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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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↗
PubMedDate not supplied

[Adrenocorticotropic function of the pituitary gland in endocrine diseases].

In examination of 123 patients with diabetes mellitus. Itsenko-Cushing disease, Addison's disease, thyrotoxicosis and adiposity there was revealed an increase in the content of the adrenocorticotropic hormone (ACTH) in the blood. Comparison of the ACTH and cortizol concentration in the blood permitted to suppose a different mechanism of the derangements revealed. An increase of the adrenocorticotropic function of the hypophysis in diabetes mellitus, Itsenko-Cushing disease and thyrotoxicosis was accompanied by a rise in the blood cortizol level. A fall of glucocorticoid function of the adrenal glands in Addison's disease and a relative hypocorticism in the patients with adiposity caused a compensatory intensification of the ACTH secretion.

Addison Disease↗
PubMed1977

[Simultaneous occurrence of juvenile diabetes and Addison's disease (author's transl)].

The occurrence of diabetes mellitus and Addison's disease together is discussed by the authors. The female patient described here had diabetes at the age of four; Addison's disease appeared when the patient was 19 years old. Four years prior to the appearance of Addison's disease, an ophthalmoscopic examination revealed microaneurysms. The examination of the fundus of the eye was negative when Addison's disease, was diagnosed. An HLA-B8 antigen positivity was established. The authors discussed the pathogenetic relationship of HLA-B8 antigen positivity, diabetes mellitus, and Addison's disease.

Addison Disease↗
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↗
PubMed1979

Probable pituitary adenoma with adrenocorticotropin hypersecretion (corticotropinoma) secondary to Addison's disease.

A 50-yr-old woman with Addison's disease from the age of 14 yr was diagnosed as empty sella turcica in 1974 (Rev Clin Esp 139: 183, 1975). She subsequently continued with hyperpigmentation in spite of adequate hormone substitution therapy which permitted her to lead a normal life. When studied she showed an extreme elevation of plasma ACTH (1500--2000 pg/ml), and with dexamethasone (2 and 8 mg/day) continued to have levels of 900 pg/ml. With 60 mg hydrocortisone daily, effects of overdosage were observed (swelling and Cushingoid facies) associated with depigmentation. However, she continued to manifest levels of plasma ACTH of 700 pg/ml and an absence of circadian rhythm. It seems likely that this patient represents a case of pituitary ACTH secretory adenoma (corticotropinoma) secondary to the preexisting Addison's disease. The circulating levels of other pituitary hormones were normal.

Addison Disease↗
PubMed1976

[Thyrotropic function of the hypophysis in endocrine diseases].

The content of thyrotropic hormone of the hypophysis (by radioimmunological method) and the level of thyrotropic hormones in the blood plasma were studied in 178 patients with various endocrine pathology (thyrotoxicosis, hypothyroidism, diabetes mellitus, Itsenko-Cushing disease, Addison's disease, adiposity). Healthy persons (33) served as control. Thyrotropic function of the hypophysis proved to be decreased in thyrotoxicosis, diabetes mellitus, adiposity, Itsenko-Cushing disease. Comparison of the plasma level of thyrotropin and thyroid hormones led to a supposition on a different mechanism of the detected changes. A marked intensification on the thyrotropic function of the hypophysis was observed in primary hypothyroidism. A tendency to increase of thyrotropin discharge was noted in the patients suffering from thyrotoxicosis given antithyroid treatment and in Addison's disease.

Adolescent↗