PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “ADDISON'S DISEASE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed1985

Clinical clues to the cause of Addison's disease.

Tuberculosis and other potentially treatable diseases remain important causes of adrenal insufficiency. Knowledge of the cause of adrenal destruction, although often difficult to ascertain clinically, is necessary for appropriate management. Clinical data are reviewed in eight patients with Addison's disease who underwent computed tomographic scanning and in 31 additional patients with Addison's disease in whom autopsy was performed. Seven of eight patients (87 percent) with tuberculous Addison's disease of no greater than two years' duration had enlarged glands whereas patients with longer duration of disease had smaller or normal-sized glands. Adrenal enlargement was also found in five of six (87 percent) subjects with carcinomatous replacement of the adrenal glands. The adrenal glands were small or undetectable in each of 16 patients with idiopathic Addison's disease. Adrenal calcification was found in nine of 17 (53 percent) tuberculous patients and was not found in any of the 22 other patients. Duration of adrenal disease, adrenal size on computed tomographic scanning, and presence of adrenal calcification were useful clues to the cause of Addison's disease.

Addison Disease↗
PubMed1984

Metastases to the adrenal glands and the development of Addison's disease.

Metastases to the adrenal glands are common in patients with cancer but symptomatic Addison's disease is rarely noted in this population. The development of body computerized tomography (CT) allows the diagnosis of adrenal metastases to be made more readily antemortem. From 1980 to 1981, 19% (4/21) of patients at the Massachusetts General Hospital who had metastatic cancer and who were noted to have enlarged adrenal glands on CT also had or developed symptomatic adrenal insufficiency. The case histories of 8 patients with Addison's disease and one patient with adrenal hemorrhage on the basis of metastatic infiltration are reviewed. Since adrenal insufficiency may develop abruptly in this group of patients, it is suggested that prophylactic maintenance glucocorticoid therapy be initiated as soon as the diagnosis of adrenal metastases is made.

Addison Disease↗
PubMed2006

[Addison's disease as a rare cause of chronically elevated liver enzymes].

Common causes of chronically elevated serum liver enzymes include fatty liver disease, chronic viral hepatitis, autoimmune hepatitis, or hereditary metabolic disorders. Adrenocortical insufficiency can also cause elevated liver enzymes. Since 1990 only 11 cases have been reported. We here report a 52-year-old man with elevated liver enzymes (1.5 x upper limit of normal) over the past 10 years. Furthermore, hyponatremia and hyperkalemia were noted. He complained of fatigue and low blood pressure over the past few years. At physical examination a dark complexion was noted. After ruling out chronic viral hepatitis, autoimmune disease, metabolic or hereditary disorders, rare causes of elevated liver enzymes were considered. The endocrinological work-up revealed Addison's disease as cause of serum electrolyte disturbance and elevated liver enzymes. The patient was successfully treated with hydrocortisol and fludrocortisol. After one week, liver enzymes, serum electrolytes and arterial blood pressure had normalized. In conclusion, for patients with constantly elevated liver enzymes also rare, extrahepatic diseases have to be considered. Addison's disease is a rare but fully reversible cause for elevated liver enzymes.

Addison Disease↗
PubMed2006

[Differential diagnosis of anorexia nervosa and depression. A case report of Addison's disease in a female patient].

Similar symptoms make the differential diagnosis of anorexia nervosa and Addison's disease difficult at times: vomiting, weight loss, hypotension, depressed mood, reduced drive, and increased irritability can occur in both disorders. Psychological factors are then frequently presumed to be causative, so that the diagnosis of Addison's disease is made only years after the onset of the disease. Against this background, our case report presents important differential features, particularly with regard to consultative psychiatry.

Addison Disease↗
PubMed1987

Addison's disease: immunological aspects.

The frequency of HLA DR3 in patients with Addison's disease is increased and the relative risk factor rises to 10 when adrenocortical failure is part of a polyendocrinopathy.

Addison Disease↗
PubMed1978

Gastrin secretion in Addison's disease.

Out of a score of patients known as suffering from Addison's disease, tuberculosis was the cause in 7, and their serum fasting gastrin levels were normal, averaging 52 pg/ml. For the 14 remaining cases, with the auto-immune variety of the disease, there were high gastrin levels in 3; in 2 out the 11 others, with values within the normal range, there was total achlorhydria. Could it be that gastrin-secreting cells might occasionally be involved in auto-immune endocrine disorders?

Addison Disease↗
PubMed1985

Clinical presentation, growth, and pubertal development in Addison's disease.

The clinical course of eight boys and six girls with Addison's disease has been reviewed. Adrenal antibodies were found in five boys and five girls, and four children showed clinical evidence of other autoimmune disease (hypoparathyroidism (three); diabetes (one)). The presentation was insidious in 12 children but acute in two. On treatment, linear growth was normal and, with the exception of one girl with theca cell antibodies, pubertal development proceeded normally in the older patients.

Addison Disease↗
PubMedDate not supplied

[Hypogammaglobulinemia of variable expression, Addison's disease, Dubin-Johnson's disease].

A girl aged 12 with hypogammaglobulinaemia is described who developed Addison's disease with adrenal antibodies at the age of eight. This unusual finding is rarely seen in childhood except in the syndrome of juvenile familial polyendocrinopathy and mucocutaneous moniliasis. By chance the child also had Dubin-Johnson syndrome which could alter the metabolism of therapeutically administered drugs and steroids.

Addison Disease↗
PubMed2005

Dehydroepiandrosterone replacement in patients with Addison's disease has a bimodal effect on regulatory (CD4+CD25hi and CD4+FoxP3+) T cells.

Oral replacement of the near-total deficiency of dehydroepiandrosterone (DHEA) in patients with Addison's disease (adrenal insufficiency) enhances mood and well-being and reduces fatigue. We studied the immunological effects of 12 wk of oral DHEA treatment in ten patients with Addison's disease receiving their normal mineralo- and glucocorticoid hormone replacement. We found that baseline circulating regulatory T cells were reduced in Addison's disease patients compared to controls, a hitherto unrecognised defect in this disorder. Oral DHEA treatment had a bimodal effect on naturally occurring regulatory (CD4+CD25hiFoxP3+) T cells and lymphocyte FoxP3 expression. Oral DHEA replacement restored normal levels of regulatory T cells and led to increased FoxP3 expression. These effects were probably responsible for a suppression of constitutive cytokine expression following DHEA withdrawal. In contrast, oral DHEA treatment led to reduced FoxP3 expression induced by TCR engagement and so augmented the cytokine response, but without a bias towards the Th1 or Th2 phenotype. NK and NKT cell numbers fell during DHEA treatment, and homeostatic lymphocyte proliferation was increased. We conclude that DHEA replacement in Addison's disease has significant immunomodulatory properties and propose that it has a greater impact on the human immune system than would be expected from its classification as a dietary supplement.

Addison Disease↗