Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute to subacute vitamin D toxicosis is described in two different fattening pig herds. A few days after admixing a new batch of vitamin/mineral-premix most of the fattening hogs developed anorexia, polydipsia and polyuria. Emesis was seen in some of the animals. About two weeks after consumption of the suspected feed two thirds of the pigs had a rough hair coat and a very poor weight gain. Because of the results of haematological and metabolic findings from blood and urine samples of diseased pigs a calcinosis and tubular nephrosis was diagnosed. Patho-histological findings of the euthanatized morbid pigs included severe chronic interstitial nephritis, glomerulonephritis and mineralisation of a number of organs. Some of the animals showed degeneration of the myocardium. Feeding two healthy pigs with the incriminated feed the disease was reproduced.
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PMID:[Clinical findings in vitamin D poisoning of swine]. 175 63

Groups of 64 male and 64 female Wistar rats were given thiram at constant dietary doses of 0, 3, 30, and 300 ppm (0, 0.1, 1.2, and 11.6 mg/kg/day for males and 0, 0.1, 1.4, and 13.8 mg/kg/day for females) for 104 weeks. Eight males and eight females in each group were killed after Weeks 13, 26, and 52. For the dog study, four male and four female beagle dogs were alloted to each group and treated with the compound at 0, 0.4, 4, and 40 mg/kg/day for 104 weeks. The dogs in the 40 mg/kg/day group had severe toxic signs, including nausea or vomiting, salivation, and occasional clonic convulsion, and all were subjected to unscheduled necropsy before Day 203 of treatment. The dogs also had ophthalmological changes such as fundal hemorrhage, miosis, and desquamation of the retina which were consistent with the retinal lesions shown by histopathology. The rats of the high-dose group had retarded growth with a slightly decreased food intake. Anemia was evident in high-dose female rats and in middle- and high-dose dogs. Liver failure in male and female dogs and kidney damage in female dogs were detected in middle- and high-dose groups by blood biochemistry and/or histopathology. Regressive changes of the sciatic nerve accompanied by atrophy of the calf muscle were seen in female rats of the high-dose group but not in male rats. In high-dose rats, progression of myocardial lesions of the heart and chronic nephrosis of the kidney were depressed in males and females, respectively. Female rats of the middle- and high-dose groups had decreased occurrences of mammary fibroadenoma and decreased development of skin masses.
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PMID:Chronic toxicity studies with thiram in Wistar rats and beagle dogs. 188 9

With the advent of boric acid insecticides, accidental ingestion of the compound can be encountered in animals. Toxic levels of boric acid most commonly cause vomiting, depression, and, occasionally, diarrhea. Boric acid is, however, cytotoxic to all cells. If a sufficiently high level is ingested, seizures, renal tubular nephrosis, and, rarely, hepatotoxicity may be noted. Gastrointestinal evaluation and supportive care are usually of primary therapeutic importance, although in severe cases, exchange transfusion and/or peritoneal dialysis may be required to decrease blood boron concentrations.
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PMID:Toxicology of selected pesticides, drugs, and chemicals. Boric acid. 218 Jan 82

Two fatal cases of Japanese pieris poisoning in goats are reported. The clinical symptoms of the two animals consisted in vomiting, salivation, excitation and depression. Despite rumenotomy and symptomatic treatment, the goats died within four days after the onset of the symptoms. Pulmonary oedema accompanied by lobular aspiration pneumonia was found to be present in one goat at autopsy. Hyperaemia, pulmonary oedema and acute tubular nephrosis were observed in the other animal.
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PMID:[Pieris japonica pieris poisoning in 2 goats]. 337 72

Acute toxicosis developed in a group (n = 35) of fattening hogs and replacement gilts that had excessive vitamin D3 inadvertently added to their feed. All of the pigs were lethargic, and emesis was evident in about half of the pigs 1 to 2 days after they consumed the feed. On the 2nd day, 3 of the pigs died. The remaining pigs were given a different ration. Five additional pigs died during the next 2 weeks. Clinical toxicosis also was observed in 1 of 2 feeder pigs fed the suspect feed in the laboratory and in 2 of 2 pigs fed the suspect feed by the company that had mixed the feed. Gross necropsy findings consistently observed were hemorrhagic gastritis and diffuse interstitial pneumonia. Myocardial degeneration and nephrosis were seen in, respectively, 1 of 6 and 4 of 6 pigs necropsied. Histologically, necrosis and mineralization of variable severity were observed in the fundic gastric mucosa, lungs, kidneys, bone, heart, and small blood vessels of the lungs and heart. Less necrosis and more mineralization were observed in pigs that survived longer than 6 days. The 2 pigs fed the suspect feed in the laboratory had increased concentrations of serum calcium from the 3rd to the 9th days or the 1st to the 3rd days, after feeding the suspect feed. Serum phosphorus concentrations were increased from the 1st until the 2nd or 3rd day, and serum magnesium concentrations were increased from the 1st or 2nd to the 3rd day after feeding the suspect feed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute toxicosis in swine associated with excessive dietary intake of vitamin D. 632 15

Tetracyclines have been used as in vivo indicators of new bone formation because they form complexes with mineral at bone-forming surfaces. Four of 12 dogs in a bone-labeling study developed clinical signs of renal disease (vomiting, diarrhea, dehydration, and azotemia) within 1 to 2 days of receiving oxytetracycline at a bone-labeling dose of 25 mg/kg of body weight, once daily for 2 consecutive days. To delineate the relationship between oxytetracycline administration and renal damage, six dogs were given the bone-labeling dose intravenously and were subsequently evaluated by determination of clinical signs, serum biochemical analysis, urinalysis, and histologic examination (experiment 1). Drug administration was modified in the five dogs remaining in the bone-labeling orthopedic study. These dogs received the oxytetracycline dose as a slow intravenous infusion diluted with 250 ml of lactated Ringer's solution (experiment 2). All six dogs of experiment 1 developed persistent isosthenuria within 2 days of receiving the bone-labeling dose of oxytetracycline. Clinical illness (three of six dogs) was associated with azotemia, creatinemia, and hyperphosphatemia. All dogs had multifocal, mild to moderate flattening of renal tubular epithelium, characteristic of nephrosis. None of the dogs of experiment 2 developed any clinical indications of renal disease, and the only biochemical abnormality was isosthenuria in two of the five dogs. Thus the development of clinical signs and biochemical abnormalities associated with the intravenous administration of oxytetracycline was obviated by the slow administration of a dilution of the calculated bone-labeling dose of the antibiotic.
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PMID:Oxytetracycline-induced nephrotoxicosis in dogs after intravenous administration for experimental bone labeling. 890 81

The toxicity of cisplatin encapsulated in pegylated, long-circulating liposomes (SPI-077) was compared with nonliposomal cisplatin in male and female cynomolgus monkeys (n = 2-4 per sex per group) treated with intravenous infusions of 2.5 or 25 mg/kg SPI-077, 2.5 mg/kg cisplatin, placebo liposomes, or saline once every 3 weeks for total of five treatments. All animals survived until scheduled necropsy at 3 days after the final treatment or after a treatment-free 4-week recovery period. Emesis occurred after each treatment in all cisplatin-treated monkeys, but only once in one monkey treated with high-dose SPI-077. Dose-related mild decreases in red blood cell (RBC) count, hemoglobin, and hematocrit to or slightly below low normal range occurred in the high-dose SPI-077 and placebo liposome treatment groups after each treatment, with partial to complete recovery between treatments and no signs of correlating bone marrow toxicity. Decreases were similar in cisplatin-treated monkeys, but resolved only slightly between treatments and after the end of treatment (continuing to decrease in females) and were accompanied by bone marrow hypocellularity. Indirect, but not direct, bilirubin levels were cyclically elevated in the high-dose SPI-077 and placebo-treated animals, but not in the other treatment groups. Levels had either fully resolved or were near baseline and/or saline group values prior to the next treatment. Serum cholesterol levels were cyclically increased in SPI-077- and placebo liposome-treated animals, and minimally increased numbers of foam cells were seen in the liver, spleen, kidney, and other organs; both were considered related to the lipid dose administered. Cisplatin-treated monkeys exhibited sensory polyneuropathy and moderate irreversible toxic tubular nephrosis, but no neuropathy or nephrotoxicity was seen in either SPI-077 treatment group. Microscopically, treatment-related cell death was seen in dorsal root ganglia (DRG), affecting 15% of the cells in cisplatin-treated animals, compared to 8 and 12% in the low- and high-dose SPI-077 treatment groups. Neither drug was ototoxic. In summary, repeated administration of SPI-077 produced minimal, reversible effects related to the lipid dose administered, mostly limited to the 25 mg/kg dose group. The most notable effects in this group were cyclical decreases in hematology parameters thought to be related to increased recycling of a small fraction of RBCs and limited cell death in the DRG in the absence of any neurophysiological changes. Animals treated with a 10-fold lower dose of cisplatin (2.5 mg/kg), in contrast, exhibited myelo-, nephro-, and neurotoxicity, including sensory neuropathy, and were emetic after every dose. The SPI-077 liposomal formulation of cisplatin may provide a less toxic alternative to standard cisplatin solution.
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PMID:Comparative intravenous toxicity of cisplatin solution and cisplatin encapsulated in long-circulating, pegylated liposomes in cynomolgus monkeys. 992 79

Treatment with intravenous human immunoglobulin (IVIG) has become a routine therapeutic method in immunodeficiency states and autoimmune diseases. Although it is a relatively safe therapeutic method it may have serious undesirable effects. Knowledge of these undesirable effects is the prerequisite for coping with them and in some instances it is possible to prevent them. Undesirable effects of IVIG administration can be divided into six groups: 1. Generalized reaction, in particular fever, shiver, nausea, vomiting, tachycardia, dyspnoea, changes of blood pressure are recorded in less than 5% patients, usually during infusion and depend on the rate of administration. 2. Hypersensitivity and anaphylactic reactions may be also severe to fatal and are usually the manifestation of the action of antibodies against IgA; they may be anticipated in particular in patients with deficiency of class A immunoglobulins and in patients with autoimmune diseases. 3. Haematological: rare and usually clinically irrelevant haemolytic anaemia. 4. Neurological: frequent and minor headache, rarely relapsing aseptic meningitis syndrome. 5. Nephrological: renal failure which developed by the mechanism of osmotic nephrosis, relatively very rare, affecting almost exclusively patients with nephropathy present before administration of IVIG. 6. Thrombotic complications manifested by cerebral ischaemia. They are however extremely rare and their relationship to IVIG administration is controversial. At present we can rule out transmission of viral infection by IVIG preparations with the exception of transmission of the hepatitis C virus.
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PMID:[Adverse effects of administration of intravenous human immunoglobulins]. 1074 20

Streptococcus pneumoniae causes lobar pneumonitis but primary peritonitis can occur in cyrrotic adults as well as in children affected by nephrosis and immunopathies. In young females peritonitis can be the consequence of infection localized at genital organs. Pneumococcal sepsis is becoming rare with the antibiotic era but resistance to penicillin is actually frequent and is becoming a problem for elderly. We report a case of a young woman affected by spontaneous primary peritonitis and pneumococcal sepsis. The prevalent symptoms were gastrointestinal: diarrhea and emesis. No infectious foci could be detected on imaging studies and during surgery.
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PMID:[Primary pneumococcal peritonitis: description of a case and review of the literature]. 1075 66

Eighteen young native male and female goats were divided into 3 equal groups. Kerosene was given to Groups 1, 2 and 3 as single doses of 10, 20 or 40 ml/kg bw respectively. Clinical signs In-Group 1 were mild behavioral changes and in Group 2 were mild to moderate bloat, coughing and behavioral changes. None of the goats of Groups 1 and 2 died. Goats of Group 3 had severe signs of poisoning and died within 4 h to 11 d after dosing with clinical signs of severe bloat, frequent coughing, vomiting, and expelling of kerosene from the mouth and nose. Star-gazing, depression, recumbency and dyspnea also occurred. Postmortem changes in Group 3 were gangrenous pneumonia, pleuropneumonia, congestion in brain and kidney, perivascular and perineuronal edema in brain tissue, and renal nephrosis.
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PMID:Experimental kerosene poisoning in goats. 1111 43


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