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PubMed2003

5'-Insulin gene VNTR polymorphism is specific for type 1 diabetes: no association with celiac or Addison's disease.

The VNTR region located at the 5'-end of the insulin gene on chromosome 11p15.5 is linked to susceptibility to type 1 diabetes mellitus (T1DM), and class I alleles have been associated with increased risk of disease, whereas class III alleles are considered to be protective. Although a potential effect on the expression level of thymic insulin and a consequent abnormal tolerance have been proposed as an explanation, it is still not clear whether the association is specific for T1DM or whether it is shared by other autoimmune disorders. To investigate the contribution of INS-VNTR to the genetic susceptibility to autoimmune disorders, we analyzed 102 autoantibody-positive T1DM patients, 59 patients with celiac disease (CD), and 57 patients with Addison's disease (ADD), as well as 111 unrelated healthy individuals from the general population. When analyzing the results, class I allele frequencies were 85.8% in the T1DM group, 77% among CD patients, 71% in the ADD group, and 76.1% in the general population. Association with increased risk was seen only in the T1DM group (pc = 0.015). Risk to T1DM was associated with the class I/class I homozygous genotype (RR, 1.92; 95% CI, 1.03-3.6). In conclusion, INS-VNTR does not seem to be involved in the susceptibility to autoimmune diseases other than T1DM and can be considered a diabetes-specific locus.

Addison Disease↗
PubMed1983

Complement-fixing adrenal autoantibodies as a marker for predicting onset of idiopathic Addison's disease.

In a prospective investigation of the role of adrenal autoantibodies (AA) in predicting the onset of idiopathic Addison's disease, 9 initially non-addisonian AA-positive autoimmune subjects were followed for 42 months. In 4 of these subjects Addison's disease developed within 1-31 months. A fifth had reduced adrenocortical reserve at the start and at the end of the investigation. An AA capable of fixing the membrane attack complex of complement [(C5-C9) F-AA] was detected before onset of the disease in the sera of the 4 patients in whom Addison's disease developed. (C5-C9) F-AA may be involved in the pathogenesis of idiopathic Addison's disease and may be regarded as a marker for individuals in whom idiopathic adrenal insufficiency is likely to develop.

Addison Disease↗
PubMed2003

Prevalence of adrenal antibodies in Addison's disease among north Indian Caucasians.

OBJECTIVE: The prevalence of antibodies in different organ-specific autoimmune diseases can vary depending on the racial group studied. Data on the prevalence of antibodies against steroidogenic enzymes in Addison's disease is available only for white Caucasians. We have evaluated the frequency of antibodies against adrenal cytoplasm, 21-hydroxylase, 17-alpha-hydroxylase and side-chain cleavage enzyme in a cohort of Indian patients with Addison's disease of idiopathic and granulomatous aetiology. DESIGN: Study of all patients with Addison's disease on whom serum samples were available (84% of total), presenting to the Endocrinology Department in a teaching hospital in India, between 1990 and 1999. PATIENTS: Thirty-eight patients with Addison's disease (19 idiopathic, 19 granulomatous). METHODS: A radiobinding assay using in vitro transcribed and translated recombinant human 35S-labelled 21-hydroxylase, 17-alpha-hydroxylase and side-chain cleavage enzymes was utilized to detect the respective antibodies. Adrenal cytoplasmic antibodies were measured by indirect immunofluorescence on cryostatic sections of human adrenal cortex. RESULTS: Of the 19 patients with idiopathic Addison's disease, adrenal cytoplasmic antibodies were present in five (26%) patients, while 21-hydroxylase antibodies were present in four (21%) subjects. The frequency of 21-hydroxylase antibodies was similar among patients with isolated idiopathic Addison's disease (3/13, 23%), and those associated with other organ-specific autoimmune diseases (1/6, 17%). 17-alpha-hydroxylase and side-chain cleavage antibodies were present in four (21%) and three (16%) patients, respectively. Overall, at least one of the three antibodies was present in eight (42%) subjects. All four female patients with premature ovarian failure had antibodies against 17-alpha-hydroxylase and/or side-chain cleavage enzyme. Two (11%) patients with granulomatous Addison's disease had adrenal antibodies. Of these, one patient with enlarged and calcified adrenal gland secondary to tuberculosis had a high titre of antibodies against all three steroidogenic enzymes. CONCLUSIONS: Antibodies to 21-hydroxylase enzyme are less frequent in idiopathic Addison's disease in north Indians, when compared with other Caucasians. In contrast, the prevalence of 17-alpha-hydroxylase and side-chain cleavage enzyme antibodies is similar to those reported. High titre antibodies against steroidogenic enzymes may occasionally be present in patients with clinical evidence of tuberculous Addison's disease.

Addison Disease↗
PubMed1992

[Addison's disease in the framework of poly-glandular autoimmune syndromes: 3 case reports].

Case reports of three patients with idiopathic Addison's disease combined with other associated autoimmune endocrine and non-endocrine disorders are presented. In the first patient, a young man with a long-standing history of mucocutaneous candidiasis, latent Addison's disease was discovered by diagnostic screening tests. In the two other patients, women aged 39 and 20 respectively, overt Addison's disease combined with primary hypothyroidism was diagnosed. One of them also had a pre-existing ovarian failure. The polyglandular autoimmune syndromes with Addison's disease are classified into two different subtypes, on the basis of characteristic patterns of disease combinations and on different modes of inheritance. Patients with autoimmune Addison's disease are at relatively high risk for other endocrine disorders or non-endocrine autoimmune diseases. Therefore, these patients--and in some instances also their relatives--need lifelong supervision and advice to ensure timely recognition of any associated diseases.

Addison Disease↗