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)

IL-6 is a 26-kDa protein cytokine with pleiotropic activities in both hematopoietic and immune systems. It is one of the major mediators of the acute phase inflammatory response. Recently it has been demonstrated that pharmacological doses of human recombinant IL-6 (rhIL-6) inhibit certain murine tumors as well as stimulate thrombopoiesis in mice, dogs, nonhuman primates, and humans. The purpose of our study was to evaluate the effects and toxicity of rhIL-6 administration in nonhuman primates with particular reference to subject age. We treated 10 female monkeys of two age groups (midle-aged and old) with rhIL-6 (15 micrograms/kg/day) for 28 days. The monkeys were observed to be somewhat lethargic and lost an average of 10% of their body weights. The white blood cell count rose transiently whereas the levels of hemoglobin and hematocrit fell significantly and remained depressed for the same period. Importantly, platelet count rose and remained elevated for the duration of treatments. Serum alkaline phosphatase levels increase significantly and certain parameters of clinical immune competence were altered by IL-6 treatment. Treatment effects were similar in both age groups, but the changes in immune functions were different between the midle-aged and old monkeys. We observed a pattern in which the middle-aged group had a significant decrease in immune functions as a result of IL-6 administration and recovered to pretreatment level despite continuous treatment, whereas the old monkeys had a more protracted but less significant decline in these same immune functions during the trial.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of recombinant human interleukin-6 on blood and immune parameters in middle-aged and old rhesus monkeys. 812 61

Two thousand Panama X Rambouillet ewes from a flock of 2,200 developed signs of acute toxicosis after being moved to a field that had been sprayed 16 hours earlier with elemental sulfur. Acute signs were lethargy, abdominal discomfort, and prostration. Two hundred six (10%) of the affected ewes died within 24 hours. Polioencephalomalacia that was unresponsive to thiamine treatment developed in another 40 (2%) of the ewes; 28 (70%) of the ewes with polioencephalomalacia recovered. Sulfur is converted to hydrogen sulfide in the rumen. Signs of sulfur toxicosis are a result of absorption of hydrogen sulfide and interaction with the cytochrome system and hemoglobin. Sulfide is detoxified in the RBC and by the liver.
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PMID:Elemental sulfur toxicosis in a flock of sheep. 862 20

Anemia can be defined as a reduction in the hemoglobin concentration and red blood cell mass compared with age-matched normal values. Anemia is caused by poor production of red blood cells, destruction of red blood cells, or loss of red blood cells. Pediatric nurse practitioners will encounter patients in their practice who have anemia resulting from each of these causes. Common clinical presentations include the child who is feeling well but is found to have a low hemoglobin concentration on a routine screening test, the child who is "tired" and does not eat well, the infant or child who is being evaluated for other chronic problems and is found to have a low hemoglobin concentration, and last, the child who is obviously pale, lethargic, and requires immediate assessment and evaluation.
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PMID:A practical approach to the child with anemia. 884 25

A 2 1/2-y-old spayed female cat was presented for lethargy and weakness. The cat was hypokalemic (3.1 m Eq K/L) and severely anemic (60% PVC, 1.3 g hemoglobin/dL). The cat was known to ingest bentonite-containing cat litter. It recovered with treatment of i.v. fluids, electrolytes and whole blood transfusion and was discharged. Two months later the cat was presented again with signs similar to those seen previously. This occurred 1 mo after the owner resumed the use of bentonite-containing cat litter. The signs were remarkably similar to those reported in humans from the chronic ingestion of bentonite clays. Bentonite toxicosis is suggested by the coexistence of hypokalemia hypochromic anemia in cats presented with lethargy and muscle weakness.
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PMID:Suspected bentonite toxicosis in a cat from ingestion of clay cat litter. 916 53

We evaluated the efficacy and safety of and compliance with rH-EPO (150 U/kg three times a week subcutaneously for up to 12 weeks) for treatment of anemia in childhood Crohn's disease (n = 4). The mean hemoglobin level before rH-EPO therapy was 109 gm/L (10.9 gm/dl) (range, 103 to 115 gm/L). The mean hemoglobin level in the three compliant children increased to 138 gm/L (13.8 gm/dl) after treatment. Response time for the correction of anemia ranged from 6 to 12 weeks (mean, 9.5 weeks). Resolution of symptoms of lethargy, poor appetite, and irritability occurred with correction of the anemia. The only adverse effect observed was transient local pain at the injection site.
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PMID:Recombinant human erythropoietin for treatment of anemia of chronic disease in children with Crohn's disease. 947 19

Signalment, clinical signs, and physical examination and clinicopathologic findings in dogs diagnosed with Hepatozoon canis parasitemia (n = 100) were compared with those in Hepatozoon-negative dogs (n = 180). A subset (n = 15) of Hepatozoon-positive dogs with unusually high (> 800 H canis gametocytes/microL of whole blood) parasitemia was compared with dogs that had low parasitemia (n = 85) and with Hepatozoon-negative dogs (n = 180). Hepatozoon-positive dogs significantly differed from Hepatozoon-negative dogs in body temperature, total red blood cell count, hemoglobin concentration, hematocrit, and platelet count. Dogs with high H canis parasitemia significantly differed from those with low parasitemia in hemoglobin concentration, hematocrit, and total neutrophil count. Clinical findings from dogs with high H canis parasitemia included emaciation, lethargy, hyperglobulinemia, hypoalbuminemia, and increased serum alkaline phosphatase and creatine kinase activities. Findings at necropsy included hepatitis, pneumonia, and glomerulonephritis associated with H canis schizonts and extensive parasitism of bone marrow, spleen, and lymph nodes. Low hemoglobin concentration, low platelet count, and concurrent parvovirus infection together represented the best predictor variables for Hepatozoon positivity in dogs presenting to the hospital.
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PMID:Retrospective case-control study of hepatozoonosis in dogs in Israel. 947 Jan 63

Gadobenate dimeglumine formulation (E7155), at doses of 0 (physiological saline), 0.25, 0.5, 1 and 2 mmol/kg/day of body weight, was administered intravenously to male and female beagle dogs once daily for 4 consecutive weeks in order to evaluate the subacute toxicity of the test article. Reversibility of toxicity was evaluated during a 4-week recovery period at 1 and 2 mmol/kg/day. No toxicologically significant changes were observed at 0.25 and 0.5 mmol/kg/day. In animals receiving 1 or 2 mmol/kg/day, transient swelling and redness of the facial and eye areas, lethargy, decreased activity, emesis, retching, watery or unformed stool, decreased body weight or body weight gain, decreased food consumption, decreased hematocrit and hemoglobin concentration, increased APTT, increases in plasma ALP, GPT or gamma-GT, decreased plasma inorganic phosphorus, total protein or albumin, increased liver or kidney weight, subacute inflammatory infiltrates, loss of centrilobular hepatocytes or hepatocellular cytoplamic vacuolation in the liver, vacuoles in the epithelial cells of the renal tubles and/or hypocellularity in the bone marrow were seen. The results of toxicokinetic analysis showed that systemic exposure was similar in males and females, and there was no accumulation of the test material over the treatment period, although AUC tended to be enhanced by slightly more than the proportionate dose increase. These effects were recovered or tended to be reversed after a post-dosing period for 4 weeks. In conclusion, the No Observed Adverse Effect Level (NOAEL) was 0.5 mmol/kg/day.
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PMID:[General toxicity study of gadobenate dimeglumine formulation (E7155) (4)--4-week repeated dose intravenous toxicity study followed by 4-week recovery period in dogs]. 1063 79

Methemoglobinemia is a condition characterized by increased level of methemoglobin in the erythrocytes and brownish cyanosis. Acquired methemoglobinemia is diagnosed by elevated methemoglobin with normal hemoglobin electrophoresis and normal NADH cytochrome b5 reductase. We report a patient who developed lethargy, confusion, and cyanosis during post-operative period. He had arterial methemoglobin level of 40.6% and oxygen saturation of 59%. No other cause could be found for his methemoglobinemia other than metoclopramide, even though it is rarely reported to cause methemoglobinemia in adults compared to infants. He had an excellent clinical response to treatment with methylene blue with which his clinical symptoms improved and the methemoglobin level returned to normal within 24 hours. Here we discuss the clinical features, diagnosis, and treatment of acquired methemoglobinemia induced by metoclopramide.
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PMID:Metoclopramide-induced methemoglobinemia in an adult. 1087 Mar 38

Heart failure is associated with an increase in plasma nitrate and nitrite (NOx). To date there is still some controversy regarding the causes of nitrate accumulation during the development of heart failure. The goal of this study was to analyze the underlying mechanisms that cause accumulation of plasma nitrates during the development of heart failure in dogs. Dogs were chronically instrumented for measurement of hemodynamics and renal function. Hearts were paced initially at 210 bpm for 3 weeks and then at 240 until the development of heart failure. Hemodynamics, renal function, renal blood flow, arterial blood gases, hemoglobin, plasma and urine NOx levels, and creatinine levels were measured weekly. Heart failure was assessed by hemodynamic alterations, physical signs such as lethargy, ascites, cachexia, and postmortem evidence of cardiac hypertrophy. LVSP (from 127 +/- 3 to 106 +/- 3 mmHg), LV dP/dt (from 2658 +/- 173 to 1439 +/- 217 mmHg/s), MAP (from 101 +/- 1.9 to 83 +/- 1.8 mmHg) fell, whereas LVEDP tripled (from 6.4 +/- 0.9 to 20 +/- 2.6 mmHg), and heart rate rose (from 101 +/- 4.2 to 117 +/- 6.3 bpm), all changes P < 0.05. RBF (from 146 +/- 10 to 96 +/- 9.9 ml/min), urine output (V) (from 0.26 +/- 0.02 to 0.16 +/- 0.02 ml/min), GFR (from 63 +/- 1.8 to 49 +/- 2 ml/min), and Na excretion (from 45 +/- 4.5 to 14 +/- 4.6 microEq/min) all decreased (P < 0.05), whereas RVR increased (from 0.68 +/- 0.05 to 0.94 +/- 0.1 mmHg/ml/min). These changes took place during a rise in plasma NOx (from 3.7 +/- 0.5 to 16+/-3.3 microM), a decrease in urine NOx (from 33 +/- 9.9 to 8.1 +/- 4.9 microM), and a concurrent increase in NOx reabsorption (from 221 +/- 31 to 818 +/- 166 nmol/min). There was a direct correlation between the increase in plasma NOx levels and an increase in filtered load (r(2) = 0.97, P = 0.02), a negative correlation between NOx levels and NOx excretion (r(2) = 0.65 P < 0.09), and a direct correlation between plasma NOx levels and NOx reabsorption (r(2) = 0.97, P = 0.02). These results indicate that elevated plasma NOx during heart failure are most likely the result of an impairment of the renal function and not increased NOx production. Furthermore, without knowing changes in renal function the measurement of plasma NOx in and of itself is a meaningless index of NO formation.
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PMID:Plasma nitrate accumulation during the development of pacing-induced dilated cardiac myopathy in conscious dogs is due to renal impairment. 1117 32

Long-term exposure to benzene vapors is associated with hematological diseases such as leukemia, lymphoma and aplastic anemia. CD(1) male mice were randomly assigned to six groups: 1B(10), 1B(15), 1B(20), 2B(10), 2B(15), and 2B(20.) 1B mice were administered 2 ml/kg (1940 mg/kg) subcutaneous injection (in the dorsal region) of benzene 5 days a week, and 2B mice were exposed 3 days a week (Monday, Wednesday and Friday) until a total of 10, 15 and 20 doses were completed. About 48 h after treatment completion, leukocyte, erythrocyte, and bone marrow cells were counted, and spleen histopathology was analyzed. 1B(15) and 1B(20) mice showed lethargy and irritability, 80% body and 42% spleen weight loss (P<0.001), while body and spleen weight loss were less severe in 2B mice (12 and 48%, respectively). After exposure to 20 benzene doses, 1B(20) and 2B(20) mice showed decreased hemoglobin concentrations, and erythrocyte, leukocyte and bone marrow cell counts (37, 34, 80 and 50%, respectively in group 1B(20); P<0.001; and 12, 48, 62 and 62%, respectively in group 2B(20)). Thrombocytopenia occurred only in group 2B. Both benzene-treatment schemes caused aplastic anemia, however, the disease was masked by spleen toxicity in group 1B. Scheme 2 allowed mice survival and caused less non-hematological effects. We establish here a reproducible and inexpensive experimental model to induce aplastic anemia in mice by subcutaneous injection of 2 ml/kg benzene, using two short-term treatment schemes.
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PMID:A model for the induction of aplastic anemia by subcutaneous administration of benzene in mice. 1136 14


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