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PubMed1999

Microsatellite polymorphism of the MHC class I chain-related (MIC-A and MIC-B) genes marks the risk for autoimmune Addison's disease.

The major histocompatibility complex class I chain-related MIC-A and MIC-B genes are located on chromosome 6 between the histocompatibility leucocyte antigen (HLA)-B and the B-associated transcript genes. The presence of 21-hydroxylase autoantibodies is a sensitive and specific marker of autoimmune Addison's disease. We studied the polymorphism of exon 5 of the MIC-A gene, of intron 1 of the MIC-B gene, and of HLA-DRB1, -DQA1, and -DQB1 genes in 28 autoimmune (21-hydroxylase autoantibody positive) Addison's disease patients and in 75 healthy subjects from central Italy. The MIC-A5.1 allele was significantly more frequent in Addison's disease patients (79%) than in healthy subjects (36%) [odds ratio (OR) = 6.52, corrected P (Pc) = 0.0015], whereas MIC-A6 was significantly reduced in affected subjects (15% vs. 56%, OR = 0.13, Pc = 0.002). The A5.1/A5.1 genotype had an OR for autoimmune Addison's disease as high as 18.0 and an absolute risk of 1 per 1131. In the presence of MIC-A5.1, MICB-CA-25 was significantly increased in Addison's disease patients (25% vs. 4%, OR = 8.0, P = 0.0039, Pc = 0.047). The MICB-CA-17 allele was absent in Addison's disease patients, but present in more than 25% healthy individuals (OR = 0.10, P = 0.0025, Pc = 0.03). Among HLA-DR and -DQ haplotypes, only DRB1*03-DQA1*0501-DQB1*0201 (DR3/DQ2) was significantly more frequent in Addison's disease patients than in healthy subjects, but only in the presence of MIC-A5.1. The frequency of MIC-A5.1 was significantly increased in Addison's disease patients only in the presence of HLA-DR3-DQ2. Our study demonstrates that susceptibility to autoimmune Addison's disease is linked to the MIC-A microsatellite allele 5.1 and that both MIC-A5.1 and HLA-DR3/DQ2 are necessary to confer increased genetic risk for Addison's disease.

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PubMed1984

Addisons's disease in pregnancy.

The Authors show a rare case of Addison's disease in pregnancy, in a 27 year old patient, under cortisonic therapy. They propose the current diagnostic therapeutic orientations relating to maternal foetal risks.

Addison Disease↗
PubMed2000

[Adrenomyeloneuropathy as the cause of Addison's disease].

The authors describe adrenoleukodystrophy and adrenomyeloneuropathy found in one family. This disease is a less frequent cause of Addison's disease, but it is very serious from the prognostic aspect. The authors recommend therefore to examine very long chain fatty acid plasma levels in patients with adrenal insufficiency.

Addison Disease↗
PubMed1991

[Radioimmunologic determination of pituitary autoantibodies in patients with Addison's disease].

The occurrence of pituitary autoantibodies was investigated in 34 patients, 25 females and 9 males, with Addison's disease of autoimmune origin and in 10 patients with tuberculous etiology of the disease. In both groups adrenal autoantibodies were also determined. Autoantibodies were determined by radioimmunoassay using solid phase technique in tubes coated with proteins of human adrenal and pituitary microsomal fractions. Pituitary autoantibodies were detected in 28 of 34 patients (20 females and 8 males) with autoimmune Addison's disease but only in 3 patients (2 females and one male) with nonimmune etiology of the disease. Both antipituitary and antiadrenal antibodies remain present in the circulation for many years as they were detected in autoimmune Addison's disease even after 10 or more years after the onset of the disease. There was a close relationship between the occurrence of pituitary antibodies and adrenal autoantibodies: they both appeared in the same patients and high titres of pituitary autoantibodies were associated with high titres of adrenal autoantibodies. This suggests a close similarity or identity of pituitary and adrenal autoantigens.

Addison Disease↗
PubMed1994

High prevalence of thyroid autoimmunity in idiopathic Addison's disease.

We have determined the incidence of autoimmune thyroid disorders in patients with Addison's disease. The material comprised 212 patients, 128 women and 84 men, aged 9-74 years. In 58 patients tuberculosis and in six patients other adrenal disorders were diagnosed. In the remaining 148 patients the auto-immune mechanism was the most probable cause of adrenocrotical insufficiency. In order to evaluate the thyroid abnormalities seen in patients with Addison's disease the T3, T4 (RIA), TSH (ELISA) and anti-thyroid autoantibodies were determined apart from routine clinical examination. Antimicrosomal, anti-thyroglobulin and anti-thyroperoxidase antibodies were measured in 91, 188 and 81 cases respectively. Thyrotoxicosis was diagnosed in 17 and primary hypothyroidism in 18 cases. Moreover, eight patients had evidence of subclinical hypothyroidism. The anti-thyroglobulin antibodies with titer ranging from 1:80 to 1:10,000 were detected in 66 patients, whereas antimicrosomal antibodies were found in 51 patients at a titer ranging from 1:80 to 1:9720. Autoantibodies against thyroid peroxidase were found in sera of 67 patients, with titer ranging from 1:2000 to 1:25,6000.

Addison Disease↗
PubMed1997

Duplex Doppler measurements of renal blood flow in a dog with Addison's disease.

Abnormal intrarenal flow in a seven-year old female Tibetan terrier with Addison's disease was demonstrated by duplex Doppler examination. Abnormal flow may reflect renal vasoconstriction due to increased activity of the renin-angiotensin system. Although not pathognomonic, an increased resistive index (> 0.70) in an otherwise ultrasonographically normal kidney can be due to Addison's disease and the technique may prove valuable as a quick non-invasive tool in the management of this disease.

Addison Disease↗
PubMed1982

Addison's disease, adrenal autoantibodies and computerised adrenal tomography.

The present study describes 53 patients with Addison's disease, who attended Auckland hospitals between 1971-1980, 32 of whom presented for the first time during this period, when the mean annual incidence of Addison's disease was 4.5 cases/million population, and the respective frequency of idiopathic (auto-immune) and tuberculous aetiologies was 92 percent and 4 percent for caucasians, but 25 percent and 63 percent for Polynesians. In addition, adrenal reserve was tested by ACTH stimulation in 20 clinically non-Addisonian patients in whom circulating adrenal antibodies had been incidentally demonstrated and present for periods of up to six years, and was normal in all cases. Such antibodies therefore lack functional disease specificity. The diagnostic value of CT adrenal scanning in illustrating the contrasting appearances between tuberculous and auto-immune adrenalitis is shown in four patients.

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PubMed1984

Auto-immune Addison's disease associated with hyperprolactinaemia.

Four cases of auto-immune Addison's disease are reported in association with hyperprolactinaemia. Two of the females had galactorrhoea. In three cases complete resolution of hyperprolactinaemia occurred with corticosteroid replacement, but it was only partial in the fourth. We suggest that hyperprolactinaemia was due to cortisol deficiency operating directly or indirectly at the level of the pituitary. These data support the animal and in vitro evidence for the influence of corticosteroids on prolactin release.

Addison Disease↗
PubMedDate not supplied

[Addison's disease: principal clinical associations and description of natural history of the disease].

From 1967 to 1988 we studied 75 cases of Addison's disease (AD). An autoimmune etiology was found in 68%, while previous tubercular infection was demonstrated in 21% of the cases; minor causes were involved in 3%, and in 8% of the cases the disease remained of unknown origin. Autoimmune adrenalitis has become the most frequent cause of AD as a consequence of decreased tubercular infection. Autoimmune AD prevailed in children or in young people, and tubercular AD in adults. The finding of calcifications in adrenals and/or other organs was the specific diagnostic sign for the identification of tubercular forms. On the other hand, the finding of circulating adrenal autoantibodies (AA) and/or other organ specific autoantibodies was the fundamental diagnostic marker of autoimmune forms. In 72% of the cases autoimmune AD is associated with other organ-specific autoimmune diseases. Subjects with AA but without clinical signs of hypoadrenalism were considered to have "potential AD", because they showed a high risk of developing clinical hypoadrenalism. This condition develops over a long period characterized by different stages of subclinical adrenal hypofunction. Steroid cell autoantibodies (StCA) are frequently detectable in patients with autoimmune AD, in whom they are markers of autoimmune premature ovarian failure. The study of StCA-positive cases without hypogonadism will be important to clarify whether or not these autoantibodies could be markers of potential autoimmune hypogonadism.

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PubMed1978

[Whited Addison's disease. Eight cases (author's transl)].

In 8 cases of Addison's disease due to adrenal tuberculosis, the substitutive treatment appeared unnecessary since more than one year. Urinary 17-OHCS were in the normal range but did not rise after ACTH injection except in two cases. In all the cases, plasma ACTH was elevated but lower than in severe adrenal insufficiency, and in the range of those observed in congenital adrenal hyperplasia. The nycthemeral variation of plasma ACTH were maintained. Therefore, an apparently normal basal cortico-adrenal function was obtained by an excessive stimulation by endogenous ACTH. The one year prescription of anti-tuberculosis chimiotherapy to 6 of these patients was possibly responsible for the partial reversal of adrenal insufficiency. However the substutive therapy appears needless in every day life, such a treatment would eventually be necessary during stress conditions.

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PubMed2004

[A case of Addison's disease presented with depression as a first symptom].

This report describes a 52-year-old male patient with idiopathic Addison's disease presenting depression as a first symptom. His psychomotor inhibition, depressive mood, sleep disturbances, general fatigue, muscular pain, and arthralgia were considered to be due to intense work in a stressful environment. Neither his physician nor his orthopedist found any physical disease. Therefore, he was diagnosed with endogenous depression by a psychiatric clinic, and antidepressants were prescribed. Antidepressants were not sufficient for improving his symptoms, and he was admitted to our hospital. Endocrine blood examination revealed primary adrenocortical insufficiency. Treatment with glucocorticoid induced rapid improvement in both the psychiatric and physical symptoms. It is well known that psychiatric symptoms occur in the progressive stage of Addison's disease. At present, however, the occurrence of psychiatric symptoms is very rare, mainly because of a decrease in the incidence of this disease or an increase in mild cases. In addition, Addison's disease presenting with psychiatric features in the early stage has the tendency to be overlooked and misdiagnosed. Thus, we suggest the necessity of blood work for ACTH and cortisol in the field of psychiatry.

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PubMedDate not supplied

Reversible cardiomyopathy in paediatric Addison's disease--a cautionary tale.

A 13 year-old girl with clinical features of Addison's disease developed acute cardiac failure after initiation of treatment and after initial clinical improvement. Large doses of i.v. hydrocortisone and oral fludrocortisone, in addition to inotropic and ventilatory support, were required to achieve cardiovascular stability. The cardiomyopathy improved over one week and her condition then remained stable on oral glucocorticoid and mineralocorticoid replacement therapy. Reversible cardiomyopathy is a rare and potentially life-threatening complication of Addison's disease. The second reported paediatric patient is presented, the only one reported to require ventilatory support.

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PubMedDate not supplied

Atypical Addison's disease in the dog: a retrospective survey of 14 cases.

Fourteen dogs diagnosed with Addison's disease and having atypical serum electrolyte levels are described. Seventy-eight percent were female, and most showed signs of inappetence, weakness, or vomiting. Ninety-three percent of the cases had either hyponatremia without hyperkalemia or normal serum electrolyte concentrations. Hemogram features were variable and were not useful in suggesting a diagnosis of hypoadrenocorticism. The results of this study show that normal or mild serum electrolyte changes in a dog with clinical signs compatible with Addison's disease should not exclude this diagnosis from consideration. Definitive diagnosis depends on the demonstration of inadequate adrenocortical response to adrenocorticotropic hormone (ACTH) stimulation.

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