Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of intestinal obstruction due to intramural hematoma of the duodenum following therapeutic endoscopy for a bleeding duodenal ulcer in a patient with liver cirrhosis. A 44-year-old man was admitted to our hospital with severe epigastralgia, nausea and tarry stool. Two years previously he had undergone endoscopic sclerotherapy for esophageal varices caused by alcoholic liver cirrhosis. Endoscopy revealed an open ulcer with a bleeding vessel in the duodenal bulb, and sclerotherapy was performed by clipping the vessel and injecting 20 ml of 0.2% epinephrine. His platelet count was 3.5x10(4)/mul. Twelve hours later, he again developed epigastralgia and hypotension. Emergency computed tomography and ultrasonography revealed an intramural hematoma, 15x18 cm in diameter, at the dorsal and lateral duodenum. Endoscopy and upper gastrointestinal series revealed severe stenosis of the duodenal lumen caused by intramural hematoma. He received parenteral feeding for 22 days and within 8 weeks the hematoma was gradually absorbed using conservative management. Intramural duodenal hematoma may be diagnosed as a complication of the endoscopic procedure in a patient with a bleeding tendency, such as liver cirrhosis.
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PMID:Intramural duodenal hematoma after endoscopic therapy for a bleeding duodenal ulcer in a patient with liver cirrhosis. 1625 10

A 69-year-old man had radiofrequency ablation therapy (following RFA) for type C cirrhosis with hepatoma (following HCC) of S7 in November 2001. Afterward the patient was followed as an outpatient, but he had been admitted to our hospital due to jaundice confirmed in March 2004. His abdominal wall appeared to be soft and flat, and we could not detect a tumor mass by palpating either. Even though he exhibited no actual symptom of anemia, jaundice was found in the bulbar conjunctiva at the time of admission. Laboratory findings showed a mild inflammation and anemia on his admission, and biochemical data showed a rise of hepatobiliary enzyme with jaundice. A rise of tumor marker (AFP, PIVKA-II) was recognized, too. We performed percutaneous transhepatic bile duct drainage (following PTBD) to decrease jaundice because abdominal echography and CT showed an extension of tumor thrombosis in bile duct and right hepatic duct by HCC of S8. However, a check of T-Bil. was 7.29 mg/dl and showed some slight decrease. Therefore, we administered prostaglandin E1 (following PGE1) at first with an intra-arterial injection catheter aiming to protect the hepatocyte. One week later, we performed hepatic artery injection chemotherapy (CDDP+5-FU) for four weeks. We confirmed a manifested improvement in T-Bil to be 1.92 mg/dl at the end of hepatic artery injections as well as a manifested decrease in hepatobiliary enzyme. We confirmed a decrease of HCC of S8 by abdominal CT, and the response rate was PR. Afterward the patient was conservatively treated even though pancytopenia was present, and was discharged from the hospital in June 2004. The hepatic artery injection chemotherapy used together with PGE1 was effective for the HCC patient with jaundice.
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PMID:[The hepatic artery injection chemotherapy and prostaglandin E1 administration for hepatocellular carcinoma invading the biliary tract with jaundice]. 1631 59

A fifteen-month-old boy, born to consanguineously married couple, presented with asymptomatic hepatomegaly. Investigations revealed mildly deranged liver functions, necroinflammatory changes and cirrhosis on liver biopsy, a markedly raised alpha feto protein and tyrosine levels in plasma and a generalized aminoaciduria. His diagnosis of hereditary tyrosinemia was established on findings of raised serum and urine succinylacetone and a deficient activity of fumaryl acetoacetate hydroxylase enzyme. Prenatal diagnosis of hereditary tyrosinemia was performed in a subsequent pregnancy in this family from India.
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PMID:Tyrosinemia type I--diagnostic issues and prenatal diagnosis. 1651 30

Copper-histidine is the treatment of choice in Menkes disease but bears the potential risk of copper overload and induced liver cirrhosis. We report normal copper concentrations of liver tissue over an 8-year treatment period with copper-histidine.
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PMID:Copper concentration of liver tissue under long-term copper-histidine therapy in a patient with Menkes disease. 1678 54

Hepatopulmonary syndrome (HPS) is a clinical state defined by a chronic hepatic disorder, intrapulmonary vascular dilatation, and altered gas exchange resulting in hypoxemia. Cirrhosis of the liver is the most common condition associated with HPS. A 3-year-old boy who presented with end-stage liver disease and severe hepatopulmonary syndrome underwent orthotopic liver transplantation (OLT). The findings of HPS resolved immediately after OLT. His status is within normal limits at 6 months after liver transplantation.
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PMID:Liver transplantation of a child with child a cirrhosis and severe hepatopulmonary syndrome. 1679 24

We experienced a case manifesting progressive multifocal leukoencephalopathy (PML) in a hemodialytic patient with hepatitis C virus-induced liver cirrhosis and human T-cell lymphotropic virus type-1 (HTLV-1)-associated uveitis. A 57-year-old male patient had received chronic hemodialysis therapy for 10 years, during which he received multiple blood transfusions and HTLV-1-associated uveitis developed. He complained of visual disturbance and disorientation. Brain CT scan showed diffuse and multifocal low density areas in occipital and temporal lobes, with gray matter relatively spared. MRI imaging showed high intensity lesions in the same areas. Cerebrospinal fluid culture was negative, but using nested PCR, rearranged regulatory region of JC virus DNA was detected. His consciousness level gradually deteriorated and complete paraplegia developed. Seven months after admission, he died of pneumonia. An autopsy confirmed the diagnosis of PML. Notably, mononuclear cell infiltration, gliosis and demyelinating lesions but no nuclear inclusion bodies were observed in the thoracic cord, which suggested HTLV-1-associated myelopathy. Because JC virus is activated under immunocompromised conditions, precipitating factors in this case appear multifactorial; depressed immune system induced by chronic hemodialysis as well as blood-borne hepatitis C virus/HTLV-1 infection might contribute to the activation of dormant JC virus and the development of florid clinical manifestation of PML.
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PMID:A case report of progressive multifocal leukoencephalopathy in a human T-cell lymphotropic virus type 1-infected hemodialytic patient. 1681 97

Hepatitis C virus is a major global health problem affecting an estimated 170 million people worldwide. Chronic infection is common and can lead to cirrhosis and liver cancer. There is no vaccine available and current therapies have met with limited success. The viral RNA genome encodes a polyprotein that includes two proteases essential for virus replication. The NS2-3 protease mediates a single cleavage at the NS2/NS3 junction, whereas the NS3-4A protease cleaves at four downstream sites in the polyprotein. NS3-4A is characterized as a serine protease with a chymotrypsin-like fold, but the enzymatic mechanism of the NS2-3 protease remains unresolved. Here we report the crystal structure of the catalytic domain of the NS2-3 protease at 2.3 A resolution. The structure reveals a dimeric cysteine protease with two composite active sites. For each active site, the catalytic histidine and glutamate residues are contributed by one monomer, and the nucleophilic cysteine by the other. The carboxy-terminal residues remain coordinated in the two active sites, predicting an inactive post-cleavage form. Proteolysis through formation of a composite active site occurs in the context of the viral polyprotein expressed in mammalian cells. These features offer unexpected insights into polyprotein processing by hepatitis C virus and new opportunities for antiviral drug design.
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PMID:Structure of the catalytic domain of the hepatitis C virus NS2-3 protease. 1713 77

University of Wisconsin (UW) solution has been the standard for preservation of liver transplantation grafts since 1989. However, some studies demonstrated that histidine-tryptophan-ketoglutarate (HTK) solution is also effective. The purpose of this study was to compare the efficacy of both solutions in liver transplantation. From January 2003 to August 2004 the livers of deceased donors were randomized into HTK and UW groups. The 102 studied patients included 65 (63.7%) in the UW group and 37 (36.3%) in the HTK group. Sex, race, hemodynamic state, use of adrenergic drugs, and presence of steatosis in the donor were similarly distributed in the two groups (P > .05). The mean age of the donors was 38.1 years (SD +/-14.4) in the UW group and 44.6 years (SD +/-14.2) in the HTK cohort (P = .036). Sex, race, age, etiology of the cirrhosis, retransplant, acute liver failure, portal thrombosis, and Child-Pugh and MELD scores in the recipients were similarly distributed in the two recipient samples (P > .05). Among 89 patients who completed 4 months of follow-up, the HTK group included eight cases (25.8%) of biliary complications versus five cases (8.6%) in the UW group (P = .033; OR = 2.0 95% CI = 1.2-3.5). The incidence of graft dysfunction was 2.8% in the HTK group and 9.4% in the UW group (P = .15). In conclusion, UW and HTK solutions were equally effective for the preservation of the hepatic graft. The routine use of HTK solution can reduce the costs of liver transplantation.
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PMID:Randomized clinical assay for hepatic grafts preservation with University of Wisconsin or histidine-tryptophan-ketoglutarate solutions in liver transplantation. 1690 10

Human hepatitis B virus (HBV) can cause acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma. HBV e antigen (HBeAg), a secreted protein and not required for viral replication, is thought to play an immunoregulatory role during viral infection. However, the functional involvement of HBeAg in host immune response has not been fully elucidated. We report in this study that HBeAg can bind to interleukin-1 receptor accessory protein (IL-1RAcP). Interleukin-1 (IL-1) plays an important role in inflammation and regulation of immune response, and membrane form of IL-1RAcP (mIL-1RAcP) is an essential component of trimeric IL-1/IL-1 receptor/mIL-1RAcP complex. We show that glutathione S-transferase- or polyhistidine-tagged recombinant HBeAg can interact with endogenous mIL-1RAcP in vitro. Purified (His)6-HBeAg added in the culture medium can interact with overexpressed FLAG-tagged mIL-1RAcP in vivo. Indirect immunofluorescence and confocal microscopy show that HBeAg colocalizes with mIL-1RAcP on the cell surface. Furthermore, HBeAg is able to induce the interaction of IL-1 receptor I (IL-1RI) with mIL-1RAcP and trigger the recruitment of adaptor protein myeloid differentiation factor 88 (MyD88) to the IL-1RI/mIL-1RAcP complex. Assembly and activation of IL-1RI/mIL-1RAcP signaling complex by HBeAg can activate downstream NF-kappaB pathway through IkappaB degradation, induce NF-kappaB-dependent luciferase expression, and induce the expression of IL-1-responsive genes. Silencing of IL-1RAcP by small interfering RNA dramatically abolishes HBeAg-mediated NF-kappaB activation. These results demonstrate that HBeAg can trigger host IL-1 response by binding to mIL-1RAcP. The interaction of HBeAg with mIL-1RAcP may play an important role in modulating host immune response in acute and chronic HBV infection.
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PMID:Human hepatitis B viral e antigen interacts with cellular interleukin-1 receptor accessory protein and triggers interleukin-1 response. 1697 26

We describe a 40-year-old male patient with Hunter's syndrome. His main manifestations were ascites and esophageal varices due to cirrhotic liver. We obtained hepatic biopsy samples and examined them. Ultrastructurally, the features of the hepatocytes and Kupffer cells were the same as those reported in young patients. The passage of 40 years led to gradual progression to fibrosis, and ultimately liver cirrhosis. Namely, with a longer survival time, the complications of liver cirrhosis become more remarkable. Hepatic fibrosis in Hunter's syndrome is slowly progressive and patients who are expected to have a longer life span should be continuously monitored for hepatic complications.
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PMID:An adult case with Hunter's syndrome presenting prominent hepatic failure: light and electron microscopic features of the liver. 1710 56


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