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)

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

A case of fulminant hepatitis with microvesicular steatosis resembling Labrea's fever, diagnosed in Vitoria (ES) is reported. The 16 year old boy presented with severe epistaxis, agitation, jaundice and hemorrhagic vomiting and died two days after admission to the emergency unit of the University Hospital. The disease started five days before with fever, myalgias, dark urine and jaundice and progressed with psychic agitation, torpor and coma. The liver and spleen were not palpable. HBsAg was negative in the serum. The autopsy showed acute hepatitis with lytic necrosis confluent in the midzonal and periportal areas with massive microvesicular steatosis in the remaining hepatocytes. Mononuclear cells predominated in the exudate. The reticulum showed condensation in the necrotic areas without typical bands of collapse. The portal tracts were edematous with mononuclear infiltration and mild bile duct proliferation. Absence of cholestasis. Except for the confluent midzonal and periportal necrosis this case showed several clinical and morphological aspects of the Labrea fever described from the East Amazon, demonstrating that the anatomical picture of this disease probably is not in related to a factor peculiar to the Amazon region.
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PMID:Labrea-like hepatitis in Vitoria, Espirito Santo State, Brazil: report of a case. 815 25

Interleukin-3 treatment of juvenile rhesus monkeys elicits a dose- and time-dependent syndrome that includes urticaria, palpable lymph nodes, splenomegaly, thrombocytopenia, anemia, vomiting, diarrhea, intestinal bleeding, edema, and arthritis, apart from a strong stimulation of hemopoiesis. Arthritis was found to occur significantly more often in animals expressing the major histocompatibility complex alleles B9 and Dr5. Histological analysis revealed an abundance of mast cells in urticaria and, to a lesser extent, in lungs and synovia of arthritic joints. Active osteoclasts were abundant in ribs and arthritic joints. Extramedullary hemopoiesis was encountered in liver, spleen, and kidneys. The spleen showed deposits of hemosiderin, and in the liver, Kupffer cells were loaded with iron, indicating enhanced turnover of hemoglobin. Lymph nodes and bone marrow showed macrophages involved in hemophagocytosis, which probably contributed to the development of anemia and thrombopenia. Biochemical parameters in sera were indicative of parenchymal liver damage, with cholestasis and increased erythrocyte destruction. The side effects were strongly reduced in monkeys subjected to total body irradiation just before interleukin-3 treatment. Histamine antagonists were not significantly effective in preventing side effects, which is explained by the perpetual stimulation of basophilic granulocytes by exogenous interleukin-3. The nature of the side effects indicates that interleukin-3 may be involved in the pathogenesis of acute type hypersensitivity reactions and arthritis.
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PMID:Acute side effects of homologous interleukin-3 in rhesus monkeys. 825 52

Twelve episodes of acute fatty liver of pregnancy (AFLP) were diagnosed in 11 patients during the past 18 years in a general hospital in Santiago, Chile, with a prevalence of 1 per 15,900 deliveries. Acute fatty liver of pregnancy started between the 31st and 38th weeks of pregnancy, with malaise, vomiting, jaundice, and lethargy as the main clinical manifestations. Polydipsia (in nine episodes) and skin pruritus (in seven episodes) were unusual clinical findings. In two patients, pruritus started two and four weeks before AFLP, suggesting that an intrahepatic cholestasis of pregnancy preceded AFLP in those patients. Considering the current prevalence of both diseases in Chile, their association should be considered fortuitous. In another patient, two consecutive pregnancies were affected by AFLP, raising to three the number of reported patients with recurrent AFLP. In 11 episodes, liver biopsies supported the diagnosis of AFLP by showing small and midsized vacuolar cytoplasmic transformation as the most prominent histopathological feature. Positive intracellular fat staining was found in the four samples analysed. Studies by electron microscopy showed megamitochondria with paracrystalline inclusions in four samples. All the mothers survived, but fetal mortality was 58.3%. Several extrahepatic complications delayed maternal recovery for up to four weeks after delivery. This study confirms an improvement in maternal prognosis in AFLP, discusses the possibility of an epidemiological association with intrahepatic cholestasis of pregnancy, and increases the number of patients reported with recurrent AFLP.
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PMID:Acute fatty liver of pregnancy: a clinical study of 12 episodes in 11 patients. 830 28

Medical records of 29 dogs with cholelithiasis were reviewed. Aged female small-breed dogs were overrepresented. Mean age was 9.5 years, and mean weight was 12 kg. Vomiting, anorexia, weakness, polyuria/polydipsia, weight loss, icterus, fever, and signs of abdominal pain were the most common clinical signs. Leukocytosis, neutrophilia with left shift, monocytosis, high activity of serum hepatic enzymes, hypoalbuminemia, and high concentrations of serum total bilirubin were common. Radiopaque choleliths were evident on abdominal radiography of 13 of 27 dogs. Microbial culturing of bile isolated organisms in 15 of 20 dogs. Gram-negative bacteria were most common. Surgery was performed in 22 dogs. Four dogs were treated medically, and 3 dogs were euthanatized without treatment. Surgical treatment consisted of cholecystectomy in 11 dogs, choledochotomy in 5 dogs, cholecystotomy in 4 dogs, and cholecystojejunostomy in 1 dog. Sphincter of Oddiotomy was performed in 1 dog. Five dogs had concurrent generalized peritonitis attributable to bile. Multiple choleliths were detected in most of the dogs. Choleliths were located in the gallbladder in 20 dogs and in the bile ducts in 14 dogs. The most common abnormalities of the gallbladder, identified histologically, were chronic cholecystitis, mucosal hyperplasia, and pericholecystic inflammation. The most common abnormalities of the liver were cholestasis, hepatocellular degeneration, and periportal fibrosis. Survival rate of dogs that underwent cholecystectomy tended to be higher (86%) than that of dogs treated via cholecystotomy (50%) or cholecystectomy in combination with choledochotomy (33%). Dogs that underwent medical treatment, abdominal exploratory, cholecystojenunostomy, choledochotomy, and sphincter of Oddiotomy died or were euthanatized because of redevelopment of clinical signs associated with cholelithiasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cholelithiasis in dogs: 29 cases (1980-1990). 847 31

The main complications of endoscopic retrograde cholangiography and sphincterotomy are bleeding, pancreatitis, perforation and sepsis. Two cases of unexplained prolonged cholestatic jaundice in patients who underwent endoscopic retrograde cholangiography (ERC) for biliary obstruction due to choledocholithiasis are reported. The patients were admitted because of right upper quadrant pain, vomiting and jaundice. Laboratory tests showed increased levels of total and conjugated serum bilirubin and increased alkaline phosphatase. Ultrasound examination showed cholelithiasis and choledocholithiasis with bile duct dilatation. ERC with sphincterotomy was performed and gallstones obstructing the common bile duct were removed endoscopically. Following ERC and despite complete patency of the biliary tree, a progressive increase of total and conjugated bilirubin and of alkaline phosphatase was noted, associated with itching and total stool discoloration. The insertion of nasobiliary drain did not improve the jaundice. Prednisolone treatment for 12 days was associated with progressive restoration of serum bilirubin alkaline phosphatase to normal levels. It was postulated that the radiocontrast material used may have acted toxically on the liver with disruption of the canalicular plasma membrane. It is proposed that intrahepatic cholestasis should be added in the list of complications of endoscopic retrograde cholangiography.
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PMID:Prolonged cholestatic jaundice after endoscopic retrograde cholangiography. 922 70

Benign recurrent intrahepatic cholestasis (BRIC or Summerskill-Walshe-Tygstrup-syndrome) is a rare autosomal recessive form of liver disease, which usually becomes manifest in childhood. Characteristic are recurrent episodes of jaundice and itching of different duration. Number and duration of episodic attack and asymptomatic period develop individually. For diagnosis of BRIC following criteria are proposed: At least three episodes of severe jaundice and pruritus with biochemical evidence of cholestasis, normal intra-and extrahepatic bile ducts on cholangiography, absence of a factor known to produce intrahepatic cholestasis and symptom-free intervals of several months or years. Often the diagnosis of BRIC is made very late and patients have to suffer invasive investigations (explorative laparotomy). Because of the unknown pathophysiological mechanism there is no specific treatment. We report on a 53-year-old patient with jaundice, severe pruritus, vomiting, loss of hair and weight, extreme sleeplessness and intractable cough. At the onset of the attack an increase of serum bilirubin concentration and serum alkaline phosphatase was observed, whereas aspartate and alanine aminotransferase and gamma-glutamyltransferase were normal. Histological findings of liver biopsy revealed accumulation of bile plugs in bile canaliculi. The long-term follow-up of our patient confirms that the prognosis is good.
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PMID:[Follow-up of benign recurrent intrahepatic cholestasis (Summerskill-Walshe-Tygstrup syndrome) over 46 years]. 965 5

Isovaleric acidemia, an autosomal recessive disorder, is due to isovaleryl-coenzyme A dehydrogenase deficiency and is one of the branched-chain aminoacidopathies. Isovaleric acidemia may present in the neonatal period with an acute episode of severe metabolic acidosis, ketosis, and vomiting and may lead to coma and death in the first 2 months of life. This report concerns an infant who presented at 10 days of age because of lethargy, poor feeding, hypothermia, cholestasis, and thrombocytopenia, leukopenia, and profound pancytopenia. Death occurred at 19 days of age. Autopsy showed mild fatty change in the liver and extramedullary hematopoiesis, generalized Escherichia coli sepsis, and myelodysplasia of the bone marrow with arrest of the myeloid series at the promyelocytic stage. The appearance resembled promyelocytic leukemia, but the diagnostic 15:17 translocation was not present. The maturation arrest in granulopoiesis in isovaleric acidemia appears to be most likely due to a direct metabolic effect on granulocyte precursor cells.
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PMID:Isovaleric acidemia with promyelocytic myeloproliferative syndrome. 1019 53

The liver has a central role in the metabolism of many drugs, since this organ is the main site of biotransformation of endo- and xenobiotics. Water-soluble drugs have a small volume of distribution and can be eliminated unchanged in the urine. By contrast, lipid-soluble drugs have a larger volume of distribution and require conversion to water-soluble metabolites for their elimination in urine or bile. The liver with its specific receptors, transporters and enzymes is responsible for the uptake, transformation and excretion of the lipophilic drugs. While most of the drugs are transformed into stable metabolites, other drugs form reactive, potentially toxic, metabolites producing liver cell damage. Liver injury caused by drugs may mimic almost any kind of liver disease. Clinical findings are gastrointestinal symptoms with nausea, vomiting and abdominal pain, cholestatic liver injury with jaundice and pruritus of severe inflammatory and cirrhotic liver damage with signs of liver failure, encephalopathy and cerebral edema. The morphological changes vary from hepatitis, cholestasis, fatty liver, granulomatous hepatitis, peri-/portal inflammation, to fibrosis with cirrhotic alterations and vascular lesions and tumors. The most commonly used drugs causing severe liver injury are discussed in detail. These are anabolics, oral contraceptives, antituberculous and antifungal agents, nonsteroidal anti-inflammatory drugs, ring substituted amphetamins ("designer drugs"), antiarrhythmics and antibiotics.
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PMID:[Liver damage caused by drugs]. 1041 44

This case report concerns a 35-year-old woman suffering from gravidic cholestasis, thrombocytosis and iterative vomiting episodes who underwent an elective cesarean section at week 35 because of recent herpetic vulvitis. Large bilateral ovarian tumors were observed which were interpreted as pregnancy luteomas. Nevertheless a biopsy of the right ovary was performed. Histologic examination revealed massive luteinization of the ovarian stroma. In addition, large tumor cells were found dispersed throughout the ovary as well as in vascular spaces as either isolated or clustered signet-ring cells. In search of the primary tumor, gastroscopy revealed a gastric ulcer in the antrum. The biopsies of the ulcer margins as well as those taken at distance demonstrated signet-ring cells in the lamina propria. Bilateral salpingo-oophorectomy and total gastrectomy were performed. In spite of postoperative chemotherapy, the patient died of disease 5 months after diagnosis.
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PMID:Bilateral Krukenberg tumor of the ovary during pregnancy. 1072 20


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