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At least 847 records · Page 47Linked to original sources
PubMed1985

Effect of angiotensin II on plasma ACTH in patients with Addison's disease.

Short-term angiotensin II (AII) infusions (3 ng/kg/min) were performed in 5 patients with Addison's disease in order to assess the effect of AII on ACTH secretion. Base line ACTH levels were elevated due to a 9-h time lag between hydrocortisone administration and onset of the study. In 2 separate infusion periods of 30-min duration, AII had no unidirectional effect on plasma ACTH. Mean ACTH increased slightly but insignificantly. Mean blood pressure rose by about 10 mmHg. The degree of angiotensinaemia induced is probably similar to the state of moderate to severe sodium deficiency. Short-term changes of AII in this order of magnitude have obviously no major effect on ACTH secretion.

Addison Disease↗
PubMed2000

Brittle Addison's disease: a new variation on a familiar theme.

Unstable and unpredictable disease control in diabetes or asthma, with frequent hospitalisations, is frequently referred to as 'brittle'. We describe two cases of Addison's disease with recurrent hospitalisations in hypo-adrenal crises. Both patients had significant psychosocial disruption, and failure to take hydrocortisone replacement therapy was admitted in one and biochemically proven in the other. We propose that 'brittle' Addison's disease in these cases was due to poor treatment compliance related to psychosocial factors. These features have particular similarities with the syndrome of brittle diabetes.

Addison Disease↗
PubMed1989

Lithium treatment of a patient with Addison's disease and affective psychosis.

A female patient born in 1941, who suffers from affective psychosis and Addison's disease, first received lithium carbonate in 1983 during a severe, therapy-resistent depression. With lithium treatment she showed a considerable improvement. In the following months, with a daily dosage of 24.4 mmol, the blood lithium levels were between 0.8 and 0.9 mmol/l. One year later she suffered a severe lithium intoxication after a virus infection. Shortly afterwards, she had a manic and then a depressive phase. She was now put on a regimen of with 12.2 mmol lithium carbonate per day, which produced blood levels between 0.3 and 0.4 mmol/l. In the following years, values of about 0.9 mmol/l were observed several times, therapy and clinical condition remaining unchanged. These spontaneous fluctuations of the blood lithium level, a hitherto unreported phenomenon are discussed as a possible cause of the lithium intoxication. The consequences for clinical practice are outlined.

Addison Disease↗
PubMed1978

Auto-immune Addison's disease in identical twins.

Identical male twins are described, one of whom presented with clinical symptoms of Addison's disease whereas the other was shown to have a deficient adrenal cortical response to stimulation tests. Both had positive adrenal cortex antibodies.

Addison Disease↗
PubMed1984

A case of tuberculous epididymitis associated with Addison's disease.

A 68-year-old man was admitted to the hospital because of loss of appetite, easy fatigability, and skin pigmentation. Physical examination revealed that the bilateral epididymides were enlarged and hard without tenderness. At 7 a.m., the basal cortisol level in the plasma was 22.4 ng/ml and ACTH 318 pg/ml. The clinical diagnosis was Addison's disease. Biopsy of the right epididymis revealed evidence of active tuberculosis. Hydrocortisone (18 mg/day) and anti-tuberculous drugs were administered, and the patient became well and regained his appetite in a week. In this case, laparotomy was not performed, but all clinical findings and the course indicated that adrenal tuberculosis was the most likely cause of Addison's disease. CT scanning of the adrenal region demonstrated large, bilateral, homogeneous, low density, and non-enhancing mass. This is the first report dealing with CT findings of Addison's disease with tuberculous epididymitis.

Addison Disease↗
PubMed1990

Adrenomyeloneuropathy presenting as Addison's disease in childhood.

Adrenoleukodystrophy, a sex-linked peroxisomal disorder that results in the impaired oxidation of long-chain saturated fatty acids and causes neurologic impairment, is a rare cause of Addison's disease in children. Adrenomyeloneuropathy is the name given to a biochemically identical but milder and more slowly progressive variant of adrenoleukodystrophy that affects young adults, in whom adrenal insufficiency may long precede nervous system dysfunction. The transmission of adrenomyeloneuropathy, like that of most cases of adrenoleukodystrophy, is sex-linked. Because of a preponderance of male patients among a group of patients with the onset of adrenal failure in childhood, we questioned whether this condition might be the initial manifestation of adrenomyeloneuropathy. We therefore measured the plasma concentrations of very-long-chain saturated fatty acids in eight patients with adrenal insufficiency; of these, five had elevated plasma hexacosanoic acid concentrations (range, 2.42 to 6.43 mumol per liter; mean normal level [+/- SD], 0.83 +/- 0.45), confirming the presence of adrenomyeloneuropathy. Magnetic resonance imaging showed clear evidence of brain involvement in all five patients. Reexploration of the family histories revealed additional missed cases. We conclude that the possibility of adrenomyeloneuropathy should be considered in any boy with Addison's disease.

Addison Disease↗
PubMed1989

[Addison's disease as a continuously difficult diagnostic problem].

A case of latent adrenocortical insufficiency is described, which had various masks in the initial period. The progressing course of the disease and two operations as well as other trials of elucidating the cause of the disease failed to give the final diagnosis. Only an adrenocortical crisis during virus hepatitis confirmed the earlier suspicion of Addison's disease.

Addison Disease↗
PubMed1988

The pancreas in idiopathic Addison's disease--a search for a prediabetic pancreas.

Autopsy pancreases were studied from 14 patients who had idiopathic Addison's disease. One patient had been diabetic for 12 years and three patients were found to be diabetic during their terminal admission. While there was no evidence of diabetes or destruction of insulin-secreting beta cells in the remaining 10 patients, islets in one pancreas exhibited many of the histological and immunohistochemical features seen in the patients with recent onset diabetes. These included the presence of alpha-interferon in endocrine cells, hyper-expression of class I major histocompatibility complex molecules by endocrine cells in islets where alpha-interferon was also present, aberrant expression of class II major histocompatibility complex molecules by endocrine cells and the presence of insulitis. Since the combination of these changes has only been described in type 1 diabetes it is thought that the appearances seen in this pancreas were those of prediabetes.

Addison Disease↗