Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The endocrine response to stress is complex. Elevations in the serum concentrations of the "classic" stress hormones, epinephrine and cortisol, occur following many kinds of physiologic challenge and are accompanied by elevations in corticotropin, GH, and glucagon levels. These changes are probably responsible for the hyperglycemia and hypercatabolism common to most critical illness. If volume depletion is present, vasopressin, renin, and aldosterone secretion are also likely to be stimulated. These hormones, if present in excess, may produce fluid retention and hyponatremia. In some critically ill patients, there is a dissociation of renin and aldosterone production called hyperreninemic hypoaldosteronism, but the clinical importance of this syndrome is poorly understood. Thyroid hormone metabolism is commonly affected by critical illness, which results in characteristic abnormalities of thyroid function testing known as the euthyroid sick syndrome. The reproductive axis is exquisitely sensitive to physiologic stress; hypogonadotropic hypogonadism is a common finding in critical illness. The ongoing challenge to the clinician is to determine whether seemingly abnormal hormone measurements in critically ill patients reflect an appropriate homeostatic response to severe illness or, instead, whether they denote an independent metabolic disorder that might actually cause or contribute to the patient's unstable condition. In view of the exceedingly complex (and poorly understood) interactions involved in the human response to a severe illness, a thoughtful approach to the whole patient is essential and far preferable to indiscriminate hormone testing. Such testing, at best, may be uninterpretable in light of the clinical circumstances or, at worst, may lead to therapeutic misadventures.
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PMID:The endocrine response to critical illness. 780 93

Selective iron deposition in the zona glomerulosa of the adrenal cortex is observed in hemochromatosis. Hypoaldosteronism should be excluded before starting venesection, to avoid long-term volume depletion. We evaluated the aldosterone status in patients with hemochromatosis. As other endocrine organs can be affected by the disease as well, we simultaneously evaluated anterior pituitary, gonadal, thyroid and pancreatic beta-cell activity. Nine patients with hereditary or acquired hemochromatosis and highly increased plasma ferritin levels were investigated. In patients, liver cirrhosis had been confirmed histologically. Five patients complained of sexual dysfunction, and one had impaired glucose tolerance. Plasma aldosterone (PA) and renin activity (PRA) were measured after a period of normal (100 mmol/day) and low (10 mmol/day) sodium intake. A combined anterior pituitary function test and a glucagon stimulation test were undertaken to evaluate other endocrine functions. Both PA and PRA levels were decreased in one patient with liver cirrhosis, who also presented attenuated cortisol, prolactin and gonadotrophin secretion. No patients had signs of primary hypoaldosteronism with hyperreninemia. Hypogonadotropic hypogonadism was observed in 3 males and 1 female. Pituitary ACTH reserve was impaired in 2, GH and prolactin response in 1, and thyroid function in none of the patients. Glucagon-stimulated plasma C-peptide was impaired in one patient. In conclusion, primary aldosterone deficiency was not observed in patients with severe iron overload. Hyporeninemic hypoaldosteronism was found in one patient who also presented other endocrinopathies. Hypogonadotropic hypogonadism is the most frequent endocrine abnormality in hemochromatosis.
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PMID:Mineralocorticoid status and endocrine dysfunction in severe hemochromatosis. 1040 11