Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The chronic oral toxicity of propiverine hydrochloride (P-4), a new anti-pollakiuria agent, was studied in beagle dogs. Groups of 6 males and 6 females were treated with P-4 at doses of 0, 0.3, 1, 3, 9 mg/kg/day for one year and thereafter 2 animals of both sexes in each group were placed on withdrawal for one month. During administration and recovery period, no death occurred in any dosed animals. As a toxic sign, only the frequency of vomiting was increased in animals of 1, 3 and 9 mg/kg/day groups. Body weight, food and water consumption were not affected by the P-4 administration. In serum chemical examinations, gamma-GTP activity was increased in both sexes of 9 mg/kg/day group at 6 month of administration. Further decrease in total and free cholesterol, triglyceride and phospholipid, increase in GPT activity were detected in some animals of 9 mg/kg/day group at 12 month of administration. In addition decreasing tendency in levels of albumin was noted in males of 9 mg/kg/day group at 9 and 12 month of administration. And also, a gradual increase in total protein level and a gradual decrease in alkaline phosphatase activity were seen in control group, but in females or males of 9 mg/kg/day group, those changes were mild. Urine pH rised slightly in females of 3 mg/kg/day group and in both sexes of 9 mg/kg/day group. No specific findings attributable to P-4 treatment were detected in ECG, heart rate, funduscopy, hematology, fecal occult blood test and necropsy. The absolute and/or relative liver weight in males of 3 and 9 mg/kg/day groups were significantly increased. Light-microscopically, the hypertrophy of hepatocytes characterized by homogenization and enlargement of cytoplasmic space, and concentric inclusions in hepatocytic cytoplasm were detected in both sexes of 3 and 9 mg/kg/day groups. Corresponding to these microscopical findings, the following changes were observed electron-microscopically, the proliferation of smooth surfaced endoplasmic reticulum in hepatocytes in both sexes of 1, 3 and 9 mg/kg/day groups, lamellar bodies in hepatocytes in females of 3 mg/kg/day group, and in both sexes of 9 mg/kg/day group, and annulate lamellae in hepatocytes were detected in one female of 9 mg/kg/day group. After the recovery period, the above mentioned abnormalities were markedly attenuated or disappeared except the changes in hepatocytes. From these results, it seemed that 9 mg/kg/day of P-4 might be safety dose.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[One-year chronic oral toxicity study of propiverine hydrochloride in dogs followed by one-month recovery]. 260 51

Methyl tertiary butyl ether (MTBE) rapidly dissolves cholesterol gall stones in vitro and in vivo. To further characterise tolerability and safety of this aliphatic ether, either MTBE (1 ml/kg body wt daily for two days) or an equal amount of saline was infused into the common bile duct (CBD) of eight cholecystectomised rabbits. Transient vomiting, dyspnoea and somnolence developed during MTBE instillation. Post-treatment values of serum transaminases and alkaline phosphatase were significantly higher in MTBE than in saline treated animals. Cholangiography one week after the last intraductal infusion showed a five-fold increase of CBD size in MTBE v control rabbits. At autopsy histological signs of chemical cholangitis and mild duodenitis were noted in MTBE treated animals. Prompted by these findings, we performed a cholangiography in two patients who had received intraductal MTBE (about 0.2 ml/kg body wt daily for one or two days) one year before: an abnormal dilatation of the CBD was present, which might represent a specific, hitherto undescribed permanent sequela of MTBE administration.
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PMID:Unexpected dilatation of the common bile duct after methyl tertiary butyl ether (MTBE) in rabbits. Possible implications to findings in man. 275 85

The authors reviewed the liver histopathology and the clinical features of eight patients with liver metastases from colorectal cancer who were treated by hepatic arterial infusion chemotherapy (HAIC) via an implantable pump (Infusaid). Before HAIC, these patients had no evidence of hepatitis, and results of liver biopsies performed on three patients showed only minor morphologic alterations. All the liver tumors responded to HAIC, but all patients developed hepatitis. Clinical findings included nausea, vomiting, abdominal pain and jaundice. Serum transaminases, alkaline phosphatase and bilirubin levels were increased. Clinical observations suggested that 5-fluoro-2'-deoxyuridine (FUDR), the predominant drug given, was the hepatotoxic agent. Toxic effects were hepatocyte necrosis, steatosis, cholestasis, central vein sclerosis, and alterations in the portal triad. In addition, central vein lesions like those in veno-occlusive disease, and micronodular cirrhosis resembling that induced by alcohol, were encountered. Although individual susceptibility to FUDR appeared to vary, portal triad fibrosis was present in all eight cases and, together with central vein sclerosis and cirrhosis, appeared to be related to the dose and duration of HAIC.
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PMID:Liver pathology following hepatic arterial infusion chemotherapy. Hepatic toxicity with FUDR. 294 Nov 40

Differential diagnosis of viral hepatitis begins with a check for darkened urine and bile in the urine. These hallmarks of conjugated hyperbilirubinemia immediately rule out prehepatic liver disease. Next, studies are done for the elevated transaminase levels that are characteristic of hepatitis infection, and a thorough history is taken to rule out drug- and toxin-induced hepatitis that may mimic acute viral hepatitis. Elevated alkaline phosphatase is a good marker of cholestasis. Ultrasonography can clarify this diagnosis. The classic presenting symptoms of viral hepatitis are jaundice, nausea, vomiting, malaise, anorexia, and dull right upper quadrant pain. However, serologic studies are needed to detect the presence of specific viral agents.
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PMID:Viral hepatitis. The alphabet game. 305 Sep 28

Pancreatic abscess was diagnosed by exploratory celiotomy in 6 dogs. The most common clinical signs included acute onset of lethargy (n = 5), anorexia (n = 6), vomiting (n = 5), and diarrhea (n = 2). Physical examination revealed pain response to abdominal palpation (n = 5), depression (n = 5), icterus (n = 3), fever (n = 3), and cranial abdominal mass (n = 2). Consistent preoperative clinicopathologic abnormalities included leukocytosis with left shift, observance of toxic neutrophils on the blood smear, hyperlipasemia, hyperamylasemia, hyperbilirubinemia, and increased serum alkaline phosphatase activity. In 5 of 6 dogs, abdominal radiography revealed increased soft tissue density in the cranial portion of the abdomen. Ultrasonography performed on 4 dogs confirmed pancreatic mass. In all dogs, exploratory celiotomy revealed a cavitary pancreatic mass that contained sterile, mucopurulent material. Histopathologic diagnoses included acute necrotizing or chronic-active pancreatitis and steatitis. Two dogs were euthanatized at the time of diagnosis, and the remaining 4 were treated by use of pancreatic debridement(s), open abdominal drainage, and intensive administration of fluids and antibiotics. One dog was euthanatized 4 days after surgery, because of progressive pancreatic abscessation. Three dogs recovered and were discharged.
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PMID:Pancreatic abscess in dogs: six cases (1978-1986). 319 66

174 patients with chronic pancreatic diseases, 30 patients with pancreatic carcinoma and 144 with chronic relapsing pancreatitis, 50 of them with calcifications, were observed in the Department of Internal Medicine of the University of Marburg/FRG between 1972 and 1982. In order to differentiate between carcinoma and relapsing pancreatitis the data of these patients were analysed retrospectively with regard to patient history, actual complaints, findings of laboratory, sonography, ERCP and X-ray investigations. The following results were obtained: Of discriminating value are steatorrhoe, local palpatory pain, alcohol ingestion, a history of earlier attacks and relapsing pain situations; however, general abdominal pain, nausea, vomiting and weight loss (if not exactly specified) are not. Within the laboratory findings bilirubin, GOT, alkaline phosphatase, gamma-GT, serum potassium, blood sugar and chymotrypsin content of the stool were significant while serum and urine amylase were similarly distributed within the groups of patients. Carcinoma and chronic relapsing pancreatitis can be identified by sonography in the majority of patients, but calcifications of the pancreas were rarely demonstrated during this observation period. The obstruction of the extrahepatic bile ducts--mostly due to a carcinoma of the pancreas head--was usually well documented by sonography. Intraabdominal air proofed to be the most disturbing factor. In carcinoma patients, the ERCP is important in demonstrating a complete obstruction of the pancreatic duct and stenosis and dilatation of the extrahepatic bile ducts. In patients with chronic relapsing pancreatitis the pancreatic duct alterations such as dilatations and partial stenosis are well documented by ERCP especially if calcifications occur. In patients without calcifications, dilatation of the branches of the main duct are less relevant in the diagnosis of pancreatic diseases. Radiological demonstration of calcification of the pancreatic area is important for the differential diagnosis. Longstanding characteristical complaints, symptoms and calcifications within the pancreatic area are the most relevant factors in discriminating carcinoma and chronic relapsing pancreatitis.
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PMID:[Differential diagnostic evaluation of chronic pancreatitis in relation to pancreatic cancer based on clinical, laboratory chemical and diagnostic parameters. Studies of 174 patients in 10 years]. 353 95

Eight homosexual men with the acquired immunodeficiency syndrome (AIDS) presented with clinical, biochemical, and radiologic features of stenosis of the papilla of Vater and sclerosing cholangitis. This newly recognized complication of AIDS produces abdominal pain, nausea, and vomiting and may predispose patients to superimposed bacterial cholangitis. Marked elevation of serum alkaline phosphatase levels and lesser changes in hepatic aminotransferase levels are common. Although abdominal ultrasonography and computed tomography detect ductal abnormalities, endoscopic retrograde cholangiography best shows precise ductal irregularities and provides therapeutic intervention. Prompt relief of symptoms follows endoscopic sphincterotomy, often with resolution of biochemical evidence of cholestasis. Biliary tract infection with cytomegalovirus or cryptosporidia and resultant viral or coccidial cholangitis are the proposed pathophysiologic mechanisms.
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PMID:Papillary stenosis and sclerosing cholangitis in the acquired immunodeficiency syndrome. 354 23

A 68-year-old man without previous hepatobiliary or pancreatic disease was admitted after five attacks of nausea, vomiting, abdominal pain and high fever. Laboratory investigations indicated cholestatic liver disease and pancreatitis. For 1.5 years the patient had occasionally been taking a non-steroidal anti-inflammatory drug, sulindac (clinoril, MSD, New York), for osteoarthritis. On suspicion of a drug-associated disease, a rechallenge experiment was performed with sulindac. Five hours after drug administration symptoms recurred. There was a pronounced increase in serum alkaline phosphatase and amylase. A liver biopsy 3 d later showed portal tract inflammatory infiltration and abnormal interlobular bile ducts with degeneration and necrosis of the epithelium and neutrophilic infiltration of the ducts. Sulindac-induced cholangitis has not been described previously. The pathogenetic mechanism is considered to be an immunoallergic idiosyncratic reaction to the active metabolite of sulindac absorbed by the bile duct epithelium. The lesion is apparently reversible.
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PMID:Acute cholangitis and pancreatitis associated with sulindac (clinoril). 362 32

Thirteen patients with systemic mast cell disease were studied in order to define the hepatic changes in this disease and to correlate the histologic lesions in the liver with the clinical findings. These patients often presented with multisystem disorders and 10 had hepatomegaly. Microscopically, the liver tissues in all patients showed fibrosis and chronic inflammatory cellular infiltration with plasma cells, lymphocytes, eosinophils, and mononuclear fibroblast-like cells in the portal area. The hepatic sinusoids were not significantly involved. A histologic diagnosis of systemic mast cell disease is seldom entertained in liver biopsy specimens embedded in paraffin and stained with hematoxylineosin, but can be facilitated in biopsy specimens embedded in plastic such as methacrylate. Tissue mast cells in the cellular infiltrate can be demonstrated best by special staining techniques with Giemsa, toluidine blue, and chloroacetate esterase. The severity of the histologic changes in the liver does not correlate well with the size of the liver or biochemical changes in the blood. Abnormal serum biochemical values were noted primarily in those with dehydration caused by diarrhea and vomiting, and in those with malnutrition. Hepatic function test results were usually normal, except for alkaline phosphatase level, which was elevated in all 13 patients. Although the clinical significance of hepatic involvement in systemic mast cell disease cannot be established with certainty in this study, it is believed that the prognosis of systemic mast cell disease is most intricately related to the systemic effects of mast cell involvement in many other organs, and not to hepatic involvement per se.
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PMID:Hepatic involvement in systemic mast cell disease. 370 70

To delineate the spectrum of clinical expressions of distal, type 1 renal tubular acidosis in children and to update progress in diagnosis, therapy, and prognosis, the medical records of 14 girls and 10 boys, seen over a 7 year period, who met the following criteria, were examined: persistent urinary pH more than 6, net acid excretion less than 70 microEq/min/1.73 m2, simultaneous serum total CO2 less than 17.5 mEq/1, and normal or mild impairment of the glomerular filtration rate. The mean age at diagnosis was 8 months. The presenting signs and symptoms were failure to thrive (50%), vomiting and/or diarrhea (37.5%), dehydration (12.5%), and poor feeding (8.3%). Mean values +/- SD of serum calcium (9.8 +/- 0.8 mg/dl), inorganic phosphate (5.6 +/- 0.8 mg/dl), and alkaline phosphatase (222.6 +/- 96.1 U/l) were normal. Hyperkalemia (serum potassium above 5.0 mEq/l) was present at diagnosis in 13 children. Type 4 renal tubular acidosis was ruled out by the inability to achieve a minimum urine pH. With a mean follow-up period of 28.1 +/- 25.3 months, after alkali therapy at 3.3-3.5 mEq/kg/day had been administered for at least 12 months, the growth parameters improved as follows: the percentile weight (mean +/- SD) increased from the initial 11.8 +/- 7.5 to the final 27.6 +/- 31.3 (p less than 0.003), and the length/height percentile increased from 11.5 +/- 7.3 to 29.7 +/- 24.2 (p less than 0.03). The relationship between urine calcium/creatinine ratio and serum total CO2 showed poor correlation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal tubular acidosis in children. Diagnosis, treatment and prognosis. 377 38


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