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)

Hyperthyroidism was diagnosed in 131 cats during a 3 1/2-year period. The cats ranged in age from 6 to 20 years; there was no breed or sex predilection. The most frequent clinical signs included weight loss, polyphagia, increased activity, polydipsia, polyuria, and vomiting. Common serum biochemical abnormalities included high values for alkaline phosphatase activity (75%), lactate dehydrogenase activity (66%), aspartate transaminase activity (66%), and alanine transaminase activity (54%). Electrocardiographic changes included tachycardia (greater than or equal to 240 beats/min) and increased R-wave amplitude in lead II (greater than or equal to 0.9 mV) in 66% and 29% of the 131 cats, respectively. Thoracic radiography in 82 cats revealed cardiomegaly in 40 (49%) of these cats; 16 cats with congestive heart failure also had pulmonary edema or pleural effusion. In 5 cats with markedly increased fecal volume, mean 48-hour fecal fat content was significantly greater than normal, with daily fat excretion 2 to 15 times the upper limit of normal. Base-line serum thyroxine concentrations were increased above normal range in all cats, whereas triiodothyronine concentrations were increased in 127 (97%) of the 131 cats. In 11 cats tested, mean thyroxine concentration did not increase significantly after thyroid-stimulating hormone administration. Mean 24-hour percentage of thyroid radioiodine uptake in 32 hyperthyroid cats was significantly higher (39.1%) than normal (9.2%). Thyroid scans, performed on 126 cats, showed enlargement and increased radionuclide accumulation in 1 thyroid lobe in 36 (29%) and both lobes in 90 (71%) of the cats.
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PMID:Feline hyperthyroidism: pretreatment clinical and laboratory evaluation of 131 cases. 687 10

Acute pancreatitis in a patient on oral contraceptive therapy is reported, and the relationship of estrogen administration to hyperlipemia and pancreatitis is discussed. A 23-year-old white woman was admitted to a hospital with epigastric pain, nausea, and vomiting. Three previous episodes of abdominal pain had been diagnosed as acute pancreatitis. On the present and previous admissions, she had just completed a cycle on her combination norethindrone 1 mg, mestranol 8 micrograms contraceptive. Laboratory results showed mild leukocytosis and elevated concentrations of blood glucose, alkaline phosphatase, serum amylase, and urine amylase. Serum cholesterol and triglycerides were elevated, and lipoprotein electrophoresis showed a type IV pattern. Abdominal sonogram revealed a normal pancreas, and all other test results were normal. The patient was treated with i.v. fluid replacement, dimenhydrinate, and meperidine hydrochloride. Within 72 hours she was asymptomatic, and serum amylase, triglyceride, and cholesterol concentrations had decreased. She was discharged with a diagnosis of acute pancreatitis secondary to oral-contraceptive-induced hyperlipidemia. Oral contraceptive therapy was not resumed. Predisposing factors, symptoms, and laboratory findings associated with estrogen-induced acute pancreatitis are presented, and the mechanisms through which serum lipid elevations and subsequent pancreatitis occur are discussed. Monitoring serum lipid concentrations before and during estrogen therapy is recommended. Research suggests that patients who are over 40 years old or have family histories of hyperlipemia are at particular risk, and that estrogen therapy should be discontinued if pancreatitis occurs.
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PMID:Estrogen-induced pancreatitis. 688 34

Case report on a 48-year-old Swiss male living in Burundi who suddenly fell ill with vomiting and anorexia, followed by pappy stools, weakness and impotence. He presented with hepatomegaly, while sedimentation rate and alkaline phosphatase were both elevated. Stool examination revealed cysts and vegetative forms of Entamoeba histolytica, while amebic serology was negative. Treatment with ornidazole and later with diloxanide furoate was given. Sonography showed two cystoid areas in the right lobe of the liver. In the third sonographically guided fine-needle puncture both lesions were fully aspirated. Amebic serological tests were now positive for the first time. Six weeks later the sonogram showed a normal liver feature. The symptomatology and diagnosis of hepatic amebic abscess are discussed, with special reference to the important role of sonographically guided fine-needle puncture and drainage. Sonographic technique and differential diagnosis are briefly demonstrated.
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PMID:[Use of ultrasound, ultrasound-directed fine needle puncture and aspiration in amebic abscess of the liver. Case report and short overview]. 715 63

Mebendazole was administered to 7 adult Dachshunds and 2 adult Doberman Pinschers at 6-month intervals for routine parasite control. Two weeks after the 1st treatment, a 3-year-old Dachshund died of acute hepatic failure. Approximately 2 weeks following the 2nd treatment, two 5-year-old Dachshunds and one 3-year-old Dachshund had evidence of acute hepatic necrosis; 1 of these dogs died of fulminant hepatic failure. Typical clinical signs in affected dogs included anorexia, depression, vomiting, icterus, and hemorrhagic diarrhea. Two additional Dachshunds had biochemical evidence of hepatic dysfunction, ie. high serum alanine aminotransferase and serum alkaline phosphatase activities. One Dachshund and 2 Doberman Pinschers had no clinical or laboratory evidence of hepatic disease.
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PMID:Acute hepatic necrosis associated with the administration of mebendazole to dogs. 734 57

Coupling of anthracyclines to high-molecular-weight carriers may alter drug disposition and improve antitumor effects. We have performed a clinical phase I trial of doxorubicin coupled to dextran (70000 m.w.). The drug was administered as single dose i.v. every 21-28 days. Thirteen patients have received a total of 24 courses (median 2; range 1-3). At the starting dose of 40 mg/m2 doxorubicin equivalent (DOXeq), WHO grade IV thrombocytopenia was noted in 2/2 patients. WHO grade IV hepatotoxicity and WHO grade III cardiotoxicity were noted in a patient with preexisting heart disease. Five patients were treated with 12.5 mg/m2 DOXeq. Maximal toxicity at this dose level was WHO grade III thrombocytopenia and local phlebitis (WHO grade II) in 1/5 patients, elevation of alkaline phosphatase (WHO grade III) and WHO grade III vomiting in another patient. Subsequently, five patients received 20 mg/m2 DOXeq. Hepatotoxicity was noted in 5/5 patients (1 x WHO grade IV, 1 x WHO grade III). Thrombocytopenia was noted in 3/5 patients (1 x WHO grade IV, 2 x WHO grade III). At 12.5 mg/m2 DOXeq, a patient diagnosed with a malignant fibrous histiocytoma had stable disease for 4 months. Pharmacokinetic analyses of total and free doxorubicin were performed in plasma and urine. The maximum peak plasma concentration (ppc) for total DOX was 12.3 micrograms/ml at 40 mg/m2 DOXeq. The area under the plasma concentration time curve (AUC) ranged from 28.83-80.21 micrograms/ml*h with dose-dependent elimination half lives (t1/2 alpha: 0.02-0.87 h; t1/2 beta: 2.69-11.58 h; t1/2 gamma: 41.44-136.58 h).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I clinical and pharmacokinetic trial of dextran conjugated doxorubicin (AD-70, DOX-OXD). 750 68

A six-month-old, female German shepherd dog was presented because of depression, anorexia, vomiting, polyuria, and polydipsia of approximately 10 days' duration. The puppy was depressed, and pain could be elicited on palpation of both shoulders and hips. The most significant results of serum chemistries and hematology were hypercalcemia; increased blood urea nitrogen, creatinine, and alkaline phosphatase; and leukocytosis with neutrophilia. Thoracic radiographs revealed a large thymic mass, diagnosed on histological examination as a thymic lymphoma. Radiographs of the shoulders revealed destructive bone lesions involving the proximal metaphyses of the humeri, causing slipped epiphyses. Bone lesions were found at necropsy on the proximal and distal aspects of both humeri and femurs. Bone resorption was due to local neoplastic infiltration and presumed humoral factors secreted locally and systemically by neoplastic thymic lymphocytes.
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PMID:Multiple metaphyseal involvement of a thymic lymphoma associated with hypercalcemia in a puppy. 782 Jul 70

A preliminary dose-range finding study, two 13-week studies and a 52-week study were performed in beagle dogs with polaprezinc (catena-(S)-[mu-[Na-(3-aminopropionyl)histidinato (2-)-N1,N2,O:N tau]-zinc], CAS 107667-60-7, Z-103), a novel anti-peptic ulcer agent, as part of a safety evaluation program. In the preliminary single-dose study, treatment-related findings were confined to one animal treated with 200 mg/kg and consisted in emesis and mucosal lesions in the stomach and upper small intestine. Based on these data, dosages were selected for the main 13-week study (0, 50, 120 and 300 mg/kg/day) and additional 13-week study (0, 8 and 20 mg/kg/day). The dosages for the 52-week study were 8, 20 and 50 mg/kg/day. In the 13-week studies, dosages of 50 mg/kg/day and above resulted in emesis, mild diarrhea and salivation; reduced food consumption and associated reduction in body weight gain for high dosed females; increased blood alkaline phosphatase and decreased urinary specific gravity; histopathological changes in the kidney of the high dosed group in males and females. These changes were no longer apparent following the withdrawal period. In the 52-week study, similar but milder and transient results were noted at the high dose of 50 mg/kg/day. From these results, the no-effect dose level was estimated to be 20 mg/kg b.w./day.
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PMID:Toxicity of the novel anti-peptic ulcer agent polaprezinc in beagle dogs. 789 70

Piroxantrone, a synthetic intercalating agent, was studied in patients with advanced, measurable gastric adenocarcinoma who had not received prior chemotherapy. The starting piroxantrone dose was 150 mg/m2 given intravenously over 1 hour on day 1 and repeated every 21 days. Response and toxicity could be evaluated in 15 patients. No complete, partial, or minor responses were observed. Toxic effects included granulocytopenia, anemia, vomiting, nausea, anorexia, fatigue, stomatitis, alopecia, hyperbilirubinemia, and increased alkaline phosphatase levels. At the stated dose and schedule, piroxantrone does not possess significant activity against advanced gastric cancer.
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PMID:Phase II trial of piroxantrone in metastatic gastric adenocarcinoma. 789 47

Serum levels of total alkaline phosphatase increase during pregnancy but the presently available methods are not very precise. We used the CHEM 1 Bayer Diagnostic test in all the consecutive patients admitted to our unit between June 1 and October 16, 1990. Exclusion criteria were twin pregnancies, pruritus, liver disease or parasitosis. A multifactorial analysis was used to discriminate between general, obstetric, pathologic and drug parameters. There were 373 serum samples, 91% were obtained during the last three months of pregnancy. The mean serum alkaline phosphatase level was 68.2 U/l and 75.9 U/l during the first two trimesters respectively and rose to 126.7, 178.8 and 234 U/l during the last three months respectively. The elevation was greater in cases of vomiting during the first trimester, alpha-methyldopa intake. It was less after hypodroxyapatite intake and was positively correlated with weight gain. Age, parity, pregestational weight, neonatal weight, other pathologies and other drug intake did not affect the results. Knowledge of these physiological levels will be useful for evaluating most liver diseases occurring during pregnancy. Assay of the enzyme fractions would be ordered secondarily.
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PMID:[Serum alkaline phosphatase levels in pregnancy]. 804 May 75

A 27-yr-old Jamaican male presented with a 2-month history of jaundice, pruritus, intermittent diarrhea, and right upper quadrant abdominal pain. Over the next month, his abdominal pain and diarrhea improved, but his jaundice and pruritus worsened. He was afebrile and profoundly jaundice, with a benign abdominal examination. Medical workup included a normal abdominal ultrasound, iron studies, ceruloplasm, and serum electrophoresis. Negative viral (Epstein-Barr virus, cytomegalovirus, mononucleosis, hepatitis A, B, C) studies, ANA, AMA, ASMA, RPR were noted. He denied any alcohol, drug, or toxin exposure. Liver tests revealed total bilirubin of 25.6 mg/dl, direct bilirubin of 13.9 mg/dl, alkaline phosphatase 278 IU/L, AST 45 IU/L, and ALT 71 IU/L. Liver biopsy demonstrated centrilobular zonal necrosis and cholestasis most consistent with a toxic reaction. The patient was again interviewed regarding potential toxins, and he admitted to the ingestion of ackee fruit, a native Jamaican fruit that is illegal in the United States. Shortly after he had ceased intake of the fruit, his symptoms resolved and his liver function tests returned to normal. We present a case of chronic ackee fruit ingestion that led to cholestatic jaundice, vomiting, and abdominal pain.
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PMID:Cholestatic jaundice due to ackee fruit poisoning. 807 44


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