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)

Ten dogs with neuroendocrine carcinoma of the liver were selected for inclusion in the study. Clinical signs were anorexia (7), vomiting (5), polydipsia/polyuria (3), icterus (2), lethargy (2), weight loss (2), paresis (1), ataxia (1), weakness (1), collapse (1), and urinary tract infection (1). Hematologic and biochemical abnormalities included anemia (2/8), leukocytosis (4/8), high liver enzyme activity (serum alkaline phosphatase, 7/9; alanine transaminase, 7/9; aspartate transaminase, 8/9), and high total bilirubin (6/9). Grossly, the tumors were diffuse, involving all liver lobes in six dogs, and two dogs had various-sized nodules in addition to diffuse involvement. Histologically, there were eight tumors with solid or trabecular pattern (group A), one tumor with cords or rows of neoplastic cells (group B), and one tumor with multiple rosette-like structures (group C). Immunohistochemical studies revealed that all 10 neoplasms were positive for at least one of the endocrine markers used: neuron-specific enolase (NSE; 8/10), synaptophysin (5/10), and chromogranin-A (3/10). A panel of NSE, chromagranin-A, and synaptophysin detected 100% of the tumors in our series. Electron microscopy confirmed the diagnosis by the presence of intracytoplasmic neurosecretory granules in the two examined cases. Our results show that neuroendocrine markers commonly used in humans can be used for the diagnosis of hepatic neuroendocrine carcinoma in dogs, preferably a panel of synaptophysin, chromagranin-A, and NSE because chromogranin-A alone is not as useful in dogs as in humans.
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PMID:Canine hepatic neuroendocrine carcinoma: an immunohistochemical and electron microscopic study. 1575 67

An 8-year-old, male domestic shorthair cat was referred to the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania with a 3-day history of lethargy, inappetance, hyperemic skin nodules, coughing, and vomiting. Laboratory results included nonregenerative anemia, lymphopenia, thrombocytopenia, hypoalbuminemia, hyponatremia, and increased alanine aminotransferase and aspartate aminotransferase activities. Cytology of the skin nodules revealed many spindle- to crescent-shaped protozoal organisms, with morphology consistent with Toxoplasma gondii or Neospora caninum. Gross necropsy, histopathologic, immunohistochemical, and transmission electron microscopic findings confirmed a systemic protozoal infection; however, the organism exhibited characteristics of both N caninum and T gondii. Diagnosis of a T gondii-like infection was based on internal structures of the organism and positive reaction to rabbit polyclonal antibodies to T gondii. Reports of toxoplasmic dermatitis are rare in the cat and dog, and this is the first reported diagnosis of T gondii-like protozoa in skin aspirates.
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PMID:Toxoplasma gondii-like organisms in skin aspirates from a cat with disseminated protozoal infection. 1590 69

The patient was a 57-year-old woman presenting with jaundice as the chief complaint. She began vomiting on July 10, 2003. Jaundice was noted and admitted to our hospital for thorough testing. Tests on admission indicated severe hepatitis, based on: aspartate aminotransferase (AST), 1 076 IU/L; alanine aminotransferase (ALT), 1 400 IU/L; total bilirubin (TB), 20.9 mg/dL; and prothrombin time rate (PT%), 46.9%. Acute hepatitis A (HA) was diagnosed based on negative hepatitis B surface antigen and hepatitis C virus RNA and positive immunoglobulin (Ig) M HA antibody, but elevation of anti-nuclear antigen (X320) and IgG (3 112 mg/dL) led to suspicion of autoimmune hepatitis (AIH). Plasma exchange was performed for 3 d from July 17, and steroid pulse therapy was performed for 3 d starting on July 18, followed by oral steroid therapy. Liver biopsy was performed on August 5, and the results confirmed acute hepatitis and mild chronic inflammation. Levels of AST and ALT normalized, so dose of oral steroid was markedly reduced. Steroid therapy was terminated after 4 mo, as the patient had glaucoma. Starting 3 mo after cessation of steroid therapy, levels of AST and ALT began to increase again. Another liver biopsy was performed and AIH was diagnosed based on serum data and biopsy specimen. Oral steroid therapy was reinitiated. Levels of AST and ALT again normalized. The present case was thus considered to represent AIH triggered by acute HA.
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PMID:Autoimmune hepatitis triggered by acute hepatitis A. 1627 28

We have developed a group of 4-substituted-1-nitroacridines with potent anti-tumor activity against prostate cancer and less toxic than parent 1-nitroacridines. The most active 9-(2'-hydroxyethylamino)-4-methyl-1-nitroacridine (C-1748) was selected for pre-clinical studies. The current study was undertaken to evaluate clinical and/or morphological adverse effects of C-1748 as a single intravenous dose at concentrations ranging from 0.16 to 4.6 mg/kg administered to male Beagle dogs. The maximum tolerated dose was 1.5 mg/kg. Emesis was observed in all groups lasting an average of 30 min to 12 h post-dosing. At high dose, extreme aggression was observed in one dog followed by disorientation and depression lasting for 48 h a frequent observation with chemotherapy. Reductions in platelets and white blood cells were observed which was similar to that seen with other chemotherapeutic agents. A compensatory hyperplasia of lymph nodes and a transient and limited extravasation in the intestinal mucosa were also observed. Increases in aspartate aminotransferase, alkaline phosphatase and creatine phosphokinase were transient with normal levels restored by day 9. These enzyme increases were accompanied by epithelial hypertrophy of larger bile ductules in the periportal triads of the liver. The low toxicity profile and high tumor target activity make this novel class of drug a promising chemotherapeutic agent.
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PMID:Pre-clinical toxicology and pathology of 9-(2'-hydroxyethylamino)-4-methyl-1-nitroacridine (C-1748), a novel anti-cancer agent in male Beagle dogs. 1671 73

Miltefosine (2.5 mg/kg/day for 28 days) was investigated for treatment of New World cutaneous leishmaniasis in Colombia and Guatemala. The data from a controlled study was remarkably similar to the data of a prior uncontrolled pilot study. In the controlled study, the per-protocol 6-month cure rate for Leishmania panamensis disease was 91% compared with a concomitant placebo cure rate of 38%. In Guatemala, the cure rate for L. braziliensis and L. mexicana disease was approximately 50% compared with approximately 20% for placebo. In both countries, nausea but not 'motion sickness' and vomiting but not diarrhoea were experienced by approximately 30% more miltefosine patients than placebo patients. Mild elevation of creatinine, but not of aspartate aminotransferase or alanine aminotransferase, was also more frequently seen in the miltefosine group than in the placebo group. Miltefosine was well tolerated, and as effective as historic values of antimony for treatment of L. panamensis disease.
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PMID:Treatment of New World cutaneous leishmaniasis with miltefosine. 1693 Jun 49

It is generally accepted that the risk for fetal infection is greatest with maternal primary cytomegalovirus CMV infection and much less likely with recurrent infection. Here, we report a fatal case of congenital CMV infection following recurrent maternal infection after a 7-year interval. A 3-month-old female baby presented with fever, jaundice, vomiting and stopping breast-feeding. Physical examination revealed mild respiratory distress, hepatosplenomegaly, microcephaly and growth retardation. Laboratory examination included bilirubin concentrations Total: 7.17 mg/dl; conjugated 6.67 mg/dl, aspartate transaminase 141 IU, and alanine transaminase 499 IU. Enzyme-linked immunosorbent assay test results revealed + CMV IgM and + CMV IgG. She died on the 10th day of admission with the diagnosis of CMV hepatitis, pneumonia, and multi-organ failure. Nuclear and cytoplasmic inclusions were demonstrated in the lung, liver and brain on postmortem biopsy. This case highlights that the outcome of babies born to mothers with recurrent maternal CMV infection may be more severe and fatal than previously thought.
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PMID:Fatal congenital cytomegalovirus infection following recurrent maternal infection after a 7-year interval. 1726 7

Rotavirus is one of the leading causes of acute gastroenteritis among children. While clinical complaints are generally intestinal including vomiting and diarrhea, there is evidence to suggest that disease outside the gastrointestinal tract occurs. This study examines the frequency of hepatic transaminase elevation in children with rotavirus gastroenteritis. Patients identified with rotavirus gastroenteritis by stool antigen testing between November 2005 and March 2006 had available serum analyzed for alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, total bilirubin, direct bilirubin, and creatinine phoshosphokinase (CPK). Chart review was conducted to identify patients with possible liver injury unrelated to rotavirus. Among the 92 patients identified with rotavirus during the study period, 75 had serum specimens available for testing. Fifteen patients (20%) had elevated ALT and AST, including one patient with an increase in AST, ALT, alkaline phosphatase, and total and direct bilirubin. The mean ALT elevation was 56 IU/L (range, 44 to 114 IU/L), and the mean AST elevation was 80 IU/L (range, 57 to 126 IU/L). Fifty-three patients (71%) had an increase in AST alone, and three patients (4%) had an increase in AST and alkaline phosphatase. The mean AST values in these groups were 61 IU/L (range, 42 to 110 IU/L) and 79 IU/L (range, 59 to 96 IU/L), respectively. In conclusion, rotavirus commonly causes elevation of liver transaminases.
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PMID:Rotavirus causes hepatic transaminase elevation. 1826 61

We report a case of acute hepatotoxicity in a 42-year-old woman after administration of clindamycin for a dental infection. After 6 d of treatment, she had fatigue, nausea, vomiting, anorexia, pruritus and jaundice. Her laboratory analysis showed alanine aminotransferase (ALT), 1795 IU/L (normal range 0-40); aspartate aminotransferase (AST), 1337 IU/L (normal range 5-34); alkaline phosphatase (ALP), 339 IU/L (normal range 40-150); gamma-glutamyl transpeptidase (GGT), 148 IU/L (normal range 9-64 IU/L); total bilirubin, 4.1 mg/dL; direct bilirubin, 2.9 mg/dL and prothrombin time (PT), 13.5 s, with international normalized ratio (INR), 1.04. She was hospitalized, with immediate drug discontinuation. Her liver biopsy specimen showed mixed-type (both hepatocellular and cholestatic) hepatic injury, compatible with a diagnosis of drug-induced hepatitis. An objective causality assessment using the Naranjo probability scale suggested that clindamycin was the probable cause of the acute hepatitis. In susceptible individuals, clindamycin use may lead to acute mixed-type liver toxicity. Complete recovery may be possible if the drug is discontinued before severe liver injury is established.
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PMID:Clindamycin-induced acute cholestatic hepatitis. 1787 18

Isopropanol (IPA) is a volatile solvent that is used in many industrial process. The major symptoms of acute isopropanol toxicity include dizziness, incoordination, headache, hypothermia, eye ataxia, irritation of upper respiratory tract and shortness of breath. Vomiting, hematemesis, diarrhoea and hypotension may occur following accidental ingestion of IPA. No data regarding subchronic or chronic toxicity of IPA were identified. The aim of this study was to measure the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and of gamma-glutamyltransferase (gamma-GT) of the last five years in 40 printer workers after the removal of IPA from the industry. The serum levels of ALT, AST and gamma-GT were higher in the exposed workers than in non exposed. In conclusion, the results of this study show that the removal of IPA from the industry had a positive health effect improving the hepatic function of the workers.
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PMID:[Modifications of hepatic transaminases in workers exposed to low doses of isopropanol]. 1840 81

Tigecycline (TGC), a glycylcycline, has expanded activity against Gram-positive and Gram-negative, anaerobic, and atypical bacteria. Two phase 3 studies were conducted. Hospitalized patients with community-acquired pneumonia (CAP) were randomized to intravenous (IV) TGC (100 mg followed by 50 mg bid) or IV levofloxacin (LEV) (500 mg bid). In 1 study, patients could be switched to oral LEV after at least 3 days intravenously. The coprimary efficacy end points were as follows: clinical response in clinically evaluable (CE) and clinical modified intent-to-treat (c-mITT) populations at test-of-cure (TOC). The secondary end points were as follows: microbiologic efficacy and susceptibility to TGC for CAP bacteria. Safety evaluations were included. Eight hundred ninety-one were patients screened: 846 mITT (TGC 424, LEV 422), 574 CE (TGC 282, LEV 292). Most patients had Fine Pneumonia Severity Index II to IV (80.7% TGC, 74.4% LEV, mITT). At TOC (CE), TGC cured 253/282 patients (89.7%) and LEV cured 252/292 patients (86.3%); the absolute difference of TGC-LEV was 3.4% (95% confidence interval [CI], -2.2 to 9.1, noninferior [P < 0.001]). In c-mITT, TGC cured 319/394 patients (81.0%) and LEV cured 321/403 patients (79.7%); the absolute difference of TGC-LEV was 1.3% (95% CI -4.5 to 7.1, noninferior [P < 0.001]). The drug-related adverse events (AEs) of nausea (20.8% TGC versus 6.6% LEV) and vomiting (13.2% TGC versus 3.3% LEV) were significantly higher in TGC; elevated alanine aminotransferase (2.8% TGC versus 7.3% LEV) and aspartate aminotransferase (2.6% TGC versus 6.9% LEV) were significantly higher in LEV. Discontinuations for AEs were low (TGC, 26 patients [6.1%]; LEV, 34 patients [8.1%]). TGC appeared safe and achieved cure rates similar to LEV in hospitalized patients with CAP.
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PMID:Integrated results of 2 phase 3 studies comparing tigecycline and levofloxacin in community-acquired pneumonia. 1850 26


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