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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The development of anuric renal failure associated with zinc intoxication was detected in a dog following ingestion of an ornamental brass knob from a toilet paper holder. The 3-y-old, male neutered, 15.4 kg Welsh Corgi presented to a local veterinary clinic with a 2-w history of intermittent vomiting, inappetance and lethargy. The dog was transferred to a veterinary teaching hospital where surgery was performed to remove the foreign body. The dogwas euthanized 24 h post-surgery due to the development of anuric renal failure. Whole blood drawn at the time of surgery had a serum zinc concentration of 89.8 ppm (normal 0.7-2.0 ppm). The serum zinc concentration in this dog is the highest reported concentration in the literature. Ingestion of any zinc-containing metal object can potentially result in a severe intravascular hemolysis with subsequent renal impairment. Zinc intoxication should be suspected when hemolysis is accompanied by the finding of a metallic object in the gut.
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PMID:Anuric renal failure associated with zinc toxicosis in a dog. 1548 54

The purpose of this study is to evaluate the acute toxicity of oral exposure to nanoscale zinc powder in mice. The healthy adult male and female mice were gastro-intestinally administered at a dose of 5 g/kg body weight with two size particles, nanoscale zinc (N-Zn) and microscale zinc (M-Zn) powder, while one group mice treated with sodium carboxy methyl cellulose was used as the control. The symptoms and mortality after zinc powder treatment were recorded. The effects of particles on the blood-element, the serum biochemical level and the blood coagulation were studied after 2 weeks of administration. The organs were collected for histopathological examination. The N-Zn treated mice showed more severe symptoms of lethargy, vomiting and diarrhea in the beginning days than the M-Zn mice. Deaths of two mice occurred in the N-Zn group after the first week of treatment. The mortalities were confirmed by intestinal obstruction of the nanoscale zinc aggregation. The biochemical liver function tests of serum showed significantly elevated ALT, AST, ALP, and LDH in the M-Zn mice and ALT, ALP, and LDH in the N-Zn mice compared with the controls (P<0.05), which indicated that the liver damage was probably induced by both micro- and nano-scale zinc powders. The clinical changes were observed in the two treated group mice as well. The levels of the above enzymes were generally higher in the M-Zn mice than in the N-Zn mice, which implied that M-Zn powder could induce more severe liver damage than N-Zn. The biochemical renal function tests of serum BUN and CR in the M-Zn mice markedly increased either compared with the N-Zn mice or with the controls (P<0.05), but no significant difference was found between the N-Zn and the control mice. However, severe renal lesions were found by the renal histopathological examination in the N-Zn exposed mice. Therefore, we concluded that severe renal damage could occur in the N-Zn treated mice, though no significant change of blood biochemical levels occurred. Blood-element test showed that in the N-Zn mice, PLT and RDW-CV significantly increased, and HGB and HCT significantly decreased compared to the controls, which indicated that N-Zn powder could cause severe anemia. Besides the pathological lesions in the liver, renal, and heart tissue, only slight stomach and intestinal inflammation was found in all the zinc treated mice, without significant pathological changes in other organs.
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PMID:Acute toxicity of nano- and micro-scale zinc powder in healthy adult mice. 1616 31

Pellagra is a systemic disturbance caused by a cellular deficiency of niacin, resulting from inadequate dietary nicotinic acid and/or its precursors, the essential amino-acid tryptophan. In Europe and North America cases of pellagra are rarely encountered, but in some developing countries this disease is frequent, and is the most frequent clinical feature of nutritional deficiency of adult. The principal causes of pellagra are: nutritional niacin deficiency; chronic alcoholism; gastro-intestinal malabsorption; some medications (5-fluoro-uracil, isoniazid, pyrazinamide ehtionamide, 6-mercaptopurine, hydantoins, phenobarbital and chloramphenicol). The diagnosis of pellagra is based on the patient's history and the presence of "3 D syndrome": dermatitis, diarrhea, and dementia. The dermatitis caused by pellagra is a bilaterally symmetrical erythema at the sites of solar exposure. The dermatitis begins in the form of an erythema with acute or intermittent onset gradually changing to an exsudative eruption on the dorsa of the hand, face, neck, and chest with pruritus and burning. Acute dermatitis of pellagra resembles sunburn in the first stages, sometimes with vesicles and bullae. The gastro-intestinal disturbances are: anorexia, nausea, epigastric discomfort and chronic or recurrent diarrhea. Anorexia and malabsorbative diarrhea lead to a state of malnutrition and cachexia. Stools are typically watery, but occasionally can be bloody and mucoid. Neuropsychologic manifestation included photophobia, asthenia, depression, hallucinations, confusions, memory loss and psychosis. As pellagra advances, patient become disoriented, confused and delirious; then stuporous and finally die. Pathological changes in the skin is non-specific, there are no chemical tests available to definitively diagnose pellagra. However low levels of urinary excretion of N-methylnicotinamide and pyridone indicates niacin deficiency. The treatment of pellagra consisted to exogenous administration of niacin or nicotinamide cures. Topical management of skin lesions with emollients may reduce discomfort. The therapy should also include other B vitamins, zinc and magnesium as well as a diet rich in calories. The prevention is based in the nutritional education (food sources of niacin: eggs, bran, peanuts, meat, poultry, fish, red meat, legumes and seeds), and the eviction of alcohol.
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PMID:[Pellagra]. 1620 85

A 6-year-old Labrador retriever was referred for investigation of severe lethargy and suspected immune-mediated haemolytic anaemia. Clinical examination revealed pale mucous membranes and jaundice. Haematology demonstrated large numbers of Heinz bodies and a marked anaemia, which was strongly regenerative. Serum zinc concentrations were markedly elevated. Analysis of a metal toy vomited by the dog 3 days prior to presentation revealed it to be composed of almost pure zinc. A diagnosis of haemolytic anaemia secondary to acute zinc toxicity was made and supportive therapy instigated. There was a subsequent decrease in numbers of Heinz bodies and a rise in the haematocrit, and the dog made an uneventful recovery. Acute zinc toxicity resulting in haemolytic anaemia is rarely observed, and this case was also unusual in that the main clinicopathological finding was the presence of numerous Heinz bodies without other evidence of oxidative damage to red blood cells.
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PMID:Heinz body haemolytic anaemia in a dog secondary to ingestion of a zinc toy: a case report. 1730 71

Lethargy, poor attention, and the high rate and severity of infections in malnourished children affect their educational achievement. We therefore studied the association between visuomotor abilities and intelligence quotient (IQ) and their relationship with iron, zinc, and copper. A cross-sectional study was carried out on a sample of 89 healthy children (age range, 4-10 years). Evaluations of visuomotor ability and IQ were performed with the Developmental Test of Visual Motor Integration (VMI) and the Scale for Measurement of Intelligence for children aged 3-18 years, respectively. Nutritional status was assessed using anthropometry and biochemical assessments, which included serum ferritin, zinc and copper levels, and Hb. The sample was classified as having low or normal VMI scores: 47 children (52.8%, mean age 7 +/- 1.5 years) had low VMI, and 42 (47.2%, mean age 7 +/- 2.06 years) had normal VMI. There were no statistically significant differences in socioeconomic and cultural condition between both groups. We found significantly higher serum copper and ferritin levels in normal as compared to low VMI, but we did not find any differences with zinc. IQ was significantly higher in normal vs low VMI children. The fact that children with abnormal VMI presented low mean serum copper and ferritin concentrations could indicate that copper and iron deficiencies in this sample could be related with visuomotor abilities.
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PMID:Acquisition of visuomotor abilities and intellectual quotient in children aged 4-10 years: relationship with micronutrient nutritional status. 1791 59

A 57-year-old schizophrenic woman presented with lethargy, nausea, vomiting, and anorexia after coin ingestion. She was found to have multiple organ dysfunction manifested as hepatitis, pancreatitis, severe anemia with markedly depressed bone marrow response, extravascular hemolysis, and acute renal failure. Prolonged exposure to zinc from massive coin ingestion was responsible. Zinc poisoning is an unusual consequence of coin ingestion in the adult human literature. A detailed discussion on zinc poisoning, as well as the pitfalls in radiological diagnosis of massive coin ingestion, is presented.
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PMID:Massive penny ingestion: the loot with local and systemic effects. 1818 Jan 30

Presented is an African giant rat (Cricetomys gambianus) following zinc ingestion. The sick rat was lethargic, withdrawn, had soft, mucus-impregnated faeces and diahorrea, foot twitching and icterus. Comparative age, sex and body weight (b.wt.)-matched analyses were made with a healthy giant rat. Twelve-hourly Urine volume (UV), Haematocrit (Hct), urinary glucose, plasma zinc and Alkaline Phosphatase (ALP) were performed over an 8-week period. Full blood counts were performed and differential WBC counts and microscopic observations were made on blood smears obtained from both healthy and sick rats. Consecutive blood samples were drawn at the end of each week (Weeks <2-6 treatment; Weeks 7-8 post-treatment). Treatment involved oral vitamin B12 supplement at 4 microg/day and 2 ml diethylenetriaminepentaacetic acid (DTPA) intramuscular injections at 1 ml/450g b.wt./5 wks (Week 2 - 6). Day 1 showed neutropaenia, Heinz bodies on RBCs (reticulocytes and immature forms). Zinc (Day 1 - end Week 7), glucose (Day 1 - end Week 4), ALP (Day 1 -Week 4) and UV were elevated (Day 1 - end Week 6). Indications of moderate zinc toxicosis following ingestion and stress-associated glucosuria were concluded.
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PMID:Hyperzincaemia in a pet African giant rat (Cricetomys gambianus Waterhouse, 1840). 1823 41

Zinc deficiency induces a striking reduction of food intake in animals. To elucidate the mechanisms for this effect, two studies were connectedly conducted to determine the effects of peripheral administration of zinc on food intake in rats fed the zinc-adequate or zinc-deficient diets for a 3-week period. In study 1, two groups of male Sprague-Dawley rats were provided diets made either adequate (ZA; 38.89 mg/kg) or deficient (ZD; 3.30 mg/kg) in zinc. In study 2, after feeding for 3 weeks, both ZA and ZD groups received intraperitoneal (IP) injection of zinc solution with three levels (0.5, 1.0, and 2.0 microg zinc/g body weight, respectively) and cumulative food intake at 0.5, 1, 2, 4, and 24 h, and plasma hormones concentrations were measured. The results in study 1 showed rats fed the ZD diets revealed symptoms of zinc deficiency, such as sparse and coarse hair, poor appetite, susceptibility to surroundings, lethargy, and small movements. Zinc concentrations in serum, femur, and skeletal muscle of rats fed the ZD diets declined by 26.58% (P < 0.01), 27.32% (P < 0.01), and 24.22% (P < 0.05), respectively, as compared with ZA control group. These findings demonstrated that rat models with zinc deficiency and zinc adequacy had been fully established. The results in study 2 showed that IP administration of zinc in both ZA and ZD rats did not influence food intake at each time points (P > 0.05), although zinc deficiency suppressed food intake. Plasma neuropeptide Y (NPY) was higher, but insulin and glucagon were lower in response to zinc deficiency or zinc administration by contrast with their respective controls (P < 0.05). Leptin, T3, and T4 concentrations were uniformly decreased (P < 0.05) in rats fed the ZD diets in contrast to ZA diets; however, no differences (P > 0.05) were observed during zinc injection. Calcitonin gene-related peptide was unaffected (P > 0.05) by either zinc deficiency or zinc administration. The present studies suggested that zinc administration did not affect short-term food intake in rats even in the zinc-deficient ones; the reduced food intake induced by zinc deficiency was probably associated with the depression in thyroid hormones. The results also indicated that NPY and insulin varied conversely during the control of food intake.
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PMID:The effect of peripheral administration of zinc on food intake in rats fed Zn-adequate or Zn-deficient diets. 1842 33

A 5-year old, intact male Yorkshire Terrier was presented due to lethargy, vomiting and diarrhea. Clinical signs included shock, icterus and a painful abdomen. Laboratory examination revealed a severe intravascular hemolytic anemia, a thrombocytopenia and a leukocytosis. The radiographic examination revealed the presence of metallic foreign bodies in the stomach and in the intestine. After stabilisation of the patient with crystalloids, packed red blood cells, ranitidine, metamizole, amoxicilline/clavulanic acid and marbofloxacine, surgery was performed and 5 coins (10 cent, 5 cent, 2 cent) were removed via esophagus and via enterotomy. In the course of disease the dog developed acute renal failure and pancreatitis. The zinc concentration in the serum was 2200 microg/dl, which was 30 times higher compared to a healthy control dog. After 21 days the dog was discharged from the hospital. On day 28 all laboratory values were within the reference range.
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PMID:[Zinc intoxication in a Yorkshire Terrier due to Euro cent ingestion]. 1918 52

A litter of 3-month-old Pharaoh Hound puppies presented to the referring veterinarian with severe generalized erythematous-crusted papules with pruritus, accompanied by exfoliation and erythema of footpads, inappetence, lethargy, and retarded growth. Three of 5 puppies (2 male and 1 female) were affected. Representative areas were biopsied from 1 affected male puppy and were routinely processed. Histologically, there was marked epidermal hyperplasia with a disorganized appearance of the epidermis and massive parakeratotic hyperkeratosis, compatible with zinc-responsive dermatosis. Low serum zinc concentrations were documented, and the affected animals partially responded to intravenous zinc supplementation but did not respond to oral supplementation. One male puppy died as a result of unrelated causes and was necropsied. The remaining 4 puppies were followed over 2 years. Growth was stunted, and enamel hypoplasia of permanent dentition developed compared with unaffected littermates. Intravenous zinc supplementation at 3-4 week intervals was required to prevent further skin lesion development. One dog died at 3 years of age of renal failure.
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PMID:Severe zinc responsive dermatosis in a litter of Pharaoh Hounds. 2062 48


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