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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↗
PubMed1985

The presence of methionine-enkephalin in plasma and urine in normal human subjects and various patients.

The present study was performed to investigate whether or not there were enkephalins in plasma and urine in normal subjects and in patients with various diseases. Two kinds of antisera were developed to detect M-enk and L-enk. One has specific affinity with the C-terminus of methionine-enkephalin sulfoxide (M-O-enk), the oxidized form of M-enk, and the other with the N-terminus of L-enk. M-enk-like substance (MELS) was present in blood and urine in normal subjects, but not L-enk-like substance (LELS). Plasma MELS and its urinary output averaged 38 +/- 14 pg/ml (N = 19) and 605 +/- 235 ng/day (N = 15, M. +/- S.D.), respectively. There was a significant increase in plasma MELS and its urinary output in patients with pheochromocytoma. Plasma MELS did not show any significant increase or decrease in Cushing's disease. Addison's disease, panhypopituitarism or chronic glomerulonephritis. The urinary output of MELS was significantly increased in patients with essential hypertension, renovascular hypertension and primary aldosteronism, but was decreased in central diabetes insipidus.

Addison Disease↗
PubMed1987

Myopathy in Addison's disease.

Since the first description of primary adrenocortical insufficiency by Thomas Addison in 1855 several large series of patients with Addison's disease have been published. The common signs and symptoms include: weakness, hyperpigmentation, weight loss, gastrointestinal complaints, and hypotension. It is rare for patients with Addison's disease to present with musculoskeletal symptoms including flexion contractures, hyperkalaemic neuromyopathy, Guillain-Barré syndrome, migratory myalgia, sciatica-like pain, and low back pain. Myopathy has not been previously described in Addison's disease. Herein we report a patient presenting with severe hyponatraemia and myopathy which resolved after steroid replacement therapy.

Addison Disease↗
PubMed2002

The importance of testing for adrenoleucodystrophy in males with idiopathic Addison's disease.

X linked adrenoleucodystrophy (X-ALD) is considered to be a rare cause of Addison's disease, although several small series suggest a high incidence in young Addisonian males. A survey in the south west of England identified 12 male patients diagnosed with Addison's disease in the period 1987-99. In 10 of these (83%) X-ALD was the underlying cause; the other two were of autoimmune aetiology. Five boys had developed Addison's disease subsequent to the diagnosis of X-ALD. Of the remaining five, in three boys the diagnosis of X-ALD was considerably delayed (by six months to two years from that of Addison's disease) and in two it was only made as a result of this survey. We also identified a patient who presented with Addison's disease at the age of 5 years but was only diagnosed as having X-ALD at the age of 34 years; in the interim his diagnosis of adrenomyeloneuropathy had been missed. Our experience highlights the absolute necessity of measuring very long chain fatty acids in all males with idiopathic Addison's disease.

Addison Disease↗
PubMed1980

Chromatographic characterization of adsrenocorticotrophin in human plasma.

A chromatographic procedure has been developed for the characterization of ACTH- and lipotrophin- (LPH) related peptides in human plasma under acid-dissociating conditions to minimize artifacts of protein binding. The recovery and sensitivity of this method permits identification of ACTH at normal physiological levels in the circulation. Plasma profiles obtained from normal subjects and patients with pituitary dependent Cushing's disease, Addison's disease and Nelson's syndsrome showed only one significant peak of ACTH activity eluting in the position of purified native human 1--39 ACTH. However, the plasma profiles obtained from all the patients with the ectopic ACTH syndrome demonstrated a second peak of immunoreactive larger-molecular-weight ACTH and in some plasma samples this was the only form of ACTH observed. This larger-molecular-weight ACTH eluted midway between the void volume and 1--39 ACTH and co-eluted with a protein marker of molecular weight 22 000.

ACTH Syndrome, Ectopic↗
PubMed1985

Addison's disease due to metastases to the adrenal glands.

A 43 year old patient with Addison's disease secondary to extensive metastases to both adrenal glands is presented. Thirty two previously reported cases are reviewed; in only 13 cases was the diagnosis of Addison's disease confirmed biochemically. Reasons for the apparent rarity of Addison's disease in spite of the frequency of adrenal metastases are discussed. The need to consider the possibility of Addison's disease complicating known malignant disease arising in other tissues is stressed.

Addison Disease↗