Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The viral hepatitis is a serious public health problem worldwide. Some problem is hepatitis B, particularly superinfection HBV-HDV and least hepatitis C (HCV), because they are transmitted via parenteral routes. About 20% of patients becomes a chronic carrier. Some chronic carriers are healthy: and they have no functional deficiencies. Others however, chronic active hepatitis develops and can lead to cirrhosis of the liver and finally to hepatocellular carcinoma, that is one of the major cancers of the world today. The immunocomplexes play a role in pathogenesis of several syndromes, such as: polyarthritis nodosa, glomerulonephritis, acrodermatitis. In the study based on questionnaires mailed 645 persons after acute viral hepatitis they were observed: cholecystitis--13.9%, stomach and/or duodenum ulcer--11.5%, and cholelithiasis--8.1%. An important results of the investigation is the conclusion that hepatitis caused distinct decrease of the health condition and change of the lifestyle. After the viral hepatitis 9% of patients shifted to a lighter job for a time, 3.8% for good and 5.6% patients after hepatitis B were receiving disability payment. In the light of the problems discussed here the vaccination would prevent not only the acute liver illness but also the sequelae of the disease.
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PMID:[Viral hepatitis sequelae]. 133 49

Extrahepatic manifestations due to an immunologic response to a surface antigen of hepatitis B virus have been identified. These include a serum sicknesslike syndrome and a necrotizing vasculitis. The latter is far more important and in indistinguishable histologically from nonhepatitis related polyarteritis. At least 90 cases have been reported in the decade since 1970, and five are added here. The necrotizing vasculitis syndrome results from fibrinoid necrosis and inflammation of small and medium-sized arterial walls recognizable angiographically by arterial microaneurysms and often by visceral infarction and hemorrhage. Renal failure is common and often associated with pulmonary edema. Gastrointestinal symptoms are a prominent feature due to bowel ischemia. Infarction and perforation are significant causes of morbidity and mortality. Necrotizing vasculitis is also one cause of pancreatitis and of cholecystitis. Plain films, contrast studies, computed tomography, and sonography have been shown to be useful in the recognition of these complications.
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PMID:Radiologic recognition of extrahepatic manifestations of hepatitis B antigenemia. 611 55

A 48-year-old asymptomatic male hepatitis B virus carrier presented with a 2-day history of fever, chills, right upper quadrant abdominal pain, and jaundice. Shock was detected on admission. Emergency abdominal computed tomography (CT) scanning without contrast enhancement showed the features of acute pancreatitis. Hemobilia, edematous pancreatitis, cholestasis and cholecystitis were found on exploratory laparotomy. Neither stone nor active bleeding were detected on intraoperative choledochoscopic examination. Postoperative T-tube cholangiography one month later revealed non-opacification of the left intrahepatic duct. The patient's abdominal pain and hemobilia recurred. Celiac angiography and CT scanning with contrast showed two hepatocellular carcinomas (HCC) in the left lobe of the liver. This is the first case report in the English literature of HCC presenting as jaundice, hemobilia, and acute pancreatitis.
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PMID:Hepatocellular carcinoma presenting as jaundice, hemobilia, and acute pancreatitis: a case report. 972 62

A case of hepatobiliary dysfunction as the initial manifestation of disseminated cryptococcosis is described. The patient was admitted with symptoms of hepatitis with cholestatic jaundice. Antibody tests for hepatitis B and C and human immunodeficiency virus were negative. The patient continued to deteriorate clinically. Eventually, the patient succumbed to hepatic failure. Autopsy disclosed systemic cryptococcosis that caused extensive necrosis of the liver. In review of the literature, only nine cases of cryptococcal infection presenting as hepatitis, cholangitis, and cholecystitis as initial manifestation were reported. Four of these patients had been subjected to exploratory laparotomy for clinical suspicion of acute abdomen. One patient developed cirrhosis as a result of cryptococcal hepatitis. Two patients succumbed to hepatic failure. Cryptococcosis is known to occur commonly in immunocompromised patients, yet only two reported cases presenting as hepatitis were associated with immunocompromised status.
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PMID:Hepatobiliary dysfunction as the initial manifestation of disseminated cryptococcosis. 1019 23

Infections of the liver and biliary tract are common during the course of AIDS. A variety of viral, bacterial, fungal, and other opportunistic infections can present with hepatobiliary involvement as either the primary site of infection or secondary to a disseminated process. Coinfection with hepatitis B and C are particularly common due to the shared means of transmission of these viruses with HIV. The typical presenting features of hepatobiliary infections are right upper quadrant (RUQ) pain and abnormal liver function tests. Initial evaluation should include an RUQ ultrasonogram, which will usually identify abnormalities in the biliary tract and may demonstrate some parenchymal abnormalities as well. A liver biopsy is necessary to determine the etiology of focal hepatic lesions or opportunistic infections within hepatic parenchyma when other less invasive tests are negative or inconclusive. Special stains and culture techniques are required to identify specific organisms in the biopsy specimen. HIV-related biliary disorders include acalculous cholecystitis, which is a potentially serious condition requiring prompt recognition and gallbladder decompression. AIDS-cholangiopathy is a form of cholangitis involving the intra- and/or extrahepatic biliary tree. Endoscopic retrograde cholangio-pancreatography (ERCP) is the test of choice, demonstrating the stricturing, dilatation, and beading of bile ducts seen in this condition. Endoscopic sphincterotomy of the papilla of Vater may provide symptomatic relief for patients with papillary stenosis. Opportunistic infections of the pancreas have been reported. Evaluation should include a computerized tomogram of the abdomen and possible pancreatic tissue aspiration or biopsy. Management of pancreatitis is supportive.
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PMID:Hepatobiliary and pancreatic infections in AIDS: Part one. 1136 70

Acquired factor X deficiency has been described in patients with amyloidosis but acquired factor V deficiency is quite rare. We report here a case of life-threatening bleeding and acquired factor V deficiency associated with primary amyloidosis. A 50-year-old man who had no previous hemorrhagic diathesis was referred to our hospital because of recurrent epistaxis, gingival bleeding and hemospermia. The laboratory examination revealed that both the prothrombin time (PT) and the activated partial thromboplastin time (aPTT) were significantly prolonged, and factor V activities were markedly decreased to 14-39% of the normal value. Other coagulation factors such as fibrinogen, prothrombin, factor VII, factor VIII, factor IX and factor X were subnormal and normal. Transaminases were slightly elevated but serological tests of hepatitis B and hepatitis C were negative. Mild hepatosplenomegaly was noted without sign of liver cirrhosis. The PT and aPTT obtained 8 years ago when he received a cholecystectomy due to cholecystitis were both normal. Specific assays for the detection of factor V inhibitor were repeatedly performed but no factor V inhibitor was found. Furthermore, a significant recovery of the infused factor V was noted shortly after an intravenous administration of 5-10 U fresh frozen plasma, but it did not last more than 6 h. Melena, bleedings into the left shoulder and buttock, and finally mortal retroperitoneal hemorrhage developed despite repeated infusions of large amounts of fresh frozen plasma. Acquired factor V deficiency associated with primary amyloidosis was suspected but histological diagnosis was not obtained because of the severe bleeding tendency. Autopsy revealed hepatosplenomegaly and massive deposits of AL amyloid in the liver, spleen, heart and other parenchymal organs. Perivascular amyloid deposition and factor V deficiency are both thought to be the cause of the severe hemorrhagic tendency seen in this patient.
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PMID:Life-threatening bleeding and acquired factor V deficiency associated with primary systemic amyloidosis. 1219 8

We reviewed the medical records of 62 patients with systemic small and medium-sized vessel vasculitides and gastrointestinal tract involvement followed at our institution between 1981 and 2002. This group included 46 men and 16 women (male:female ratio, 2.9), with a mean age of 48 +/- 18 years. Vasculitides were distributed as follows: 38 polyarteritis nodosa (21 related to hepatitis B virus), 11 Churg-Strauss syndrome, 6 Wegener granulomatosis, 4 microscopic polyangiitis, and 3 rheumatoid arthritis-associated vasculitis. Gastrointestinal manifestations were present at or occurred within 3 months of diagnosis in 50 (81%) patients and were mainly abdominal pain in 61 (97%), nausea or vomiting in 21 (34%), diarrhea in 17 (27%), hematochezia or melena in 10 (16%), and hematemesis in 4 (6%). Gastroduodenal ulcerations were detected endoscopically in 17 (27 %) patients, esophageal in 7 (11%), and colorectal in 6 (10%), but histologic signs of vasculitis were found in only 3 colon biopsies. Twenty-one (34%) patients had a surgical abdomen; 11 (18%) developed peritonitis, 9 (15%) had bowel perforations, 10 (16%) bowel ischemia/infarction, 4 (6%) intestinal occlusion, 6 (10%) acute appendicitis, 5 (8%) cholecystitis, and 3 (5%) acute pancreatitis. (Some patients had more than 1 condition.) Sixteen (26%) patients died.The respective 10-month and 5-year survival rates were 71% (95% confidence interval [CI], 52-90) and 56% (95% CI, 35-77) for the 21 surgical patients; and 94% (95% CI, 87-101) and 82% (95% CI, 70-94) for the 41 patients without surgical abdomen (p = 0.08). Peritonitis (hazard ratio [HR] = 4.3, p < 0.01), bowel perforations (HR = 5.7, p < 0.01), gastrointestinal ischemia or infarctions (HR = 4.1, p < 0.01), and intestinal occlusion (HR = 5.5, p < 0.01) were the only gastrointestinal manifestations significantly associated with increased mortality in multivariate analysis. For this subgroup of 15 patients, 6-month and 5-year survival rates were 60% (95% CI, 35-85) and 46% (95% CI, 19-73), respectively (p = 0.003). None of the other gastrointestinal or extraintestinal vasculitis-related symptoms, or angiographic abnormalities (seen in 67% of the 39 patients who underwent angiography), was predictive of surgical complications or poor outcome. However, prognosis has dramatically improved during the past 30 years, probably owing to better management of these more severely ill patients, with prompt surgical intervention when indicated, and the combined use of steroids and immunosuppressants.
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PMID:Presentation and outcome of gastrointestinal involvement in systemic necrotizing vasculitides: analysis of 62 patients with polyarteritis nodosa, microscopic polyangiitis, Wegener granulomatosis, Churg-Strauss syndrome, or rheumatoid arthritis-associated vasculitis. 1575 41

A 64-year-old man was admitted for alithiasic cholecystitis. Necrotizing vasculitis was detected in a gallbladder obtained at the cholecystectomy. Slight elevation of transaminases, HBe antigens and hepatitis B-DNA (HBV-DNA) were detected in the patient. Intrahepatic necrotizing vasculitis was also detected in the liver biopsy specimen, and he also suffered from peripheral neuropathy of suddenly onset. Based on the diagnosis of hepatitis B-related polyarteritis nodosa, lamivudine was initially administered, followed by plasmapheresis and glucocorticoid steroid therapy. These treatments brought satisfactory improvement of polyarteritis nodosa without exacerbation of liver function.
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PMID:Hepatitis B-related polyarteritis nodosa presenting necrotizing vasculitis in the hepatobiliary system successfully treated with lamivudine, plasmapheresis and glucocorticoid. 1650 28

Polyarteritis nodosa (PAN) is a necrotizing, focal segmental vasculitis that affects predominantly medium-sized arteries in many different organ systems. It is associated with hepatitis B virus (HBV) in about 7% of cases, a decline from about 30% before the mandatory testing of blood products and the widespread vaccination programs. HBV PAN is an early postinfectious process. The hepatitis is silent in most cases, with mild transaminase level increases in 50% of patients. Gastrointestinal involvement occurs in 14% to 65% of patients with PAN. Postprandial abdominal pain from ischemia is the most common symptom. When transmural ischemia develops, there may be necrosis of the bowel wall with perforation, associated with a poor prognosis. Liver involvement occurs in 16% to 56% of patients, although clinical manifestations related to liver disease are quite rare. Acalculous gangrenous cholecystitis may develop owing to arteritis involving the wall of the gallbladder. Microaneurysms on arteriography or computed tomography angiography are characteristic of PAN, but are seen in other conditions. Tissue biopsy may confirm the diagnosis, although involvement is segmental. Corticosteroids are used for non-HBV PAN with cyclophosphamide added for severe disease. For PAN related to HBV, a 2-week course of corticosteroids is begun, with plasma exchanges and an antiviral agent. Corticosteroids and cyclophosphamide have improved patient outcome so that the 1-year survival rate is now about 85%.
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PMID:Gastrointestinal involvement in polyarteritis nodosa. 1858 77

Chemotherapy drugs, biological medications that are used to treat cancer, may cause hepatic side effects. Patients with pre-existing viral hepatitis may be more susceptible to exacerbation of their underlying liver disease, and risk of drug-induced hepatotoxicity. We conducted a search on immunosuppression, and its impact on reactivation of viral hepatitis, using the electro-nic medical databases. Before starting chemotherapy, it is recommended to record the past history of liver disease and check for hepatitis B virus (HBV) and hepatitis C virus (HCV) serology. In immunosuppressed patients, radiation toxicity, graft versus host disease, hepatic veno-occlusive disease, acalculous cholecystitis, tumor infiltration, ischemia, other viruses such as CMV and her-pes virus, and systemic infection should also be considered. Transplant recipients with serologic evidence of previous infection with hepatitis B or C, or those who receive organs from a seropositive donor, should have viral load levels monitored before and after transplantation and, may also require treatment. We believe that there is a role for prophylactic use of antiviral treatment in patients at risk for HBV reactivation.
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PMID:Impact of immunosuppression and chemotherapy on reactivation of viral hepatitis. 2058 63


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