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)

In a double-blind, randomized study the efficacy of lactulose was compared with neomycin-sorbitol in 45 episodes of acute nitrogenous portal-systemic encephalopathy (PSE) induced by dietary protein, azotemia, or gastrointestinal hemorrhage. All patients had underlying cirrhosis, and at the time of randomization had encephalopathy of at least grade 2 severity and arterial ammonia concentrations greater than 150 microgram/100 ml. Two thirds of the patients in each group returned to normal mental status and more than 80% in each group showed at least one grade improvement in mental state. In addition, there was equivalent improvement in asterixis, in the performance of the Number Connection Test, in the electroencephalographic pattern, and in arterial ammonia concentration. The principal difference between the two groups was a greater reduction in stool pH after lactulose therapy than after neomycin-sorbitol therapy. One patient randomized to neomycin-sorbitol had to be withdrawn from the study because of persistent vomiting related to the administration of the medication. Otherwise there were no complications attributable to therapy in either group. These data suggest that neomycin-sorbitol and lactulose are equally effective in the treatment of acute nitrogenous portal-systemic encephalopathy.
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PMID:Neomycin-sorbitol and lactulose in the treatment of acute portal-systemic encephalopathy. A controlled, double-blind clinical trial. 35 73

The authors report a case of toxic hepatitis in a woman of 22 years of age in the third trimester of her first pregnancy treated by methyldopa for hypertension of pregnancy which was diagnosed at 33 weeks of amenorrhoea. The prodromal symptoms were mild and consisted of nausea, vomiting and rise in temperature and this phase was associated with febrile jaundice without pruritus and it was only associated with coagulation disorders in the third stage of labour. This was a case of mixed cytolytic hepatitis (ASAT x 3N) and cholestasis (x 1.5N). The outcome was fatal. The patient died three days after delivery following haematemesis and renal failure as well as hepatic encephalopathy. The main diagnostic feature was acute hepatic stasis in spite of the absence of pruritus and the presence of a raised temperature after hematolytic, viral and obstructive causes had been eliminated. Histology confirmed that there was toxic hepatitis. This aetiology was suggested by the timing of the symptoms after MD (methyldopa) had been taken. Elkington described methyldopa hepato-toxicity in 1969. Fatal cases in the literature were in patients who were over 40 years of age. Methyldopa is used in pregnant women because of its safety as far as the fetus is concerned. Mechanism by which it causes toxic hepatitis is a combination of abnormal metabolism (the cytochrome P450 chain produces an antigen) and an immune reaction in response to this antigen and these explain why such severe and potentially fatal forms of the condition exist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Fatal toxic hepatitis in pregnancy. A discussion of the role of methyldopa]. 232 42

Idiopathic hepatic lipidosis was diagnosed in 11 cats. Cats were treated by delivery of balanced nutrients supplemented with L-carnitine via a surgically placed gastrostomy tube. Feeding through the gastrostomy tube was initiated in the hospital and was continued at home in all cats. The mean duration of gastrostomy tube feeding was 48 days (range, 22 to 98 days). Vomiting associated with feeding (3 cats) and localized cellulitis at the gastrostomy site (2 cats) were the most frequent complications. Vomiting was controlled by reducing the volume of food administered at each feeding or by administration of metoclopramide. Cellulitis was treated successfully by parenteral administration of antibiotics and local wound cleansing. Seven of 11 cats (65%) survived and have remained clinically healthy for 15 to 29 months (mean, 20 months) since diagnosis. The other 4 cats died of peritonitis (n = 1), pneumonia (n = 1), hepatic encephalopathy (n = 1), or cardiopulmonary arrest (n = 1) between 0 and 10 days after surgery.
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PMID:Treatment of idiopathic hepatic lipidosis in cats: 11 cases (1986-1987). 250 62

Cisplatin suspension in Lipiodol (LPS) was prepared for the treatment of hepatocellular carcinoma by intra-hepatic arterial injection. In a rabbit liver cancer model, concentrations of cisplatin in tumor were more than 20 times higher than those in a nontumorous part of the liver at 5 min after LPS injection into the hepatic artery. Cisplatin at high concentrations was detected at 7 days after injection. The concentrations in other organs were lower except in the gall-bladder. In clinical trials for 71 patients with hepatocellular carcinoma, partial response was observed in 33 cases (46.5%) and minor response in 20 cases (28.2%). The survival rate was 77% at 6 month and 55% at one year. Although fever, nausea, vomiting and epigastralgia were observed as side effects, these were temporary. Acute gastroduodenal mucosal lesions, cholecystitis, pancreatitis, delayed jaundice and hepatic encephalopathy were observed as complications and super selective cannulation was necessary for their prevention.
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PMID:[Intra-arterial injection of cisplatin suspension in Lipiodol (LPS) in the treatment of hepatocellular carcinoma]. 255 Dec 47

Five infants admitted consecutively with severe hepatitis B were treated with exchange transfusion, correction of coagulation defects and supportive measures. All were born to HBsAg carrier mothers and one had received hepatitis B immune globulin (HBIG) within 24 hours after birth. All of them presented with nonspecific symptoms such as vomiting, loose stools, low grade fever and progressed to acute liver failure. Three of them survived with full recovery and two died from hepatic encephalopathy one and two weeks after admission. Early recognition of hepatic failure and prompt exchange transfusions with intensive supportive treatment may save these infants.
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PMID:Severe hepatitis B in infants born to HBsAg carrier mothers. 273 54

A 39 year old woman was admitted to a maternity unit at 34 weeks' gestation with nausea, vomiting, and jaundice. Her condition deteriorated, and she was transferred to hospital, deeply unconscious and hypotensive. The diagnosis of acute fatty liver of pregnancy was initially suggested by the typical history of prodromal malaise and vomiting and the rapid onset of hepatic encephalopathy with profound hypoglycaemia and only small increases in transaminase activities. Computed tomography was performed: there was no enlargement of the liver or spleen, but the attenuation value over the liver indicated appreciable fatty infiltration of the liver, establishing the diagnosis of acute fatty liver of pregnancy. Computed tomography is of value in the diagnosis of liver disease of late pregnancy, and this technique may become the method of choice for the investigation of acute fatty liver of pregnancy.
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PMID:Acute fatty liver of pregnancy and diagnosis by computed tomography. 308 Jan 42

The authors analyse 115 cases of acute fatty liver of pregnancy, proven histologically. Characteristics of the condition is the finding of central nuclei in the hepatocytes containing microvesicular droplets. The disease occurs more frequently in primiparous women (54 per cent) and usually occurs in the third trimester of the pregnancy. A pre-icteric phase usually precedes the jaundice and during that time there is usually vomiting and/or nausa with abdominal pain or anarexia. In 92 per cent of case there is transient loss of consciousness with hepatic encephalopathy. Further tests show that there is more defective liver function than would be expected from the extent of cell lysis; and there is defective renal function. The worst complications are intestinal haemorrhages (48 per cent of cases)--genital bleeding (43 per cent of cases)--shock--diffuse intravascular coagulation and complications associated with coma. Maternal mortality at present runs at 25 per cent and fetal mortality at 60 per cent. The condition does not recur. Early evacuation of the uterus is recommended by most authors and does probably improve the outlook. The various hypotheses concerning the aetiology are discussed.
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PMID:[Acute fatty liver of pregnancy]. 354 2

Acute hepatic failure is characterized by a sudden catastrophic compromise of hepatic failure that causes clinical signs such as anorexia, depression, vomiting, diarrhea, icterus, and encephalopathy. Injurious hepatotoxins, drugs, infectious agents, or metabolic disturbances can cause acute hepatic failure; however, in many cases, the inciting cause is not determined. Treatment is aimed at controlling complications such as fluid-electrolyte imbalances, hepatic encephalopathy, hypoglycemia, bleeding diathesis, gastric ulcer, sepsis, and endotoxemia, in order to provide time for liver regeneration and recovery.
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PMID:Acute hepatic failure. 387 99

Inborn errors of ureagenesis must be considered in the differential diagnosis of recurrent vomiting and lethargy in childhood. Elevations of liver enzyme levels are often present during these episodes and may lead to an erroneous diagnosis of hepatic encephalopathy. We studied two cases of urea cycle defects.
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PMID:Detection of urea cycle enzymopathies in childhood. 674 67

The authors report a case of fatal hepatic failure in a 19-year old young man suffering from absence seizures and treated for two months with valproic acid (VPA). The duration of VPA therapy before onset of clinical manifestations was four weeks. The prodromal symptoms were weakness, anorexia, and vomiting, then in a few weeks occurred a jaundice and an hepatic encephalopathy leading to death. Among laboratory findings disturbance of liver tests and particularly depressed levels of clotting factors were observed. The histologic study of the liver showed an extended centrolobular necrosis associated with fatty change and fibrosis. The mechanism of this hepatic failure remains unknown. The seriousness of this complication necessitates to respect any contraindications.
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PMID:[Fatal hepatic necrosis during treatment with sodium valproate]. 758 2


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