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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an average 30 years of follow-up study, seven of 22 patients with primary adrenal insufficiency have had cardiac failure. Comparison of these seven with the 15 who remain free of this complication revealed that the former group were somewhat older and had higher incidences of unrelated cardiac disease and of nonsteroid-dependent hypertension, but that their replacement regimens, with respect to sodium supplementation and sodium-retaining steroids, were identical with the latter. Coincident with the appearance of cardiac failure, all seven patients had a decrease in sodium requirements. Adequate control of the adrenal disease was subsequently possible with elimination of mineralocorticoid support in one of the six who had initially required this therapy and a reduction in dosage in the other five. In all seven, dietary sodium supplements were no longer required. In three patients with severe failure, sodium restriction was imposed and diuretics were added, although the latter therapy has required close monitoring to avoid sodium depletion.
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PMID:Cardiac failure in Addison's disease. 683 6

We report on 2 newborns with adrenal cysts who were treated successfully with an operation. One patient had been well after birth with no adrenal insufficiency. However, 2 large and 2 small cysts were found, all of which were attached to the adrenal gland without a clear vascular stalk. The other patient had adrenal cortical insufficiency. His mother had had gestational diabetes and hypertension during pregnancy. The adrenal cyst was partially resected. Both patients were in good condition 5 years postoperatively.
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PMID:Adrenal cysts in the newborn. 685 47

Nephrotic syndrome in children is a very common disease in Thailand. Most of the patients respond well to oral prednisolone treatment but side effects of the drug especially adrenal insufficiency remains a threat to all. We studied the adrenal function by studying the response to ACTH stimulation test in 14 Thai children, nine girls and five boys, with idiopathic nephrotic syndrome: immediately, 3, 6 and 9 months after discontinuation of oral prednisolone treatment. Average age on entry to the study was 104.4 months (25-183 months). Prednisolone was given every day for 29 days (6-64 days) then every other day for 542 days (178-1,562 days). Side effects of steroid treatment were gross obesity BMI > 30 (one patient), moderate hypertension (one patient), and marked cushingoid features (two patients). ACTH stimulation tests were normal in 64 per cent of patients within 7 days, 64 per cent at 3 months, 73 per cent at 6 months, and 90 per cent at 9 months after discontinuation of oral prednisolone. We suggest that adrenal insufficiency has to be considered in all children on prolonged prednisolone unit at least 9 months of treatment-free period.
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PMID:Adrenal function after prednisolone treatment in childhood nephrotic syndrome. 779 46

Seventy-two long-surviving liver transplant recipients were evaluated prospectively, including a baseline allograft biopsy for weaning off of immunosuppression. Thirteen were removed from candidacy because of chronic rejection (n = 4), hepatitis (n = 2), patient anxiety (n = 5), or lack of cooperation by the local physician (n = 2). The other 59, aged 12-68 years, had stepwise drug weaning with weekly or biweekly monitoring of liver function tests. Their original diagnoses were PBC (n = 9), HCC (n = 1), Wilson's disease (n = 4), hepatitides (n = 15), Laennec's cirrhosis (n = 1), biliary atresia (n = 16), cystic fibrosis (n = 1), hemochromatosis (n = 1), hepatic trauma (n = 1), alpha-1-antitrypsin deficiency (n = 9), and secondary biliary cirrhosis (n = 1). Most of the patients had complications of long-term immunosuppression, of which the most significant were renal dysfunction (n = 8), squamous cell carcinoma (n = 2) or verruca vulgaris of skin (n = 9), osteoporosis and/or arthritis (n = 12), obesity (n = 3), hypertension (n = 11), and opportunistic infections (n = 2). When azathioprine was a third drug, it was stopped first. Otherwise, weaning began with prednisone, using the results of corticotropin stimulation testing as a guide. If adrenal insufficiency was diagnosed, patients reduced to < 5 mg/day prednisone were considered off of steroids. The baseline agents (azathioprine, cyclosporine, or FK506) were then gradually reduced in monthly decrements. Complete weaning was accomplished in 16 patients (27.1%) with 3-19 months drug-free follow-up, is progressing in 28 (47.4%), and failed in 15 (25.4%) without graft losses or demonstrable loss of graft function from the rejections. This and our previous experience with self-weaned and other patients off of immunosuppression indicate that a significant percentage of appropriately selected long-surviving liver recipients can unknowingly achieve drug-free graft acceptance. Such attempts should not be contemplated until 5-10 years posttransplantation and then only with careful case selection, close monitoring, and prompt reinstitution of immunosuppression when necessary.
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PMID:Weaning of immunosuppression in long-term liver transplant recipients. 783 42

Tests for adrenal hormone abnormalities are important in the investigation of endocrine hypertension and adrenal insufficiency. This article assesses the suitability of the available tests. Particular attention is paid to the specificity and sensitivity of tests to exclude phaeochromocytoma and Cushing's syndrome.
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PMID:Adrenal profiles. 808 67

A 46-year-old man with known arterial hypertension for 10 years had, over the last two years, developed increasing obesity, particularly of the trunk, with other symptoms typical of Cushing's syndrome. Hormone analysis demonstrated hypercortisolism and decreased plasma ACTH concentration. The dexamethasone inhibition test failed to show any significant suppression of serum cortisol. Plasma ACTH was not increased in the corticotrophin-releasing hormone and the metyrapone tests. In the short ACTH test there was an excessive cortisol increase. Abdominal computed tomography revealed both adrenals to be enlarged (6 x 4 cm) and coarsely nodular. Adrenolytic treatment with ketoconazole (400 mg daily) caused symptoms of adrenal insufficiency, but a reduced dosage of 200 mg daily lowered the cortisol level to between 5 and 11 micrograms/dl and normalized the blood pressure and clinical signs of Cushing's syndrome disappeared. Subsequent bilateral adrenalectomy confirmed the diagnosis of massive macronodular adrenal hyperplasia. Substitution treatment with twice daily 25 mg cortisone acetate and 0.05 mg fludrocortisone was started postoperatively.
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PMID:[Bilateral massive macronodular adrenal gland hyperplasia. A rare cause of Cushing's syndrome]. 830 53

In its classical form, congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency is characterized by hypertension and abnormal sexual development. Suppression of ACTH secretion by means of administering glucocorticoids fulfills the therapeutic goal of reducing blood pressure and decreasing androgen production. The present report describes the case of a patient suffering from congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency who developed an acute adrenal crisis, unprovoked by stress, following interruption of glucocorticoid replacement therapy. It is suggested that patients on a suppressive dose of glucocorticoids for adrenal hyperplasia are at increased risk for acute adrenal insufficiency if therapy is interrupted, and that deoxycorticosterone (DOC) in the absence of a glucocorticoid is insufficient to prevent manifestations of adrenal crisis.
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PMID:Acute adrenal crisis complicating hypertensive congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency. 844 9

We reviewed 14 male and 9 female patients with adrenal tumor discovered incidentally by imaging studies in an attempt to assess adrenal function, mainly cortical function. Pathological diagnosis consisted of cortical adenoma in 12 patients, cortical nodular hyperplasia in 2, medullary hyperplasia in 1, cavernous hemangioma in 1, metastatic tumor in 4 and cyst in 2. Another adrenal cyst was diagnosed by percutaneous puncture. In all patients peripheral levels of plasma cortisol and aldosterone were normal. Plasma catecholamine levels were also normal except for 1 patient with medullary hyperplasia who had equivocal elevation. Among the patients with cortical adenoma and hyperplasia, however, 5 of 10 (50%) had excessive excretion of 24-hour urinary 17-hydroxycorticosteroids, 4 of 13 (31%) had a loss of plasma cortisol circadian rhythm and 7 of 14 (50%) had insufficient suppression on the dexamethasone test. Furthermore all patients had an increased ipsilateral uptake that was not suppressed after dexamethasone on 131iodine-adosterol scintigraphy, while a diminished contralateral uptake was noted in 5 of 15 (33%). Postoperatively, hypertension decreased to normal in 2 of 3 patients and impaired glucose tolerance was improved in 1 of 2. Two patients with cortical adenoma who exhibited a loss of plasma cortisol circadian rhythm experienced postoperative adrenal insufficiency. These data indicate that a considerable number of incidentally discovered adrenal tumors are not nonfunctioning particularly in reference to glucocorticoid secretion, and adrenalectomy seems to be beneficial in some of those patients with hypertension or impaired glucose tolerance.
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PMID:Clinical experience of incidentally discovered adrenal tumor with particular reference to cortical function. 851 Feb 81

As a potent antagonist of glucocorticoid and progesterone receptors, mifepristone (RU-486) has potential use in the treatment of Cushing's syndrome. Initial research in this area has demonstrated that RU-486 acts as an anti-glucocorticoid by antagonizing the negative feedback on the pituitary of endogenous and exogenous glucocorticoids. Since 1985, the literature has reported four studies of the feasibility of RU-486 treatment in Cushing's syndrome patients. In the largest of these studies, 11 patients with inoperable adrenal cancer or ectopic adrenocorticotrophic hormone-secreting neoplasms received 5-22 mg/kg/day of RU-486 for 1-12 months. In seven of these patients, treatment resulted in marked improvement in the Cushingoid phenotype, psychiatric status, hypertension, and carbohydrate intolerance. Three patients discontinued RU-486 because of clinical manifestations of adrenal insufficiency. The most common side effect was nausea. Titration of RU-486 dosing remains imprecise due to the lack of an acceptable rapid biochemical measurement to monitor glucocorticoid action. Regrettably, further research in this area has been hindered by the political controversy regarding RU-486's use as an abortifacient agent.
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PMID:Mifepristone: treatment of Cushing's syndrome. 873 15

Neurofibromatosis type 1 is the most common autosomal dominant inheritable disease, which is often associated with secondary forms of hypertension and with tumors of neuroectodermal origin. The authors present the results of evaluation of 60 members of 3 families. Of the 60 family members, 13 subjects had symptoms of neurofibromatosis type 1 disease, of which 7 subjects were evaluated. The case histories of patients are discussed: (1) An incidentally discovered adrenal tumor was proved to be a pheochromocytoma. (2) Because of complaints similar to thyrotoxicosis, thyrostatic drugs were administered for years without effect and, finally, an adrenal phaeochromocytoma was diagnosed after the presence of neurofibromatosis was established. (3) Preeclamptic pregnancy of a young primigravida complicated with severe HELLP syndrome (hemolysis-elevated liver enzymes-low platelet count) led to thorough evaluation which revealed renal artery stenosis. In this patient, percutaneous renal artery angioplasty resulted in a complete cessation of hypertension. (4) Glucocortocoid replacement therapy in a patient with neurofibromatosis type 1 resulted in a complete normalization of both secondary adrenal insufficiency and a previously unexplained iron-refractor iron-deficient anemia. The case histories of the patients demonstrate a lack of in-depth knowledge of neurofibromatosis in clinical practice. A regular follow-up of neurofibromatosis patients is suggested in specialized health centers.
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PMID:[Endocrinologic complications of neurofibromatosis type 1]. 899 16


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