Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Management of accidental overdosage with oral hypoglycemic agents in toddlers may be difficult when the history of ingestion is overlooked. We report a 21-month-old girl who presented with lethargy and generalized seizures 12 hours after ingestion of an unknown number of glibenclamide pills. The blood glucose on admission was 0.5 mM/l. Symptoms resolved promptly after an intravenous bolus of glucose. Metabolic and infectious causes of hypoglycemia were ruled out. The parents denied drug ingestion initially, but further investigation revealed that she had ingested several glibenclamide pills used by her diabetic father 12 hours prior to admission. This case illustrates the problem involved in diagnosis and management of accidental drug overdosage in children when no such history is elicited and symptoms are delayed.
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PMID:[Overdosage of glibenclamide presenting with lethargy and seizures in a child]. 142 74

Diuretics can result in various undesired biochemical changes, such as impotence, skin rashes, nausea, dizziness and lethargy as well as subjective side effects. The side effects are mostly predictable, their effects depending on both the circulatory blood volume and on the transport of water and solute in the renal tubules. Two of the commonest side effects are mild hypovolaemia, when any diuretic is used, and mild hypokalaemia when the non-potassium-sparing diuretics, such as thiazides and frusemide are used. Its occurrence is dose dependent and can be corrected by potassium supplements, but potassium-retaining diuretics, which also correct the often associated fall in serum magnesium, are preferable. Many reports link hypokalaemia with cardiac arrhythmias, but some dispute this association in the absence of the concomitant use of digoxin. Hyponatraemia rarely occurs, but can be life threatening. Calcium excretion is markedly reduced, but unlike other electrolyte disturbances from diuretics, this may be valuable: some suggest diuretics have an anti-osteoporotic action. Diuretics increase glucose and insulin resistance and should be used sparingly in diabetics. They rarely cause a non-ketotic hyperosmolar coma. Urate is raised, but clinical gout is not common. Cholesterol elevation has been reported in some studies, but long-term studies indicate that lipid changes are minor. Other rare side effects are not predictable from their pharmacological actions and these include the occurrence of skin rashes, thrombocytopenia, pancreatitis and interstitial nephritis; and ototoxicity from frusemide.
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PMID:Adverse reactions to diuretics. 148 14

A total of 2248 infants born at All India Institute of Medical Sciences Hospital, New Delhi were selectively screened for hypoglycemia over a period of 15 months. Hypoglycemia (blood glucose less than 30 mg/dl) was diagnosed in 107 cases (4.8%). Preterm babies had three times increased risk (12.8%) as compared to term babies (3.6%). Small-for-dates (SFDs) and large-for-dates (LFDs) infants were at increased risk of manifesting hypoglycemia (7 and 10 times, respectively) as compared to the appropriate-for-dates (AFDs) babies (2.7%). Approximately two-thirds of the hypoglycemic babies (67.3%) had one or more risk factors including birth asphyxia (24.2%), diabetic mothers (23.8%), respiratory distress (13.9%) and septicemia (11.6%). A total of 59.8% cases were asmyptomatic while the rest had one or more symptoms. The most common symptom observed was lethargy (81.4%), followed by jitteriness (67.4%), respiratory abnormalities (41.9%), hypotonia (39.5%) and seizures (30.2%). The amount of glucose (mg/kg/min) needed to maintain a stable blood sugar in various categories of hypoglycemic babies was observed to be in the following decreasing order of amount; symptomatic babies with seizures (Gp IV), IGDM's/IDM's and symptomatic babies with other features (Gp III), SFDs and LFDs (Gp II) and AFDs (Gp I). Such a categorization of hypoglycemic babies will help to treat them more precisely.
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PMID:Neonatal hypoglycemia--clinical profile and glucose requirements. 159 96

We have established an improved model of fulminant hepatic failure in dogs. Buthionine sulfoximine is used to inactivate glutathione synthesis, and small increments of acetaminophen are given intravenously to maintain the plasma level at approximately 200 micrograms/ml for 20 hr. This regimen produces severe liver injury along with many of the features seen in humans with acetaminophen poisoning. The first sign of impending liver failure is hypoglycemia. This occurs about 15 hr into the experiment and requires treatment with a continuous infusion of glucose. Between 15 and 20 hr, serum ALT activity begins to rise, indicating the onset of liver necrosis. Over the following 15 to 20 hr ALT activity continues to rise and is accompanied by an increase in bilirubin, a prolongation of the prothrombin time and the development of fetor hepaticus. Thirty to 48 hr after the initial acetaminophen dose, the animals begin to exhibit symptoms of encephalopathy and progress from lethargy to the inability to maintain posture and then coma, seizures and death. Liver biopsy specimens obtained at several stages throughout the study showed progressive necrosis, ultimately resulting in the complete destruction of zones 2 and 3.
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PMID:An improved model of acetaminophen-induced fulminant hepatic failure in dogs. 173 38

From January 1981 to December 1988, we collected 11 cases of neonatal meningitis caused by Flavobacterium meningosepticum. The 6 male and 5 female newborns ranged from 3 days to 20 days old. Birth body weight varied from 1100 gm to 3600 gm. Seven cases were premature or small for date. Nosocomial infection was noted in 7 of these 11 cases. Clinically, lethargy and poor activity were the most common symptoms. Cyanosis, fever and convulsion were the next. There were 9 cases showing pleocytosis, increased protein and decreased glucose level in the cerebrospinal fluid examination. The organisms isolated in all 11 cases were susceptible to piperacillin, resistant to ampicillin, aminoglycosides and cephalosporin. Five patients were treated with antibiotics other than piperacillin for 5 to 18 days. Three patients died; hydrocephalus was the cause of death in 2 of them. Two patients were discharged against advice. Among the remaining 6 cases we gave piperacillin for 3 weeks, one case developed hydrocephalus but eventually succumbed to K. pneumoniae sepsis. Out of five surviving cases, 3 developed hydrocephalus (VP shunt performed in two). The other two patients were discharged without neurological deficit. In conclusion, neonatal Flavobacterium meningosepticum meningitis was more frequent in premature or small for date babies, and it usually appeared in nosocomial infection. The prognosis was poor and piperacillin was proved to be the drug of choice.
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PMID:[Clinical observation of neonatal meningitis caused by flavobacterium meningosepticum]. 177 41

Recent research clearly shows that fusion genes can be microinjected into a pronucleus of an ovum and integrate into the pig genome. Animals with such fusion genes are called 'transgenic'. The percentage of injected ova that developed into transgenic pigs varied among experiments from 0.31% to 1.73%. The percentage of transgenic pigs that expressed the fusion gene ranged from 17% to 100%. Eleven different regulatory sequences have been used for fusion genes transferred into pigs. Some of these regulatory sequences directed strong gene expression, but control over level of expression was inadequate. Other regulatory sequences directed weak expression, but imparted only brief spikes of induced expression. The predominant gene coding sequences transferred were for growth-related hormones. Elevation of growth hormone (GH) in expressing transgenic pigs enhanced plasma concentrations of insulin-like growth factor-I (IGF-I), insulin, and glucose, improved feed efficiency about 15%, and markedly reduced subcutaneous fat compared to nontransgenic siblings. Growth rate was enhanced in some transgenic GH pigs but not in others, possibly due to dietary limits. The 'over-expression' of GH was detrimental to the general health of most transgenic pigs. The most prevalent problems were lethargy, lameness, and gastric ulcers. Gilts that expressed foreign GH genes were anoestrous. Boars that expressed foreign GH genes lacked libido, but their semen was fertile when used by artificial insemination. Six different fusion genes have been transmitted from transgenic founders to progeny. Most of the transgenic pigs that produced progeny transmitted the fusion gene as an autosomal dominant trait to about half of their progeny. Regulatory sequences that will permit full control of gene expression must be developed before the full potential of gene transfer in pigs can be realized.
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PMID:Expression and performance in transgenic pigs. 219 41

We have produced transgenic pigs that harbour structural genes for bovine and human growth hormone (bGH and hGH) ligated to a mouse metallothionein-I (MT) promoter, human growth hormone-releasing factor (hGRF) ligated to the MT or mouse albumin (ALB) promoter, and human insulin-like growth factor-I (hIGF-I) ligated to MT promoter. From 0.31 to 1.03% of microinjected ova developed into transgenic pigs with the various fusion genes. Foreign GH was present in plasma of 61% of the MT-hGH and 89% of the MT-bGH transgenic pigs. Two of 7 pigs with MT-hGRF and all 3 ALB-hGRF transgenic pigs had high concentrations of GRF in their plasma, but plasma concentrations of porcine GH (pGH) were not higher in GRF transgenic pigs than in littermate control pigs. In contrast, plasma concentrations at birth ranged from 3 to 949 ng hGH/ml for MT-hGH transgenic pigs and 5 to 944 ng bGH/ml for MT-bGH transgenic pigs. Presence of the foreign GH depressed endogenous pGH to non-detectable levels. In MT-bGH transgenic pigs, plasma IGF-I was elevated more than 2-fold, plasma glucose was elevated about 30 mg/dl, and plasma insulin was 20-fold higher than in littermate or sibling control pigs. Two lines of pigs expressing the MT-bGH transgene gained 11.1% and 13.7% faster, and were 18% more efficient in converting feed to body weight gain than were sibling control pigs. Expression of the MT-bGH transgene caused a marked repartitioning of nutrients from subcutaneous fat into other carcass components, including muscle, skin, bone and certain organs. The persistent excess hGH or bGH in transgenic pigs was detrimental to general health; lameness, lethargy and gastric ulcers were the most prevalent problems. Gilts that expressed the hGH or bGH transgenes were anoestrous. Germ-line transmission was obtained in 4 of 5 expressing transgenic boars and 4 of 5 nonexpressing transgenic boars and gilts. From 2% to 73% of progeny inherited a transgene from founder transgenics. All transgenic progeny of MT-hGH, MT-bGH and MT-hGRF founder males expressed the transgene if their sire also expressed the gene. The concentration of bGH or hGH in plasma of transgenic progeny was similar to the concentration present in the founder transgenic.
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PMID:Integration, expression and germ-line transmission of growth-related genes in pigs. 221 18

The effect of intracranial microdialysis on brain glucose metabolism in control and kainic acid-treated rats was assessed by semi-quantitative [14C]2-deoxyglucose autoradiography. A dialysis fiber loop was implanted into the piriform cortex or a horizontal Vita fiber into the hippocampus, and 24 h later, fibers were perfused with Krebs-Ringer bicarbonate solution before and after injection of kainic acid (16 mg/kg, i.p.) [14C]2-Deoxyglucose was injected i.p. 3 h after the injection of kainic acid. Rats injected with kainic acid were initially lethargic and then proceeded through behavioral phases of staring, "wet-dog shakes", Straub tail, rearing, forepaw clonus, and, in some cases, tonic-clonic convulsions. Three hours after kainic acid, the fiber presence in the piriform cortex enhanced kainic acid-induced metabolic activity in areas adjacent to the fiber assembly, whereas the fiber in hippocampus attenuated kainic acid-induced metabolic activity in areas adjacent to the fiber assembly. The results indicate that intracranial microdialysis alters the already abnormal brain metabolism in a kainic acid-induced seizure state, but has no significant effect in the non-seizure control state.
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PMID:Effects of microdialysis on brain metabolism in normal and seizure states. 224 90

A 3 year old boy who had glutaric aciduria diagnosed at 22 months of age was admitted with a history of lethargy, vomiting, and fever. He had been receiving glucose polymers as part of his dietary management. He was severely hypernatraemic, but after resuscitation and rehydration made a good recovery. The possible aetiology of his hypernatraemia is discussed.
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PMID:Glucose polymer regimens and hypernatraemia. 224 22

In 32 hypertensive diabetic patients a study was performed to determine the effects of indoramin on blood pressure and blood glucose, plasma insulin, C-peptide, serum total cholesterol, and triglyceride levels. All patients evaluated showed a significant fall in blood pressure with daily doses of 50 to 200 mg of indoramin. In six insulin-dependent diabetic patients there was no change in diabetic control and no effect on the incidence of hypoglycaemia. In 18 noninsulin-dependent diabetics monitored for 3 months and in 14 followed for 12 months, there was no significant change in glucose tolerance after a 75 g glucose dose; mean plasma C-peptide levels and 2 h insulin levels were increased at 12 months. Mean weight and mean fasting cholesterol and triglyceride concentrations were unchanged. Nine patients withdrew because of side effects, mainly drowsiness and lethargy.
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PMID:Indoramin in the hypertensive diabetic patient. 242 5


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