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At least 937 records · Page 52Linked to original sources
PubMed1993

[B cell malignant lymphoma complicated with partial Addison's disease, report of a case].

A 58-year-old man was admitted in May 1988, because of high fever, skin, pigmentation and body weight loss. Abdominal ultrasonography and generalized computed tomography examinations showed swelling of general lymph nodes and bilateral adrenal glands, splenomegaly, and lesion in the liver. Serum cortisol, urinary 17-OHCS and 17-KS level were within the normal range, while the ACTH level was elevated (189.9 pg/ml). ACTH overload test showed a non-reactive pattern, leading to a diagnosis of partial Addison's disease. He was also diagnosed as non-Hodgkin lymphoma, diffuse, large cell type (B) by a biopsy of the left supraclavicular lymph node. After combination chemotherapy, swelling of the supraclavicular lymph node diminished, followed by normalization of ACTH level and improvement of symptoms. Abdominal lymphadenopathy, hepatosplenomegaly and swelling of adrenal glands also decreased in size. Although involvement of tumor cells in adrenal glands sometimes occurs in malignant lymphoma, it is reported that more than 90% destruction of adrenal gland tissue is necessary to develop Addison's disease. It was suggested that the involvement of many lymphoma cells in both adrenal glands resulted in the development of partial Addison's disease in this case.

Addison Disease↗
PubMed1987

Effects of fludrocortisone withdrawal on plasma angiotensin II, ACTH, vasopressin, and potassium in patients with Addison's disease.

UNLABELLED: We attempted to answer to the question whether excessive rises in endogenous plasma angiotensin II (AII) stimulate ACTH secretion by measuring PRA, AII, AVP, ACTH, and cortisol in 8 patients with Addison's disease before and after withdrawal of fludrocortisone substitution. Blood was drawn at 14.30 h, exactly 6 1/2 h after the morning dose of hydrocortisone had been taken. PRA and AII were initially higher than normal in 4 patients. After withdrawal of fludrocortisone for 1 or 2 weeks, PRA and AII rose markedly in 4 patients (up to 260 ng/l) without concomitant changes in plasma ACTH levels (r = -0.081, AII vs ACTH). Changes in plasma cortisol could not have obscured a stimulatory effect of AII on ACTH by variable feedback inhibition of ACTH release. The increase in plasma AII levels in the 4 patients was larger than that observed in a previous study in normal subjects after rigorous dietary sodium restriction. In all patients, hyperkalaemia developed after fludrocortisone withdrawal, independent of changes in PRA and AII. Rises in PRA, AII, and plasma potassium were partially reversed by increased sodium intake and further suppressed by resumption of fludrocortisone therapy. Plasma AVP remained in the normal range after fludrocortisone withdrawal, but was slightly elevated after increasing salt intake without fludrocortisone administration. CONCLUSIONS: Rises of endogenous plasma AII to levels tenfold higher than normal do not stimulate ACTH release. AII is probably not a physiological modulator of ACTH secretion. Mineralocorticoid substitution in Addison's disease should be monitored by plasma potassium measurement. Hyperkalaemia may coexist with normal PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

Addison Disease↗
PubMed1975

Bilateral adrenal enlargement in Addison's disease caused by tuberculosis. Nephrotomographic demonstration.

Nephrotomography showed markedly enlarged adrenal glands in a 67-year-old man with acute Addison's disease due to tuberculosis. Other causes of acute adrenal insufficiency associated with enlarged adrenals are histoplasmosis and, rarely, bilateral metastatic carcinoma, amyloidosis, or hemorrhage. Radiologic demonstration of large adrenal glands in a patient with acute Addision's disease should strongly suggest an infectious etiology.

Addison Disease↗
PubMed1981

Addison's disease presenting as a hypercalcemic crisis in a patient with idiopathic hypoparathyroidism.

A patient with idiopathic hypoparathyroidism complicated by Addison's disease is described. The development of adrenal insufficiency was accompanied by a hypercalcaemic crisis. The hypercalcaemia appeared to result from a reduction in the filtered load and enhanced renal tubular reabsorption of calcium. Cortisone therapy was followed by the characteristic renal tubular leak of calcium associated with hypoparathyroidism and a return of the serum calcium to normal. The possible mechanisms for these changes in calcium homeostasis are discussed.

Addison Disease↗
PubMed1996

X-linked adrenoleukodystrophy is a frequent cause of idiopathic Addison's disease in young adult male patients.

X-Linked adrenoleukodystrophy (ALD) is a genetic disease associated with demyelination of the central nervous system, adrenal insufficiency, and accumulation of very long chain fatty acids in tissue and body fluids. ALD is due to mutation of a gene located in Xq28 that encodes a peroxisomal transporter protein of unknown function. The most common phenotype of ALD is the cerebral form (45%) that develops in boys between 5-12 yr. Adrenomyeloneuropathy (AMN) involves the spinal cord and peripheral nerves in young adults (35%). Adrenal insufficiency (Addison's disease) is frequently associated with AMN or cerebral ALD and may remain the only clinical expression of ALD (8% of cases). The prevalence of ALD among adults with Addison's disease remains unknown. To evaluate this prevalence, we performed biochemical analysis of very long chain fatty acids in 14 male patients (age ranging from 12-45 yr at diagnosis) previously diagnosed as having primary idiopathic adrenocortical insufficiency. In 5 of 14 patients (35%), elevated plasma concentrations of very long chain fatty acids were detected. None of these patients had adrenocortical antibodies. By electrophysiological tests and magnetic resonance imaging it was determined that two patients had cerebral ALD, one had adrenomyeloneuropathy with cerebral involvement, and two had preclinical AMN. Our data support the hypothesis that ALD is a frequent cause of idiopathic Addison's disease in children and adults.

Addison Disease↗