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At least 775 records · Page 43Linked to original sources
PubMed1989

Immunoglobulins of patients with idiopathic Addison's disease block the in vitro action of adrenocorticotropin.

The presence of serum immunoglobulins (Ig) blocking ACTH-induced adrenal DNA synthesis and/or cortisol production was studied in 25 patients with idiopathic Addison's disease. For this purpose guinea pig adrenal segments kept in organ culture were exposed to ACTH and graded concentrations of patient IgG. After a 5-h culture period the cortisol present in the culture fluid was measured by RIA, and DNA synthesis in the adrenal cells was measured using Feulgen densitometry on frozen sections of the cultured adrenal segments. Addition of ACTH alone in concentrations of 0.1-10 pmol/L to the culture system stimulated in vitro cortisol secretion; the maximal stimulation was 63 +/- 35% (+/- SD; n = 5) at a concentration 0.1 pmol/L. ACTH also increased (in concentrations of 1 fmol/L to 1 pmol/L) the percentage of fasciculata cells in S-phase from 0-4% (nonstimulated) to 5-12%. IgG preparations from all but 2 of the 25 patients with idiopathic Addison's disease blocked these in vitro ACTH-induced adrenal responses in a dose-dependent fashion. IgG from 2 patients with tuberculous adrenalitis, 1 patient with secondary adrenal insufficiency, and 7 normal subjects had no blocking activity. Among 5 non-Addisonian autoimmune endocrinopathy patients who had adrenal cytoplasmic autoantibodies, 4 had no ACTH-blocking IgGs. Two of 9 patients with miscellaneous adrenal disorders (Cushing's disease, pigmented adrenal micronodular dysplasia, and adrenal nodules) had ACTH-blocking activity. These results demonstrate the existence of IgGs blocking the in vitro effects of ACTH and suggest their involvement in the pathogenesis of idiopathic Addison's disease.

Addison Disease↗
PubMed2004

A promoter polymorphism of the CYP27B1 gene is associated with Addison's disease, Hashimoto's thyroiditis, Graves' disease and type 1 diabetes mellitus in Germans.

BACKGROUND: CYP27B1 hydroxylase catalyzes the conversion of 25 hydroxyvitamin D(3) (25OHD(3)) to 1,25(OH)(2)D(3), the most active natural vitamin D metabolite, which plays a role in the regulation of immunity and cell proliferation. We therefore investigated two single nucleotide polymorphisms in the CYP27B1 hydroxylase gene for an association with Addison's disease, Hashimoto's thyroiditis, Graves' disease and type 1 diabetes mellitus. METHODS: Patients with Addison's disease (n=124), Hashimoto's thyroiditis (n=139), Graves' disease (n=334), type 1 diabetes mellitus (n=252) and healthy controls (n=320) were genotyped for the promoter (-1260) C/A polymorphism and for the intron 6 (+2838) C/T polymorphism of the CYP27B1 gene. Patients and controls were compared using genotype-wise and allele-wise X(2) testing. RESULTS: A significant association was found between allelic variation of the promoter (-1260) C/A polymorphism and Addison's disease, Hashimoto's thyroiditis, Graves' disease and type 1 diabetes mellitus (P=0.0062, P=0.0173, P=0.0094 and P=0.0028 respectively). Significant differences were also observed for the intron 6 (+2838) C/T polymorphism (P=0.0058) in Hashimoto's thyroiditis but not for the other autoimmune endocrine diseases. CONCLUSIONS: The CYP27B1 promoter (-1260) C/A polymorphism appears to be associated with endocrine autoimmune diseases but the CYP27B1 intron 6 (+2838) C/T polymorphism appears to be associated only with Hashimoto's thyroiditis. These results imply a regulatory difference of the CYP27B1 hydroxylase to predispose to endocrine autoimmunity.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed2000

Autoantibodies against aromatic L-amino acid decarboxylase identifies a subgroup of patients with Addison's disease.

Autoantibodies against aromatic L-amino acid decarboxylase (AADC) are present in about 50 percent of sera from patients with autoimmune polyendocrine syndrome type I (APS I) but absent in sera from patients with different organ-specific autoimmune diseases, such as insulin-dependent diabetes mellitus, Hashimoto's thyroiditis, and Graves' disease. AADC is expressed in the pancreatic beta-cells, the liver, and the nervous system; and the presence of AADC antibodies has been shown to correlate to hepatitis and vitiligo in APS I patients. Among 101 investigated patients with autoimmune Addison's disease, 15 had high titers of AADC antibodies. According to the clinical characteristics of these patients, only 3 had APS I. The remaining 12 had either isolated Addison's disease or associated diabetes mellitus, hypothyroidism, vitiligo, alopecia, gonadal failure, and pernicious anemia. Autoantibodies against 21-hydroxylase were present in 9 of 12, whereas autoantibodies against side-chain cleavage enzyme and 17alpha-hydroxylase were present in 3 of 12. Two patients had only autoantibodies against AADC. DNA was available from 3 of these 12 patients. One of the patients, a woman with Addison's disease, autoimmune thyroiditis, and premature menopause was heterozygous for a point mutation (G1021A, Val301Met) in the first plant homeodomain zinc finger domain of the autoimmune regulator (AIRE) gene. The presence of AADC autoantibodies identifies patients with APS I and a subgroup of Addison patients who may have a milder atypical form of APS I or represent a distinct entity. Measurement of autoantibodies against AADC should be included in the evaluation of Addison's disease.

17-Hydroxysteroid Dehydrogenases↗
PubMed2006

Saliva cortisol measurement: simple and reliable assessment of the glucocorticoid replacement therapy in Addison's disease.

No ideal parameter is available for assessment of the glucocorticoid replacement therapy in Addison's disease. Serum cortisol day-curves can be used to monitor the therapy, but this technique is cumbersome and expensive. We evaluated the potential for saliva cortisol measurement in this setting. We found excellent correlation between serum and saliva cortisol after oral intake of cortisone acetate (no. 7) or iv administration of hydrocortisone (no. 4) (Pearson's R=0.83-0.98, p<0.002). A morning dose of 12.5 mg cortisone acetate yielded wide interindividual variations in cortisol levels in saliva. Saliva cortisol measurements were successfully adopted to evaluate and adjust doses in outpatients. We conclude that cortisol measurement in saliva is practical and reliable, and is preferable to serum cortisol measurement in the assessment of the glucocorticoid replacement therapy. Our results confirm that only a minority of patients require more than 12.5 mg of cortisone acetate (equivalent to 10 mg hydrocortisone) in the morning to have sufficient cortisol levels during the first part of the day.

Addison Disease↗
PubMed1992

The renin-secreting cell and the glomerular peripolar cell in renal artery stenosis and Addison's disease.

The glomerular peripolar cell may be a secretory component of the juxtaglomerular apparatus. To investigate this hypothesis we studied kidneys with the renin-angiotensin system activated by two different stimuli in order to compare the responses of peripolar cells and renin-secreting cells. We examined 10 human kidneys, removed for renal artery stenosis and 11 autopsy cases of Addison's disease with appropriate controls. We counted granulated peripolar cells in serial paraffin-embedded sections and renin-containing cells were quantified using an immunoperoxidase technique with an antiserum to human renin. There was a five-fold increase in the number of renin-containing cells in both renal artery stenosis and in untreated, but not in treated, Addison's disease. Peripolar cells were increased in number in three cases of renal artery stenosis, but were unaltered in both treated and untreated Addison's disease. Therefore, neither a reduction in renal perfusion pressure (renal artery stenosis), nor sodium depletion (Addison's disease) consistently affect peripolar cells in humans. These findings do not support the hypothesis that the peripolar cell is part of the juxtaglomerular apparatus.

Addison Disease↗
PubMed1993

Role of glucocorticoid in excretion of an acute potassium load in patients with Addison's disease and panhypopituitarism.

Glucocorticoid (GC) has been shown to stimulate potassium (K) excretion in various conditions, but it is still incompletely resolved whether its presence is essential for the normal K homeostasis. We addressed this question in patients with selective GC deficiency (panhypopituitarism) and with combined GC and mineralocorticoid deficiency (Addison's disease), studied 24 hours after withdrawal of their regular substitution therapy. Compared to data in healthy subjects, both basal K excretion and the kaliuresis after a KCl load (1 mmol/kg body wt orally) were impaired in either patient group (P < 0.05). Physiological cortisol supplementation (20 mg 3 hr prior to test, and 1 mg/hr during test) increased basal K excretion (from 10.6 +/- 1.8 to 19.2 +/- 1.9 mmol/5 hr, P < 0.01) and KCl stimulated kaliuresis (from 47.9 +/- 6.1 to 54.8 +/- 4.7 mmol/5 hr, P = 0.06) to normal levels in panhypopituitarism. Cortisol also improved basal K excretion (from 10.2 +/- 1.5 to 16.9 +/- 3.5 mmol/5 hr, P < 0.05) and KCl-stimulated K excretion (from 31.6 +/- 2.5 to 45.2 +/- 3.8 mmol/5 hr, P < 0.05) in Addison's disease, although KCl-stimulated K excretion remained below normal (P < 0.01). The effects of cortisol on sodium excretion differed between the two patient groups (P < 0.05) in that only in Addison's disease the improved K excretion was associated with sodium retention. Additional experiments with the purely GC compound dexamethasone (0.5 mg 3 hr prior to test, and 0.03 mg/hr during test) in the patients with Addison's disease also improved K excretion (P < 0.05), but without the concomitant sodium retention observed after cortisol.(ABSTRACT TRUNCATED AT 250 WORDS)

Addison Disease↗
PubMed1991

Association of Addison's disease with autoimmune disorders--a long-term observation of 180 patients.

This study aimed at evaluating the frequency of autoimmune disorders in Addison's disease. We have observed 180 patients (113 females, 67 males, aged 9-74 years) for 1 to 26 years. Tuberculosis was noted in 54 patients. Autoimmune disorders were found in 80 patients (44%); however, 125 (69%) patients were believed to have an autoimmune origin of adrenocortical insufficiency. In 20 patients two or more autoimmune disorders were found to coexist with Addison's disease.

Addison Disease↗