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At least 811 records · Page 45Linked to original sources
PubMed1977

Immunological studies in the neonate of a mother with Addison's disease and diabetes mellitus.

In a baby born to a mother who had idiopathic (autoimmune) Addison's disease and gestational insulin-dependent diabetes, antibodies to adrenal cortex and to pancreatic islet cells were demonstrated in the cord blood and serum for at least 41 days. There was no clinical or objective evidence of adrenocortical failure or of disturbed carbohydrate tolerance in the baby.

Addison Disease↗
PubMed1987

Addison's disease secondary to lymphomatous infiltration of the adrenal glands. Recovery of adrenocortical function after chemotherapy.

This case represents the first known instance of reversal of Addison's disease after antineoplastic therapy. Malignant infiltration of the adrenal glands was demonstrated by cytologic findings of needle biopsy in a 57-year-old man suffering from disseminated large cell lymphoma and Addison's disease. He was treated with combination chemotherapy and adrenal hormone replacement. Improvement shown in his computed tomography (CT) scan and clinical status led to the successful discontinuance of cortisone and 9-alpha fluorohydrocortisone. Basal adrenal function and response to ACTH stimulation recovered.

Addison Disease↗
PubMed1983

Case 47, part II: Oral hyperpigmentation associated with Addison's disease.

This case is interesting in several respects. Although diffuse oral hyperpigmentation is suggestive of Addison's disease and should prompt the latter to be a prominent potential diagnosis in any setting, diagnosis was delayed by lack of constitutional and systemic symptoms, normal preliminary hematologic and electrolytic laboratory data, and the strong opinion of the pathologist that the oral mucosal biopsy specimen represented a fixed drug eruption. A subsequent orthopedic complaint and the resultant cooperative efforts of staff persons from several disciplines led to the proper diagnosis.

Addison Disease↗
PubMed2001

Screening for an AIRE-1 mutation in patients with Addison's disease, type 1 diabetes, Graves' disease and Hashimoto's thyroiditis as well as in APECED syndrome.

OBJECTIVE: Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare systemic autoimmune disorder of monogenic and autosomal-recessive inheritance. To date, 29 APECED causing mutations have been identified in the responsible gene AIRE-1, coding for a regulator of transcription. The aim of this study was to examine whether mutations in AIRE-1, in their heterozygous form, predispose to the more common isolated autoimmune endocrinopathies Addison's disease, type 1 diabetes mellitus, Graves' disease and Hashimoto's thyroiditis. DESIGN: Patients with isolated autoimmune endocrine disorders as well as healthy controls were analysed for two of the most common AIRE-1 mutations, mutation R257X in exon 6 and a 13-bp deletion in exon 8. Mutations were detected by polymerase chain reaction based techniques. PATIENTS: In total, 726 individuals were investigated for mutation R257X. Subjects comprised patients with Addison's disease, IDDM, Graves' disease and Hashimoto's thyroiditis. With regard to the 13 bp deletion we could screen 91 patients with Addison's disease. In addition, six patients with the APECED syndrome including one family were analysed for both mutations. RESULTS: Out of the 12 alleles in APECED patients six contained either mutation R257X or the 13 bp deletion, confirming that these mutations prevail in Europe. R257X was found in one subject with Hashimoto's thyroiditis in its heterozygous form. The 13 bp deletion was not detected in any subject with Addison's disease. CONCLUSIONS: The two studied AIRE-1 mutations are so rare in the general population that they can not contribute to susceptibility for the more common isolated autoimmune disorders.

Addison Disease↗