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PubMed1999

Bone mineral density in patients with treated Addison's disease.

Some studies have reported low bone mineral density (BMD) in patients with Addison's disease, whereas others have found BMD to be normal. It is possible that over-replacement of corticosteroids and adrenal androgen deficiency may contribute to a reduction in BMD in these patients. The aims of this study were to examine BMD using dual-energy X-ray absorptiometry in patients with treated Addison's disease at multiple skeletal sites and to investigate the relationships between these measurements and corticosteroid dose. Nineteen men, 3 premenopausal and 7 postmenopausal women with Addison's disease were studied and data from these patients were analyzed separately and as a group. The mean SEM age and duration of Addison's disease of the men were 44 +/- 3.8 years and 15 +/- 2.2 years, in the premenopausal women 40 +/- 2 years and 5 +/- 2.4 years, and in the postmenopausal women 68 +/- 4 years and 20 +/- 5 years, respectively. Eight men were unexpectedly hypogonadal (serum testosterone <13 nmol/l). BMD was expressed as a percent of values in normal controls (n = 418) adjusted for age, sex, ethnic origin, menopausal status and body weight. In the whole group (n = 29), mean BMD of the patients with Addison's disease was not different from normal at any site [mean (+/- SEM) lumbar spine 99.5% +/- 2.9%; femoral neck 99.3% +/- 2.5%; Ward's triangle 96.2% +/- 3.5%; trochanter 99.2% +/- 2.9%; radius 99.8% +/- 2.1%; total body 98.5% +/- 1.4%]. However, there was a wide range of bone densities, with some patients having a low BMD at multiple sites. Bone density was negatively correlated with current and cumulative corticosteroid dose per kilogram body weight and duration of Addison's disease. In conclusion, BMD in patients with Addison's disease is little different from normal, but may be lower in patients with disease of long duration and a high cumulative corticosteroid dose. Unexpected hypogonadism in men with Addison's disease is common.

Absorptiometry, Photon↗
PubMed1996

Reversible cardiomyopathy in a child with Addison's disease.

An 11-year-old boy in acute adrenal crisis was subsequently diagnosed with Addison's disease and presumably had an unrecognized preceding chronic adrenal insufficiency. His adrenal insufficiency and hypovolemic shock were promptly diagnosed and treated in the emergency room. However, 24 h later, signs of congestive heart failure developed and an echocardiogram revealed cardiomyopathy. He responded to i.v. dopamine and his cardiomyopathy resolved over some days. Acute adrenal insufficiency and actual ventricular dysfunction had not been described in humans until last year; this is the second reported case of cardiomyopathy in a patient with acute adrenal insufficiency.

Acute Disease↗
PubMed1981

Two types of autoimmune Addison's disease associated with different polyglandular autoimmune (PGA) syndromes.

A review of 295 patients with autoimmune Addison's disease which occurred as part of a polyglandular autoimmune syndrome is presented. Information of 41 cases was obtained from our clinics and from the examination of medical records, while 254 cases were culled from the literature. We report that autoimmune Addison's disease in association with other autoimmune diseases occurs in at least two distinct types. Addison's disease occurring in Type I polyglandular autoimmune disease (PGA) is associated with chronic mucocutaneous candidiasis and/or acquired hypoparathyroidism. The age of onset is predominately in childhood or in the early adult years. Type I PGA syndrome is also frequently associated with chronic active hepatitis, malabsorption, juvenile onset pernicious anemia, alopecia and primary hypogonadism. Insulin requiring diabetes and/or autoimmune thyroid disease are infrequent. In contrast, Addison's disease in Type II PGA is associated with insulin requiring diabetes and/or autoimmune thyroid disease(s). Although the age of onset of Addison's disease in Type II PGA syndrome is not confined to any age group or any specific sex, it occurs predominately in the middle years of life in females. The associated autoimmune diseases found in Type I disease, such as chronic active hepatitis, etc. (see table II) are rare in Type II PGA disease except for a low frequency of gonadal failure. We provide evidence to support the concept that the Addison's diseases in Type I and II PGA syndromes have different genetic bases, as related to HLA haplotypes, and possibly have different underlying pathogeneses.

Addison Disease↗
PubMed1996

Adrenal autoantibodies and organ-specific autoimmunity in patients with Addison's disease.

OBJECTIVE: Autoimmune destruction of the adrenal gland is the major cause of Idiopathic Addison's disease, but the significance of 21-hydroxylase autoantibodies and their correlation with the presence of other autoantibodies have not so far been investigated in a larger population of patients with Addison's disease. We have now characterized a cohort of patients with idiopathic Addison's disease (n = 97) regarding the specificity of autoantibodies against the adrenal cortex and, as Addison's disease can be either an isolated condition or part of a polyendocrine disorder, we investigated the presence of organ-specific polyendocrine autoimmunity in this patient population. DESIGN: Cross-sectional study. MEASUREMENTS: Autoantibodies were analysed with indirect immunofluorescence (IF) on tissue preparations, ELISA and in Western blots using bacterially expressed proteins. RESULTS: Eighty-four per cent (81/97) of the patient sera recognized the steroid-producing cells of the adrenal cortex in indirect IF. The antigen was identified as 21-hydroxylase by 72% (70/97) of the patient sera in Western blots. Seven sera that were negative on adrenocortical IF identified 21-hydroxylase on Western blot, while eight IF-positive sera were 21-hydroxylase-negative. Five sera weakly recognized 17 alpha-hydroxylase in Western blots, but all of these were also positive for 21-hydroxylase. In 13 cases (12 women), the sera also reacted with testicular Leydig cells, and nine of these identified the side-chain cleavage (SCC) enzyme. Other clinically evident organ-specific autoimmune disorders were present in 40% of the 97 patients and abnormal titres of organ-specific antibodies were found in 60% of the patients. CONCLUSIONS: In idiopathic Addison's disease, auto-antibodies against 21-hydroxylase are found in a majority of cases and this represents an important diagnostic tool. The enzyme 17 alpha-hydroxylase does not seem to constitute a major autoantigen in Addison's disease. In a subgroup of patients with autoantibodies to gonads, antibodies to SCC are produced, often in parallel with antibodies to 21-hydroxylase. In yet another subgroup the specificity of autoantibodies giving positive immunofluorescence is still unknown. Three patients revealed a polyendocrine syndrome which clinically resembles autoimmune polyendocrine syndrome (APS) type I, but serologically corresponds to APS type II. Polyendocrine disorders are often associated with Addison's disease, and screening, including quantification of autoantibodies, may help to identify those at risk of developing associated autoimmune disorders.

Addison Disease↗
PubMed1994

Bone mineral density is reduced in female but not male subjects with Addison's disease.

AIMS: Bone mineral density (BMD) may be potentially reduced in Addison's disease as a result of excessive glucocorticoid replacement, loss of adrenal androgens or concomitant gonadal or thyroid disease. We have examined clinical and biochemical parameters, and BMD in a group of subjects with Addison's disease. METHODS: Fourteen patients (9 female mean age 56 years, 5 male mean age 56.6 years) with primary adrenocortical failure (median duration 8.5 yrs) on replacement therapy were studied. Four had hypothyroidism on thyroxine doses (0.1 to 0.15 mg/d). Seven of the 9 females were post menopausal. Mean plasma cortisol levels were calculated from at least five samples in each subject drawn between 3 and 5 hours post dose, and the cortisol replacement dose calculated per unit body mass (mg/kg). BMD was measured by dual energy X-ray absorptiometry (DEXA) at femoral neck and lumbar spine (L2-4) and compared with local reference data. RESULTS: For women (n = 9) at L2-4 the mean Z score was -1.21 (95% CI -1.69, -0.73), and at femoral neck -0.57 (95% CI -1.15, 0.00). For men (n = 5) at L2-4, the mean Z score was 1.32 (95% CI -0.86, 3.50) and at femoral neck 0.62 (95% CI -0.18, 1.42). For all patients, there was no significant correlation between mean plasma cortisol and Z scores at L2-4 and femoral neck, r = -0.003 and -0.095 respectively; and between duration of Addison's disease and mean Z scores at L2-4 and femoral neck r = -0.043 and 0.143 respectively. CONCLUSIONS: Women with Addison's disease therefore have a greater than expected reduction in BMD. We postulate that this may be related to loss of adrenal androgens.

Absorptiometry, Photon↗
PubMedDate not supplied

[Proceedings: Plasma renin activity in management of Addison's disease (author's transl)].

13 patients with Addison's disease, 7 men and 6 women, 19 to 61 years old, were investigated. Plasma Renin Activity (P.R.A.) is measured by radioimmunoassay of Angiotensin I (ng/ml/h) in the supine (S) and the upright (U) position. These patients are studied before treatment and under normal sodium diet in 11 cases: the P.R.A. value is constantly increased [5 men: MS = 10,09 (range: 6,2-12,5) and MU = 23,22 (range : 17,1-31,09), 6 women : MS = 24,48 (range : 3,46-45,04) and MU = 42,23 (range : 42,23 (range 17,37-69,34), to be compared with our normal values (M +/- S.D.) : MS = 1,02 +/- 0,39 and MU = 2,56 +/- 0,99 for men - MS = 0,82 +/- 0,14 and MU = 2,32 +/- 0,93 for women in follicular phase - MS = 1,45 +/- 0,56 and MU = 4,59 +/- 1,63 for women in luteinic phase. After dietary sodium restriction (10 mEq/24 h) in 2 cases, the P.R.A. is significantly increased with respect to the basal value]. Under Hydrocortisone alone (25 to 30 mg/24 h) and normal sodium diet, 4 patients kept significantly increased P.R.A. values. Under Hydrocortisone (20 to 40 mg/24 h) and 9-alpha-fluorohydrocortisone (50 to 100 microgrammes/24 h) for 6 days to 14 months, the P.R.A. value decrease into the normal range [men : MS = 1,02 (range : 0,54-1,92) and MU = 1,68 (RNAGE : 0,81-2,57) - 2 Menopausal women : MS = 1,55 and MU - 1,16. The P.R.A. measurement seems useful in the adaptation of Addision's disease treatment.

Addison Disease↗