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Results for “ADDISON'S DISEASE”

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At least 793 records · Page 44Linked to original sources
PubMed1986

Loperamide, an opiate analogue, inhibits plasma ACTH levels in patients with Addison's disease.

The effects of loperamide, an opiate analogue of the piperidine class on pituitary hormone secretion were evaluated in eight patients with Addison's disease. In all patients loperamide administration (16 mg orally) induced a marked fall in plasma ACTH levels (P less than 0.01), without affecting GH, PRL and LH levels. Plasma ACTH concentration fell significantly from 854 +/- 167 pg/ml (mean +/- SEM) to 460 +/- 123 pg/ml at 60 min (P less than 0.01). The inhibition persisted throughout the whole test period, the nadir being reached at 300 min. Low dose naloxone infusion 180 min after loperamide administration caused plasma ACTH to rise from 181 +/- 61 pg/ml to 539 +/- 99 pg/ml (P less than 0.01). The present data suggest that the opiate analogue loperamide is a potent inhibitor of ACTH secretion in patients with Addison's disease, which may be acting on mu receptors, since its effect is blocked by low doses of naloxone.

Addison Disease↗
PubMed2004

Polymorphisms in the cytotoxic T lymphocyte antigen-4 gene region confer susceptibility to Addison's disease.

The cytotoxic T lymphocyte antigen-4 (CTLA4) gene on chromosome 2q33 encodes a key regulator in the adaptive immune system. The CTLA4 surface molecule is expressed on activated T lymphocytes and involved in down-regulation of the immune response. Previous studies on a possible association between autoimmune Addison's disease and CTLA4 polymorphisms have shown conflicting results. A recent study identified new candidate polymorphisms in the CTLA4 region, influencing gene splicing and thereby the relative abundance of soluble CTLA4. We genotyped 134 patients with Addison's disease and 413 healthy controls from Norway and United Kingdom for these newly identified polymorphisms. Our data demonstrate that the same polymorphisms that have recently been demonstrated to confer susceptibility to autoimmune thyroid disease and type 1 diabetes also confer susceptibility to Addison's disease. This finding suggests that polymorphisms in CTLA4 confer general risk to develop autoimmunity and identifies a potential therapeutic target in the prevention of autoimmune endocrine disorders.

Addison Disease↗
PubMed1993

[Clinical usefulness of adrenal gland computed tomography in the etiologic diagnosis of Addison's disease].

BACKGROUND: The aim of this study was to evaluate adrenal gland morphology by computerized tomography (CT) in the etiologic diagnosis of Addison's disease. METHODS: Twenty-two patients were grouped according to their etiology based on the study of antiadrenal antibodies at diagnosis of the disease: 7 were positive (autoimmune etiology or EAA), 11 were negative (tuberculous etiology or EAT) and in four serologic study was not available (undetermined etiology or EAI). Adrenal gland CT was performed with contiguous sections every 5 mm. In eight cases the examination was carried out upon diagnosis of the disease (initial stage) and in 14 between 2 and 17 years following diagnosis (evolutive stage). RESULTS: In all the patients of the EAA group, examined in either the initial or evolutive stages, the adrenal glands appeared atrophic without calcifications. In the patients of the EAT group adrenal masses of proven tuberculous origin were found in five who were studied in the initial stage and with atrophic glands with calcifications in the remaining patients examined in the evolutive stage, with the exception of two cases with atrophic adrenal glands without calcifications which could serologically be considered as false negatives having autoimmune etiology. The patients in the EAI groups were studied in the evolutive stage with three having atrophic glands with calcifications and one atrophic adrenal glands without calcifications. CONCLUSIONS: Adrenal gland computerized tomography is an useful examination to differentiate between autoimmune or tuberculous origin in Addison's disease. Clinical application may be justified in all patients of recent diagnosis when the study of the antiadrenal antibodies is negative or not possible.

Addison Disease↗