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

Two patients who developed Wernicke's Encephalopathy with subsequent hypothermia are described. Both patients responded rapidly to thiamine administration and one later had hypothalamic-pituitary function tests performed. This patient demonstrated depressed TSH response to TRH and a sluggish early cortisol response to adequate hypoglycaemia compared to 17 control subjects. These findings may suggest that previously described hypothalmic-pituitary abnormalties in chronic alcoholics may be mediated via thiamine deficiency and may also reflect hypothalamic damage contributing to the hypothermic state. The importance of intravenous thiamine administration in cases of coma of unknown aetiology is emphasised.
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PMID:Coma and hypothermia in Wernicke's encephalopathy. 693 37

The reported failure of serum TSH to rise in response to the low serum T3 of severe systemic illness may be due to the known stress inhibition of TSH secretion. We therefore measured TSH and total and free thyroid hormones during the course of recovery from severe illness. During recovery, TSH increased at a time when T3 was rising but still below normal (mean TSH during recovery, 6.5 +/- 0.8 SEM microU/ml, n = 41 vs. normal, 2.5 +/- 0.2 SEM microU/ml; n = 31; P less than 0.001), TSH concentrations were negatively correlated with total and free T3 and less strongly correlated with total T4 but not with free T4. Average TSH concentrations were also significantly elevated in severely ill patients with hypothermia that was unrelated to cold exposure (mean TSH, 5.6 +/- 1.3 microU/ml; n = 11; P less than 0.005). The T3 concentrations in these sera were lower than those of other severely ill patients. Thus, during recovery from severe illness and during hypothermia not induced by cold, the relationship between serum T3 and TSH is qualitatively similar to that seen in primary hypothyroidism and may imply a pituitary response to a deficiency of thyroid hormone.
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PMID:The relationship between serum triiodothyronine and thyrotropin during systemic illness. 707 98

Plasma growth hormone (GH) and thyrotropin (TSH) levels were measured in freely behaving rats for 6 h on three consecutive days. On the 1st and 3rd days there was no treatment, and on the 2nd day endotoxin (150 mg/kg) was administered intravenously. Endotoxin causes a biphasic temperature response: an initial hypothermia persisting for 1 h, followed by hyperthermia evident from 5 to 8 h after injection. Normal pulsatile GH release observed on the 1st day was abolished on the 2nd day by the endotoxin treatment. On the 3rd day, however, GH secretion was greater than on the initial control day. TSH release was also suppressed by endotoxin and showed a rebound release on the subsequent day. The suppression of GH secretion by endotoxin was reversed in all animals by antisomatostatin serum, and the suppression of TSH secretion by endotoxin was reversed in some animals. These results suggest that endotoxin is a potent stimulus for hypothalamic somatostatin release in the rat. Endotoxin profoundly alters adenohypophyseal hormone release.
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PMID:Altered release of growth hormone and thyrotropin induced by endotoxin in the rat. 712 45

Female rats were killed 15 days, 2 months, and 4 months after surgical thyroidectomy that was followed by injection of 100 microCi 131I. The concentrations of T3 and T4 were measured in tissues (liver, kidney, brain, heart, and hindleg muscle) specific RIAs. Results were compared to those found in intact rats. Thyroidectomy resulted in severe hypothyroidism by 2 and 4 months after the operation, as assessed by undetectable levels of T4 and T3 in unextracted plasma, high circulating TSH, hypothermia, stasis of body weight increase, and depletion of pituitary GH content. Concentrations of T4 and T3 in plasma, as determined after extraction and concentration, were very low, being less than 5% of the normal value by the earliest observation period (15 days). In contrast, although tissue concentrations and total organ contents also decreased after thyroidectomy, they were still clearly detectable 4 months after thyroidectomy. The rates of decrease of T4 and T3 concentrations in most tissues were markedly slower than expected from their rapid decrease in plasma. Some tissues still contained 20% of the normal level 2-4 months after ablation of the thyroid. Tissue levels of thyroid hormones were hardly detectable in rats thyroidectomized 6 months before, having decreased in most tissues to less than 5% of the normal value. Several animals from this group had died. It is concluded that tissues from severely hypothyroid thyroidectomized rats may contain higher concentrations of T4 and T3 than previously thought. The idea that thyroid hormone is not essential for life, based on the assumption that thyroidectomized animals survive without thyroid hormones, might have to be reevaluated.
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PMID:Presence of L-thyroxine and 3,5,3'-triiodo-L-thyronine in tissues from thyroidectomized rats. 726 25

Sleep deprivation is associated with poor cognitive ability and impaired physical health, but the ways in which the brain and body become compromised are not understood. In sleep-deprived rats, plasma total T4 and T3 concentrations decline progressively to 78% and 47% below baseline values, respectively, brown adipose tissue 5'-deiodinase type II activity increases 100-fold, and serum TSH values are unknown. The progressive decline in plasma thyroid hormones is associated with a deep negative energy balance despite normal or increased food intake and malnutrition-like symptoms that eventuate in hypothermia and lethal systemic infections. The purpose of the present experiment was to evaluate the probable causes of the low plasma total T4 during sleep deprivation by measuring the free hormone concentration to minimize binding irregularities and by challenging the pituitary-thyroid axis with iv TRH to determine both 1) the pituitary release of TSH and 2) the thyroidal response of free T4 (FT4) and free T3 (FT3) release to the TSH increment. Sleep-deprived rats were awake 91% of the total time compared with 63% of the total time in yoked control rats and 50% of the total time during the baseline period. Cage control comparison rats were permitted to sleep normally. Sustained sleep deprivation resulted in a decline from baseline in plasma FT4 of 73 +/- 6% and FT3 of 45 +/- 12%, which were similar to the declines in total hormone concentrations observed previously; nonstimulated TSH was unchanged. In the yoked and cage control groups, FT4 also declined, but much less than that of the sleep-deprived group. The relative changes in free compared with total hormone concentrations over the study were also less parallel than those in the sleep-deprived group. The plasma TSH response to TRH was similar in all groups across experimental days. The plasma FT4 and FT3 concentrations in sleep-deprived rats increased after TRH-stimulated TSH release to an extent comparable to control values. Taken together, low basal FT4 and FT3 hormone concentrations and unchanged TSH and thyroidal responses to TRH suggest a pituitary or hypothalamic contribution to the hypothyroxinemia during sleep deprivation.
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PMID:Pituitary and peripheral thyroid hormone responses to thyrotropin-releasing hormone during sustained sleep deprivation in freely moving rats. 789 53

Central and peripheral compartments of hypophyseo-adrenal regulation, the state of renin-angiotensin-aldosterone system (RAAS) and thyroid-stimulating functions of hypophysis have been assessed in 72 patients with heart valve defects operated under profound hypothermal perfusion. It has been established that cardiopulmonary bypass surgery with profound hypothermia is accompanied by moderate and reversible changes in the above parameters. The activity of hypophyseo-adrenal system and RAAS reaches the maximum during a warming-up period and then gradually decreases. TSH content considerably decreases in the early postoperative period. Cardiopulmonary bypass surgery with profound hypothermia causes more pronounced changes in neurohormonal regulation than heart valve correction under hypothermal perfusion, which might be associated with blood flow arrest in major vessels causing changes in peripheral metabolic processes.
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PMID:[Hormonal regulation during cardiac surgery operations on the "dry" heart]. 806 1

A patient with mild hypothyroidism underwent a repair of abdominal aortic aneurysm. Although the serum TSH level of this patient was very high and T4, free T4 levels were low, T3 level remained within normal ranges. Inhalation anesthesia with continuous epidural block was selected and there was no complication such as hypotension or hypothermia during perioperative period. Recently, several reports demonstrate that the preoperative supplemental therapy of the thyroid hormone should not be necessary in the case of mild hypothyroidism. Moreover, the biological potency of T3 is higher than that of T4. Thus, in patients whose T3 level is kept within normal ranges even if serum T4 level is low and serum TSH level is high, we may say that they are in euthyroid state. We think these patients can be anesthetized safely.
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PMID:[Anesthetic management of a patient with mild hypothyroidism]. 807 61

Eleven patients with severe head injuries were treated by artificial moderate hypothermia (32.0-33.0 degrees C). Measurement of the serum levels of anterior pituitary hormones (LH, FSH, TSH, and PRL) and the response of these hormones to the respective releasing hormones was done in the 11 patients before and during hypothermia. All 11 patients were under GCS 5. Those with brain death during hypothermia were excluded. Moderate hypothermia was performed for 3-7 days and involved cooling to 32.0-33.0 degrees C (Jugular venous blood temperature). The peak value of LH, FSH, TSH and PRL to administration of TRH or LH-RH during hypothermia were significantly lower than those before hypothermia, while basal values of those hormones were not affected by this treatment. These findings suggested that anterior pituitary function were suppressed by moderate hypothermia.
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PMID:[Anterior pituitary functions in patients with severe head injuries treated with moderate hypothermia]. 904 26

Myxedema coma is the most severe form of hypothyroidism and is characterized by extreme hypothermia, bradycardia, central hypoventilation and hypoxia. Common causes are intercurrent diseases, interruption of thyroid hormone treatment, or an overdose of sleeping pills or sedatives. The diagnosis is usually readily established on the basis of very high serum TSH and low T4 levels. Consideration must also be given to an extra-thyroidal influence on the hormone levels. Intensive care treatment involving intravenous high-dose L-thyroxine and the reversal of hypoxia improve the prognosis of the serious disease.
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PMID:[Coma in myxedema--a rare complication of hypothyroidism. Possible iatrogenic factors should be taken into account]. 908 99

Since the introduction of neonatal mass screening for congenital hypothyroidism (CH), numerous cases have been detected. It is of interest that even severely hypothyroid neonates rarely exhibit bradycardia, hypothermia, or inactivity, which have been recognized as typical signs of CH. Regarding neonates and young infants, few reported data are available on the effects of thyroid hormones on energy expenditure. Plasma free fatty acids (FFAs), markers for lipolysis, play essential roles in maintaining physiologic homeostasis. To study fuel utilization in CH neonates, we measured heart rates, plasma FFA, and thyroid hormones before and after levothryoxine (LT4) replacement therapy. Fifty-five screen-detected CH neonates and 29 age-matched normal neonates for controls were enrolled. The CH neonates were divided into two groups according to serum thyroid hormone levels: a mildly hypothyroid group (n = 37), serum thyrotropin (TSH) less than 100 microIU/mL and free thyroxine (FT4) 0.6 ng/dL or more; and a severely hypothyroid group (n = 18), TSH 100 microIU/mL or more and FT4 less than 0.6 ng/dL. Twenty-four of the 55 patients had their heart rates measured by electrocardiography. Fasting blood samples were taken from the subjects during physical movements. Serum levels of TSH, FT4, FFA, and other blood chemicals, measured on an autoanalyzer system in our hospital, were compared before and after LT4 substitution therapy. The following results were obtained. The mean plasma FFA values before LT4 replacement were 208.5 +/- 89.4 microEq/L in the mildly hypothyroid group, 228.5 +/- 114.7 microEq/L in the severely hypothyroid group, and 213.9 +/- 97.7 microEq/L in controls. No statistical differences were noted among the three values. Two months after LT4 replacement therapy, at the age of 3 months, plasma FFA concentrations significantly increased in both groups compared with those before the therapy. Control infants also showed a significant increase in plasma FFA concentrations from 1 to 3 months of age. There were no significant differences in plasma FFA concentrations among the three groups at the age of 3 months. No significant correlations were found between plasma FFA and serum thyroid hormones. From these results it is suggested that in neonates and young infants, thyroid hormones do not play major roles in mobilization of fats through the adrenergic regulation of lipolysis for energy supply. This may be one of the reasons for the unexpectedly mild signs and symptoms in the screen-detected hypothyroid neonates.
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PMID:Plasma free fatty acids in neonates with congenital hypothyroidism. 1127 1


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