Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of chronic hepatitis (CH) should include the information on CH etiology, the presence or absence of CH activity as well as its morphological characteristics. CH may be of a viral etiology (the type of the virus should be mentioned in the diagnosis), autoimmune, drug-induced and alcoholic. The etiology can be established by means of the clinicomorphological analysis using immunological and immunohistochemical techniques. Sometimes it is possible to do so after routine staining of biopsies. Portal, lobular and periportal hepatitis are distinguished morphologically. Instead of the indefinite term chronic persisting hepatitis it is recommended to recognize active and non-active hepatitis.
 ...
PMID:[Morphologic classification of chronic hepatitis]. 767 77

We present a case of dramatic radiation enterocolitis inducing portal venous air diagnosed by Doppler sonography only. The sonographic pattern consisted of multiple irregular hyperechoic areas into the liver, with internal repetitive noisy bidirectional peaks superimposed on the usual continuous Doppler display of the portal flow. Although portal hyperechoic moving foci alone may reflect only slow portal velocity, they do not create any Doppler distortion as do moving bubbles. Portal air may have multiple causes such as abdominopelvic abscesses, sepsis, intestinal distension, fulminant hepatitis, cholangitis, cholecystitis, diabetic acidosis..., but mesenteric infarct, necrotic enterocolitis, and radiation enteritis are life-threatening conditions that have to be diagnosed as soon as possible. Although large quantities of portal air may be demonstrated on plain film of the abdomen or by computed tomography, Doppler sonography may detect smaller quantities, allowing earlier diagnosis of intestinal pathology requiring immediate surgical treatment. Therefore, Doppler sonography of the liver should be performed in any patient with acute abdominal pain or distension, especially if being treated by abdominal radiotherapy.
 ...
PMID:[diagnostic ultrasonography of air in the portal venous system: apropos of a case of colonic radionecrosis and literature review]. 782 61

Portal vein aneurysm (PVA) includes focal dilatation of the portal vein, and was formerly thought to be a rare disease. We report a 46-year-old man with chronic aggressive hepatitis and intrahepatic portal vein aneurysm communicating with the hepatic vein. Hemangiomas in the liver and intracranial arteriovenous malformation (AVM) were also found. To our knowledge, this is the first report of a case of PVA in a patient with congenital intracranial AVM. As the PVA in this patient communicated with the hepatic vein, and as hemangiomas in the liver and intracranial AVM were also present, the pathogenesis in this patient seems to have been congenital anomaly of the vasculature.
 ...
PMID:Portal vein aneurysm in the liver associated with multiple vascular malformations. 787 76

Met-enkephalin is known to circulate in human and animal plasma in low levels. However, the source(s) of plasma met-enkephalin have not been completely elucidated. It has been proposed that the adrenal gland, sympathetic nerves, pancreas and the gut might be implicated. Recently, markedly elevated levels of met-enkephalin have been documented in the presence of liver disease. To investigate potential sources of met-enkephalin in liver disease, rats with acute cholestatic hepatitis 24 h after gavage with alpha naphthylisothiocyanate (ANIT) 100 mg/kg were studied. Plasma met-enkephalin levels were determined by radioimmunoassay in plasma samples from normal, adrenalectomized, or chemically sympathectomized animals. In control rats, ANIT treatment resulted in a striking 8.7-fold increase in systemic venous met-enkephalin levels (inferior vena cava) (P < or = 0.0005) and a significant increase in peptidase-derived met-enkephalin levels (determined after trypsin/carboxypeptidase B digestion of plasma samples) (P < or = 0.05). ANIT-treatment also resulted in a 5.6-fold increase in portal vein met-enkephalin levels (P < or = 0.005). Portal vein met-enkephalin levels were only 1.2-fold higher than IVC levels in ANIT-treated rats (P < or = 0.05). Plasma activities of the two main enkephalin degrading enzymes, aminopeptidase and enkephalinase, were similar in control and ANIT-treated rats. Chemical sympathectomy, prior to ANIT treatment, decreased the elevation in inferior vena caval met-enkephalin levels by 35% (P < or = 0.005). Adrenalectomy did not alter ANIT-induced increases in circulating met-enkephalin levels (pNS).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Sympathetic nerves, but not the adrenal gland, contribute to elevated plasma levels of met-enkephalin in rats with acute cholestatic hepatitis. 821 May 12

Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections are common complications after orthotopic liver transplantation (OLT), but the liver pathology and clinical outcomes of HBV infection with HCV coinfection have not been thoroughly examined. In this study, we used the polymerase chain reaction (PCR) to detect HBV and HCV in pre- and post-OLT sera of 38 patients and correlated the findings with clinical outcome and liver pathology. Of 13 patients who were HBV and HCV negative before OLT, 9 acquired HBV infection, and 4 developed acquired HBV and HCV coinfections after OLT. Persistent HBV infections were present in 10 patients. Three patients with pre-OLT HBV infections developed persistent HBV and acquired HCV coinfections after OLT; 5 with pre-OLT HCV infections developed acquired HBV and persistent HCV coinfections after OLT, and 7 had persistent HBV and HCV coinfections before and after OLT. Portal/periportal inflammation was the same in all groups; however, lobular inflammation and fibrosis were more severe in patients with persistent HBV infections and in those with acquired HBV and HCV coinfections. Two major histopathological patterns were present in patients with HBV and HCV coinfections, one with predominant features of HCV infection, and the other with those of HBV infection. Patients with post-OLT HBV and HCV coinfections had survival rates similar to those with acquired HBV infection, whereas patients with persistent HBV infections experienced more allograft loss caused by chronic hepatitis or fibrosing cytolytic hepatitis, and had a more dire clinical outcome than the others. Although the limited numbers reported in this study prevent a definitive conclusion, our data suggest that in patients with HBV and HCV coinfections, the presence of HCV may improve the clinical outcome as compared with the expected outcome of persistent HBV infection alone.
 ...
PMID:Hepatitis B and C coinfections and persistent hepatitis B infections: clinical outcome and liver pathology after transplantation. 861 17

To evaluate the histological findings in patients with chronic hepatitis C and autoimmune features, liver tissue specimens from 60 patients were graded under code for individual features and composite patterns that denoted autoimmune, viral, combined autoimmune and viral, and nondiscriminative changes. Portal, interface, and acinar hepatitis in any combination with plasma cell infiltration connoted an autoimmune pattern that was associated with higher serum levels of gamma-globulin (2.4 +/- 0.2 g/dL vs. 1.7 +/- 0.1 g/dL; P = .0003) and immunoglobulin G (2,211 +/- 227 mg/dL vs. 1,508 +/- 83 mg/dL; P = .001) than patients with other patterns. Patients with the autoimmune pattern also had a greater frequency of cirrhosis (43% vs. 8%; P = .003), higher mean Knodell score (13.2 +/- 0.9 vs. 6.8 +/- 0.9; P < .0001), and a greater occurrence of high-titer smooth muscle antibodies (SMA) (13% vs. 0%; P = .05) than patients with other histological findings. HLA DR3 also occurred more frequently in these individuals than in other patients (48% vs. 15%; P = .01) and normal subjects (43% vs. 16%; P = .01). Patients with nondiscriminative patterns and interface hepatitis had clinical findings similar to those with autoimmune patterns, except for a lower mean serum level of gamma-globulin. We conclude that the composite histological pattern that resembles autoimmune hepatitis is associated with greater immunoreactivity, inflammatory activity, and disease severity than other patterns. Interface hepatitis may be the most important histological finding associated with these clinical manifestations.
 ...
PMID:Histological findings in chronic hepatitis C with autoimmune features. 925 59

The histopathology and clinical picture of hepatocellular carcinoma (HCC) varies between individual patients and regions. These variations are perhaps due to differences in the genetic alterations that precede hepatocarcinogenesis. In this study, the clinicopathological features of HCC were compared between southern African blacks and Japanese, indicating large differences in the frequency of underlying cirrhosis, grade of cancer cell differentiation and clinical course. Intra-abdominal bleeding and febrile, rapidly progressive HCC are more common among blacks. Such a difference is accounted for, in part, by frequent encapsulation of the tumour which is well differentiated, and grows slowly in an expanding fashion in Japan. Encapsulated HCC was not seen among the black patients studied. Other distinct clinicopathological types discussed in this paper include diffuse-type HCC which is usually caused by multiple portal spread occurring almost simultaneously; the clinical course is fulminant. Sclerosing carcinoma is frequently associated with hypercalcaemia in the United States, but not in Japan. Fibrolamellar carcinoma is nearly non-existent in Asia, whereas it is common among young adults in the West. Its prognosis is generally better than ordinary HCC. Hepatocellular carcinoma has a strong propensity to invade vessel and duct systems. Portal invasion does not produce distinct clinical signs although it may aggravate portal hypertension. Patients with tumour occlusion in the major portal vein may give rise to ischaemic hepatitis when blood pressure drops suddenly in the preterminal stage. Liver parenchyma develops submassive necrosis and clinically there is an acute rise in alanine aminotransferase (ALT). Invasion into a major hepatic vein and the inferior vena cava also occurs, but less frequently compared with portal invasion. The patient can live even with a tumour thrombus in the atrium crossing the tricuspid valves. Intraductal invasion causes acute jaundice as well as an occasional haemobilia with pain. We recently found that a distinct pathological type called 'extrahepatic growth' or 'pedunculated HCC' develops as a result of fusion of right-sided adrenal metastasis of HCC and the liver, perhaps through the 'adreno-hepatic fusion' which is rather common in cirrhotic livers.
 ...
PMID:Hepatocellular carcinoma: clinicopathological aspects. 940 52

We report on the significance of percutaneous transhepatic portal vein embolization (PTPE) for hepatocellular carcinoma based on the results in 111 patients who underwent PTPE in our hospital. All patients tolerated the procedure without major complications, although transient elevations in serum transaminase levels were noted. Immediately after PTPE, the portal pressure increased. Portal venous flow at the main portal trunk decreased, but the flow in the nonembolized part of the liver increased. PTPE produced regenerative hypertrophy in the nonembolized part of the liver, which was mainly predicted by the volume of the embolized area and the morphological score of the hepatitis or cirrhosis. PTPE increased the safety of subsequent hepatectomy and expanded the indications for hepatectomy. PTPE is also useful as a type of multiplicative therapy for hepatocellular carcinoma.
 ...
PMID:[Percutaneous transhepatic portal vein embolization for hepatocellular carcinoma]. 964 92

Evidence has been accumulating in favour of a role for hepatitis C virus (HCV) in the pathogenesis of human lymphoproliferative disorders. HCV infection has been documented in the majority of patients with essential mixed cryoglobulinaemia type II (MC-II); in patients with HCV infection, B-cell clonal expansion have been detected in peripheral blood and bone marrow, and a high prevalence of B-cell non-Hodgkin's lymphomas has been documented. Liver biopsies in chronic hepatitis C frequently show portal lymphoid infiltrates with features of B follicles, whose clonality has not yet been investigated. This study has analysed the B-cell clonality of portal lymphoid infiltrates from 16 patients with chronic HCV hepatitis. Portal tracts showing obvious lymphoid infiltrates were microdissected from the paraffin-embedded liver tissue sections and the clonality of lymphoid B-cells was tested using a polymerase chain reaction (PCR) approach designed to identify immunoglobulin heavy chain gene (IgH) rearrangements. A successful IgH-PCR analysis was achieved in 35 lymphoid infiltrates from 11 patients (seven with the four without MC-II) and yielded a single band in 21 cases, two bands in ten cases, and three bands in four cases. Comparison of the IgH-PCR amplification bands obtained from the different lymphoid aggregates of the same biopsy revealed that they differed in size. This finding indicates that each aggregate derives from the proliferation of one or a few founder B-cells, which are not related to each other. The results obtained in patients with and without MC-II were similar, suggesting that the presence of B-cell clonal proliferations in liver biopsies is independent of the occurrence of B-cells producing monoclonal IgMk cryoglobulins.
 ...
PMID:Clonality of B-cells in portal lymphoid infiltrates of HCV-infected livers. 971 64

Fluoxetine-induced hepatotoxicity is generally considered of minimal clinical importance and is not well recognized. Asymptomatic increases in liver enzyme values have been observed in 0.5% of patients who take long-term fluoxetine therapy. This report details 2 cases of acute hepatitis believed to be caused by fluoxetine. Three cases of acute hepatitis caused by fluoxetine have been reported previously. The mechanism of fluoxetine-induced hepatotoxicity is unknown. Although routine monitoring of liver function may not be cost-effective, physicians should be alert to the possibility of fluoxetine-associated hepatitis and consider early discontinuation of the drug if this condition is suspected.
 ...
PMID:Acute hepatitis due to fluoxetine therapy. 1040 99


<< Previous 1 2 3 4 5 Next >>