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)

Studies of depression associated with oral contraceptive use present conflicting results. Individual susceptibility may affect psychiatric symptoms more than biochemical composition of the pill. In the authors' study 40 women without previous histories of depression were assigned to 4 regimens: 1) mestranol 80 mcg, norethisterone 1.0 mg; 2) pill 1 and pyridoxine; 3) mestranol 5 mcg, norethisterone 1.0 mg; and 4) pill 3 and pyridoxine. Alcohol and other chemicals were avoided. The 40 subjects completed self-reporting ratings on depression and a libido rating. 24 hour urine samples were collected on day 14 and 21 of the menstrual cycle. A brief psychiatric interview was conducted monthly. Adrenaline, noradrenaline, and 5 HIAA were measured throughout the year long study. 10 women completed 3 cycles. 20 of 10 complained of lethargy, loss of libido, irritability, and moodiness. The study concludes that biochemical and pharmacological effects affect a minority of women. A psychologic and negative placebogenic effect is possible. Depending on the composition of the contraceptive, a differential effect may occur. Sequential pills caused less depression than combination types.
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PMID:Oral contraceptives and depression. 44 Dec 35

Social drinkers, when drinking, are expected to feel better and to be kinder, more fun to be with and more energetic and active than they would be if they were not drinking; inebriated alcoholics are expected to be meaner, less fun to be with and more lethargic than they would be if they were not inebriated.
J Stud Alcohol 1979 May
PMID:College students' expectations of the results of drinking. 47 Mar 97

Twenty-one patients developed acute renal failure in association with nontraumatic rhabdomyolysis and myoglobinuria. The illness followed an overdose of ethanol, heroin, or other depressant drug in 18 patients. Lethargy or coma was present in 17 patients and muscle swelling in 11. Evidence of rhabdomyolysis included markedly elevated creatine phosphokinase, myoglobinuria, and aldolase in blood. Initial biochemical findings were similar to those of acute renal failure due to other causes, but the abnormalities were exaggerated. There was a disproportionate rise in serum creatinine concentration in relation to serum urea nitrogen concentration. Profound hyperuricemia was present in most patients. Transient hypercalcemia developed during the diuretic phase in 5 patients. One patient died. We conclude that nontraumatic myoglobinuria with acute renal failure is not infrequent and may occur after an overdose of ethanol or heroin. The disease has good prognosis despite severe hypercatbolism and untreated profound hyperuricemia.
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PMID:Acute renal failure due to nontraumatic rhabdomyolysis. 93 19

A case of lactic acidosis associated with phenformin therapy for diabetes mellitus is reported, and 34 previously reported cases of lactic acidosis associated with phenformin therapy are reviewed to determine if any predisposing factors to lactic acidosis were apparent. Observations of sex, age, duration of diabetes, pathologic conditions, dosage, duration of phenformin therapy and the onset of symptoms preceding lactic acidosis were made. Renal impairment, urinary tract infections, hepatic impairment, ethanol ingestion and poorly controlled congestive heart failure were found to be predisposing factors to lactic acidosis. The appearance of a syndrome of impending lactic acidosis consisted of anorexia, nausea, vomiting with abdominal pain or lethargy.
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PMID:Phenformin-associated lactic acidosis; a review. 114 21

Ethylene glycol (EG) is a toxic chemical found in antifreeze and heat exchangers. Standard therapy for EG intoxication in administration of ethanol (ETOH) to inhibit its metabolism by alcohol dehydrogenase (ADH). Studies indicate 1,3-butylene glycol (BG) binds to ADH more efficiently than EG and is orally less toxic than EG or ETOH. Male rats were divided into 5 groups of 6 animals. Groups received by oral intubation a single dose of EG (32 mmole/kg), BG (39 mmole/kg) initially and every 6 h up to 72 h, ETOH (39 mmole/kg) initially and every 6 h up to 72 h, or EG initially and then either BG or ETOH every 6 h up to 72 h. Administration of ETOH produced hepatotoxicity and pulmonary pathology as indicated by changes in clinical chemistry, urinalysis, and histopathology, while BG did not. Neither ETOH nor BG produced any apparent nephrotoxicity. ETOH produced ataxia, lethargy and central nervous system depression while BG did not. BG produced a higher concentration of urinary EG indicating a better inhibition of ADH metabolism of EG. Ethanol produced a higher EG blood concentration than BG. Ethanol's higher EG blood concentration may be partially attributed to dehydration and a decreased urine output as well as inhibition of ADH metabolism. Ethanol produced mortality in all animals prior to 72 h. The EG/ETOH combination produced mortality more quickly due to additive toxicity of the combination. Lack of any significant toxicity produced by BG and the production of significant toxicities by ETOH indicates that BG is potentially a better antidote than ETOH.
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PMID:The toxicokinetics of 1,3-butylene glycol versus ethanol in the treatment of ethylene glycol poisoning. 162 60

A one-month-old child was referred to our hospital for unexplained lethargy. She was found to be intoxicated from ethanol-soaked gauze pads which had been applied to the umbilical stump and contiguous skin for several days for the purpose of promoting umbilical cord detachment. We emphasize the importance of considering the risk of percutaneous alcohol absorption, especially in young infants, and the necessity of toxicology screening in every child with drowsiness of unknown etiology.
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PMID:Percutaneous ethyl alcohol intoxication in a one-month-old infant. 178 21

Three patients had neurologic signs due to isopropyl alcohol (IPA) intoxication. Over a several-week period, a known alcoholic developed apathy, confusion, ataxia, and hyperreflexia. During this period, there was no ethanol available to him, and he denied use of other intoxicants. He was found stuporous in the hospital after drinking IPA and admitted to IPA abuse during the preceding weeks. Two other men were admitted in a stupor after large ingestions of IPA. Intoxication with IPA has two different presentations: stupor in a known alcoholic and encephalopathy of unknown cause in individuals who hide their addiction. Ethanol, methanol, IPA, and ethylene glycol intoxications are associated with different clinical and laboratory findings.
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PMID:Isopropyl alcohol intoxication. 198 19

Intravenous nitroglycerin is frequently used in the treatment of acute myocardial infarction for its vasodilating effect on lowering both preload and afterload and in the control of ischemic heart pain. The end point for doses of nitroglycerin infusion is either relief of persistent or recurrent angina or controlling congestive heart failure by lowering left ventricular end diastolic pressure and volume. Nitroglycerin accomplishes these end points primarily through its venodilating property. Intolerable headaches or symptomatic hypotension may prevent achieving the clinical end point. Nevertheless, high doses of intravenous nitroglycerin may need to be administered to achieve a desired hemodynamic and therapeutic effect. Changes in mental status, i.e., lethargy and confusion, should be a warning sign of possible ethanol intoxication. An alcohol blood level verifies the clinical impression and gradually withdrawing the intravenous nitroglycerin is all that is necessary to effect a total recovery from this reaction.
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PMID:An unusual complication of intravenous nitroglycerin. 309 6

A tetrodotoxin-like substance, denoted ephippiotoxin, was obtained from the tissue of Brachycephalus ephippium, a small pumpkin-coloured frog collected in the Atlantic Forest of the southeast region of Brazil. Ephippiotoxin is a dialyzable substance soluble in water, methanol and ethanol, but insoluble in organic solvents such as chloroform and other apolar solvents. After treatment with active charcoal (Norit-A) and purification with ion-exchange Amberlite IRC-50 resin (NH4 + form), a freeze-dried residue was obtained, with a toxicity of c. 117 micrograms/kg (mice, i.p.). Ephippiotoxin showed the same mobility as crystalline tetrodotoxin (Sankyo) when submitted to thin-layer chromatography (silica gel G) using seven different solvent systems. White mice (20 +/- 1 g) injected i.p. with either B. ephippium tissue extracts or semi-purified toxin showed partial paralysis of the hind limbs, lethargy, altered breathing rhythm and clonic convulsions. Death occurred within 1.5-30 min after injection, depending on the dose. Ephippiotoxin induced atrioventricular diastolic blockade in the toad heart. It also inhibited the response of toad striated muscle to direct and indirect electric stimulation and blocked the compound action potential of isolated frog sciatic nerve.
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PMID:A tetrodotoxin-like substance found in the Brazilian frog Brachycephalus ephippium. 377 95

Previous studies have shown that manganese (Mn) deficiency in rats results in reduced activity of manganese superoxide dismutase (MnSOD) and increased levels of mitochondrial lipid peroxidation. These findings suggested to us that the Mn-deficient rat may be especially susceptible to the toxic effects of ethanol, as the metabolism of this compound results in production of superoxide anion. Offspring from Mn-sufficient and Mn-deficient adult rats were given either 20% (wt/vol) ethanol or distilled-deionized water as their drinking fluid for 14 d. Response to ethanol feeding was different between Mn-sufficient and deficient rats as evidenced by severe reductions in caloric intake and body weight observed in the Mn-deficient rats. Furthermore, after 14 d of ethanol feeding, these rats were extremely lethargic and in poor physical condition. Although Mn-sufficient rats responded similarly to the deficient rats during the first 6 d of ethanol feeding, they increased their caloric intake and body weight during the remainder of the experimental period. MnSOD activity in the ethanol-fed Mn-sufficient and Mn-deficient rats was similar, thus the alcohol-induced toxicity observed in the deficient rats was not due to reduced MnSOD activity. Iron-induced lipid peroxidation may be one of the mechanisms leading to the toxicity observed, as ethanol feeding resulted in liver Fe levels that were 30% higher than those in Mn-deficient rats that were not fed ethanol.
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PMID:Manganese deficiency: effects on susceptibility to ethanol toxicity in rats. 398 Dec 64


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