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At least 613 records · Page 34Linked to original sources
PubMed1982

Etiology of hypercalcemia in a patient with Addison's disease.

A case is reported of a hypercalcemic patient with primary Addison's disease. A combination of increased calcium input into the extracellular space and reduced calcium removal by the kidney accounted for the hypercalcemia. The mechanisms responsible for the reduction in calcium removal were decreased glomerular filtration and increased tubular calcium reabsorption. Both renal factors were secondary to volume depletion and improved rapidly during rehydration with saline infusion. The enhanced calcium mobilization was probably of skeletal origin. It persisted irrespective of volume status until hydrocortisone treatment was instituted. Serum 1,25-dihydroxyvitamin D3 levels were below 10 pg/ml, even after normalization of the glomerular filtration rate, but returned slowly to the normal range during corticosteroid substitution. Serum 25-hydroxyvitamin D3 and parathyroid hormone levels were within the normal range. Our case report therefore demonstrates that physiological amounts of glucocorticoids reduce bone resorption, normalize serum calcium, and restore the production of 1,25-dihydroxyvitamin D3.

Addison Disease↗
PubMed1998

Detection of adrenocortical autoantibodies in Addison's disease with a peroxidase-labelled protein A technique.

Adrenocortical autoantibodies (ACA), present in 60-80% of patients with idiopathic Addison's disease, are conventionally detected by indirect immunofluorescence (IIF) on frozen sections of adrenal glands. The large-scale use of IIF is limited in part by the need for a fluorescence microscope and the fact that histological sections cannot be stored for long periods of time. To circumvent these restrictions we developed a novel peroxidase-labelled protein A (PLPA) technique for the detection of ACA in patients with Addison's disease and compared the results with those obtained with the classical IIF assay. We studied serum samples from 90 healthy control subjects and 22 patients with Addison's disease, who had been clinically classified into two groups: idiopathic (N = 13) and granulomatous (N = 9). ACA-PLPA were detected in 10/22 (45%) patients: 9/13 (69%) with the idiopathic form and 1/9 (11%) with the granulomatous form, whereas ACA-IIF were detected in 11/22 patients (50%): 10/13 (77%) with the idiopathic form and 1/9 (11%) with the granulomatous form. Twelve of the 13 idiopathic addisonians (92%) were positive for either ACA-PLPA or ACA-IIF, but only 7 were positive by both methods. In contrast, none of 90 healthy subjects was found to be positive for ACA. Thus, our study shows that the PLPA-based technique is useful, has technical advantages over the IIF method (by not requiring the use of a fluorescence microscope and by permitting section storage for long periods of time). However, since it is only 60% concordant with the ACA-IIF method, it should be considered complementary instead of an alternative method to IIF for the detection of ACA in human sera.

Addison Disease↗
PubMed1976

Control of mineralocorticoid substitution in Addison's disease by plasma renin measurement.

In 7 out-patients with Addison's disease, plasma renin activity (PRA), plasma concentrations of angiotensin II (AT II), renin substrate (PRS), potassium, sodium and total protein, hematocrit, blood pressure, heart rate and body weight were studied after 2 weeks each on 2 mg of dexamethasone, 25 mg hydrocortisone (HC), 25 mg HC + 0.05 mg 9-alpha-fluorohydrocortisone (FC), 25 mg HC + 0.1 mg FC and 25 mg HC + 0.2 MG FC. Four further patients were less extensively studied. Mean PRA (upper normal limit, ambulatory: 12 ng AT I-ml-1-h-1) after the 5 steps of incremental substitution, starting with dexamethasone, was 192, 59, 38, 24 and 9 ng AT I-ml-1-h-1 rsp. PRS did not change with increasing substitution. PRA and AT II were significantly correlated (r = 0.91; p less than 0.0001) and proved to be the most sensitive parameters of insufficient mineralocorticoid substitution. With decreasing significance, PRA also correlated with plasma protein concentration, plasma sodium concentration (negative), delta body weight (negative), heart rate, delta mean blood pressure (negative) and plasma potassium concentration. PRA or AT II measurements are useful clinical tools to control mineralocorticoid substitution in Addisonian patients. Inappropriately high substitution can be prevented by keeping PRA in the upper normal range.

Addison Disease↗
PubMed1997

A case of Addison's disease associated with the Lambert-Eaton myasthenic syndrome.

Nonneoplastic Lambert-Eaton Myasthenic Syndrome (LEMS) is rare. A 27-year-old man as initially having the diagnosis of Addison's disease was admitted to the hospital because of fatigue, dry-mouthness and proximal limb weakness for 1 year. A diagnosis of LEMS was made from electrophysiological studies. Clinical and laboratory studies revealed no malignancy. We report the first case of Addison's disease associated with non-neoplastic LEMS. It is possible that subclinical LEMS might be present in patients with Addison's disease more frequently than currently believed, since the prominent symptoms of LEMS may be confused with symptoms of Addison's disease.

Addison Disease↗
PubMed1987

Osmoregulation of arginine-8-vasopressin secretion in primary hypothyroidism and in Addison's disease.

The osmoregulation of arginine-8-vasopressin (AVP) was investigated in 14 patients with primary hypothyroidism and in 6 with Addison's disease. Plasma AVP was measured by radioimmunoassay. Patients with primary hypothyroidism were classified into subgroups with elevated (6.81 +/- 1.12 pmol/l) or normal (3.92 +/- 0.96 pmol/l) basal levels of plasma AVP. Following the infusion of 2.5% saline, a positive correlation was established between plasma AVP and plasma osmolality. A decreased osmotic threshold was found in hypothyroid patients with augmented basal AVP levels (pAVP = 0.37 (pOs-265), r = 0.71, P less than 0.01) as compared with that in hypothyroid patients with a normal AVP level (pAVP = 0.42 (pOs-280), r = 0.93, P less than 0.001). A relationship was demonstrated between the alteration in the AVP osmoregulation and the severity of the thyroid insufficiency. Patients with Addison's disease exhibited an increased basal level of plasma AVP (9.59 +/- 1.25 pmol/l) and a decreased osmotic threshold (pAVP = 0.42 (pOs-261), r = 0.63, P less than 0.01) contrasted to that of healthy volunteers (pAVP = 0.41 (pOs-280), r = 0.83, P less than 0.001). The osmoregulation disturbance of the AVP secretion may play a major role in the impaired water metabolism in primary hypothyroidism and in Addison's disease.

Addison Disease↗
PubMed1999

A conformation-dependent epitope in Addison's disease and other endocrinological autoimmune diseases maps to a carboxyl-terminal functional domain of human steroid 21-hydroxylase.

Idiopathic Addison's disease develops as a consequence of autoimmune destruction of steroid-producing cells in the adrenal gland. A major autoantigen is 21-hydroxylase (21OH; P450c21), which is involved in the biosynthesis of cortisol and aldosterone in the adrenal cortex. We selected a number of functionally important 21OH amino acid substitutions, found in patients with congenital adrenal hyperplasia, to study their effects on the binding of 21OH autoantibodies (21OHAb) to 21OH. The ability of 21OHAb to bind in vitro transcribed and translated wild-type 21OH and five different 21OH mutant proteins was quantified by liquid-phase assays. Sera from 21OHAb-positive patients with idiopathic Addison's disease (n = 24), Graves' disease (n = 3), and insulin-dependent diabetes mellitus (n = 1) were used. While the P105L, delE196, and G291S mutations had no effect on autoantibody binding, the P453S mutation had a considerable effect, and the R483P mutation almost completely abolished binding. Synthetic peptides corresponding to linear epitopes defined by amino acids 447-461 and 477-491 were unable to compete with wild-type 21OH for binding to autoantibodies. Direct 21OH DNA sequencing could not reveal any specific genetic variation in alleles found in 21OHAb-positive patients. We conclude that the region involving R483 plays a key role in the formation of a three-dimensional epitope in a functionally important C-terminal domain of the enzyme.

Addison Disease↗
PubMed1985

High serum levels of angiotensin-converting enzyme in untreated Addison's disease.

Serum angiotensin-converting enzyme (ACE) in four patients with untreated Addison's disease was significantly higher [79.7 +/- 17.5 (SD) nmol min-1 ml-1] than in normal subjects (37.7 +/- 8.9 nmol min-1 ml-1, P less than 0.02). During corticosteroid hormone replacement therapy the enzyme levels returned within the normal range (44.0 +/- 7.6 nmol min-1 ml-1). In two additional patients the enzyme was assayed only while they were receiving therapy and found normal (38 and 52 nmol min-1 ml-1, respectively). In one of them, an increase ACE level (70 nmol min-1 ml-1) was found after therapy was reduced by 50%. Primary adrenal insufficiency is another disease in which ACE levels may be increased.

Addison Disease↗
PubMed1989

Addison's disease and pregnancy.

Five case reports are presented illustrating that pregnancy and Addison's disease are not incompatible, provided adequate substitution therapy is given.

Addison Disease↗
PubMed1989

Raised plasma levels of atrial natriuretic peptides in Addison's disease.

Plasma levels of atrial natriuretic peptides (ANP) were significantly higher in 7 patients with treated Addison's disease (15.8 +/- 8.8 pg/ml, mean +/- SD) than in 7 control subjects (6.1 +/- 3.8 pg/ml) matched for sex, age, body weight and blood pressure. All subjects were studied on their usual sodium intake and had similar urinary sodium excretions. These findings indicate inappropriately high levels of plasma ANP in patients with treated Addison's disease and are possibly due to the lack of adrenal control on ANP synthesis and/or secretion in these patients.

Addison Disease↗
PubMed1998

Circulating levels of adrenomedullin in patients with Addison's disease before and after corticosteroid treatment.

BACKGROUND AND OBJECTIVE: A novel hypotensive peptide, adrenomedullin (AM), had recently been isolated, purifed and its encoding gene sequenced from a human phaeochromocytoma. In humans AM circulates in physiological levels and possesses a distinct vasodilatatory activity. The purpose of this study was to examine the behaviour of AM levels in primary adrenal failure. DESIGN: Plasma AM levels were measured in patients with proven Addison's disease using a specific radioimmunoassay and compared to those in healthy normotensive subjects. PATIENTS: Eighteen patients with Addison's disease (10 men and eight women; ages 21 to 72 years) and 21 healthy control subjects (13 men and eight women; ages 20 to 71 years) were enrolled in the study. All patients were studied under basal conditions and 10 were reassessed following corticosteroid treatment. RESULTS: All patients with Addison's disease showed increased levels of AM compared to the control group. Mean plasma AM levels were correspondingly higher in patients with Addison's disease than in normal subjects (102.1 +/- 33.4 (SD) ng/l versus 13.7 +/- 6.1 ng/l; P < 0.0001). In 10 patients studied after corticosteroid treatment, plasma AM levels were significantly reduced (P < 0.0001: 110.3 +/- 35.8 ng/l versus 32.4 +/- 10.3 ng/l) after 2 weeks of treatment. A weak correlation (r = 0.458; P = 0.048) was observed between systolic blood pressure and plasma AM concentrations in all patients with Addison's disease. CONCLUSIONS: These results indicate a consistent but reversible increase of adrenomedullin in patients with Addison's disease.

Addison Disease↗