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Query: UMLS:C0020672 (hypothermia)
17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a rare case of hypothermia with acute renal failure in a patient suffering from diabetic nephropathy. A 71-year-old male who had been receiving insulin therapy for the treatment of diabetes mellitus complicated with advanced diabetic nephropathy since 1998 was malnourished with an extremely decreased muscle mass. Without any prolonged exposure to excessively low external temperatures or hypothyroidism, pituitary insufficiency, adrenal insufficiency, sepsis, hypoglycemia, and diabetic ketoacidosis, acute hypothermia appeared together with an aggravation of diabetic nephropathy. His skin temperature fell to below measurable levels and his rectal temperature fell to 30.0 degrees C. His consciousness was drowsy and the hypothermia was not accompanied by shivering. Skeletal muscle is known to play an important role as a center of heat production and shivering thermogenesis in skeletal muscle mainly operates on acute cold stress. Therefore, in this case, hypothermia may have occurred because the shivering thermogenesis could not fully act on the acute cold stress due to the dramatically reduced muscle mass. We should always keep in mind that older, malnourished diabetic patients can easily suffer from impairments of the thermoregulatory system.
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PMID:Hypothermia with acute renal failure in a patient suffering from diabetic nephropathy and malnutrition. 1080 30

Thyroxine (T4) and 3,5,3'-triiodothyronine (T3) are secreted by the thyroid gland, while T3 is also generated from the peripheral metabolism of T4 by iodothyronine deiodinases types I and II. Several conditions like stress, diseases, and physical exercise can promote changes in local TH metabolism, leading to different target tissue effects that depend on the presence of tissue-specific enzymatic activities. The newly discovered physiological and pharmacological actions of T4 and T3 metabolites, such as 3,5-diiodothyronine (3,5-T2), and 3-iodothyronamine (T1AM) are of great interest. A classical thyroid hormone effect is the ability of T3 to increase oxygen consumption in almost all cell types studied. Approximately 30 years ago, a seminal report has shown that 3,5-T2 increased oxygen consumption more rapidly than T3 in hepatocytes. Other studies demonstrated that exogenous 3,5-T2 administration was able to increase whole body energy expenditure in rodents and humans. In fact, 3,5-T2 treatment prevents diabetic nephropathy, hepatic steatosis induced by high fat diet, insulin resistance, and weight gain during aging in Wistar male rats. The regulation of mitochondria is likely one of the most important actions of T3 and its metabolite 3,5-T2, which was able to restore the thermogenic program of brown adipose tissue (BAT) in hypothyroid rats, just as T3 does, while T1AM administration induced rapid hypothermia. T3 increases heart rate and cardiac contractility, which are hallmark effects of hyperthyroidism involved in cardiac arrhythmia. These deleterious cardiac effects were not observed with the use of 3,5-T2 pharmacological doses, and in contrast T1AM was shown to promote a negative inotropic and chronotropic action at micromolar concentrations in isolated hearts. Furthermore, T1AM has a cardioprotective effect in a model of ischemic/reperfusion injury in isolated hearts, such as occurs with T3 administration. Despite the encouraging possible therapeutic use of TH metabolites, further studies are needed to better understand their peripheral effects, when compared to T3 itself, in order to establish their risk and benefit. On this basis, the main peripheral effects of thyroid hormones and their metabolites in tissues, such as heart, liver, skeletal muscle, and BAT are discussed herein.
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PMID:Similarities and Differences in the Peripheral Actions of Thyroid Hormones and Their Metabolites. 3007 51