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)

A 77-year-old woman with refractory multiple myeloma was treated with a 4-day continuous intravenous infusion of vincristine and doxorubicin and 4 days of oral dexamethasone. Nine days after her second cycle she presented with lethargy and weakness associated with hyponatremia. Evaluation revealed the syndrome of inappropriate secretion of antidiuretic hormone, which was attributed to the vincristine infusion. After normal serum sodium levels returned, further doxorubicin and dexamethasone chemotherapy without vincristine did not produce this complication.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone after infusional vincristine. 142 76

An overdose of up to 850 levothyroxine sodium tablets (0.2 mg) in a healthy 6-year-old 16.8-kg dog induced an episode of vomiting and hippus within 9 hours of ingestion. The dog was treated with activated charcoal and saline (magnesium sulfate) cathartic. Initially the serum concentration of thyroxine (T4) 4,900.9 nmol/L. On the second day, serum concentration of triiodothyronine (T3) was 5.3 nmol/L. Serum T4 concentration decreased slowly and was not determined to be normal until day 36. Serum T3 concentration was found to be normal on day 6. Serum alanine transaminase activity peaked on day 6 at 345 U/L. Significant abnormalities were not found during the following 36 days. Clinical signs of thyroid hormone toxicosis in dogs and cats include hyperactivity, lethargy, tachycardia, tachypnea, dyspnea, abnormal pupillary light reflexes, vomiting, and diarrhea. High overdoses of levothyroxine sodium in dogs should be managed by initial decontamination and administration of activated charcoal with a cathartic followed by supportive care.
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PMID:Acute overdose of levothyroxine in a dog. 161 89

Cyclosporin-A-treated renal allograft recipients have demonstrated an improved graft survival rate, when compared to that of patients treated with conventional azathioprine and steroid therapy. Cyclosporin-A has been used for immunosuppressive therapy after renal transplantation at the National Taiwan University Hospital since November 1985. Since then, the one-year graft survival rate has been 78%, and the patient survival rate is 91%. At our service, acute rejection is confirmed mainly by an increase in the serum creatinine level of 0.5 mg% per day and a subsequent return of kidney function to normal after pulse steroid therapy. Twenty patients receiving cyclosporin-A and suffering from acute rejection episodes were chosen for comparison with 18 patients receiving conventional azathioprine and steroid therapy. Compared to conventional therapy, the classical systemic manifestations of rejection, such as malaise, lethargy, apathy, general weakness, vague discomfort, increase in body weight, swelling of graft with tenderness, were all more mild and less frequent in the cyclosporin-A-treated group. Episodes of rejection appeared earlier and the duration of rejection was shorter than in those of the conventional group. The urinary sodium concentration and the ratio of urine urea nitrogen to blood urea nitrogen were reliable references during the acute rejection episode in the conventional group, but it cannot be used as indices in the cyclosporine group. These findings can help us understand the changes which occurred in acute rejection in patients who receive renal transplantation during the cyclosporine era.
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PMID:Clinical manifestations of acute rejection in renal allograft recipients receiving cyclosporin-A therapy. 168 Sep 67

A protein toxic to mice was isolated from the venom of the Mexican beaded lizard Heloderma horridum horridum by a combination of gel filtration (Sephadex G-75) and ion exchange chromatography (both diethylaminoethyl-cellulose [DE-cellulose] and carboxymethyl-cellulose [CM-cellulose]). The purified polypeptide component has an apparent mol. wt of 25,500 and is composed of approximately 220 amino acid residues. It has an isoelectric point (pI) of 6.8 and its N-terminal amino acid sequence was shown to be: Glu-Ala-Ser-Pro-Lys-Leu-Pro-Gly-Leu-Met-Thr-Ser-Asn-Pro-Asp-Gln-Gln-Thr- Glu-Ile. The sequence has no significant similarity with any other protein previously reported in the literature. Enzymatic activities such as phospholipase, hyaluronidase and proteinase, commonly present in venoms, could not be demonstrated in this protein. Patch-clamp experiments conducted with excitable membranes show no effects on Na+, K+ or Ca2+ ion channels. Among the constant physiological effects observed in mice injected with this toxin are lethargy, partial paralysis of rear limbs and lowering of body temperature, suggesting that it might be a hypothermic toxin. We propose calling this toxin Helothermine.
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PMID:Isolation and characterization of helothermine, a novel toxin from Heloderma horridum horridum (Mexican beaded lizard) venom. 169 19

Two male siblings presented in the first 6 weeks of life with emesis, diarrhoea, metabolic acidosis and lethargy. A male sibling had previously died at 14 months of age from liver failure of unknown aetiology. Both of the current cases had mild hyperammonaemia with normal orotic acid, organic acid and argininosuccinic acid levels. Citrulline and arginine levels were normal or mildly decreased. One of the brothers was biopsied and had no detectable N-acetylglutamate synthetase activity and normal values for other enzymes of the urea cycle in liver. Treatment with a low-protein diet and sodium benzoate/sodium phenylacetate resulted in near normal blood ammonia levels, except during viral illness. Subsequent neurological development has been normal to mildly delayed. These patients differ from those previously described with N-acetylglutamate synthetase deficiency in that their presentation and subsequent course were relatively benign.
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PMID:N-acetylglutamate synthetase deficiency: clinical and laboratory observations. 177 15

A study was carried out to compare the haemodynamic and respiratory effects, as well as the quality of recovery, of anaesthesia with ketamine, sodium gamma-hydroxybutyrate (GOH) and etomidate in children undergoing cardiac catheterization. Thirty children, mean age 48 +/- 35 months, ranked ASA 2 or 3 on account of congenital heart disease, were assigned to one of three groups (n = 10). They were given: in group E1, a 0.3 mg.kg-1 bolus of etomidate, followed by 0.1 mg.kg-1.min-1 for 10 minutes, and 0.026 mg.kg-1.min-1 thereafter; in group G2, a 50 mg.kg-1 bolus of GOH, and in group K3, a 4 mg.kg-1 bolus of ketamine followed by a continuous infusion of 0.083 mg.kg-1.min-1. The patients breathed spontaneously. Monitoring included heart rate, systolic, diastolic and mean blood pressure, pulse oximetry, and capnography. Femoral venous or arterial catheterization was performed after local anaesthesia (with no more than 2 mg.kg-1 of lidocaine). Measurements were performed before induction, and then 1, 10, 30 and 60 minutes afterwards. The quality of anaesthesia was assessed according to Steward's scale. The investigation lasted between 50 and 100 min in all three groups. There were no significant differences in haemodynamic and respiratory parameters during the investigation between the groups. Recovery was shorter and of better quality in group E1. On the opposite, 30 minutes after the end of the catheterization, all the patients in group K3 were stuporous, with 5 of them displaying involuntary movements. The patients of the other two groups reacted correctly to stimuli, but those in group G2 went back to sleep very rapidly. There were no complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anesthesia for heart catheterization in children. Comparison of 3 techniques]. 178 1

In order to minimize heat loss cold stress induces peripheral vasoconstriction via the sympathetic nervous system. This effect is most pronounced in the extremities. Vasoconstriction does not appear in the head-neck region--a fact of great importance in emergency situations. In order to compensate for heat loss shivering is an early event, where involuntary muscle contractions increase metabolic rate 2-6 fold. Early tachycardia and elevated blood-pressure, followed by progressive bradycardia and lowered pressure are common cardiovascular effects of hypothermia. Death due to ventricular fibrillation or asystole occurs between 28 degrees-25 degrees C. Cold stress causes an osmolal diuresis with sodium and chloride as the main constituents. The natriuresis is of tubular origin and could be due to impaired autoregulation in the kidney and/or depend on the natriuretic polypeptide. The augmented urine flow decreases blood volume, lowers physical working capacity and increases blood viscosity--all negative events in a hazardous situation. Sudden immersion initiates hyperventilation for 1-2 minutes with an increasing risk of drowning. Thereafter ventilation decreases to rates consistent with metabolic requirements. In severe hypothermia carbon dioxide retention causes respiratory and metabolic acidosis. Hypothermia induces progressive depression of mental functions starting with apathy and bizarre behaviour and ending in lethargy and coma often between 30 degrees-28 degrees C. The paradoxal feeling of heat with undressing in agony could depend on cerebral receptor disturbances.
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PMID:Human physiology under cold exposure. 181 74

A 24-year-old Italian male presented with a nephrotic syndrome in September 1984. In February 1985 renal biopsy showed amyloid disease with tubular atrophy and interstitial fibrosis. Edema was treated with furosemide, and cholchicine was started. Because he feared side effects of drug therapy, the patient stopped all medication by July 1985. Instead, he decided to restrict severely fluids in order to fight edema. In early November 1985 his family noted he was becoming increasingly lethargic. Two weeks later, on his admission to the hospital, he had a serum sodium concentration of 193 mmol/l and serum osmolality of 397 mosm/kg. Apart from mild mental status changes neurological examination was normal. The fluid deficit was slowly corrected. He was discharged three weeks later with normal serum electrolytes. This case demonstrates that (1) severe hypernatremia can present with mild neurological symptoms and (2) it can be survived provided that it develops slowly and is corrected cautiously.
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PMID:Excessive hypernatremia in a patient with renal amyloid disease. 194 55

A patient presented without symptoms 30 minutes after ingesting acetonitrile, also known as methylacyanide. He had prompt gastric lavage and activated charcoal administration. Hours later, the onset of clinical toxicity was heralded by mental status abnormalities and vomiting prior to a generalized seizure. Following administration of sodium thiosulfate, the patient made an uneventful recovery. A blood cyanide level drawn shortly after presentation, but reported after the patient had been discharged, documented significant exposure. During hospitalization, cyanide toxicity was inferred from the history of ingestion of acetonitrile, plus a significant absence of venous blood hemoglobin desaturation. Because even small amounts can be harmful and toxicity is delayed, all acetonitrile ingestions should be presumed dangerous. Patients should be observed and repeatedly evaluated for at least 24 hours. In the absence of cyanide level determinations, lethargy, vomiting, seizures, and the lack of normal venous blood hemoglobin desaturation are clues to cyanide toxicity.
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PMID:Cyanide toxicity from acetonitrile-containing false nail remover. 201 1

Propionic acidemia is a rare hereditary disease which is an autosomal recessive disorder. Defect of propionyl CoA carboxylase results in abnormal accumulation of propionate and its metabolites which interfere the pathway of glycine cleavage and the urea cycle. This organic acidemia is characterized by a wide spectrum of clinical and biochemical findings, including recurrent vomiting, difficult feeding, lethargy, hypotonia, metabolic ketoacidosis, hyperglycinemia and hyperammonemia during the acute episodes. We present a male newborn infant who sustained this disorder and was managed successfully with blood exchange transfusion, peritoneal dialysis, supplemented with sodium benzoate and sodium bicarbonate therapy. Urine gas chromatography disclosed significant elevation of propionate and its metabolites which subsided 2 days after peritoneal dialysis. Special designed formula was then given with restriction of protein intake and supplement with sodium benzoate and sodium carbonate. Prenatal genetic counseling is necessary in further pregnancy. Diagnosis can be obtained when propionyl CoA carboxylase activity is low in cultured amniotic fluid cells or chorion villi sample or when there is abnormally high methylcitrate level in amniotic fluid.
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PMID:[Propionic acidemia: report of a case that is successfully managed by peritoneal dialysis and sodium benzoate therapy]. 217 70


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