Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double-blind trial of (+)-cyanidanol-3 (2 g/day) versus placebo tablets was carried out in 100 patients with acute viral hepatitis. 51 received the drug and 49 placebo. (+)-Cyanidanol-3 accelerated the disappearance of HBsAg from the blood, lowered serum-bilirubin, and relieved symptoms such as anorexia, nausea, and pruritus. The drug was well tolerated. None of the patients had a relapse of acute hepatitis. Chronic active hepatitis developed in 1 of the placebo-treated patients. Thus, (+)-cyanidanol-3 seems to be of benefit in acute viral hepatitis.
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PMID:Treatment of acute viral hepatitis with (+)-cyanidanol-3. 7 62

Non-A, non-B hepatitis has been diagnosed in 12 blood donors in a plasmapheresis unit. The course of the disease has been symptomatic, accompanied by jaundice, fatigue, and nausea in 8 cases, and subclinical in the remaining 4 patients. Nine patients were followed-up to 2 years and only 2 patients liver biochemical tests were normalized permanently. The biopsies performed, a year after the acute phase of hepatitis period revealed chronic active disease in patients, chronic persistent hepatitis in 2 patients, acute hepatitis in one, and normal liver in one patient. Repeated liver biopsies, performed one year later, have basically shown similar lesions except one patient in whom chronic active hepatitis progressed to incipient liver cirrhosis. No symptoms of the disease have been usually noted in patients with chronic form of the disease, and liver function tests have occasionally been normal.
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PMID:[Epidemic focus of non-A, non-B viral hepatitis in a plasmapheresis unit]. 143 24

Two patients developed cardiac tamponade from delayed hemorrhage into the pericardial sac following open heart surgery. The initial clinical manifestations of tamponade included nausea and dramatic elevations of serum aminotransferases, simulating acute hepatitis. To our knowledge, this presentation of cardiac tamponade has not been previously reported.
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PMID:Post-cardiac surgery tamponade mimicking acute hepatitis. Report of two cases. 155 26

Ranitidine was first marketed in 1981; since then many patients have been treated such that much experience has been accumulated on the safety of this histamine H2-receptor antagonist in the treatment of gastroduodenal disease. A wide array of ranitidine-associated side effects has been described, but infrequently. As so much information is now available, the aim of this review is to assess the weight of evidence for a causal link between ranitidine and the reported side effects. Overall, ranitidine is well tolerated. The incidence of general side effects at less than 2% is very similar to placebo. Headaches, tiredness, dizziness and mild gastrointestinal disturbance (e.g. diarrhoea, constipation and nausea) are among the most frequent complaints, but have very seldom resulted in stopping treatment. Cardiovascular side effects are extremely rare and unpredictable with the usual doses of oral ranitidine (at most 1 in 1 million patients). They mostly comprise sinusal bradycardia and atrioventricular blockade, especially after rapid intravenous administration, receding after cessation of the drug. Clinical studies, however, have not shown a significant pharmacological effect of ranitidine on the cardiovascular system via H2-receptors, even though individual sensitivities cannot be ruled out in a few isolated reports. Ranitidine is unlikely to be directly hepatotoxic: a transient change in liver function tests has been noted in only 1 in 100 to 1 in 1000 patients. Several cases of mixed hepatitis have been reported, but very few were fully documented. The incidence of ranitidine-associated acute hepatitis has been estimated to be less than 1 in 100,000 patients. Neuropsychiatric complications may be less common and clinically quite similar to those reported with cimetidine, i.e. confusion, disorientation, hallucinations, delirium. These side effects have occurred especially in critically ill and multiple-therapy patients, or patients with chronic renal or hepatic failure, so that the direct causal link with ranitidine treatment was often difficult to ascertain. Even though an H2-receptor-mediated effect is an attractive hypothesis (since similar complications were noted with other H2-receptor antagonists), other mechanisms have been suggested to play a role, e.g. cholinergic or histaminic effects. The overall incidence of neuropsychiatric complications is probably markedly less than 1%. White cell injury (i.e. agranulocytosis) appears to be the most frequent haematological complication, even though case reports are very few and poorly documented.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Side effects of ranitidine. 204 87

Cases are reported of two patients in whom acute hepatitis and cholestatic jaundice were induced by a tricyclic antidepressant, amineptine. A 29-year old woman received amineptine for 10 days before the onset of acute hepatitis. Slight jaundice and pruritus were preceded by fever, nausea and anorexia. The case is documented by a rapid return to normality of the liver function tests after amineptine was discontinued. We also report the case of a 55-year old woman to whom amineptine was administered for 4 weeks: she was admitted to our Department due to a 14-day history of pruritus and painless jaundice. Histological examination, in this case showed marked cholestasis without inflammatory infiltration. After suspending the treatment, it took 3 weeks for the liver function tests to return to normal. These observations, and the features of the cases published in the literature, suggest that amineptine can produce a wide spectrum of liver injuries, in different patients, taking the form of hepatocellular necrosis, cholestasis or a combination of both.
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PMID:Hepatic injury associated with amineptine therapy. 213 27

Seven patients developed acute hepatitis after receiving Plethoryl for obesity for 4 to 16 weeks. Jaundice was generally associated with or preceded by asthenia, nausea and pruritus. Serum aminotransferase activities were markedly increased whereas alkaline phosphatase and gamma-glutamyltransferase activities were moderately elevated. There was no hepatic failure. In all cases, Plethoryl administration was promptly discontinued. In 6 cases, jaundice disappeared within 2 to 4 weeks, and recovery occurred within 2 to 5 months. In one case, however, jaundice disappeared within 12 weeks and recovery took 10 months.
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PMID:[Hepatitis probably caused by Plethoryl. Apropos of 7 cases]. 337 97

An 80-year-old woman developed acute hepatitis following her first exposure to nifedipine. This adverse effect was characterised by fever, chills, anorexia, nausea, liver tenderness, hepatitic liver function tests and peripheral blood eosinophilia. On liver biopsy the portal tracts were expanded with a mixed inflammatory cell infiltrate rich in eosinophils. The potential for the occurrence of this adverse effect must increase with the current expansion of indications for the use of nifedipine.
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PMID:Nifedipine hepatitis. 343 25

The clinical features, laboratory investigations and histopathology of 12 patients with idiopathic acute fatty liver of pregnancy are presented. Repeated vomiting, starting in the last trimester, was the cardinal symptom. Seven patients had proteinuria, hypertension and peripheral oedema before jaundice appeared. Caesarian section and induction of labour led to a lower than expected maternal mortality (33 X 3 per cent) and foetal mortality (66 X 7 per cent). There was a high incidence of twin and male births. Neutrophilia, thrombocytopenia and normoblasts were a uniform feature and uric acid levels were universally high. These findings may be useful in diagnosis in conjunction with liver function tests. Hepatic histology showed pathognomonic microvesicular fat in swollen hepatocytes with central nuclei and centrilobular distribution. However, a diffuse pattern and the presence of significant inflammation and fibrin deposits led to an initial misdiagnosis in two patients. Histology of fetal livers and five placentae was normal. Seven subsequent normal pregnancies occurred in four patients. Acute fatty liver of pregnancy may be confused with acute hepatitis or toxaemia on both clinical and histological grounds. Accurate diagnosis should lead to improved management and lessen maternal and fetal mortality. This justifies more intensive and urgent investigation of nausea, vomiting and jaundice in the last trimester of pregnancy.
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PMID:Idiopathic acute fatty liver of pregnancy in 12 patients. 715 26

A 42-year-old female was admitted to a hospital, because of acute hepatitis A. Laboratory data were GOT 8210mU/ml. GPT 4650mU/ml, LDH 11860mU/ml, total bilirubin 4.7mg/dl, BUN 19.5mg/dl and creatinine 1.9mg/dl. Urinalysis showed proteinuria 3+ and occult blood 1+. Soon after admission, she suffered from anuric acute renal failure and was transferred to our hospital for hemodialysis. Her urine-volume was under 20 ml per day. Urinalysis showed proteinuria 4+, occult blood 1+ and casts. Laboratory data showed BUN 58.2mg/dl and creatinine 8.5mg/dl. She was treated by hemodialysis for 35 days, before recovering from renal failure. However, her renal function did not recover perfectly and her 24-hour creatinine clearance remained at 50ml/min after 6 months. Renal biopsy was performed on the 17th day after admission. Examination by light microscopy revealed the findings of acute tubular necrosis and examination by immunofluorescence antibody method was negative. Urinalysis of 8 patients with acute hepatitis A showed that all patients had proteinuria at the onset. Patients with acute hepatitis A have symptoms of appetite-loss, nausea, vomiting and/or diarrhea. These symptoms cause hypovolemia, and hepatic dysfunction causes discontrol of vasoactive hormones, which gives rise to disturbance of renal circulation. Subsequently, acute tubular necrosis and acute renal failure occur.
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PMID:[A case of acute hepatitis A associated with acute renal failure from the onset]. 823 Aug 22

Pericarditis is a frequent and serious complication of chronic uremia. The uremic pericarditis can get much improvement by aggressive heparin-free hemodialysis therapy. However, the presenting symptoms and signs are too nonspecific to identify at early stage. Cardiac tamponade is the late and fatal complication, and need the immediate & adequate management. A 35-year-old female patient suffered from nausea, vomiting and right upper quadrant dull pain in November 1993, and was admitted to a local hospital. Uremia (BUN: 210 mg/dl, serum Cr.: 13.2 mg/dl) and abnormal liver function (SGOT: 330 IU/L, SGPT: 449 IU/L) were found, then she received regular hemodialysis therapy. About 10 days later, acute exacerbation of liver function (SGOT: 2,488 IU/L, SGPT: 1,048 IU/L), consciousness disturbance and hypotension occurred during hemodialysis. She was referred to our ER immediately. At ER, she had been on comatous, shock state with pulseless electric activity. After resuscitation and serial evaluation, cardiac tamponade was diagnosed. Emergent pericardiocentesis and then bilateral partial pericardiectomy were done about 2 hours later. The pericardial effusion was bloody without evidence of malignancy, bacterial or TB infection. The pathology of pericardium revealed chronic inflammation only. HBsAg, Anti-HCV Ab, and anti-HAV IgM were undetectable. So the etiology of acute hepatitis was diagnosed as ischemic hepatitis. Her general condition and vital sign became stable thereafter. The liver function also improved rapidly. She was discharged one month later and received maintainance hemodialysis therapy and no evidence of recurrence till now.
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PMID:[Acute uremic pericarditis presented as cardiac tamponade with acute ischemic hepatitis: a case report]. 904 74


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