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

Although the conditions that cause hypoglycemia in adults may also be present in infants and children, there are many entities unique to the pediatric age group. This reflects the delicate balance that exists in the newborn and young child between glucose production and utilization. During fasting in infants and children, hepatic glucose production is normally two to three times that of adults when expressed on the basis of weight. In the newborn and young infants, hypoglycemia usually presents with irritability, feeding difficulties, lethargy, cyanosis, tachypnea, and/or hypothermia rather than the typical adrenergic or neuroglucopenic symptoms seen in the adult. The hypoglycemia may be due to abnormalities in hormone secretion, substrate interconversion, or mobilization of metabolic fuels. The hypoglycemia associated with hyperinsulinemia may be transient neonatal, sustained, or drug-induced. Inborn errors of metabolism caused by enzymatic defects are responsible for hypoglycemia associated with abnormalities of production and utilization of metabolic fuels. These can involve carbohydrate, protein, and fat metabolism. In addition, there may be acquired or transient defects in carbohydrate metabolism secondary to other diseases or ingestion of certain substances. Finally ketotic hypoglycemia appears to be due to abnormalities in substrate availability. A variety of tests are useful for establishing the etiologic basis of the hypoglycemia, and the appropriate treatment depends upon the underlying cause.
 ...
PMID:Hypoglycemia in infants and children. 264 28

Sepsis remains a significant cause of morbidity and mortality in newborn infants. From January 1983 to April 1988, 166 cases of neonatal sepsis with positive blood cultures were collected at V.G.H.--Taichung. Among them 140 newborn babies were delivered at private clinic (outborn babies), 26 cases were inborn babies. Of the inborn babies, 20 cases (76.9%) were early onset sepsis (the onset of illness within 96 hours of life) and 6 cases (23.1%) were late onset sepsis (the onset of illness beyond 96 hours of life). Off the outborn babies, 64 cases (45.7%) were early onset sepsis and 76 cases (54.3%) were late onset sepsis. The Gram positive organism (51.9%) was more common than the Gram negative organism in the inborn babies, on contrary, the Gram negative organism (59.0%) was more common in the outborn babies. The most common pathogenic organism of the inborn babies was Enterococcus (22.2%) and E. coli (22.2%), followed by Pseudomonas spp (11.1%) and Staphylococcus aureus (11.1%). The most common pathogenic organism of the outborn babies was Enterococcus (17.4%), followed by E. coli (16.1%), Staphylococcus aureus (9.9%) and Klebsiella spp (8.1%). The antibiotics sensitivity tests to the pathogens didn't show any significant difference between these two group babies. In this clinical study, we found that the first choices of antibiotics were ampicillin plus aminoglycosides. The clinical symptoms and signs were nonspecific. The most common findings were lethargy, fever, hypothermia and poor feeding. Of the inborn babies, 17 cases (65.4%) had the predisposing factor(s). Of the outborn babies, 42 cases (30%) had the predisposing factor(s).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Clinical observation of neonatal sepsis]. 281 81

Nine dogs with primary gastrointestinal disease had clinical and laboratory findings resembling hypoadrenocorticism. The dogs had histories of anorexia, weakness or lethargy, diarrhea, vomiting, and weight loss. Hypothermia, dehydration, and emaciation also were detected on physical examination. Hyponatremia, hyperkalemia, and abnormally low Na/K ratios were found on laboratory evaluation, but results of ACTH-response tests were not compatible with hypoadrenocorticism. The primary diagnoses were trichuriasis and salmonellosis in 2 dogs, trichuriasis in 5 dogs, and perforated duodenal ulcer in 2 dogs. Most dogs responded to medical or surgical treatment of their primary gastrointestinal disease, and the original electrolyte abnormalities resolved. These findings emphasize the importance of the ACTH-response test in the diagnostic evaluation of dogs with clinicopathologic findings similar to those of hypoadrenocorticism.
 ...
PMID:Clinicopathologic findings resembling hypoadrenocorticism in dogs with primary gastrointestinal disease. 299 Nov 78

This article attempts to cover the more specific pruritic problems encountered in rabbits, rodents, and ferrets. There are certainly other causes of pruritus in these animals. Dermatophytes in guinea pigs are not reported to be pruritic, but because they are pruritic in other species, they should be considered in a differential diagnosis. A cryptococcal dermatitis in a guinea pig that was pruritic has been reported. Although mites were not seen on scraping, the animal was treated for sarcoptid mites and apparently the pruritus lessened. Because the cryptococcis was still present, it is questionable whether it was causing the pruritus. Pruritic ulcerative dermatitis over the back and shoulders has been seen in some lines of rats. Staphylococcus aureus was cultured from many of the lesions. Clipping the toenails on the feet helped lessen the severity of the lesions. Syphacia spp. have been reported in rats, gerbils, and hamsters and should be considered if there is perineal pruritus. MOBS, or "move over buddy syndrome," is seen especially in mice and may be seen in hamsters, gerbils, and rats that are overcrowded or stressed. The lesions are actually bite wounds that have been inflicted around the tail base and the perineum and on the tail, but these wounds can be mistaken for self-inflicted trauma from pruritus. All of the recommended treatments are extralabel, and clients should be informed of this. I have observed a guinea pig become lethargic and anorexic after only one application of a flea powder approved for use in cats. Brushing most of the powder off and offering dandelion greens to stimulate appetite helped. The second dusting was done with the same flea powder diluted with baby powder. Whenever these animals are dipped, it is important to let them dry in a warm, draft-free area. Again, it is important to be aware that the ratio of surface area to body weight is much higher in these small animals than in the species routinely seen in veterinary practice especially to prevent toxicoses from topically applied medications and iatrogenic hypothermia or hyperthermia.
 ...
PMID:Pruritus in rabbits, rodents, and ferrets. 305 47

The divalent cationic ionophore A23187 (calimycin) facilitates the transport of calcium ions across biological membranes, resulting in an increase of cytosolic calcium. A23187 has been used extensively in vitro to activate calcium-dependent neurocellular processes. Because of its potential usefulness as a neurotoxicological probe, our laboratory conducted a series of studies to characterize the neurofunctional consequences of A23187 in the intact organism. In addition to approximating the LD50, the effects of acute parenteral administration of A23187 on conditioned avoidance, nociceptive shock threshold, open-field activity, consummatory behavior, body temperature and neuromotor function, including general activity, coordination, balance and grip strength, were assessed in the rodent. The LD50 of A23187, administered intraperitoneally to adult male rats, was 9.2 mg/kg. The predominant overt signs of toxicity included lethargy, limb weakness and apnea. Lower doses, from 0.5 to 0.03 mg/kg, produced a variety of more subtle neurobehavioral effects, including a selective depression of motor activity, a moderate elevation of shock threshold, altered conditioned avoidance behavior and hypothermia.
 ...
PMID:Neurobehavioral effects of the calcium ionophore A23187. 311 83

A new patient with neonatal lactic acidosis due to pyruvate carboxylase deficiency is described. Since birth he developed vomiting, hypothermia, lethargy, irritability, hypoglycemia and severe metabolic acidosis. During admission a progressive deterioration was observed. Despite different attempted therapies patient died at 4 1/2 months of age. High levels of plasma and urine lactate and pyruvate were detected. Enzymatic studies in cultures skin fibroblasts and postmortem tissues showed a severe deficiency of pyruvate carboxylase.
 ...
PMID:[Neonatal lactic acidosis caused by severe pyruvate carboxylase deficiency]. 314 24

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Sudden unexplained death may be seen with treatment of craniovertebral anomalies and surgery of the upper cervical spine. Death is due to sleep-induced apnea, premonitored by periods of confusion, lethargy, and asthenia. There may be associated hypotension, bradycardia, hyponatremia, hypothermia, inappropriate antidiuretic hormone secretion, and difficulty in micturition. The potential for respiratory failure may be predicted if a CO2 response test demonstrates an attenuated or abnormal response. Apnea during sleep may be reversed by arousal or may require ventilatory support for a period of time. The condition is self-limiting, but remains the major life-threatening complication. Both apnea and autonomic dysfunction are treatable and curable with appropriate diagnosis and management.
 ...
PMID:Occult respiratory and autonomic dysfunction in craniovertebral anomalies and upper cervical spinal disease. 375 66

Antitumor effects of i.v. injected human recombinant tumor necrosis factor (rTNF) against solid Meth A tumors in mice appeared to be critically dependent on the dose and were limited by its toxicity. Extensive necrosis and complete cures were only induced by doses having untoward effects, such as diarrhea, hypothermia, ruffled fur, and lethargy. Murine tumor necrosis serum (TNS, 0.5 ml) had about the same antitumor potential and induced all side effects except diarrhea. More extensive necrosis and approximate doubling of the incidence of complete regression in the absence of gross side effects were observed upon administration of a low dose of rTNF combined with detoxified endotoxin, nontoxic poly A:U, or submicrogram doses of toxic endotoxin. The separate constituents had little antitumor effects, if any at all. Increasing the dose of toxic endotoxin resulted in a further potentiation of necrosis, overt toxicity, but no cures. Muramyl dipeptide and interferon alpha/beta did not potentiate effects of rTNF. In vitro growth of Meth A cells was not inhibited by toxic endotoxin, rTNF or the combination, although TNS was highly inhibitory. Data show that therapeutic effects of rTNF and its synergy with endotoxin are not due to direct effects on the tumor cells and that the extent of prompt in vivo tumor necrosis does not predict the course of tumor growth. Therapeutic effects of both TNS and toxic endotoxin probably involve a synergy between low levels of TNF and other factors/effects induced by endotoxin. Detoxified endotoxin and poly A:U probably induce the latter effects and little or no TNF, so explaining the absence of side effects, their weak antitumor potential, and their powerful synergistic action with rTNF. A role for interferon alpha/beta as an induced synergistic factor is not likely. Muramyl dipeptide and TNF might share properties needed for synergy with endotoxins.
 ...
PMID:Synergistic action of human recombinant tumor necrosis factor with endotoxins or nontoxic poly A:U against solid Meth A tumors in mice. 382 51

Phorbol esters, in particular 12-O-tetradecanoyl-phorbol-13-acetate (TPA), have been shown to have profound effects on most biological systems including tumor promotion. Presented here are studies on the acute toxic effects of TPA, and the effects of phorbol esters on the in vivo and in vitro, T cell-dependent, antigen-specific antibody response in the mouse. The LD50 of a single i.v. dose of TPA in the mouse was 309 micrograms/kg. Acute toxic effects included lethargy, hypothermia and enlarged, hemorrhagic spleens at the higher doses. TPA was shown to be a potent inhibitor of the in vivo primary antibody response as measured by the IgM antibody-forming cell (AFC) response to sheep red blood cells (sRBC). The ED50 of a cumulative i.v. dose was 145 micrograms/kg administered the day before and the day of immunization (72.5 micrograms/kg/day). A cumulative dose of 500 micrograms/kg (250 micrograms/kg/day) resulted in a 100% suppression of the response. This in vivo exposure to TPA did not alter B cell/T cell ratio in the spleen. Phorbol ester analogs inactive in other biological systems were also inactive in the in vivo AFC response. The in vitro AFC assay was used to determine what cell type was being affected by TPA. Separation of the adherent spleen cells into B and T cell populations was done using nylon wool columns and anti-theta plus complement treatment. Experiments with these cell populations indicated that TPA produced suppression of the response due to an effect on the nylon wool adherent cell population.
 ...
PMID:Suppression of the antibody response by phorbol esters in the mouse is due to an effect on the nylon wool adherent cell population. 387 72


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>