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)

Alprazolam is a benzodiazepine anti-anxiety agent that acts at the limbic, thalamic, and hypothalamic level of the CNS and has anxioytic. sedative, hypnotic, skeletal muscle relaxant, and anticonvulsant properties. A retrospective study was conducted of 415 alprazolam ingestions in dogs reported to the ASPCA Animal Poison Control Center between January 1998 and August 2000: 238 suspected alprazolam toxicoses in dogs were evaluated. Clinical signs were ataxia/disorientation, depression, hyperactivity, vomiting, weakness, tremors, vocalization, tachycardia, tachypnea, hypothermia, diarrhea, and increased salivation that developed within 10-30 min post-ingestion. Treatment included standard decontamination procedures, such as emesis and activated charcoal: the specific benzodiazepine antagonist, flumazenil, may be used for severe CNS depression.
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PMID:Accidental ingestion of alprazolam in 415 dogs. 1182 68

Melia azedarach fruits were administered at single doses ranging from 5 to 30 g/kg bw to 10 calves. The animals dosed with 25 g/kg bw and 30 g/ kg bw died, as well as 1/2 cattle that received 15 g/kg bw. Clinical signs were depression, ruminal stasis, anorexia, diarrhea, incoordination, muscle tremors, difficulty to stand, sternal recumbence, hypothermia and dyspnea. Serum AST and CPK were increased. Signs appeared 4 to 24 h after dosing and the clinical manifestations continued for 20 to 72 h. Macroscopic findings included congestion of the intestine, focal or diffuseyellow discoloration of the liver, and brain congestion. LiQuid content was in rumen, reticulum and intestines. The liver had swollen and vacuolated hepatocytes, and necrotic hepatocytes were scattered throughout the parenchyma or concentrated in the periacinar zone. Degenerative and necrotic changes were in the epithelium of the forestomachs. There was also necrosis of lymphoid tissue. Skeletal muscles had hyaline degeneration and fiber necrosis.
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PMID:Intoxication of cattle by the fruits of Melia azedarach. 1204 65

187 babies born elsewhere and referred to the Pediatric Department of the Christian Medical College and Hospital, Ludhiana, for management of prematurity over a period of 6 years were studied. Babies with hypothermia and those below 1200 g were given iv fluids. Preterm babies delivered in the institution and managed in the neonatal special care nursery over 1 year were also studied for comparison. The preterm babies were evenly distributed in the different gestation age groups between 28 and 36 weeks. About half the babies were appropriate for gestational age, while 47% were small for gestational age. The weight ranged from 760 to 2260 g. Males (166) outnumbered females (21) by a ratio of 8:1. There was a high incidence of hypothermia (54%) at the time of admission, more so in babies with gross prematurity. In babies less than 30 weeks old, 80% had become hypothermic during transit to the hospital. A fatal outcome was seen in 69% of babies with hypothermia as compared to 38% of babies admitted without hypothermia. 85% of babies were born in circumstances of potential infection in the form of prolonged rupture of membranes, multiple unsterile vaginal examinations, foul smelling liquor, fever of the mother, or a combination of these. Septicemia, purulent meningitis, bronchopneumonia, and diarrhea were the common infections. Other common morbidities were hyaline membrane disease, necrotizing enterocolitis, and metabolic disturbances. The overall mortality was 54% and it was inversely proportional to the gestational age, increasing from 36% at 35-36 weeks to 82% at 28-30 weeks. On the other hand, there was only a 21% mortality rate among preterm babies delivered at the hospital and managed in the neonatal nursery. Mortality was 9% in babies at 35-36 weeks. Intracranial hemorrhage was the most common cause of death in the study group, accounting for 42% of total deaths (59% of deaths at 28-30 weeks gestation, decreasing to only 4% at 35-36 weeks), followed by septicemia in 31%. On the other hand, septicemia caused about one-third of deaths at 35-36 weeks.
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PMID:Outcome of hospitalised out-born preterm babies. 1228 86

This article offers a protocol for reducing high case fatality rates from malnutrition. Most child deaths from malnutrition occur in the first few days of treatment. Treatment should involve stabilization followed by rehabilitation. The article describes the treatment procedures for hypoglycemia, hypothermia, dehydration, and missed infections and discusses feeding during the stabilization and rehabilitation phases of treatment. All severely malnourished children have excess body sodium but high intracellular and low plasma levels. Malnourished children have deficiencies of potassium and magnesium that may take 2 weeks to correct. Edema is partly due to deficiencies in potassium and magnesium. A high sodium intake can be corrected by rehydrating with a modified oral rehydration solution and the special starter formula. Family food should be prepared without salt. Magnesium and potassium should be added directly to foods. All severely malnourished children have vitamin and mineral deficiencies. Deficiencies may include vitamin A, zinc, copper, selenium, and folic acid. Multivitamin supplements can correct for micronutrient deficiencies. It is advised that zinc should not be ignored, since it is responsible for repair of intestinal mucosa, halting diarrhea, healing of ulcerated skin lesions, restoration of appetite, improved immune function, and lean tissue synthesis. Iron should not be given until growth starts, infections are controlled, and antioxidant status is improved (usually 1 week after admission). Early introduction of iron poses a risk of enhancing pathogen increases and stimulating production of toxic free radicals. Relapses can be reduced by training parents how to feed their child frequently with energy and nutrient dense foods. The regimen was tested in a South African project and found to reduce mortality from 30% to 20%. After greater hospital attention to treatment of sepsis and hypoglycemia, case fatality declined to 6%.
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PMID:Severe malnutrition in children: high case-fatality rates can be reduced. 1232 Dec 37

Natural infection of humans with human T-cell lymphotropic virus type I (HTLV-I) and of old world nonhuman primates with the simian counterpart, STLV-I, is associated with development of neoplastic disease in a small percentage of individuals after long latent periods. HTLV-I is also the etiologic agent of a more rapidly progressive neurologic disease, HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Macaques have been used experimentally in studies to evaluate HTLV-I candidate vaccines for efficacy, but no evidence of disease was observed. Here we report experimental infection of pig-tailed macaques with STLV-I(sm) and HTLV-I(ACH), both of which were associated with a disease syndrome characterized by rapid onset, hypothermia, lethargy, and death within hours to days. Other pathologic sequelae included diarrhea, rash, bladder dysfunction, weight loss, and, in one animal, arthropathy. Both retroviruses were detected in the central nervous systems of some animals, either by culture or by direct antigen capture for p19 Gag in cerebrospinal fluid. Although virus was recovered throughout infection from peripheral blood mononuclear cells (PBMC), all infected macaques maintained low antiviral antibody titers and stable proviral burdens, which generally ranged between 10 and 100 copies per 10(6) PBMC. However, of 13 macaques infected with HTLV-I(ACH) or STLV-I(sm), seven animals (54%) died between 35 weeks and 412 years after infection. This unexpected high mortality within a relatively short time suggests that infection of pig-tailed macaques might be a useful model for studying immune responses to and pathologic events resulting from HTLV-I infection.
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PMID:Association of primate T-cell lymphotropic virus infection of pig-tailed macaques with high mortality. 1250 76

Metformin belongs to a class of drugs known as the biguanides that are widely used in the treatment of type 2 diabetes mellitus. Its association with lactic acidosis is well established, although rare. Metformin-associated lactic acidosis is recognized as a potentially lethal condition that can occur in patients with contraindications to the drug, such as renal dysfunction, liver diseases, alcoholism, and cardiopulmonary diseases. In these cases, the plasma concentration of metformin is not necessarily abnormally high. We describe a 75-year-old diabetic woman with acute renal failure and life-threatening lactic acidosis due to metformin intoxication. Clinical manifestations included vomiting, diarrhea, hypothermia, hypotension and transitory blindness. Her initial renal function was recovered after hemodialysis and she was discharged 3 months after admission.
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PMID:Metformin-associated lactic acidosis and acute renal failure in a type 2 diabetic patient. 1460 17

Studies in animals exploring the antagonism of the cholinesterase inhibitors soman and sarin have shown that pretreatment with low doses of the centrally acting cholinesterase inhibitor, physostigmine, alone or in conjunction with the centrally acting anticholinergic agent, scopolamine, is effective against their lethality and toxicity. The current study evaluated the effects of pretreatment with the oral anticholinesterase agent, donepezil (Aricept, 2.0 mg/kg), used to treat Alzheimer's disease, with and without scopolamine in decreasing the hypothermic, hypokinetic, and diarrhea-inducing effects of the irreversible long-acting cholinesterase inhibitor diisopropyl fluorophosphate (DFP, 1.0 mg/kg) in adult Flinders sensitive line (FSL) male rats. Donepezil alone and donepezil plus scopolamine (0.1 mg/kg) to a greater extent antagonized the decrease in temperature, hypoactivity, and induction of diarrhea due to DFP observed at 4 h after its administration. However, donepezil alone induced hypothermia at 1 and 2 h after treatment. Therefore, these preliminary findings are encouraging, but many additional studies are needed to establish the effectiveness of donepezil as a prophylactic agent against irreversible cholinesterase inhibition by DFP.
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PMID:Antagonism of anticholinesterase (DFP) toxicity by donepezil plus scopolamine: a preliminary study. 1475 62

To induce luteal regression-related abortion/delivery and treat pyometra in dogs, various PGF2alpha-analogues (PGAs) are administered, but a PGA most appropriate for clinical application in dogs, with a low incidence of side effects, is being investigated. In this study, we compared the effects of etiproston tromethamine (PGA-E), which has not been investigated in dogs, with those of cloprostenol (PGA-C), which is routinely used in dogs. A single dose of PGA-E at 100, 200, 400 or 800 microg or PGA-C at 12.5, 25, 50 or 100 microg was administered to beagles (n=5 per group) 25 days after ovulation, when the corpus luteum was in the functional phase. We compared the state of luteal regression by measuring plasma progesterone levels. As side effects, the incidences of salivation, vomiting, tachypnea, diarrhea and the drop in body temperature were investigated. In the 400-microg and 800-microg groups treated with PGA-E, the mean intervals from administration until luteal regression were 18.6 days and 31.2 days, respectively. In the dogs treated with 50 microg or more of PGA-C, luteal regression was noted 2 days after administration. The above side effects were observed for 3 hr after administration of PGA-E/PGA-C. In the dogs treated with 800 microg of PGA-E, the mean body temperature was 36.7 degrees C 4 hr after administration; hypothermia persisted. PGA-E may be less useful than PGA-C for promoting luteal regression in dogs in clinical application.
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PMID:Influence of a PGF2alpha-analogue, etiproston tromethamine, on the functional corpus luteum of dogs. 1569 86

Algid is a rare complication of tropical malaria and it occurs in 0.37% of cases. Algid malaria is characterized by hemodynamic disorders as shock with pronounced metabolic changes and hypothermia. A number of factors are involved in the development of algid malaria. These include: 1. Pathological phenomena that are associated with the changes in the state of red blood cells and lead to impaired microcirculation (cytoadherence, sequestration, rosetting); 2. Tumor necrosis factor (TNF) that provokes hypoglycemia, coagulopathy, and impaired erythropoiesis; 3. Altered acid-alkali balance with the development of metabolic acidosis; 4. Gastrointestinal lesion. Adherence of contaminated red blood cells in the intestinal mucosal vessels induces epithelial ischemic damage. Impaired absorption of liquid and its loss with vomiting and diarrhea result in acute hypovolemia; 5. Algid malaria is associated with the addition of gram-negative septicemia. The paper describes a case of algid malaria.
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PMID:[Algid malaria]. 1580 Dec 11

A 69-year-old woman caught a cold resulting in nausea, vomiting, diarrhea and severe anorexia. Then she suffered progressively from dyspnea and leg edema, and finally became delirious. On admission severe hypoglycemia, hypothermia, marked tachycardia, generalized edema, mild jaundice and cachexy were noted. EKG showed atrial fibrillation. A chest X-ray, chest CT and echocardiography showed congestive heart failure. Therapeutic use of diuretics induced shock leading to serious liver dysfunction and disseminated intravascular coagulation. However, combined therapy by intravenous glucose, digitalis, diuretics, anti-fibrinolytic drug and hydrocortisone were effective. Addition of antithyroid therapy brought a further favorable outcome.
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PMID:Severe starvation hypoglycemia and congestive heart failure induced by thyroid crisis, with accidentally induced severe liver dysfunction and disseminated intravascular coagulation. 1580 13


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