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Results for “ADDISON'S DISEASE”

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PubMed1993

[Hyperpigmentation in primary adrenal cortex insufficiency: Addison disease].

Diffuse hyperpigmentation of the skin may develop without preceding inflammatory skin disease or be associated with various inflammatory disorders. The differential diagnosis of the diffuse hyperpigmentation is complex and difficult. We present a 36-year-old woman with diffuse hyperpigmentation caused by adrenal insufficiency, with special reference to the diagnosis and differential diagnosis of hyperpigmentation associated with endocrine disorders. In addition, metabolic, toxic, nutritional and internal factors and the skin-associated diseases leading to hyperpigmentation are categorized. A classification of diffuse hyperpigmentation is presented.

Addison Disease↗
PubMed1996

[Asymptomatic Addison disease: cause of striking reduction of insulin requirements in a patient with diabetes, Hashimoto thyroiditis and Basedow disease].

We report a 30 years old woman with sporadic poliglandular autoimmune syndrome type II, first seen with an insulin-dependent diabetes mellitus and a Graves-Basedow disease that became spontaneously hypothyroid with positive antimicrosomal antibodies. Six years later she presented with persistent vomiting and a remarkable reduction in insulin requirements. She had low basal and stimulated-cortisol levels and the diagnosis of severe adrenal failure was reached. A CT scan showed normal adrenal glands, she did not have cutaneous hyperpigmentation nor evidences of mineralocorticoid deficit. A selective autoimmune damage of the fascicular zone was assumed but a selective damage of ACTH producing pituitary cells cannot be discarded. The importance of investigating adrenal function in cases of unexplained reduction of insulin requirements is emphasized.

Addison Disease↗
PubMed2001

[Is there an indication for dehydroepiandrosterone (DHEA) treatment in elderly women with Addison disease? Beneficial and adverse effects of DHEA].

DHEA is a cetosteroid secreted by the adrenal gland. Serum levels of DHEA decline by an average of 10% per decade whereas cortisol levels remain stable. The relative lack of DHEA secretion in elderly people has been called adrenopause. The daily administration of 50 mg of DHEA to women over 60 years old results in a two-fold increase in serum level of testosterone and androstenedione and in a 10% increase of estradiol in men. A 10 to 20% increase of IGF-1 is observed in both sexes. In women over 70 years old treated by 50 mg/day of DHEA for 6 months an improvement of bone turnover and of skin status was observed as well as an increase of overall well-being and of libido. These beneficial psychological effects have also been observed in younger men and women with adrenal insufficiency. In men 50 to 65 years old, 100 mg/day of DHEA for 6 months could slightly increase the lean body mass and the muscle strength. Moreover DHEA could increase immune function and NK cell activity. As there are no actual data about cardio-vascular and oncological risks of a prolonged treatment with DHEA, the administration of this steroid must still be considered experimental. Previous or present cancer of the breast or of the prostate is an absolute contraindication to DHEA treatment.

Addison Disease↗
PubMed2002

Coeliac disease and autoimmune Addison's disease: a clinical pitfall.

BACKGROUND: Coeliac disease has an increased prevalence in a number of autoimmune endocrine conditions. An association between coeliac disease and Addison's disease has been proposed in isolated case reports, but has not been formally studied. AIM: To investigate the extent of this association. DESIGN: Prospective screening of patients with confirmed Addison's disease. METHODS: From central computerized records, we identified all living patients with a diagnosis of autoimmune Addison's disease in the past 30 years and presently attending our affiliated hospitals. After exclusions, 44 were invited to attend for screening. RESULTS: Of 41 patients screened, five (12.2%) had coeliac disease: Three were previously diagnosed coeliacs and this was confirmed on review, including examination of biopsy material. A further two had positive IgA-endomysial antibodies. Histological confirmation was obtained in both cases. Neither had laboratory or clinical evidence of malabsorption. DISCUSSION: In this series of patients with Addison's disease, a higher co-morbidity with coeliac disease was observed than in any previously studied endocrine condition. We recommend that coeliac serology (anti-endomysial and tissue transglutaminase antibody) testing be incorporated routinely into the autoimmune screen for other conditions in patients with Addison's disease.

Addison Disease↗
PubMed1987

Dermatitis herpetiformis and celiac disease associated with Addison's disease.

We treated two patients with dermatitis herpetiformis and Addison's disease, and one patient with celiac disease without the rash, but with Addison's disease and juvenile diabetes. In two of the patients, the concomitant diseases also included a thyroid disease. The predisposing factors to the multiple endocrine disorders in these patients with gluten-sensitive skin and/or small intestinal disease remained unknown. Two of the three patients had HLA-B8, none was known to have affected relatives, and the Addison's disease appeared before, at the same time, or after the patients contracted dermatitis herpetiformis or celiac disease.

Addison Disease↗
PubMed2006

Genetic association studies of the FOXP3 gene in Graves' disease and autoimmune Addison's disease in the United Kingdom population.

Regulatory T lymphocytes play a crucial role in modulating potentially self-reactive clones, and dysfunction of this cell type contributes to autoimmune disease. FOXP3 is a critical determinant of CD(4+)CD(25+)T regulatory (T(reg)) cell development and function. The aim of this study was to investigate whether genetic polymorphisms at the FOXP3 locus predispose to autoimmune endocrinopathies. Five single nucleotide polymorphisms (SNPs) and two microsatellite polymorphisms were genotyped in our Caucasian cohorts of 633 unrelated Graves' disease (GD) subjects, 104 autoimmune Addison's disease (AAD) subjects and 528 healthy controls. SNP genotyping was performed by either restriction enzyme digestion or by primer-extension-MALDI-TOF (matrix-assisted laser desorption/ionisation time-of-flight) assay. Microsatellites were analysed using fluorescent PCR. Case-control analysis was performed using chi(2) testing on contingency tables for allele frequency. Haplotype analysis was performed using the UNPHASED package. No evidence for disease association was found with any of the seven polymorphisms in either of the GD or AAD subjects as compared with controls (P = 0.26-0.94). Haplotype analysis found a weak evidence for the association of a minor haplotype with GD; this was not significant when corrected for multiple testing. This study has found no robust evidence that FOXP3 gene polymorphism contributes to the susceptibility to GD or AAD in the UK population.

Addison Disease↗