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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight out of 246 patients with severe viral hepatitis were complicated with spontaneous abdominal viscera perforation. The eight patients all had serious digestive symptoms, orange green colour in skin, swollen abdomen with ascites, abdominal pain. All cases were diagnosed by liver function examination, colour ultrasonography, x-ray examination, abdominal puncture and one case by operation. Among these 8 cases, 3 cases had perfornation of stomach, 3 cases had perforation of gall bladder and 2 cases had perforation of small intestine. Though emergancy treatment had been applied, only one case was saved.
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PMID:[Clinical analysis of spontaneous perforation of abdominal viscera in patients with severe viral hepatitis]. 986 31

The occurrence of hepatocellular carcinoma (HCC) in renal transplant recipients has typically been associated with hepatitis B or C infection. We encountered two cases of HCC in renal transplant recipients with negative hepatitis B and C markers and no underlying liver pathology, in whom immunosuppression therapy consisted of prednisone and azathioprine (AZA). Patient no. 1 is a 66-year-old man with diabetes who underwent cadaveric renal transplantation 13 years before presentation. An ultrasound obtained for evaluation of a prolonged prothrombin time and decreased serum albumin level showed a suspicious nodular lesion in the left lobe of the liver. A computed tomographic (CT) scan confirmed a 4- x 5- x 5-cm mass that, on biopsy, was determined to be well-differentiated HCC. There was no evidence of metastasis, and the results of random biopsies of the surrounding parenchyma were normal. The patient underwent a left lateral segmentectomy, did well, and an initial alpha-fetoprotein (AFP) level of 85995 ng/mL decreased to 9 ng/mL. Approximately 20 months postoperatively, however, a surveillance CT scan showed three hypervascular lesions in the right lobe of the liver and the AFP level increased to 28,370 ng/mL. Subsequent percutaneous alcohol injections yielded good results, and the patient is alive and well 13 months later. Patient no. 2 is a 57-year-old man who underwent cadaveric renal transplantation 24 years earlier. A CT scan of the abdomen obtained for evaluation of lower abdominal pain showed a 4- x 4- x 6.5-cm mass in the right lobe of the liver that, on biopsy, was found to be poorly differentiated HCC. Multiple biopsies of adjacent liver parenchyma showed no evidence of cirrhosis, AFP level was normal, and imaging studies showed no evidence of tumor spread. The patient underwent a right hepatic lobectomy and is doing well without evidence of recurrence 27 months postoperatively. Our two patients had no evidence of viral hepatitis, cirrhosis, or metabolic liver disease, yet both developed HCC. The use of AZA may have had a role in the development of HCC. In renal transplant recipients on long-term immunosuppression therapy, particularly AZA, it is prudent to maintain a high index of suspicion for HCC when liver enzyme level or function abnormalities are encountered.
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PMID:Hepatocellular carcinoma after renal transplantation in the absence of cirrhosis or viral hepatitis: a case series. 987 92

A 62-year-old man, affected by Chronic Active Hepatitis (discovered in 1993) and treated with interferon, referred to our department with increased abdominal volume, persistent abdominal pain, continuous-remittent fever and jaundice. CT scan of the liver revealed a hypodense, not capsulated, infiltrative, solid formation in the right lobe. US guided biopsy showed multinucleated giant cells, with eosinophilic cytoplasm and pleomorphism of the nuclei, arranged in several thick trabecula lined by endothelial cells or formed bile containing acini. In our case, the rapid evolution of chronic viral hepatitis towards HCC calls for a careful evaluation of the role of IFN therapy, since this drug is widely used in chronic liver diseases.
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PMID:Rapid evolution of chronic viral hepatitis into hepatocellular carcinoma after beta-interferon treatment. 1023 Feb 60

Association of hepatitis viruses with acute pancreatitis in the setting of nonfulminant viral hepatitis is rare. We report six cases of nonfulminant viral hepatitis complicated by acute pancreatitis, including the first documented case of hepatitis E virus (HEV) associated acute pancreatitis. The other five patients had acute viral hepatitis caused by hepatitis A infection. Besides features of viral hepatitis, the presence of typical abdominal pain, high serum amylase, and ultrasound or CT scan features suggested the diagnosis of acute pancreatitis. This complication generally developed in the initial phase of the hepatitic illness. All of the patients had mild to moderate pancreatitis that recovered uneventfully with conservative treatment.
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PMID:Acute pancreatitis associated with viral hepatitis: a report of six cases with review of literature. 1044 66

Our article concentrates on two acute states, which develop less dramatically but their after-effects may be very serious: Spontaneous bacterial peritonitis and Ogilvie's syndrome. Spontaneous bacterial peritonitis is a bacterial infection of the ascitic fluid without any intraperitoneal source of infection. Ascites is a condition of the disease but need not be clinically manifested. Spontaneous bacterial peritonitis comes usually during heavy hepatic impairment. Diagnosis can be set according: 1. Positive cultivation of ascitic fluid, 2. PMN levels higher than 250/mm3, 3. No infection, which may require a surgical intervention is apparent. Liver disease, which brings about the spontaneous bacterial peritonitis can be: 1. Chronic (e.g. alcoholic cirrhosis), 2. Subacute (e.g. alcoholic hepatitis), 3. Acute (e.g. fulminant hepatic failure). Mortality of this form of peritonitis can reach up to 46%. The most frequent etiological factor is alcohol and viral hepatitis, the most frequent agents are E. coli and Klebsiella pneumoniae. The disease is most effectively cured by cefalosporins of the third generation. With inadequate treatment, prognosis may be poor. Intestinal pseudoobstruction syndrome has clinical symptomatology of a serious impairment with ileus without signs of any mechanical intestinal obstruction. Syndrome can be classified according to its development: 1. Acute form--acute intestinal pseudoobstruction syndrome--Ogilvie's syndrome, 2. Chronic form--chronic intestinal pseudoobstruction syndrome. Pathogenic mechanism of the syndrome is not known. The disease is related to immobility, administration of some drugs, electrolyte imbalance and concomitant diseases (most frequently malignant tumors). Clinical symptomatology dominates nausea, vomiting, diffuse abdominal pain, constipation or diarrhoea. For diagnostics the first step should be termination of all medication, which could have causing affects, then taking native abdominal X-ray picture where gaseous intestinal distension can be prominent (coecum distended up to 9-12 cm). Identification of fluid surfaces is not usual. Endoscopic examination can exclude obstruction in the distal part of gut minimally. The most frequent complication is perforation of coecum. Pharmacological treatment relays on prokinetics. The basic intervention remains decompression by a rectal catheter or an effective coloscopic decompression with subsequent introduction of a cannula. Mortality of the disease fluctuates between 43 and 46%.
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PMID:[Acute states in gastroenterology: spontaneous bacterial peritonitis and the acute intestinal pseudoobstruction syndrome]. 1150 91

We report the case of a 71-year-old man with mixed glomerular lesions, membranous and necrotizing changes. The patient had abdominal pain and purpurat on the extremities and trunk, followed by melena, and after admission to hospital, proteinuria and occult blood were noted. Laboratory findings were negative for autoimmune disease and viral hepatitis. Renal biopsy showed segmental necrotizing changes and mesangial proliferation with spike formation. Immunofluorescence revealed a granular deposition of IgA predominantly in the mesangial area in contrast to the granular IgG deposition along the glomerular capillary loops. Moreover, electron-microscopically, mesangial as well as subepithelial electron-dense deposits were observed. These data suggest that the patient had 2 distinct types of glomerulonephritis simultaneously: idiopathic membranous nephropathy and purpura nephritis.
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PMID:A case of mixed membranous nephropathy and purpura nephritis. 1207 54

Complications of oral contraceptives (OCs) affecting the gastrointestinal tract, liver and pancreas are rare but potentially serious. Hepatobiliary complications are by far the most frequent and varied. Hepatic lesions will probably decline in frequency as low-dose OCs replace higher dosed pills. Intrahepatic cholestasis induced by OCs resembles that of pregnancy. There may be a genetic predisposition to both conditions involving a dose-dependent estrogen effect of decreasing bile secretion. Intrahepatic cholestasis appears within 6 cycles of OC use. Symptoms include pruritus with anorexia, asthenia, vomiting, and weight loss without fever, rash or abdominal pain. Termination of OCs clears the condition without sequelae within 1-3 months, sometimes after a temporary aggravation. A moderate and asymptomatic cytolysis may appear when OC treatment is begun. Sinusoidal dilatation has been conclusively linked to OCs although few cases have been published. Clinical manifestations other than hepatomegaly are variable. Abdominal pain and fever are the most common. The condition is not related to duration of use and disappears 5-15 days after OC use is terminated. The relative risk of Budd-Chiari syndrome in OC users is estimated at 2.37. OCs increase the prevalence of hepatic adenomas as a function of duration of treatment. They are usually discovered fortuitously but may be revealed by vague abdominal pains. Hemorrhagic complications are more likely in OC users. It may be difficult to distinguish between adenomas, hepatocellular carcinoma, and focal nodular hyperplasia. A puncture biopsy guided by sonography may aid diagnosis. The natural history of adenomas is poorly understood and treatment remains controversial. OCs do not appear to increase the risk of focal nodular hyperplasia but they increase the size of the tumor and the risk of hemorrhage. OCs should be terminated because of risk of hemorrhage. Surgical resection is not indicated unless there are complication or diagnostic doubts. While hepatocellular carcinoma is very rare, its risk is increased by a factor of 7-20 in women using OCs for 8 years or more. Use of combined OCs appears to speed development of lithiasis in predisposed women. Risk of lithiasis is linked to estrogen content in women under 30. Several cases of acute pancreatitis in the 1st 3 months of treatment have been reported in women with preexisting lipid metabolic anomalies. Cases of ischemic lesions of the small intestine or colon have been reported in OC users with A positive blood type. Such lesions can be fatal without early diagnosis and termination of OCs. Gastric esophageal reflux is increased by progestins. Preexisting constipation may be aggravated and the incidence of Crohn's disease increased by OCs. It is advisable to rule out preexisting hepatic pathology before prescribing OCs. OCs should be stopped in case of viral hepatitis.
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PMID:[Contraception and hepatogastroenterology]. 1231 76

Hepatocellular carcinoma (HCC) is one of the most common internal malignancies worldwide. Until recently, it has occurred relatively rarely in the West. Now, however, it appears to be rising in incidence in the United States and other developed western countries. The most frequent underlying factors causing HCC are chronic viral hepatitis and cirrhosis. Common clinical features include abdominal pain and worsening of hepatic synthetic function. More recently, however, patients with asymptomatic tumors are being diagnosed because of more frequent screening and improvements in imaging techniques. Early detection of HCC is a key factor in improving outcomes of therapies. There is growing evidence that HCC may be prevented with strategies aimed at preventing or treating viral hepatitis.
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PMID:Epidemiology and clinical presentation of hepatocellular carcinoma. 1235 33

A 45-year-old male presented with severe abdominal pain, hyperamylasaemia and a bulky pancreas. In addition, he had deep jaundice and markedly raised serum transaminases, and his serum was positive for IgM anti-hepatitis E virus (HEV) antibodies. The common aetiologies of acute pancreatitis were excluded. The patient ran a benign course for both acute viral hepatitis and acute pancreatitis, and recovered completely. Acute pancreatitis caused by HEV infection has been reported only occasionally.
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PMID:Acute pancreatitis associated with acute hepatitis E infection. 1516 33

Polyarteritis nodosa (PAN) is a rare vasculitis in children. We report a case of 5-year-old boy with systemic PAN and cholestatic hepatitis. He had fever, abdominal pain, and gastrointestinal bleeding. Angiography revealed multiple microaneurysms in the renal, hepatic, and superior mesenteric arteries. Clinical manifestations improved slowly after immunosuppressive therapy, but liver enzyme and bilirubin levels elevated gradually. Liver biopsy findings revealed marked centrizonal canalicular cholestasis, bile duct damage, and intact hepatocyte, but there was no evidence of viral hepatitis or vasculitis. Levels of liver enzymes and bilirubin improved after two cycles of cyclophosphamide therapy. We thought that the possible etiology of elevated liver enzyme and bilirubin levels might be a manifestation of PAN.
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PMID:Successful treatment of pediatric systemic polyarteritis nodosa with cholestatic hepatitis. 1636 46


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