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)

Three rabbits from two sources died after an acute illness characterized by fever, lethargy and diarrhea in one rabbit and no clinical signs in two rabbits. The most striking lesion in all three rabbits was foci of necrosis of the spleen and liver associated with massive presence of multiplying Toxoplasma gondii tachyzoites. The diagnosis was confirmed by specific staining with anti-T. gondii serum in an avidin-biotin complex immunohistochemical stain.
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PMID:Fatal toxoplasmosis in domestic rabbits in the USA. 146 39

Severe renal oxalosis was diagnosed in 4 male and 1 female purebred Beefmaster calves from herds in southeastern and northwestern United States. Clinical signs included weakness, anorexia, lethargy, alopecia, dehydration, and diarrhea. Results of serum biochemical analysis for 2 calves were consistent with end-stage renal disease. Calves died 2 days to 6 weeks after birth. At necropsy, renal calyces were dilated and contained pale yellow granular calculi. Histologically, there was renal interstitial fibrosis, and cortical and medullary tubules were distended with calcium oxalate crystals. Oxalate crystals were also in the tracheal glands of 1 calf. Severe renal oxalosis in young purebred calves, on widely varied diets, with no known exposure to exogenous oxalates is suggestive of an inherited metabolic defect resulting in primary hyperoxaluria.
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PMID:Severe renal oxalosis in five young Beefmaster calves. 148 14

Utilizing behavioral and electroencephalographic (EEG) assessments, two inbred rat strains, Lewis (LEW) and Fischer 344 (F344), were exposed to morphine (IV) over a period of 7 days to discern differences in tolerance development. Following morphine injection, the LEW group demonstrated a greater mean total amount, as well as a greater rate of reduction, of stuporous behavior across the 7 days tested. Differences in patterns of latency to onset of slow-wave sleep between the two strains were also exposed. EEG analysis of spectral parameters utilizing an analysis of variance with repeated measures revealed that peak frequency, mean frequency, and edge frequency differed as a function of inbred rat strain. All spectral parameters differed as a function of duration of morphine injection; linear trends were indicated for both strains. Naloxone was administered (IV) following the 7 days of morphine to delineate dependence differences. LEW animals reflected a greater amount of behavioral responses, for example, wet-dog shakes, diarrhea, body stretch, and sluggish behavior. However, F344 rats demonstrated a greater alteration in two spectral parameters assessed: peak frequency and total power. Genetic variability appears to play a major role in both morphine tolerance and dependence as indicated by differences in EEG and behavioral responses.
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PMID:Effects of chronic morphine administration and naloxone on EEG, EEG power spectra, and associated behavior in two inbred rat strains. 151 64

The rapid-cycling variant of bipolar disorder constitutes about 15%-20% of all bipolar patients, and 72%-82% of these patients exhibit less than adequate response to lithium therapy. Valproate's spectrum of efficacy was examined in 78 patients with rapid-cycling bipolar disorder in a prospective, open, 15.8-month trial. Thirty patients received valproate monotherapy and 48 received combination therapy. Treatment assignment was nonrandomized and based on prior treatment history. A marked acute response was seen in 54% of the patients with mania, 87% of those with mixed states, and 19% of those with depression. Marked prophylactic responses were seen in 72% of manic patients, 94% of mixed states patients, and 33% of depressed patients. In addition, moderate acute antimanic responses were observed in another 31% of the patients, prophylactic antimanic responses in 17%, acute antimixed state responses in 0%, prophylactic antimixed state responses in 0%, acute antidepressant responses in 25%, and prophylactic antidepressant responses in mixed states in 34%. Pattern analysis was conducted to examine the spectrum of efficacy of valproate in various cells (e.g., the cohort of patients who had an acute antimanic response to the drug). Pattern analysis showed that 40% of the patients with a marked prophylactic antimanic response had a marked antidepressant response to valproate. However, among the patients with a marked antidepressant response to valproate, 91% had a marked antimanic response. The most common side effects of valproate in our study, as in earlier studies, were gastrointestinal problems (nausea, stomach cramps, diarrhea), tremors, lethargy, and hair thinning.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spectrum of efficacy of valproate in 78 rapid-cycling bipolar patients. 154 18

This phase I study investigated flavone acetic acid (FAA) given as a 12-h intravenous infusion every 3 weeks in the absence of urinary alkalinisation. Cohorts of three patients were treated at doses of 7, 10 and 13 g/m2. One subject had colon cancer; 5, renal cancer; and 3, lung cancer. The Eastern Cooperative Oncology Group (ECOG) performance status was 0 in four patients, 1 in two subjects and 2 in three cases. The maximum tolerated dose was 13 g/m2. The dose-limiting toxicities were WHO grade 3 hypotension and grade 3 diarrhoea. Other toxicities included lethargy and dizziness, nausea, temperature fluctuation, myalgia and dry mouth, but no significant myelosuppression was encountered. One patient receiving 10 g/m2 for renal cancer showed a partial response that lasted for 3 months and included the resolution of pulmonary and cutaneous metastases. The pharmacokinetics showed large interpatient variability. At 12-16 h post-infusion, the plasma elimination profile entered a plateau phase, with frequent increases in concentration suggesting enterohepatic recycling. Neither peak FAA levels nor AUC values were dose-dependent at the doses studied. Peak plasma levels were 101-402 micrograms/ml and AUC (0-48 h) values were 75-470 mg ml-1 min. Plasma protein binding varied with total concentration. Two metabolites were detected in the plasma, and both also underwent apparent enterohepatic recycling. Repeat dosing resulted in decreases of up to 48% in peak levels and AUC values for FAA in three of six patients. Of the total FAA dose, 39%-77% was excreted in the urine as FAA or metabolites within 2 days. The dose recommended for further phase II studies is 10 g/m2.
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PMID:A phase I and pharmacokinetic study of 12-h infusion of flavone acetic acid. 155 Nov 73

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

Case records of 32 neonatal calves with the antemortem diagnosis of meningitis were reviewed. Mean age at admission was 6 days (range, 11 hours to 30 days), and the most common concurrent clinical problem was diarrhea (16/32). Twenty-seven of the calves were available for necropsy. At postmortem, there was evidence of septicemia in 22 (81%) of these calves. Escherichia coli was the organism most frequently isolated (11/16; 69%) from the CNS. The major clinical signs of CNS disturbance observed over the course of hospitalization were lethargy, recumbency, anorexia, loss of suckle reflex, and coma. Leukocytosis and a left shift was evident in 11 of 15 (73%) calves. Concurrent metabolic problems that could have aggravated the CNS disturbance included hyperkalemia and respiratory acidosis. Analysis cerebrospinal of fluid from 22 of the calves, revealed pleocytosis, xanthochromia, turbidity, and high total protein concentration. Cytologically, neutrophils predominated in the CSF in calves with acute disease. Mononuclear cells dominated in calves with chronic disease. Microscopically, bacteria were evident in 10 of 22 (45%) of the antemortem CSF samples and bacteria were isolated from slightly more than half (11/19) of the specimens subjected to microbial culturing. Escherichia coli was the agent most frequently isolated from the CSF. Two of the 9 E coli isolates were resistant to trimethoprim potentiated sulfonamide drugs and all (4/4) of the CSF E coli isolates tested for susceptibility to triple-sulfonamide drugs were resistant. Twenty-seven of the 32 calves died or were euthanatized within 2.43 days after hospitalization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Meningitis in neonatal calves: 32 cases (1983-1990). 164 35

Seventeen patients with small cell lung cancer were entered into a dose ranging phase I-II study using rhGM-CSF (Glaxo). In the phase I study patients received 50, 150, 300 or 500 micrograms/m2 GM-CSF for 10 days by daily subcutaneous injection. Full blood counts were performed thrice weekly. After 4 days off all therapy patients then received chemotherapy with doxorubicin 50 mg/m2 i.v. bolus, day 1, ifosfamide 5 g/m2 with mesna 5 g/m2 over 24 h by continuous infusion followed by mesna 3 g/m2, and etoposide 120 mg/m2 i.v. on days 1-3. A total of six courses of chemotherapy were given. In the phase II study patients received the same dose of GM-CSF as in the phase I. GM-CSF was given 24 h after the last dose of chemotherapy for 14 days. Full blood counts were checked thrice weekly and the incidence of infections noted. Patients were randomised to receive GM-CSF with either odd or even courses of chemotherapy. The leucocyte count rose from a mean of 8.7 to 21.6 x 10(9)/l at the 50 micrograms/m2 GM-CSF dosage and from 11.4 to 39.4 x 10(9)/l at the 500 micrograms/m2 dosage during the phase I study. Phase I toxicity was: bone pain in 65% of patients, rash in 47%, fever in 24%, lethargy in 12% and diarrhoea in 12%. In the phase II study the duration of neutropenia was less during the chemotherapy courses with GM-CSF (p = 0.04) but the number of infections was similar.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recombinant human GM-CSF in small cell lung cancer: a phase I/II study. 165 15

A prospective study at two regional poison centers was undertaken in 500 children under six years of age (mean age 2.3 y) to resolve the question of whether milk has an effect on ipecac-induced emesis. When home administration of ipecac was recommended, parents were asked to select either milk or clear fluids. The mean volume of fluid +/- standard deviation administered was 159 +/- 72 mL in the milk group and 161 +/- 77 mL in the clear fluid group (p = 0.79). There was no difference in the onset of vomiting (23.4 +/- 18.5 vs. 23.3 +/- 12.9 min, p = 0.92), number of vomiting episodes (3.5 +/- 1.9 vs. 3.4 +/- 1.8, p = 0.65), or duration of vomiting (45 +/- 73 vs. 39 +/- 54 min, p = 0.31) for the milk group compared with the clear fluid group. Side effects including lethargy and diarrhea occurred with similar frequency in both groups. The substance ingested had no effect on onset of vomiting, vomiting duration or number of vomiting episodes. These findings again demonstrate that milk does not interfere with ipecac-induced emesis.
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PMID:The effect of milk on ipecac-induced emesis. 168 8

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


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