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PubMed1977

[Simultaneous occurrence of juvenile diabetes and Addison's disease (author's transl)].

The occurrence of diabetes mellitus and Addison's disease together is discussed by the authors. The female patient described here had diabetes at the age of four; Addison's disease appeared when the patient was 19 years old. Four years prior to the appearance of Addison's disease, an ophthalmoscopic examination revealed microaneurysms. The examination of the fundus of the eye was negative when Addison's disease, was diagnosed. An HLA-B8 antigen positivity was established. The authors discussed the pathogenetic relationship of HLA-B8 antigen positivity, diabetes mellitus, and Addison's disease.

Addison Disease↗
PubMed1997

The prevalence of Addison's disease in Coventry, UK.

The prevalence of Addison's disease (chronic adrenal failure) has not been widely investigated and is usually given as 39 in a million. We conducted a prevalence study using a postal survey of general practitioners in Coventry. Three quarters (139/188) replied, representing 79/85 (93%) of the practices. Thirty cases of Addision's disease were found from a total patient list of 323852, of which a third were tuberculous in origin and two-thirds non-tuberculous (12/30 autoimmune, 8/30 unclassified). We conclude that Addison's disease is 2.4 times more common than previously reported. The tuberculous group was older, 65 vs 52 years (p < 0.05), and had had the disease for longer than the non-tuberculous group, 20 vs 12 years (p < 0.05). There was no significant difference in the age at diagnosis.

Addison Disease↗
PubMedDate not supplied

Clinical profile and prognosis of Addison's disease in India.

BACKGROUND: The clinical presentation of primary adrenocortical insufficiency (Addison's disease) in India may differ from that in developed countries. We therefore studied the clinical profile and prognosis of Addison's disease, with special reference to patients with tuberculous infection. We also evaluated the utility of various clinical parameters in differentiating tuberculous from idiopathic Addison's disease. METHODS: In a retrospective and prospective study, 45 consecutive patients of Addison's disease (20 patients with tuberculous aetiology) were studied for their clinical features, autoantibody profile (adrenal cytoplasmic, thyroid microsomal and gastric parietal cell antibodies) and prognosis. RESULTS: A tuberculous aetiology was present in 47% of the patients and of these, 85% had enlargement of one or both adrenal glands. While patients with tuberculous Addison's disease had a higher prevalence of extra-adrenal tuberculosis (55% v. 9%, p = 0.001), a lower frequency of adrenal cytoplasmic antibodies (17% v. 50%, p = 0.03) and parietal cell or thyroid microsomal antibodies (11% v. 55%, p = 0.004), a considerable overlap was observed. Despite adverse circumstances, during a mean follow up of 3.3 years, only 2 (5%) patients died, neither of whom had tuberculous involvement. Five (13%) patients suffered from one or more episodes of Addisonian crises, though none of these resulted in mortality. CONCLUSION: Tuberculosis remains an important cause of Addison's disease in India. The presence of extra-adrenal tuberculosis, or lack of adrenal cytoplasmic antibodies, does not, with certainty, differentiate between a tuberculous and idiopathic aetiology. The prognosis of Addison's disease was good despite unfavourable circumstances.

Addison Disease↗
PubMed1987

Pituitary enlargement associated with Addison's disease.

We report a case of Addison's disease with pituitary enlargement which could easily have been misinterpreted as a pituitary adenoma or other pituitary disease. Serial computed tomography following replacement therapy was essential to confirm the diagnosis.

Addison Disease↗
PubMed1986

Addison's disease without pigmentation.

Four cases of Addison's disease are described in whom the diagnosis was unexpected or dangerously delayed because of the absence of pigmentation.

Addison Disease↗
PubMed1996

[Autoimmune Addison's disease. Current knowledge and prospects].

Idiopathic Addison's disease (IAD) is a chronic organ-specific autoimmune disease sometimes associated with other autoimmune endocrine diseases. The prevalence is 50-100/million with an incidence of 5-6 cases/million/year. A genetic predisposition to this disease has been reported in subjects with phenotype HLA-DR3, -DR4, -A1, -B8 or HLA-A28, -B8; a phenotype HLA-B8 has been described in subjects with adrenal autoantibodies (AA) not progressing toward an overt disease. There is strong evidence that AA can play a pathogenic role or at least can be considered good immunological markers in IAD. AA may damage adrenal function by a cytotoxic process directed at adrenal cell surface or other intracellular antigens. An antigenic activity has been recently attributed to P450c enzymes and in particular to P450c21. Clinical manifestations of IAD can be preceded by a long period of subclinical adrenocortical impairment, characterized only by the presence of AA with or without adrenocortical function findings. In our experience, where AA titers were 1:8 or higher, progression of adrenal disease was likely with time. A spontaneous remission can indeed occur with lower titers, especially in early stages of subclinical adrenal insufficiency. Finally, a reversal of previously significant AA positive titers in patients in more advanced stages of subclinical adrenal insufficiency seems to be induced by corticosteroid therapy.

Addison Disease↗