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PubMed1994

Eighty-six cases of Addison's disease.

OBJECTIVES: Since there have been no recent reviews of Addison's disease, we have undertaken a retrospective case-notes review of all identifiable cases in Nottingham to define the prevalence, incidence and causes of Addison's disease. We have also reviewed the criteria for interpretation of the short Synacthen test in diagnosis. DESIGN: A retrospective study of all patients coded for the diagnosis and admitted to Nottingham's hospitals between 1 April 1987 and 31 March 1993, identified by the hospital Information Services. PATIENTS: A total of 86 cases were identifiable of whom 66 were still alive and living in the town. RESULTS AND CONCLUSIONS: The calculated prevalence was 110 per million population. The cause was attributed to autoimmune destruction of the adrenal cortex in 81 (93%). There were two cases of metastatic malignancy and three unrelated cases of late onset adrenoleukodystrophy, but none were attributable to tuberculosis. Twenty-one new cases were diagnosed between 1987 and 1993. The calculated incidence was 5.6 per million per annum. The biochemical basis of the diagnosis was reviewed in these 21 patients and as a result firm criteria are suggested for the interpretation of the short Synacthen test; criteria for normality being baseline cortisol >250 and 30 minute peak >600 nmol/l, taking into account clinical circumstances.

Addison Disease↗
PubMed1977

Rare occurrence of Addison's disease and diabetes mellitus in children.

We report on two children with both Addison's disease and diabetes mellitus, a rare occurrence in children. One of the children first developed Addison's disease and later developed diabetes mellitus, while the other had the onset of diabetes mellitus first and later Addison's disease. In the latter patient a direct relationship was shown between the insulin dose and adrenal cortical hormone. Organ-specific antibody studies are reported and the diagnosis and management of these combined endocrinopathies are discussed.

Addison Disease↗
PubMed1997

Addison's disease and selective IgA deficiency in two coeliac patients.

Coeliac disease is associated with selective IgA deficiency and various autoimmune disorders. An association between Addison's disease and coeliac disease has been documented previously in the literature but never heretofore in coeliac patients with selective IgA deficiency. From a coeliac registry of over 700 biopsy-proven coeliac patients, studied closely over a 25-year period at University College Hospital, Galway, we now report the finding of Addison's disease and selective IgA deficiency in two patients with established coeliac disease. Previous reports of Addison's disease in coeliac patients were sporadic, and it was felt that the association between the two conditions was fortuitous. We now believe that coeliac patients, especially those who are selectively deficient in serum IgA, should be followed up with increased vigilance, as the association between IgA-deficient coeliac patients and Addison's disease is greater than can be explained by chance. Furthermore, we suggest that patients with established Addison's disease may have subclinical coeliac disease and should be screened with anti-reticulin or anti-endomyseal antibodies.

Addison Disease↗
PubMed1986

Inherited susceptibility to autoimmune Addison's disease is linked to human leukocyte antigens-DR3 and/or DR4, except when associated with type I autoimmune polyglandular syndrome.

The inherited susceptibility to autoimmune Addison's disease was found to be strongly associated with human leukocyte antigens (HLA)-DR3 and DR4 alleles. In a study of 45 white patients from the United States with the disease, the relative risks (the number of times that an individual is at risk for Addison's disease if they had a marker, compared to those without such marker) were found to be 6.0, 4.6, and 26.5 for the DR3 allele, the DR4 allele, and for DR3/DR4 heterozygotes, respectively. Frequencies of DR2, DR5, and DR7 in the patients with Addison's disease were significantly decreased in comparison to 265 individuals in the control population. These HLA-DR frequencies in patients with Addison's disease were similar to those for 723 patients with insulin-dependent diabetes (IDD). However, the above HLA-DR associations persisted even when only data from the 37 patients with Addison's disease who did not have IDD were considered. Adrenocortical autoantibodies in 23 patients with IDD who did not have Addison's disease were equally frequent among those with DR4 and DR3 alleles. In contrast, HLA-DR frequencies in 17 patients with type I autoimmune polyglandular syndrome (chronic mucocutaneous moniliasis, hypoparathyroidism, Addison's disease, etc.) were not different from control. We conclude that genetic susceptibility to autoimmune Addison's disease may involve the same HLA-associated genetic determinants as IDD, except when Addison's disease occurs as part of type I autoimmune polyglandular syndrome.

Addison Disease↗
PubMed1976

[Diabetes mellitus and Addison's disease)].

The authors diagnosed diabetes mellitus together with Addison's disease in a 38 year-old male patient. They are discussing therapeutic difficulties arising from the biglandular hypofunctional condition and the problems of the pathogenesis.

Addison Disease↗
PubMed1993

Bronchial asthma with Addison's disease.

A 14-year-old boy with bronchial asthma who was subsequently diagnosed to have coexistent Addison's disease is presented. Both diseases responded to continuous replacement steroid therapy. We suggest that worsening of bronchial asthma symptoms in this patient may be due to the hypocortisolemia produced by the coexistent Addison's disease. Patients with Addison's disease with clinical evidence of bronchial asthma have rarely been reported [1, 2]. A 14-year-old boy in whom symptoms of bronchial asthma obscured the otherwise obvious diagnosis of adrenocortical insufficiency is presented.

Addison Disease↗
PubMed1999

Liquorice, growth retardation and Addison's disease.

An 11-year-old boy had hypoparathyroidism and Addison's disease. During treatment with calcitriol, calcium, hydrocortisone and 9-alpha-fluorocortisol, he developed an apparent mineralocorticoid excess and growth retardation. Pseudohyperaldosteronism even persisted after treatment with 9-alpha-fluorocortisol was stopped and hydrocortisone was reduced to 6 mg/m(2). The boy reported an excessive daily intake of 300-400 g liquorice corresponding to 600-800 mg glycyrrhizic acid because of salt craving. After complete withdrawal of liquorice all symptoms of hypermineralocorticoidism diminished and growth velocity increased. We hypothesise that inhibition of 11beta-hydroxysteroid dehydrogenase by liquorice caused hypermineralocorticoidism and growth retardation via increased levels of free cortisol in this patient. We conclude that self-medication with liquorice in children with Addison's disease should be considered during treatment.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1984

Computed tomography of the adrenal glands in Addison's disease.

In 30 cases of chronic adrenal insufficiency (Addison's disease) CT of the adrenal glands was performed using a fourth generation scanner and a 2 mm slice thickness. Adrenal glands were visualized in all the cases. In 26 patients the adrenals were atrophied; the adrenal shape was abnormal in 21 patients. In 15 patients CT disclosed calcifications in one or both glands, which were particularly frequent in patients over the age of 50. Atrophy of adrenal glands was of high occurrence in cases of autoimmune origin.

Addison Disease↗
PubMed1989

[Pregnancy in Addison's disease].

A 29-year-old woman with Addison's disease was hospitalized in the eighth week of pregnancy because of an Addisonian crisis. The crisis was successfully treated with physiological saline infusions, as well as hydrocortisone (25 mg/d) and fludrocortisone (0.05 mg/d). The dose of fludrocortisone had to be increased to 0.1 mg/d from the 21st week of pregnancy onwards, because hyponatraemia and hypotension had once again developed. The hydrocortisone dose was raised to 37 mg/d from the 32nd week of pregnancy onwards because of a latent hypoglycaemia and raised further to 50 mg/d from the 35th week onwards because the retardation in fetal growth had become more marked. A mature infant was delivered spontaneously on the 282d day of pregnancy. At the start of labour the patient had been given 100 mg hydrocortisone intravenously and then 50 mg at the moment of delivery. The substitution treatment was gradually reduced to the original (pre-pregnancy) dosage during the first three post-partum days.

Addison Disease↗
PubMedDate not supplied

Focal segmental glomerular sclerosis in two patients with Addison's disease: any more than fortuitous development of glomerular disease?

Adjustment of the mineralocorticoid activity under substitution therapy is of primary importance in Addison's disease. We report the clinical and biological conditions of 2 patients with Addison's disease who developed nephrotic proteinuria during their deficient mineralocorticoid state. Renal biopsy was performed and the specimens processed using conventional histochemistry, Congo red staining, and indirect immunofluorescence. The renal biopsy specimens showed focal segmental glomerular sclerosis and nodular deposits of IgM and C3. Negative for Congo red staining. Serum complement, circulating immune complexes, and anti-DNA and hepatitis B and C and human immunodeficiency virus antibodies were all normal or negative. Absence of vesicoureteral reflux was assessed by X-ray studies. Our observations suggest that deficiency in mineralocorticoid substitution therapy inducing a status of hyperreninemia could play a role in the development of focal segmental glomerulosclerosis in patients with Addison's disease.

Addison Disease↗
PubMed1991

X-ray microanalysis of ossified auricles in Addison's disease.

The element content of ossified auricles in two patients with Addison's disease was determined by X-ray microanalysis. The results showed a similar element content of the ossified auricles of the Addison's patients and control bone specimens. The calcium and phosphorus content of the petrified auricles was, however, slightly decreased compared with the iliac bone biopsies of the patients. The sulfur content of the ossified auricles was higher than that of their bones, but markedly lower than control auricular cartilage. Iron, sodium, and chloride contents were similar in the ossified auricles and in the normal auricular cartilage, whereas only trace amounts of these elements were detected in the bone. The auricles of the patients with Addison's disease possessed relatively high aluminium content compared with both control bone and cartilage. The element content of the bone biopsies from Addison patients was comparable to control bone. The presence of trace amounts of aluminium in the petrified auricles of Addison's patients is probably attributed to a long period of aluminium hydroxide consumption.

Addison Disease↗
PubMed1992

[A case of latent Addison's disease with hypogonadotropic hypogonadism and dwarfism].

A case of latent Addison's disease accompanied by hypogonadotropic hypogonadism and dwarfism is described. A 20-year-old man was admitted to our department complaining of short stature and immature development of the external genitalia. Pigmentation was most evident on the fingers and face. Endocrinologically, serum ACTH level was very high, and serum cortisol level was in the lower limit of the normal range. Serum aldosterone and adrenal androgen levels were below their normal ranges. Based on these clinical and laboratory findings, the patient was diagnosed as having latent Addison's disease. Serum LH did not respond to a bolus injection of LH-RH. However, after 3 days administration of LH-RH, the response of serum LH to a bolus injection of LH-RH was enhanced. Serum testosterone level was not increased after the administration of hCG. These findings suggested a hypothalamic cause for the hypogonadism. It was indicated that short stature was apparently caused by GH neurosecretory dysfunction, since nocturnal GH secretion was below that in normal males and the response of GH to the administration of arginine was normal. In regard to the thyroid function, the peak of serum TSH after a bolus injection of TRH was delayed compared with normal subjects, and although serum T4 level was high, the basal metabolic rate was very low. This suggests that there is tissue resistance to the elevated thyroid hormone.

Addison Disease↗
PubMed1996

Autoantibodies to steroidogenic enzymes in autoimmune polyglandular syndrome, Addison's disease, and premature ovarian failure.

Autoantibodies to steroidogenic enzymes, steroid 17 alpha-hydroxylase (17 alpha-OH), cytochrome P450 side-chain cleavage enzyme (P450scc), and steroid 21-hydroxylase (21-OH), were measured using specific and sensitive immunoprecipitation assays (IPAs) in patients with various forms of autoimmune adrenal disease. Autoantibodies to 17 alpha-OH were detected in 6 of 11 (55%) patients with autoimmune polyglandular syndrome (APS) type I, 8 of 24 (33%) patients with APS type II, 11 of 56 (20%) patients with adrenal cortex antibody (ACA; measured by immunofluorescence)-positive patients without Addison's disease, and only 3 of 64 (5%) patients with Addison's disease. Autoantibodies to P450scc were found at a prevalence similar to those to 17 alpha-OH: in 5 of 11 (45%) APS type I patients, 10 of 24 (42%) APS type II patients, 11 of 56 (20%) ACA-positive patients without Addison's disease, and only 6 of 64 (9%) patients of the Addison disease group. Autoantibodies to 21-OH were found in a majority of patients with APS type I (7 of 11;64%), APS type II (23 of 24; 96%), Addison's disease (41 of 64; 64%), and ACA-positive patients without Addison's disease (48 of 56; 86%). All sera that were positive for 17 alpha-OH or P450scc were also positive for 21-OH autoantibodies, except in 1 case. There was good agreement between the presence of ACA measured by immunofluorescence and 21-OH antibodies measured by IPA in all patient groups studied, and this indicates that 21-OH is a major autoantigen in adrenal autoimmune disease regardless of whether the disease presents as isolated Addison's disease or APS type I or type II. Autoantibodies to 17 alpha-OH and P450scc appeared to be the major components of the steroid-producing cell antibodies measured by immunofluorescence. No autoantibodies to 21-OH, 17 alpha-OH, or P450scc were detected in 17 sera from patients with premature ovarian failure without evidence of adrenal autoimmunity (as judged by immunofluorescence studies), except for 1 serum in which low levels of 17 alpha-OH antibodies were found. Overall, our studies indicate that 35S-labeled 17 alpha-OH, P450scc, and 21-OH can be used successfully in IPAs for their respective autoantibodies. Assays such as these may well be valuable in the immunological assessment of patients at risk for or suspected of adrenal autoimmunity.

Addison Disease↗