Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Addison Disease”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1992

Corticotroph cell hyperplasia in a patient with Addison disease: case report.

A woman with Addison disease developed hyperpigmentation, headache, and nausea despite conventional replacement therapy with cortisone. Excessively elevated plasma adrenocorticotropic hormone (ACTH) with absence of response to administration of corticotropin-releasing factor (CRF), and roentgenological evidence of enlargement of the sella turcica, as well as detection of enlarged pituitary gland on magnetic resonance images, led to a diagnosis of ACTH-producing microadenoma, which was removed by transsphenoidal microsurgery. The specimen obtained at surgery evidenced corticotroph hyperplasia, as demonstrated by immunohistochemical staining for ACTH. Fine structure exhibited densely granulated cells with a few bundles of microfilaments and an abundance of large lysosomal bodies. Surgical removal of the hyperplasia alleviated the patient's symptoms, and hyperpigmentation faded remarkably. Her plasma ACTH level returned to normal, has remained normal for more than 3 years, and responds adequately to CRF administration.

Addison Disease↗
PubMed1991

Tuberculous Addison's disease.

Addison's disease is a possible diagnosis in any patient who presents with weakness, weight loss, hyperpigmentation, hyponatremia, and hypotension. Laboratory findings, including depressed levels of cortisol and aldosterone, help to confirm the diagnosis. Computed tomography may reveal adrenal calcification and abnormal-sized adrenal glands. In most cases, autoimmune destruction of the adrenal cortex is the cause of Addison's disease; however, as in the patient described here, tuberculosis is a possible cause.

Addison Disease↗
PubMed1975

Cytoenzymologic activities of some oxidroeductases and alkaline phosphatase of leucocytes in Basedow, Cushing and Addison diseases.

Leukocytes, approached by histoenzymological methods for demonstration of dihydrofolate dehydrogenase, NADH2-diaphorase, lactate dehydrogenase and alcaline phosphatase activities, provided information about the impaired metabolic balance of thyrotoxicosis, Cushing and Addison diseases. The most relevant variations were found in thyrotoxicosis, the most sensitive enzyme was dihydrofolate dehydrogenase and the less sensitive was alcaline phosphatase. The neutrophils and lymphocytes had more evident enzymic variations.

Addison Disease↗
PubMed1992

T and B cell reactivity to adrenal antigens in autoimmune Addison's disease.

Autoimmune Addison's disease is a rare condition of uncertain pathogenesis. To delineate potential autoantigens, an adrenal homogenate was fractioned by SDS-gel electrophoresis and used in immunoblotting and T cell proliferation assays. Antibodies specific for adrenal proteins with approximate molecular weights of 70, 55 and 45 were found in five out of 20 consecutive Addison's disease patients at routine follow-up. Five sera also reacted with a 52-kD protein shared with liver. T cells from six out of 10 Addison's disease patients proliferated in response to a range of adrenal-specific antigens including one, in particular, with a molecular weight of 18-24 kD. T and B cell reactivity to adrenal antigens did not appear to correlate and there was no relationship with time since diagnosis, associated autoimmunity or HLA-DR type. These results show that the autoimmune response to adrenal antigens in Addison's disease is heterogeneous and that such autoreactivity can only be inconsistently documented using these techniques and circulating antibodies or T cells.

Addison Disease↗
PubMed1976

Renal hemodynamics and water excretion in Addison's disease.

Patients with Addison's disease have impaired ability to excrete free water. The mechanism of this defect is still not clear. These experiments were designed to help clarify the role of altered renal hemodynamics in the genesis of the defect. Six patients with Addison's disease were studied. Enough salt and water was administered to maintain adequate hydration throughout the study but no hormonal replacement was instituted. After a water load, the urine output (V), free water clearance (CH2O), sodium excretion (UNaV), total solute clearance (COsm), inulin clearance (CIn), and para-aminohippurate clearance (CPAH) were measured by standard clearance techniques. In the control studies V and CH2O were abnormally low. The studies were repeated after administration of DOCA, 2.5 mg daily, for a week. This medication decreased UNaV and improved the plasma electrolyte profile but did not cause a significant change in V, CH2O, GFR, or RPF. The same studies were repeated once more after administration of prednisone, 5 mg daily in divided doses, for a week. This drug induced a marked water diuresis while GFR and RPF remained unchanged. It is concluded that hypovolemia and altered renal hemodynamics are not the only mechanisms of the impaired water excretion in Addison's disease. A severe defect remains after normalization of hypovolemia and this is corrected by prednisone but not by DOCA, through mechanisms which do not involve changes in GFR or RPF.

Addison Disease↗
PubMed1978

Tuberculous Addison's disease and thyrotoxicosis.

Addison's disease developed in two patients after they had tuberculosis. Thyrotoxicosis subsequently developed. In both cases, the adrenal glands were calcified, suggesting that Addison's disease was tuberculous in origin. Results of tests for antihyroglobulin, antimicrosomal, and adrenal cortex antibodies were normal. These findings do not suggest an autoimmune basis for the occurrence of the two endocrinopathies. The rarity of the simultaneous occurrence of both disorders suggests it to be fortuitous.

Addison Disease↗
PubMed1992

[The importance of computerized axial tomography in the etiological diagnosis of Addison's disease].

Sixteen cases of newly diagnosed Addison disease were studied by CT scan. An initial diagnosis was performed according to the clinical data of each patient, and a second diagnosis after examining the abdominal CT scan. According to the second diagnosis there were six patients with primary adrenal failure of probable autoimmune origin, six tuberculosis, two metastatic, one undetermined and one hemorrhagic. The second diagnosis coincided with the first one in 10 cases (62.5%), but was different in six cases (37.5%). Information obtained by CT scan modified the therapeutic attitude in 4 cases (25%). The main morphologic patterns of adrenal glands in CT scan (atrophy, calcification and enlargement) are commented as well as the importance of CT scan in the study of the more common etiologies of Addison's disease (tuberculosis, autoimmune, neoplastic metastasis and hemorrhage). It is concluded that the information obtained by CT scan is important in the etiological diagnosis of Addison disease and it is advised to perform it in all newly diagnosed cases.

Addison Disease↗
PubMed1992

Mania in association with hydrocortisone replacement for Addison's disease.

A 32 year old woman with untreated primary adenocortical insufficiency presented with prominent depressive symptoms. Upon treatment with physiological doses of glucocorticoids she developed a self-limiting acute manic illness. We suggest that up-regulation of hippocampal glucocorticoid receptors as a consequence of prolonged hypocortisolaemia resulted in increased cerebral sensitivity to exogenous corticosteroids, which are known to precipitate manic symptoms in some normal individuals when given in supraphysiological doses.

Acute Disease↗
PubMed1977

Secondary pituitary hyperplasia in Addison's disease.

In patients with Addison's disease, whether treated or untreated for the previous 24 hours, hydrocortisone produced only a partial suppression of their elevated adrenocorticotrophic-hormone (A.C.T.H.) levels. This is comparable to untreated myxoedema, in which administration of triiodothyronine fails to inhibit secretion of thyrotrophin (T.S.H.). In myxoedema, however, continued treatment produces normal T.S.H. levels. Inadequate A.C.T.H. suppressibility in patients with Addison's disease while on treatment may be due to the maintenance of a secondary pituitary hyperplasia by inadequate replacement therapy. This may be clinically important, especially in the genesis of Nelson's syndrome.

Addison Disease↗
PubMed1978

A possible ACTH secreting tumour of the pituitary developing in a conventionally treated case of Addison's disease.

A patient with Addison's disease, treated with conventional corticosteroid therapy, developed endocrine and radiological features suggestive of an ACTH secreting pituitary tumour. The negative feedback control of ACTH secretion by the inhibitory effect of hydrocortisone was shown to be preserved although attenuated. Retiming and alteration of corticosteroid therapy reinforced this feedback control, without the need for supraphysiological amounts of steroid, and resulted in the regression of the endocrine disorder.

Addison Disease↗
PubMed1977

[Idiopathic adrenal cortex dystrophy with the clinical picture of Addison's disease].

Clinical and autopsy findings are reported of three cases of Addisons disease due to idiopathic dystrophy of the adrenal cortex as seen in two women, 20 and 37 years of age respectively as well as a boy of 14 years. Idiopathic dystrophy of the adrenal cortex as a cause of Addisons disease has become aware of more and more frequently for some years. Its classification as an auto-aggression disease has been made a subject for discussion. Morphological findings and immunological investigations with three own cases confirm this conception. This disease should be reminded of with regard to the problem of clinically diagnosing it and the fatal prognosis of untreated cases.

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↗