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PubMed1983

Inhibitory effect of cyproheptadine on ACTH secretion in patients with Addison's disease.

In 14 patients with Addison's disease plasma levels of ACTH were studied after administration of a single oral dose (16 mg) of cyproheptadine. The drug administration was followed by an inhibition of ACTH release. These results support the view that cyproheptadine may exert an inhibitory effect on ACTH secretion in subjects whose corticosteroid feedback mechanism is normal. We hypothesize that the effect of cyproheptadine might be related to its anti-serotonin or anti-histaminergic action.

Addison Disease↗
PubMed1996

Atrial natriuretic peptide and plasma renin levels in assessment of mineralocorticoid replacement in Addison's disease.

Assessment of mineralocorticoid replacement therapy in Addison's disease relies on clinical features and laboratory measurements, including plasma renin and potassium. Previous studies have questioned the value of measuring the plasma renin concentration (PRC), particularly in the setting of fludrocortisone overreplacement. The aim of this study was to evaluate the usefulness of plasma atrial natriuretic peptide (ANP) measurements as a marker of sodium and volume status in Addison's disease. Fourteen patients with Addison's disease receiving their usual glucocorticoid doses were placed on various doses of fludrocortisone (FC; 0 mg, 0.05 mg, 0.1 mg and 0.2 mg) in random order for four 2-week periods. At the end of each period, blood pressure and clinical symptoms were assessed, and blood was drawn for measurement of PRC and ANP levels. PRC was significantly elevated in patients receiving placebo (54.2 +/- 57.9 ng/mL x h) compared with PRC in those receiving baseline FC (24.7 +/- 42.4 ng/mL x h), 0.1 mg FC (15.2 +/- 25.9 ng/mL x h), and 0.2 mg FC (5.5 +/- 5.7 ng/mL x h). ANP levels were measured by either an extraction method (ANP(ext)) or directly from plasma (ANP(dir)). ANP(dir) was significantly elevated at 0.2 mg FC (87.1 +/- 20.1 pg/mL) compared with baseline (63.3 +/- 8.1 pg/mL), placebo (56.1 +/- 5.5 pg/mL), 0.05 mg FC (60.5 +/- 16.0 pg/mL), and 0.1 mg FC (65.4 +/- 13.7 pg/mL) values. ANP(ext) was elevated in patients receiving 0.2 mg FC (42.7 +/- 41.8 pg/mL) compared with that in patients receiving placebo (7.9 +/- 5.4 pg/mL), 0.05 mg FC (16.2 +/- 11.2 pg/mL), or 0.1 mg FC (19.7 +/- 11.1 pg/mL). Our data suggest that PRC is of value in determining mineralocorticoid underreplacement, whereas ANP is a more sensitive index of FC overreplacement. ANP levels may, therefore, be complementary to PRC in adjustment of mineralocorticoid doses in the upper dose range, where clinical symptoms and signs appear to be of little value.

Addison Disease↗
PubMed1979

Mineralocorticoid replacement in Addison's disease.

Eight patients with treated Addison's disease were studied whilst receiving different doses of fludrocortisone together with a constant intake of glucocorticoid. Plasma renin activity (PRA), blood pressure, pulse rate and plasma potassium and urea concentrations were measured after 2-week periods on each dose. In two patients, PRA measurements indicated that mineralocorticoid replacement therapy had been inadequate. In four others, PRA remained normal throughout the study, even after fludrocortisone had been discontinued, suggesting that the drug was unnecessary for the maintenance of normal sodium balance in these patients. Asymptomatic fludrocortisone overdosage was indicated by a low plasma potassium concentration, but not by PRA measurements which failed in this study to distinguish between adequate and excessive mineralocorticoid replacement.

Addison Disease↗
PubMed2001

Quadriceps muscle function and fatigue in women with Addison's disease.

In nine patients with Addison's disease (mean +/- SE: 51 +/- 2 years) receiving conventional steroid treatment, and nine age-matched healthy controls (56 +/- 2 years), we investigated maximum voluntary quadriceps force (MVC) and contractile properties evoked with stimulation and central activation both at rest and during a submaximal intermittent fatigue task. The MVC was similar (-3%), but twitch tension (-27%) and central activation were significantly less (-7%), and tetanic half-relaxation time was approximately 40% slower in the patients. Twitch amplitudes were potentiated by 6% in the patients, but unchanged in the control group. The patients self-terminated a submaximal intermittent fatigue protocol (0.6 duty cycle) at approximately 5 +/- 1 min, whereas the controls stopped when they lost 50% of MVC force ( approximately 10 +/- 1 min). Force loss was similar between groups over the first 5 min of the fatigue task. In the patient group, maximal and submaximal relative integrated electromyogram (IEMG) increased significantly in the first minute of fatigue and remained elevated, whereas the controls exhibited a gradual increase in submaximal IEMG with little change in maximal IEMG. These results indicate that conventionally treated Addison's patients have similar MVC strength, but altered contractile properties and decreased endurance compared with controls.

Addison Disease↗
PubMed1980

Immunoregulation abnormalities in familial Addison's disease.

Three brothers, two with Addison's disease and a monozygous twin discordant for adrenal insufficiency, presented an unique opportunity to evaluate the endocrine and immunological abnormalities associated with this disorder. None of the brothers had clinical evidence of other autoimmune disease. However, each of the twins had elevated titers of antihydroglobulin and antiparietal cell antibodies, and both Addisonian siblings had cytoplasmic islet cell antibodies. We evaluated the ability of nonspecific Concanavalin A-activated suppressor cells from all three siblings to inhibit immunoglobulin biosynthesis by pokeweed mitogen-stimulated B cells, cell proliferation by phytohemagglutinin-stimulated T cells, and the proliferative response of an allogenic mixed lymphocyte culture. In comparison to normal controls, suppressor cells from the Addisonian siblings were less efficient in inhibiting both B and T cell activities. The nonAddisoninan twin had a lesser degree of impaired suppressor cell function to the B and T cell targets. Suppressor cell activity, as measured by the ability to inhibit proliferation within the mixed lymphocyte culture, was normal in all three siblings. The relationship of suppressor cell dysfunction, genetic predisposition, and the expression of the autoimmune state are discussed.

Addison Disease↗
PubMed1979

Subclinical hypothyroidism in Addison's disease.

Fourteen patients with Idiopathic Addison's disease (IAD) were studied in order to detect a possible subclinical hypothyroid state. All were clinically euthyroid with normal serum thyroxine (T4) and serum 3,5',5'-triiodothyronine (T3). Eleven had circulating thyroid microsomal antibodies in blood. The mean basal serum TSH was significantly higher than that of the control group but only three patients had values above the upper normal range. The mean value of serum T4 was decreased as compared to that of the normal persons, while serum 3,3',5'-triiodothyronine was elevated. 7.5 mU bovine thyrotrophin per kilogram body weight injected intravenously caused a rise in serum T3 not different from the response in normals. However, as well increasing serum TSH as increasing microsomal antibody titer correlated significantly to decreasing thyroidal release of T3. Our results suggest that clinically euthyroid patients suffering from IAD might have a beginning thyroidal insufficiency because of a progressive immunological damage of the thyroid.

Addison Disease↗
PubMed1999

Addison's disease in Africa--a teaching hospital experience.

OBJECTIVE: Addison's disease may present with diverse and non-specific clinical and biochemical features. Contentious issues include the appropriate criteria for the interpretation of the ACTH stimulation test and the necessary extent of investigation to identify a specific aetiology for the hypoadrenalism. The experience of Addison's disease at a South African teaching hospital was reviewed to (1) record the aetiology and spectrum of presentation, (2) examine the performance of the ACTH stimulation test and (3) determine the utility of adrenal CT scan and biopsy. METHODS: Retrospective study of patients admitted to a South African teaching hospital from 1980 to 1997 with a diagnosis of acute Addison's disease. PATIENTS AND MEASUREMENTS: Fifty patients presenting with acute Addison's disease were identified by a search of hospital records. Pretreatment biochemical and haematological parameters were recorded. The cortisol response at 20 and 60 min to an intravenous injection of 250 micrograms synacthen (Cortrosyn) was analysed. In a subgroup of affected subjects, the bone mineral density (BMD) in the lumbar spine and femoral neck was measured during long-term follow-up. RESULTS: Presenting features included hyperpigmentation (86%), weight loss (67%), abdominal pain (20%) and diarrhoea (16%). Thirty-nine patients (78%) were hyponatraemic, while 26 (53%) were hyperkalaemic. Nine patients (18%) were hypoglycaemic and 21% had hypercalcaemia. The mean basal cortisol was 148 nmol/l (range 10-487) and 16 patients (40%) had a normal basal cortisol. The mean cortisol 20 min after ACTH stimulation was 172 nmol/l (range 19-588). There was no significant increase in serum cortisol following ACTH stimulation (P > 0.05). Adrenal CT scans were performed in only 24 patients (48%) and were normal in 10, while abnormalities were detected in 14 patients (bilateral enlargement in 11, calcification in two and atrophic adrenals in one). Eight patients had a DEXA scan performed during follow-up--four were osteopaenic in the lumbar spine and five at the femoral neck. The probable aetiology of Addison's was idiopathic in 42%, related to active TB in 18%, old TB in 16%, autoimmune in 12% and malignancy with metastases in 6%--single cases were due to sarcoid, iron overload and adrenoleukodystrophy. Adrenal biopsy was performed in two patients and was diagnostic of malignancy in both cases. The mortality within the first month after hospitalization was 12%. CONCLUSIONS: In our experience, Addison's disease is frequently idiopathic, presents with protean manifestations and should be considered in patients with unexplained hyperpigmentation or gastrointestinal complaints, particularly when associated with hyponatraemia and hyperkalaemia. A normal basal cortisol does not exclude the diagnosis which requires ACTH stimulation testing.

Abdominal Pain↗
PubMed1992

21-Hydroxylase, a major autoantigen in idiopathic Addison's disease.

Sera from patients with idiopathic Addison's disease commonly react with the zona glomerulosa of adrenal cortex. We used high-resolution western blot analysis of an adrenal microsomal fraction to investigate the target of these antibodies. A protein with an apparent molecular weight of 54 kDa was recognised as the common and major component. Sera identifying this autoantigen (from 12 of 16 patients) also showed strong immunofluorescence staining of a steroid-producing human adrenal adrenocortical cell line, NCI-H295. On application of antisera specific for different cytochrome P450 steroidogenic enzymes (side-chain cleavage enzyme, 21-hydroxylase, 17 alpha-hydroxylase, 11 beta-hydroxylase) the mobility of the 54 kDa protein in western blots corresponded to that of 21-hydroxylase. This parallel behaviour was confirmed by immunoprecipitation, electrophoresis, and autoradiography with the various sera and 35S-methionine-labelled NCI-H295 cell lysates. Preabsorptions of 35S-methionine-labelled cell lysates with the antiserum to 21-hydroxylase, but not with the other enzyme antisera, abolished precipitation of the 54 kDa autoantigen with the patient sera. These results indicate that 21-hydroxylase (P450c21), prominent in the zona glomerulosa of the adrenal cortex, is a major autoantigen in idiopathic Addison's disease.

Addison Disease↗
PubMed2000

Addison's disease: the potentially life-threatening tan.

Addison's disease is a potentially life-threatening endocrine disorder. The classic dermatologic sign of Addison's disease is diffuse hyperpigmentation of the skin with focal hyperpigmentation of scars, nails, and the oral mucosa. Recognition of these dermatologic manifestations in a patient with otherwise vague constitutional symptoms warrants a consideration of Addison's disease.

Addison Disease↗
PubMed1989

Gastrointestinal manifestations of Addison's disease.

Gastrointestinal symptoms are a common feature of Addison's disease, but the diagnosis may be delayed because of the nonspecific nature of the symptoms. This report describes nine patients with Addison's disease who presented to our unit over the past 3 yr. Eight had severe or unusual gastrointestinal symptoms at presentation. One, already known to have Addison's disease, required several admissions to the hospital because of unexplained abdominal pain and vomiting before inadequate glucocorticoid replacement was diagnosed. All but one had previously attended the hospital, but the diagnosis of Addison's disease had been overlooked. Five eventually presented in crisis. It is important to exclude Addison's disease in all patients with unexplained abdominal symptoms.

Abdominal Pain↗
PubMed1990

[Addison's disease: a clinico-epidemiologic study of 45 cases].

We present the clinical-epidemiological results obtained in a series of 45 patients diagnosed of Addison disease between 1967 and 1988. The incidence was 0.83 cases/100,000 inhabitants/year and the prevalence was 10 cases/100,000 inhabitants. The etiology was unknown in 44.4% of cases tuberculous in 24.4% and in 31.1% of cases the caused could not be established with the classical clinical and radiological criteria. Amongst the studied variables in each etiological group, we highlight the association with other autoimmune processes and the development of extraadrenal tuberculous infection after Addison disease diagnosis. We discuss the approach to etiological diagnosis and the convenience of tuberculostatic treatment in EAT cases.

Addison Disease↗