tumor staging was the following: 3 (16%) stage I patients (tumor size varying from 4 to 5 cm), 7 (37%) stage II patients (tumor size 6-20 cm, mean 12 cm) and 3 (47%) stage III or IV. SO - Congresso Internazionale, I Tumore del Surrene [International Congress, Tumors of the Adrenal Glands], March 25-26, 1994, Turin, Italy, p. 40, 1994 AD - Clinique des Maladies Endocriniennes et Metaboliques, Hopital Cochin AB - We studied 105 patients (75 female and 30 male; mean age 46 years). 59 of the 80 patients who underwent surgery received mitotane therapy: 20 patients were treated before surgery (between one to six months) and 52 after surgery, including 23 patients with apparently curative surgery.

ADRENOCORTICAL CARCINOMA - March 1996 1 UI - 96051094 AU - Rossi E; Sani C; Perazzoli F; Casoli MC; Negro A; Dotti C TI - Alterations of calcium metabolism and of parathyroid function in primary aldosteronism, and their reversal by spironolactone or by surgical removal of aldosterone-producing adenomas. AB - In order to investigate the possible existence of abnormal calcium metabolism and parathyroid function in primary aldosteronism (PA), we have compared the calcium/parathyroid hormone (PTH) profile of patients with PA with the profile of healthy normotensive subjects and of patients with essential hypertension (EH). Furthermore, we have evaluated the effects of spironolactone and the surgical removal of aldosterone-producing adenomas on the calcium/PTH profile in the PA patients. Four groups of 10 subjects each participated in the study: 1) hypertensive patients with PA, 2) patients with low-renin EH (LREH), 3) patients with normal-renin EH (NREH), 4) normotensive healthy subjects (NS). In all subjects, after 1 week of a controlled intake of Na and K, the following parameters were measured: urine excretion of Na, K, Ca, Mg, and P, plasma levels of K, Mg, inorganic P, total calcium and ionized calcium, and plasma renin activity, aldosterone concentration, and intact PTH. Blood pressure and laboratory parameters were determined again in all the PA patients after 1 month of 100 mg daily spironolactone administrat- ion, and in four out of the 10 PA patients 2 months after surgical removal of aldosterone-producing adenomas. These results suggest the presence of calcium metabolism alterations in both PA and EH patients, but that these alterations are more exaggerated in PA, so that higher PTH levels are needed for maintaining low-normal levels of serum ionized calcium.

ADRENOCORTICAL CARCINOMA - October 1995 1 UI - 95612356 AU - Boscaro M; Fallo F; Barzon L; Daniele O; Sonino N TI - Adrenocortical carcinoma: epidemiology and natural history (Meeting abstract). SO - Congresso Internazionale, I Tumore del Surrene [International Congress, Tumors of the Adrenal Glands], March 25-26, 1994, Turin, Italy, p. 37, 1994 AD - Division of Endocrinology-Institute of Semeiotica Medica, University of Padova, Padova, Italy AB - Adrenocortical carcinoma is a rare and very aggressive tumor. The results of tumor staging were stage I (tumor size less than 5 cm) 1 patient (3%); stage II (local disease) 10 patients (28%); stage III-IV (locoregional disease/metastases) 24 patients (69%). Tumor staging was the following: 3 (16%) stage I patients (tumor size varying from 4 to 5 cm), 7 (37%) stage II patients (tumor size 6-20 cm, mean 12 cm) and 3 (47%) stage III or IV. SO - Congresso Internazionale, I Tumore del Surrene [International Congress, Tumors of the Adrenal Glands], March 25-26, 1994, Turin, Italy, p. 40, 1994 AD - Clinique des Maladies Endocriniennes et Metaboliques, Hopital Cochin AB - We studied 105 patients (75 female and 30 male; mean age 46 years). 59 of the 80 patients who underwent surgery received mitotane therapy: 20 patients were treated before surgery (between one to six months) and 52 after surgery, including 23 patients with apparently curative surgery.

ADRENOCORTICAL CARCINOMA - March 1996 1 UI - 96051094 AU - Rossi E; Sani C; Perazzoli F; Casoli MC; Negro A; Dotti C TI - Alterations of calcium metabolism and of parathyroid function in primary aldosteronism, and their reversal by spironolactone or by surgical removal of aldosterone-producing adenomas. AB - In order to investigate the possible existence of abnormal calcium metabolism and parathyroid function in primary aldosteronism (PA), we have compared the calcium/parathyroid hormone (PTH) profile of patients with PA with the profile of healthy normotensive subjects and of patients with essential hypertension (EH). Furthermore, we have evaluated the effects of spironolactone and the surgical removal of aldosterone-producing adenomas on the calcium/PTH profile in the PA patients. Four groups of 10 subjects each participated in the study: 1) hypertensive patients with PA, 2) patients with low-renin EH (LREH), 3) patients with normal-renin EH (NREH), 4) normotensive healthy subjects (NS). In all subjects, after 1 week of a controlled intake of Na and K, the following parameters were measured: urine excretion of Na, K, Ca, Mg, and P, plasma levels of K, Mg, inorganic P, total calcium and ionized calcium, and plasma renin activity, aldosterone concentration, and intact PTH. Blood pressure and laboratory parameters were determined again in all the PA patients after 1 month of 100 mg daily spironolactone administrat- ion, and in four out of the 10 PA patients 2 months after surgical removal of aldosterone-producing adenomas. These results suggest the presence of calcium metabolism alterations in both PA and EH patients, but that these alterations are more exaggerated in PA, so that higher PTH levels are needed for maintaining low-normal levels of serum ionized calcium.

Tumors of the Adrenal Glands], March 25-26, 1994, Turin, Italy, p. 37, 1994 AD - Division of Endocrinology-Institute of Semeiotica Medica, University of Padova, Padova, Italy AB - Adrenocortical carcinoma is a rare and very aggressive tumor. The results of tumor staging were stage I (tumor size less than 5 cm) 1 patient (3%); stage II (local disease) 10 patients (28%); stage III-IV (locoregional disease/metastases) 24 patients (69%). Tumor staging was the following: 3 (16%) stage I patients (tumor size varying from 4 to 5 cm), 7 (37%) stage II patients (tumor size 6-20 cm, mean 12 cm) and 3 (47%) stage III or IV. Tumors of the Adrenal Glands], March 25-26, 1994, Turin, Italy, p. 40, 1994 AD - Clinique des Maladies Endocriniennes et Metaboliques, Hopital Cochin AB - We studied 105 patients (75 female and 30 male; mean age 46 years). 59 of the 80 patients who underwent surgery received mitotane therapy: 20 patients were treated before surgery (between one to six months) and 52 after surgery, including 23 patients with apparently curative surgery. The mean postoperative hospital stay for the six patients with successful laparoscopic procedures was 2.3 days, and four patients were dismissed within 48 hours after the procedure.

Left ventricular mass and diastolic function in primary aldosteronism and primary hypertension (Sep 95) Hypertension AHA Council for High Blood Pressure Research Evidence for a bufodienolide Na/K pump inhibitor in human urine (Apr 96) Am J Hypert 11th Scientific Meeting, American Society of Hypertension Routine determination of TSH for the detection of hypo- and hyperthyroidism in hypertensive women referring to a specialized centre (Apr 96) Am J Hypert 11th Scientific Meeting, American Society of Hypertension Renin and aldosterone measurements after captopril and supine position in differential diagnosis of adenoma and hyperplasia in primary aldosteronism (Apr 96) Am J Hypert 11th Scientific Meeting, American Society of Hypertension The prevalence of primary aldosteronism using the response of plasma aldosterone/renin ratio to captopril as initial screening test in hypertensives (Apr 96) Am J Hypert 11th Scientific Meeting, American Society of Hypertension High concentrations of interleukin 1 beta in patients with essential hypertension before any drug therapy: a pilot preliminary study (Jun 96) Nephrol Dial Transplant 33rd Congress of the Eur Dial Transplant Assoc

Matrix Position: Breast/Risk Factors # 1 Answer: D A 42 year old single woman whose aunt had a mastectomy at age 52 wishes to know if she is at increased risk of developing breast cancer. Matrix Position: Gastrointestinal/Risk Factors # 2 Answer: B Risk factors for colorectal cancer include all of the following except: a. a personal history of adenomatous polyps of the colon. Matrix Position: Lung/Epidemiology # 20 Answer: D In considering the pathogenesis of lung cancer, all of the following are true except: a. Inheritance plays a role in lung cancer risk. Matrix Position: Breast/Epidemiology # 24 Answer: C Breast cancer is the most common cancer among women. Matrix Position: Lung/Prevention # 26 Answer: C Primary prevention practices are considered to be the most effective strategy for reducing the morbidity and mortality of lung cancer. Matrix Position: Skin/Cost-Benefit # 31-34 Answer: See below Match the following responses with items 31-34: a. Proven to be cost-beneficial to prevent melanoma.

Also published as an article in the International Journal of Social Psychiatry, 20:68-71, 1974. Cancro, R. Is Individual Psychotherapy in the Schizophrenias an Anachronism? Also published as an abstract in Abstracts, Fifth World Congress of Psychiatry. New York: AMS Press, 1976, pp. Cancro, R. and Angrist, B. Are Drugs More Than Palliative in the Management of Schizophrenia? Cancro, R. General considerations relating to theory in the schizophrenic disorders.

Back to previous level Bartter's Disease Hosp. for Sick Children, Toronto:Anaesthetic Implications for Bartter's syndrome Vanderbilt U.:Bartters syndrome Last update: 04/25/97

BARTTER'S SYNDROME A combination of fluid, electrolyte, and hormonal abnormalities characterized by renal K, Na, and Cl wasting; hypokalemia; hyperaldosteronism; hyperreninemia; and normal BP. The syndrome usually appears in childhood, either as a sporadic or a familial, usually autosomal recessive, disorder. All rights reserved.

BARTTER'S SYNDROME A combination of fluid, electrolyte, and hormonal abnormalities characterized by renal K, Na, and Cl wasting; hypokalemia; hyperaldosteronism; hyperreninemia; and normal BP. The syndrome usually appears in childhood, either as a sporadic or a familial, usually autosomal recessive, disorder. All rights reserved.

Abstract: Primary aldosteronism is a potentially curable cause of hypertension, especially when caused by an adrenal adenoma. IFN-gamma appeared in the cytoplasm of tumor cells in 7/7 cases of adrenal cortical carcinoma, 8/17 cases of cortical adenoma and endothelium in 2/7 cases of adrenal cortical carcinoma and 5/17 cases of cortical adenoma. The nonfunctional tumors were usually diagnosed in the late period, therefore the prognosis was worse, but in recent years some cases of no secretory carcinomas had been occasionally found by image diagnosis and these tumors were small, so their prognosis was favorate. In immunoelectron microscopic investigations, GSH-PO was localized not only in cytoplasm (cytosol GSH-PO) but also in mitochondria (mitochondrial GSH-PO). Based on our findings, cytosol GSH-PO may play an important role in protective effects against cell injury by lipid peroxides induced in the process of the steroid hormone synthesis or the cellular aging process, and mitochondrial GSH-PO was strongly suggested to be one of the most important enzymes for steroidogenesis, especially cortisol synthesis. Abstract: This case report deals with an insulin-dependent diabetic patient suffering peripheral adrenal insufficiency who, after 12 years of substitutive treatment exhibited resistance to mineralo- and gluco-corticoids with relapse of melanodermia and plasma ACTH levels higher than 1500 pg/ml despite increasing doses.

Abstract: Primary aldosteronism is a potentially curable cause of hypertension, especially when caused by an adrenal adenoma. IFN-gamma appeared in the cytoplasm of tumor cells in 7/7 cases of adrenal cortical carcinoma, 8/17 cases of cortical adenoma and endothelium in 2/7 cases of adrenal cortical carcinoma and 5/17 cases of cortical adenoma. The nonfunctional tumors were usually diagnosed in the late period, therefore the prognosis was worse, but in recent years some cases of no secretory carcinomas had been occasionally found by image diagnosis and these tumors were small, so their prognosis was favorate. In immunoelectron microscopic investigations, GSH-PO was localized not only in cytoplasm (cytosol GSH-PO) but also in mitochondria (mitochondrial GSH-PO). Based on our findings, cytosol GSH-PO may play an important role in protective effects against cell injury by lipid peroxides induced in the process of the steroid hormone synthesis or the cellular aging process, and mitochondrial GSH-PO was strongly suggested to be one of the most important enzymes for steroidogenesis, especially cortisol synthesis. Abstract: This case report deals with an insulin-dependent diabetic patient suffering peripheral adrenal insufficiency who, after 12 years of substitutive treatment exhibited resistance to mineralo- and gluco-corticoids with relapse of melanodermia and plasma ACTH levels higher than 1500 pg/ml despite increasing doses.

Back to previous level Adenoma, Islet Cell Med. of Wisconsin:Pancreatic Islet-Cell Tumors U. of Utah Webpath:Islet cell adenoma of pancreas, high power microscopic U. of Utah Webpath:Islet cell adenoma of pancreas, low power microscopic U. of Utah Webpath:Islet cell adenoma of pancreas, medium power microscopic Adenoma, Liver Cell U. of Utah Webpath:Hepatic adenoma, liver, gross U. of Utah Webpath:Hepatic adenoma, liver, microscopic Adenoma, Oxyphilic Adenoma, Pleomorphic Harvard U.:Pleomorphic Adenoma U. of Pittsburg Med. Ctr.:Pleomorphic Adenoma Ex Carcinoma U. of Utah Webpath:Pleomorphic adenoma, parotid gland, high power microscopic U. of Utah Webpath:Pleomorphic adenoma, parotid gland, low power microscopic Adenoma, Sweat Gland Adenoma, Villous Adenomatoid Tumor Adenomatosis, Pulmonary Adenomatous Polyps Cornell U.:Adenomatous polyp [Colon] NCI:Cigarette Smoking and Alcohol Consumption as Risk Factors for Colorectal Adenomatous Polyps U. of Pennsylvania:Adenomatous Polyp U. of Utah Webpath:Colon, adenomatous polyp (tubular adenoma) compared to normal mucosa, medium power microscopic U. of Utah Webpath:Colon, adenomatous polyp (tubular adenoma), gross U. of Utah Webpath:Colon, adenomatous polyp (tubular adenoma), low power microscopic U. of Utah Webpath:Colon, adenomatous polyp on long stalk, gross U. of Utah Webpath:Colon, multiple adenomatous polyps, gross U. of Wisconsin, Madison:Adenomatous Polyp Adenoma, Acidophil Apudoma Cystadenoma Med. Ctr.:Moderately Differentiated Adrenal Cortical Carcinoma U. of Utah Webpath:Adrenal gland, cortical adenoma with Cushing's syndrome, gross Mesothelioma Froedtert Hosp. of Wisconsin:Omental Cake Nat'l Cancer Ctr. of Japan:Malignant Mesothelioma U. of Iowa:Benign fibrous mesothelioma of the pleura U. of Pennsylvania:Malignant Mesothelioma U. of Pennsyvania Oncolink:NCI/PDQ Physician Statement: Malignant mesothelioma U. of Utah Webpath:Lung, mesothelioma, gross Prolactinoma Harvard U.:Indications for Treatment of Microprolactinomas: An Update Med. of Wisconsin:Prolactinoma NIDDK:Prolactinoma Adenoma, Basophil Adenoma, Bile Duct Adenoma, Chromophobe Last update: 04/25/97

English: To the English dictionary Technical term: hydrolysis (niet: hydrolyse) Popular term: adding water to split a compound Technical term: hydrolyse Popular term: Wasser abstoßend Popular term: excess of blood in a part Popular term: Steigerung der Durchblutung eines Organs

There is a 9 x 9mm hypodense rounded nodule within the right adrenal. The lesion measured 9 x 9mm. There is no adrenal calcification. The liver, spleen, pancreas, gallbladder and kidneys are normal. There is no lymphadenopathy. No focal bone lesion is seen.

Specimens must be collected in the GI Preservative tube. Specimens must be collected in the GI Preservative tube. Specimens must be collected in the GI Preservative tube. Specimens must be collected in the GI Preservative tube. Specimens must be collected in the GI Preservative tube. Specimens must be collected in the GI Preservative tube.

The Hypermedia PDQ project is supported, in part, by grants from the National Cancer Institute and the National Action Plan on Breast Cancer. Additional information is available regarding this project. We are in the initial phase, and welcome your input. Comments may be sent to pdq@oncolink.upenn.edu. The Hypermedia PDQ project is supported, in part, by grants from the National Cancer Institute and the National Action Plan on Breast Cancer. We are in the initial phase, and welcome your input.

Medicine Links    74%    [find similar]     70%    [find similar] Cushing's Syndrome    66%    [find similar] Cushing's Syndrome    66%    [find similar] Cushing's & Conn's Syndromes    65%    [find similar] Raymond McCaffrey    63%    [find similar]

Back to previous level Cushing's Syndrome Harvard U.:Clinical Uses of Corticotropin-Releasing Hormone in the Evaluation of Patients with Cushing's Syndrome Harvard U.:Major Diagnostic Advance: Bilateral Inferior Petrosal Sinus Sampling in Cushing's Syndrome Harvard U.:Surgery for Cushing's Disease Med. School, Houston:Cushing's Syndrome U. of Utah Webpath:Adrenal gland, cortical adenoma with Cushing's syndrome, gross U. of Utah Webpath:Adrenal gland, cortical adenoma, gross U. of Utah Webpath:Adrenal glands, comparison of atrophic (Addison's disease), normal, and hyperplastic (Cushing's syndrome) glands, g Uniformed Services U. of the Health Sciences:Cushing's syndrome Hyperaldosteronism Last update: 04/25/97

When you enter a standing order, you will be sent a pro forma invoice for each new volume in the series. Standing order customers receive a 10% discount on the cost of any title on the standing order. The book is organized into the following sections: diabetes lipids thyroid calcium and bone reproductive endocrinology adrenal pituitary The topics covered in the Clinical Endocrinology Update are presented by the leading clinicians and are selected on the basis of requests received from practicing endocrinologists, internists, and clinicians. 1996 Introduction to Molecular & Cellular Research Syllabus The 1996 Syllabus contains completely new chapters on: 148 pages, paper ISBN 1-879225-16-6 1994 Introduction to Molecular and Cellular Research 144 pages, paper ISBN 1-879225-12-3 Back to Top

URL: http://www.stepstn.com/nord/rdb_sum/628. Summary: If you order the full text version of this report from NORD, you can contact the agencies listed in the Resources section for more detailed information and avenues to support. Summary: A. ACTH B. bitemporal hemianopsia C. Conn s syndrome D. Cushings syndrome E. dexamethasone suppression test F. diabetes insipidus G. glucose tolerance test H. empty sella syndrome I. hyperprolactinemia J. insulin-like growth factor 1 K. MEN 1 L. MEN II M. myxedema N. serum angiotensin converting enzyme O. syndrome of inappropriate ADH secretion P. thyroid function tests Q. urinary . URL: http://www.stepstn.com/nord/org_sum/1011. URL: http://www.stepstn.com/nord/org_sum/78. URL: http://saltlake.thesource.net/files/librarywire/DN95_09_11/95_09_11_i.html

This test helps to distinguish patients with excess production of ACTH due to pituitary adenomas from those with ectopic ACTH-producing tumors. Since cortisol and other glucocorticoids signal the pituitary to lower secretion of ACTH, the normal response after taking dexamethasone is a drop in blood and urine cortisol levels. This test helps to distinguish between patients with pituitary adenomas and those with ectopic ACTH syndrome or cortisol-secreting adrenal tumors. Patients with pituitary adenomas usually experience a rise in blood levels of ACTH and cortisol. This response is rarely seen in patients with ectopic ACTH syndrome and practically never in patients with cortisol-secreting adrenal tumors. Conversely, pituitary tumors are not detected by imaging in almost 50 percent of patients who ultimately require pituitary surgery for Cushing's syndrome.

Research activities Research activities Aims Current research projects are focused on the following main questions: 1) How is the regioselectivity and stereospecificity of steroid hydroxylations determined? How are the electrons transferred from the electron donor to the respective steroid hydroxylases? What are the main characteristics of the adrenal ferredoxin, being the electron transfer protein from adrenal reductase to cytochromes P450? 3) Moleculargenetic characterization of steroid hydroxylases from patients suffering obviuosly from different defects of these proteins (congenital adrenal hyperplasia caused by CYP11B1 deficiency; glucocorticoid-remediable hyperaldosteronism; hyperaldosteronism) [Research activities]

[8] -- TNM definitions -- Primary tumor (T) T1: Primary tumor no more than 5 cm in size; no local invasion T2: Primary tumor greater than 5 cm in size; no invasion T3: Primary tumor of any size, locally invading to but not involving adjacent organs T4: Tumor any size, locally invading adjacent organs Nodal involvement (N) N0: No regional positive nodes N1: Positive regional nodes Distant metastasis (M) MX: Minimum requirements to assess the presence of distant metastasis cannot be met M0: No (known) distant metastasis M1: Distant metastasis present -- Stage I -- Stage I adrenocortical carcinoma is defined by the following TNM grouping: T1, N0, M0 -- Stage II -- Stage II adrenocortical carcinoma is defined by the following TNM grouping: T2, N0, M0 -- Stage III -- Stage III adrenocortical carcinoma is defined by the following TNM groupings: T3, N0, M0 T1 or T2, N1, M0 -- Stage IV -- Stage IV adrenocortical carcinoma is defined by the following TNM groupings: T3 or T4, N1, M0 any T, any N, M1 References: 1. : Adrenocortical carcinoma in surgically treated patients: a retrospective study on 156 cases by the French Association of Endocrine Surgery. The treatment of patients who have tumors with local invasion, but without clinically enlarged regional lymph nodes, is complete surgical removal as for stage I and stage II tumors. [4,5,7,8] One study reported that doxorubicin produced objective responses in 3 of 16 patients with poorly-differentiated, non-hormone-producing tumors but no responses in 15 patients whose disease did not respond to mitotane. : Phase II trial of mitotane and cisplatin in patients with adrenal carcinoma: a Southwest Oncology Group study. : Phase II trial of mitotane and cisplatin in patients with adrenal carcinoma: a Southwest Oncology Group study.

[8] -- TNM definitions -- Primary tumor (T) T1: Primary tumor no more than 5 cm in size; no local invasion T2: Primary tumor greater than 5 cm in size; no invasion T3: Primary tumor of any size, locally invading to but not involving adjacent organs T4: Tumor any size, locally invading adjacent organs Nodal involvement (N) N0: No regional positive nodes N1: Positive regional nodes Distant metastasis (M) MX: Minimum requirements to assess the presence of distant metastasis cannot be met M0: No (known) distant metastasis M1: Distant metastasis present -- Stage I -- Stage I adrenocortical carcinoma is defined by the following TNM grouping: T1, N0, M0 -- Stage II -- Stage II adrenocortical carcinoma is defined by the following TNM grouping: T2, N0, M0 -- Stage III -- Stage III adrenocortical carcinoma is defined by the following TNM groupings: T3, N0, M0 T1 or T2, N1, M0 -- Stage IV -- Stage IV adrenocortical carcinoma is defined by the following TNM groupings: T3 or T4, N1, M0 any T, any N, M1 References: 1. : Adrenocortical carcinoma in surgically treated patients: a retrospective study on 156 cases by the French Association of Endocrine Surgery. The treatment of patients who have tumors with local invasion, but without clinically enlarged regional lymph nodes, is complete surgical removal as for stage I and stage II tumors. [4,5,7,8] One study reported that doxorubicin produced objective responses in 3 of 16 patients with poorly-differentiated, non-hormone-producing tumors but no responses in 15 patients whose disease did not respond to mitotane. : Phase II trial of mitotane and cisplatin in patients with adrenal carcinoma: a Southwest Oncology Group study. : Phase II trial of mitotane and cisplatin in patients with adrenal carcinoma: a Southwest Oncology Group study.

[8] TNM definitions Primary tumor (T) T1: Primary tumor no more than 5 cm in size; no local invasion T2: Primary tumor greater than 5 cm in size; no invasion T3: Primary tumor of any size, locally invading to but not involving adjacent organs T4: Tumor any size, locally invading adjacent organs Nodal involvement (N) N0: No regional positive nodes N1: Positive regional nodes Distant metastasis (M) MX: Minimum requirements to assess the presence of distant metastasis cannot be met M0: No (known) distant metastasis M1: Distant metastasis present Stage I Stage I adrenocortical carcinoma is defined by the following TNM grouping: T1, N0, M0 Stage II Stage II adrenocortical carcinoma is defined by the following TNM grouping: T2, N0, M0 Stage III Stage III adrenocortical carcinoma is defined by the following TNM groupings: T3, N0, M0 T1 or T2, N1, M0 Stage IV Stage IV adrenocortical carcinoma is defined by the following TNM groupings: T3 or T4, N1, M0 any T, any N, M1 References: Cerfolio RJ, Vaughan ED, Brennan TG, et al. The treatment of patients who have tumors with local invasion, but without clinically enlarged regional lymph nodes, is complete surgical removal as for stage I and stage II tumors. : Impact of adjuvant mitotane on the clinical course of patients with adrenocortical cancer. [4,5,7,8] One study reported that doxorubicin produced objective responses in 3 of 16 patients with poorly-differentiated, non-hormone-producing tumors but no responses in 15 patients whose disease did not respond to mitotane. : Phase II trial of mitotane and cisplatin in patients with adrenal carcinoma: a Southwest Oncology Group study. : Phase II trial of mitotane and cisplatin in patients with adrenal carcinoma: a Southwest Oncology Group study.

Aldactone oral tablets contain 25 mg, 50 mg, or 100 mg of the aldosterone antagonist spironolactone, 17-hydroxy-7alpha-mercapto-3-oxo-17alpha-pregn-4-ene-21-carboxylic acid gamma-lactone acetate, which has the following structural formula: Spironolactone is practically insoluble in water, soluble in alcohol, and freely soluble in benzene and in chloroform. (0-24 hr, day 1) Mean Peak Serum Concentration Mean (SD) Post-Steady State Half-Life 7-alpha-(thiomethyl) spirolactone (TMS) 1.25 391 ng/mL at 3.2 hr 13.8 hr (6.4) (terminal) 6-beta-hydroxy-7-alpha-(thiomethyl) spirolactone (HTMS) 1.50 125 ng/mL at 5.1 hr 15.0 hr (4.0) (terminal) Canrenone (C) 1.41 181 ng/mL at 4.3 hr 16.5 hr (6.3) (terminal) Spironolactone 1.30 80 ng/mL at 2.6 hr Approximately 1.4 hr (0.5) (beta half-life) The pharmacological activity of spironolactone metabolites in man is not known. General: Because of the diuretic action of Aldactone (spironolactone), patients should be carefully evaluated for possible disturbances of fluid and electrolyte balance. If serum potassium increases during Aldactone administration but drops when Aldactone is discontinued, a presumptive diagnosis of primary hyperaldosteronism should be considered. The initial daily dosage should provide approximately 1.5 mg of Aldactone per pound of body weight (3.3 mg/kg) administered in either single or divided doses. Aldactone 25-mg tablets are round, light yellow, film coated, with SEARLE and 1001 debossed on one side and ALDACTONE and 25 on the other side, supplied as: NDC Number Size 0025-1001-31 bottle of 100 0025-1001-51 bottle of 500 0025-1001-52 bottle of 1000 0025-1001-55 bottle of 2500 0025-1001-34 carton of 100 unit dose Aldactone 50-mg tablets are oval, light orange, scored, film coated, with SEARLE and 1041 debossed on the scored side and ALDACTONE and 50 on the other side, supplied as: NDC Number Size 0025-1041-31 bottle of 100 0025-1041-34 carton of 100 unit dose Aldactone 100-mg tablets are round, peach colored, scored, film coated, with SEARLE and 1031 debossed on the scored side and ALDACTONE and 100 on the other side, supplied as: NDC Number Size 0025-1031-31 bottle of 100 0025-1031-34 carton of 100 unit dose Store below 77°F (25°C).

A 72 y/o man presented with a mass on routine chest x-ray. Achest/upper abdomen CT scan confirmed the chest mass and identified a 2 cm diameter right adrenal mass. Biochemical studies of adrenal functon were normal. An F-18-FDG scan depicts the chest mass (left panel, anterior coronal section, arrow) Uptake of F-18-FDG confirms the presence of lung carcinoma with metastasis to the right adrenal. In a 68 y/o man with prostate cancer, a CT scan done to screen for metastatic disease identified a 3 cm diameter incidental right adrenal mass. A C-11 acetate scan demonstrates focal uptake (left panel, coronal section,arrow, K=kidneys; right panel, arrow, transaxial section, L=liver) in the mass that was later demonstrated to be a benign adrenal adenoma.

bilateral adrenal mass bilateral adrenal mass acute granulomatous dz (eg, TB) metastases (bilateral in 15%) pheochromocytoma (bilateral in 10%) adrenal hyperplasia ("adenoma") spontaneous adrenal hemorrhage

Back to previous level Adrenal Cortex Neoplasms Med. of Wisconsin:Bilateral Adrenal Mass U. of Illinois, Urbana:Adrenal cortex, adenoma, gross U. of Pennsyvania Oncolink:NCI/PDQ Physician Statement: Adrenocortical carcinoma U. of Utah Webpath:Adrenal gland, cortical adenoma with Cushing's syndrome, gross U. of Utah Webpath:Adrenal gland, cortical adenoma, gross U. of Utah Webpath:Adrenal gland, cortical carcinoma, gross U. of Utah Webpath:Adrenal gland, cortical carcinoma, low power microscopic Last update: 04/25/97

Classical Presentation: Hypokalemia/hypochloremia Metabolic alkalosis Normal blood pressure/highplasma renin activity/ secondary hyperaldosteronism Decreased CH20/GFR; decreased maximal urine osmolality Increased urinary PGE2 and 6-keto-PGF1a Vascular insensitivity to AII Juxtaglomerular hyperplasia Delayed growth and cognitive development Minimal Diagnostic Criteria: Hypokalemia/hypochloremia Metabolic alkalosis Normal blood pressure/high plasma renin activity/secondary hyperaldosteronism Decreased CH20/GFR; decreased maximal urine osmolality Increased urinary PGE2 and 6-keto-PGF1a Decreased distal tubular chloride reabsorp-tion Renal Manifestations: Decreased CH20/GFR; decreased maximal urine osmolality Increased urinary PGE2 and 6-keto-PGF1a Decreased distal tubular chloride reabsorption Inappropriately high urine potassium Juxtaglomerular hyperplasia Associated Defects: Normal serum calcium Normal/low serum magnesium Normal/high serum creatinine Normal/high serum uric acid Differential Diagnosis: Severe potassium depletion chronic vomiting; chronic diuretic use; chronic laxative use) Familial chloride diarrhea Magnesium-losing tubulopathy Calcium-losing tubulopathy Gitelman syndrome If you feel that you have individuals who meet the minimal diagnostic criteria you may read: How to add data to the Bartter Database The Bartter disease editor is: Lisa Guay-Woodford, M.D.

[NO DESCRIPTION: Not enough sentences on document]

The information contained in the Organizational Database (ODB) is provided for informational purposes only. There is no implied endorsement by NORD. NORD does not promote or endorse participation in any specific organization. The information is subject to change without notice. Every effort is made to ensure that the details for each entry are as current as possible. The National Adrenal Diseases Foundation (NADF) is a not-for-profit organization dedicated to serving the needs of those with adrenal diseases such as Addison

Back to previous level Adrenal Cortex Neoplasms Med. of Wisconsin:Bilateral Adrenal Mass U. of Illinois, Urbana:Adrenal cortex, adenoma, gross U. of Pennsyvania Oncolink:NCI/PDQ Physician Statement: Adrenocortical carcinoma U. of Utah Webpath:Adrenal gland, cortical adenoma with Cushing's syndrome, gross U. of Utah Webpath:Adrenal gland, cortical adenoma, gross U. of Utah Webpath:Adrenal gland, cortical carcinoma, gross U. of Utah Webpath:Adrenal gland, cortical carcinoma, low power microscopic Last update: 04/25/97

HTML document for the World Wide Web - Adrenal adenoma - Adrenal cyst - Adrenal hemorrhage - Granulomatous adrenal disease - Myelolipoma

ADRENOCORTICAL CARCINOMA - September 1995 1 UI - 95331328 AU - Gross MD; Shapiro B; Francis IR; Bree RL; Korobkin M; McLeod MK; Thompson NW; Sanfield JA TI - Scintigraphy of incidentally discovered bilateral adrenal masses. AB - The purpose of this study was to determine the patterns of iodine-131 6 beta-iodomethylnorcholesterol (NP-59) imaging and the correlation with computed tomography (CT)-guided adrenal biopsy and follow-up in patients with bilateral adrenal masses. To this end we investigated a consecutive sample of 29 euadrenal patients with bilateral adrenal masses discovered on CT for reasons other than suspected adrenal disease. Among these cases the NP-59 scan demonstrated either bilaterally absent tracer accumulation (in eight, all with bilateral metastases proven by CT-guided biopsy or progression on follow-up CT) or marked asymmetry of adrenocortical NP-59 uptake (in five). In 16 patients diagnosis of adenoma was made on the basis of (a) CT-guided adrenal biopsy of the gland with the greatest NP-59 uptake of the pair (n = 4), or (b) adrenalectomy (n = 2), or (c) absence of change in the size of the adrenal mass on follow-up CT scanning performed 6 months to 3 years later (n = 10). (ABSTRACT TRUNCATED AT 250 WORDS) 2 UI - 95339250 AU - Sakamoto K; Ariyoshi A; Okazaki M TI - Metastatic adrenocortical carcinoma treated by repeated resection: a case report of long-term survival over 18 years.

Note the loss of nuclear polarity, haphazard unorderly growth pattern, and prominent nuclei and nucleoli. Note round uniform nuclei, nucleoli, and glandular-type cluster. FNA, cell block (54.5 kb) 05-11-95 (Courtesy of John Minarcik) Adenocarcinoma of the Pancreas 1. Note that almost every cell has a prominent nucleolus. Note squamous cells with intercellular bridges and columnar periphery (40.0 kb) 10-22-92 (Courtesy of Taz) 4. Courtesy UI Balis MD, deeply into pathology images and a CAP exhibitor "microcomputers roundtable" (44.1 kb) 10-31-93 (Courtesy of Web Smith) 2.

Note the loss of nuclear polarity, haphazard unorderly growth pattern, and prominent nuclei and nucleoli. Note round uniform nuclei, nucleoli, and glandular-type cluster. FNA, cell block (54.5 kb) 05-11-95 (Courtesy of John Minarcik) Adenocarcinoma of the Pancreas 1. Note that almost every cell has a prominent nucleolus. Note squamous cells with intercellular bridges and columnar periphery (40.0 kb) 10-22-92 (Courtesy of Taz) 4. Courtesy UI Balis MD, deeply into pathology images and a CAP exhibitor "microcomputers roundtable" (44.1 kb) 10-31-93 (Courtesy of Web Smith) 2.

1 UI - 96148771 AU - Doppman JL; Gill JR Jr TI - Hyperaldosteronism: sampling the adrenal veins.

adrenal mass adrenal mass lung, melanoma) primary adenocarcinoma large at diagnosis (> 5 cm) usually functional (increased corticosteroids ==> Cushing's) rapid growth benign adrenal adenoma +/- functional nonfunctional occurs in 2-8% of population diff from mets: MRI (mets bright on T2), bx, follow pheochromocytoma neuroblastoma myelolipoma cyst / pseudocyst see also: adrenal calcification, hemorrhage

"three P's" pituitary adenoma 65% ==> Cushing's, acromegaly, prolactinoma parathyroid hyperplasia / adenoma 88% ==> hyper-PTH pancreatic islet-cell tumor gastrinoma (Z-E) most common 50% of Z-E ==> MEN-1 inconstant features: bronchial/intestinal carcinoid, thyroid adenoma, adrenal cortical tumor, lipoma, thymoma

Back to previous level. UI Urbana: Adrenal cortex, adenoma, gross. Our goal is to delineate the physiology - both of the control and function - of the. Communication between cells and organs within the body is essential for the efficient control of body metabolism.

[NO DESCRIPTION: Not enough sentences on document]

ADRENAL CORTICAL HYPERFUNCTION (See also Congenital Adrenal Hyperplasia, Chapter 199 CONGENITAL ADRENAL HYPERPLASIA) Hypersecretion of one or more adrenocortical hormones produces distinct clinical syndromes. Excessive production of androgens results in adrenal virilism; hypersecretion of glucocorticoids produces Cushing's syndrome; and excess aldosterone output results in aldosteronism. These syndromes frequently have overlapping features. Adrenal hyperfunction may be compensatory, as in congenital adrenal hyperplasia, or may be due to acquired hyperplasia, adenomas, or adenocarcinomas. All rights reserved.

benign adrenal tumor hyperfunctioning adenoma can cause 1' hyperaldosteronism Cushing syndrome nonfunctional adenoma seen in 2-8% of population differentiate from metastasis MRI: mets bright on T2 bx follow see: adrenal mass

[NO DESCRIPTION: Not enough sentences on document]

Magnetic resonance imaging (MRI) is a new and innovative technique that affords anatomic images in multiple planes and may provide information on tissue characterization. The Brain TumorMRI demonstrates smaller tumors better than CT, without the need for intrathecal air or contrast material, but larger tumors are well visualized by both CT and MRI. MRI demonstrates smaller tumors better than CT, without the need for intrathecal air or contrast material, but larger tumors are well visualized by both CT and MRI. Acoustic NeuromasMRI demonstrates smaller tumors better than CT, without the need for intrathecal air or contrast material, but larger tumors are well visualized by both CT and MRI. Pituitary TumorsBoth MRI and contrast-enhanced CT are effective in defining pituitary tumors, but MRI may provide more information about the precise extent of the lesions and their effect on adjacent structures. While no large prospective studies comparing MRI with CT are available, preliminary data indicate that tumor staging with MRI is as accurate as with CT.

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Document could not be found]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Document could not be found]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Document could not be found]

[NO TEXT: Document contains no text]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Document contains no text]

[NO DESCRIPTION: Not enough sentences on document]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Document contains no text]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO DESCRIPTION: Not enough sentences on document]

[NO TEXT: Document contains no text]

[NO TEXT: Document could not be found]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Document could not be found]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Document could not be found]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Document could not be found]

[NO TEXT: Document could not be found]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Document could not be found]

[NO TEXT: Document could not be found]

[NO TEXT: Document could not be found]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]

[NO DESCRIPTION: Not enough sentences on document]

adrenal adenoma adrenal angiography adrenal calcification adrenal cyst adrenal hemorrhage adrenal imaging adrenal mass adrenal myelolipoma bilateral adrenal mass choristoma Cushing syndrome Hutchinson syndrome neuroblastoma Pepper syndrome pheochromocytoma Wolman disease

[NO TEXT: Not enough time allocated for Network Connection]

[NO TEXT: Document could not be found]

[NO TEXT: Request did not complete successfully]

[NO TEXT: Not enough time allocated for Network Connection]