Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Presented is the case of a normal two-month-old girl who developed seizures secondary to water intoxication. The infant had been fed 20 to 30 oz of water daily for three days, while her usual formula was withheld because of vomiting and diarrhea. On the day of admission, the infant exhibited signs of water intoxication in the form of lethargy, vomiting, and seizures. Hyponatremia, hypothermia, and hyperglycemia were noted on admission, and are common features of the syndrome. The patient responded well to fluid restriction and salt replacement. Previous reports have attributed water intoxication to feeding mismanagement, vigorous hydration, dilute formulas, and swimming lessons.
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PMID:Water intoxication with seizures. 396 5

A female newborn infant with Marfan-like habitus experienced lethargy and hypothermia associated with tyrosinemia that was not corrected by the administration of ascorbic acid at 50 mg/day but that subsequently responded to ascorbic acid at 500 mg/day. Cerebrospinal fluid analysis for neurotransmitter metabolites showed elevated concentrations of homovanillic acid and 5-hydroxyindoleacetic acid when the child was symptomatic and normal concentrations after successful ascrobic acid therapy. These observations suggest that a high level of tyrosine in serum can affect the metabolism in the brain of dopamine and serotonin.
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PMID:CSF neurotransmitter studies. An infant with ascorbic acid-responsive tyrosinemia. 615 67

Echoviruses cause neonatal disease following intrauterine and intrapartum acquisition of the organism or by nosocomial infection. Dizygous twins apparently became infected following transplacental transmission of echovirus 11. At 5 days of age, both twins experienced poor feeding, lethargy and hypothermia, and evidence of coagulopathy and hepatitis. During the sixth week of illness, the convalescence of twin A was complicated by peritonitis and sepsis, and the infant died. Pathologic findings included scattered foci of dystrophic myocardial calcification, distortion of hepatic architecture with fibrous connective tissue surrounding regenerative nodules and large foci of dystrophic calcification, and adrenal hemorrhagic necrosis and calcification. Twin B recovered without sequelae. The disease in twin A was unusual because of the extensive myocardial involvement. Also of interest was the variability of disease in twins who presumably had received a similar inoculum of organism by the same route.
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PMID:Dissimilar manifestations of intrauterine infection with echovirus 11 in premature twins. 634 39

In order to determine the influence of hibernation depth upon the secretion and the effect of insulin, two groups of edible dormice were maintained in winter under different climatic and nutritional conditions, and their pancreatic B-cell function was tested during the spring arousal. The first group of animals was exposed to a moderate temperature and fed ad libitum. Their periods of hypothermia were short and irregular and the active periods sometimes lasted several days; their body weight increased during the winter months; in spring, the sensitivity of B cells to glucose was low, decreasing insulin secretion in vivo and in vitro, and the adipocytes were insulin resistant. The second group of fasting animals was exposed to a low and constant temperature (5 degrees). Their phases of lethargy were long and regular (about 15 days), separated by active periods (6-8 hr); their body weight decreased during the winter months; in spring the B-cell secretion was increased and the sensitivity of the tissues to insulin ensured a high peripheral glucose utilization. These data show that the winter climatic and nutritional conditions which influence the depth of hibernation modify the edible dormouse B-cell activity during the spring arousal.
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PMID:Hibernation depth influences the edible dormouse pancreatic B cell during the spring arousal. 637 92

Episodic hyperhidrosis and hypothermia are the primary symptoms of a rare central nervous system disorder of thermoregulation which is often associated with agenesis of the corpus callosum and can present in childhood or adult years. During attacks, patients may exhibit confused, withdrawn, and lethargic behavior and ataxia or other neurologic symptoms. A 21-year-old man with temperature chronically between 30 and 32 degrees C transiently responded to phenobarbital and to cyproheptadine therapy. A 34-year-old woman with frequent, brief episodes of hypothermia and hyperhidrosis improved with chlorpromazine treatment. Episodic thermoregulatory disturbance has been attributed to "vagal attacks" or "diencephalic epilepsy," but the pathophysiology remains undefined.
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PMID:Episodic hyperhidrosis, hypothermia, and agenesis of corpus callosum. 668 46

The effects of adenosine on the acute toxicity and oncolytic activity of adriamycin (ADR) were evaluated in mice. When administered as a single i.p. injection of 17.5 mg/kg, adriamycin produced death in all mice within 12 days after treatment, with a mean survival time of 5-9 days. In contrast, the mean survival time of mice administered adenosine subcutaneously (200 mg/kg) in addition to adriamycin was significantly increased compared to adriamycin-treated mice. The protection elicited by adenosine was apparently not a generalized phenomenon of purines, however, since neither hypoxanthine nor inosine were effective protectants. Although a number of adenosine treatment schedules were tested, it was found that adenosine given immediately after adriamycin was as effective as multiple adenosine injections. Administration of adenosine had no apparent effect on adriamycin-mediated changes in ventricular weight, leukocyte count, elevated serum lactic dehydrogenase (LDH) activity or in the histopathologic changes observed in selected tissues. Two grossly observable effects of adenosine administration were lethargy and peripheral hypothermia, which were first noticed approximately 15 min after adenosine administration and which lasted for up to 2 hr. Finally, adenosine had no adverse effect on the antitumor efficacy of adriamycin against L1210 ascites cells inoculated i.p. to BDF1 mice.
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PMID:Reduction of acute adriamycin toxicity in mice treated with adenosine. 668 57

Clostridium botulinum can colonize and produce botulinal toxin in the human infant intestine, which the toxin then permeates to cause generalized flaccid paralysis, and occasionally, sudden death. This study was undertaken to test the hypothesis that toxins produced by other intestinal clostridia, e.g., C. difficile, might also cause systemic illness and sometimes death in infants (J Pediatr 100:568, 1982). Because this hypothesis could not be evaluated clinically until the systemic manifestations of C. difficile toxins in primates were known, infant rhesus monkeys were given 6 to 11 micrograms/kg of the recently purified C. difficile toxins A or B, either intravenously or intraperitoneally. The animals showed no abnormalities for several hours, but then developed lethargy, hypotonia, hypothermia, and, shortly before death, sudden elevation of serum concentrations of potassium, magnesium, and phosphorus and of enzymes that derived mainly from skeletal muscle, heart and brain. Five of six animals died quietly 3.5 to 8.0 hours after onset of symptoms. Death appeared to result from cessation of breathing, after which the sinus tachycardia then deteriorated to a flat ECG. Necropsy findings were insufficient to explain the cause of death. It appears that in infant monkeys microgram amounts of C. difficile toxins A and B can produce a rapid quiet death, the cause of which is undetectable at necropsy, a situation pathologically reminiscent of crib death in human infants, although the possible clinical identity of these two conditions has yet to be established.
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PMID:Rapid death of infant rhesus monkeys injected with Clostridium difficile toxins A and B: physiologic and pathologic basis. 669 Jun 74

Following the Exxon Valdez oil spill, 347 oiled sea otters (Enhydra lutris) were treated in rehabilitation centers. Of these, 116 died, 94 within 10 days of presentation. Clinical records of 21 otters dying during the first 10 days of rehabilitation were reviewed to define the laboratory abnormalities and clinical syndromes associated with these unexpected deaths. The most common terminal syndrome was shock characterized by hypothermia, lethargy, and often hemorrhagic diarrhea. In heavily and moderately oiled otters, shock developed within 48 hours of initial presentation, whereas in lightly oiled otters shock generally occurred during the second week of captivity. Accompanying laboratory abnormalities included leukopenia with increased numbers of immature neutrophils (degenerative left shift), lymphopenia, anemia, azotemia (primarily prerenal), hyperkalemia, hypoproteinemia/hypoalbuminemia, elevations of serum transaminases, and hypoglycemia. Shock associated with hemorrhagic diarrhea probably occurred either as a direct primary effect of oiling or as an indirect effect secondary to confinement and handling in the rehabilitation centers. Lightly oiled otters were less likely to die from shock than were heavily oiled otters (22% vs. 72%, respectively). Heavily oiled otters developed shock more rapidly and had greater numbers of laboratory abnormalities, suggesting that exposure to oil was an important contributing factor.
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PMID:Clinical and clinical laboratory correlates in sea otters dying unexpectedly in rehabilitation centers following the Exxon Valdez oil spill. 748 8

A six-year-old girl with non-Hodgkin's lymphoma who was treated with both intravenous (IV) and intrathecal (IT) methotrexate and developed brain damage secondary to the cytostatic drug is described. This patient displayed hypertension, hypothermia/hyperthermia, lethargy, deterioration and coma as clinical findings, and bilateral, focal white matter hyperintensities in the occipital lobes were seen in her magnetic resonance imaging (MRI). Treatment-related leukoencephalopathy is one such adverse effect of IT methotrexate administration on the central nervous system and usually appears in a generalized form.
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PMID:Methotrexate-induced leukoencephalopathy. A case report. 750 68

An 8-year-old, neutered, male, domestic shorthaired cat is admitted to your clinic with a complaint of lethargy and anorexia. The cat was last examined 2 months previously with a urinary tract infection and severe cellulitis at the site of a ventral abdominal urethrostomy. The urethrostomy was performed several years ago at another clinic. Euthanasia was recommended during your first examination, but the owner insisted on treatment. The cat improved after receiving fluids and systemic and topical antibiotics, but its condition suddenly deteriorated 2 days ago. Physical examination reveals severe dehydration, bradycardia, hypothermia, and an infected and fly-blown urethrostomy opening. Euthanasia is again recommended. The owner refuses and leaves the clinic, apparently intending to seek a second opinion.
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PMID:An ethicist's commentary on the case of a client who refuses euthanasia for a sick cat. 758 30


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