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

Several extrahepatic syndromes have been associated with chronic hepatitis C virus infection. In our patient (a 57-yr-old woman without risk factors for hepatitis), chronic active hepatitis C was diagnosed serologically and histologically. Three months later, membranoproliferative glomerulonephritis with compromised renal function and peripheral edema, cryoglobulinemia, and a vasculitis of the finger tips developed. During interferon treatment for 3 months, neither the clinical condition nor serological parameters improved significantly. Progressive dyspnea was due to bilobar pulmonary infiltration. Despite antibiotic, virostatic, and corticosteroid therapy, the patient died from respiratory failure. Autopsy revealed diffuse pulmonary vasculitis. Thus, this is the first description of chronic hepatitis C virus infection, glomerulonephritis, and cryoglobulinemia complicated by immunologically mediated pulmonary vasculitis. Because interferon therapy may be ineffective, immunosuppressive therapy should be considered.
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PMID:A lethal course of chronic hepatitis C, glomerulonephritis, and pulmonary vasculitis unresponsive to interferon treatment. 777 95

To investigate the effect of external radiotherapy in the control of portal vein invasion (PVI) in hepatocellular carcinoma (HCC), ten patients with cytologically confirmed unresectable HCC were recruited for study. All of the patients were assigned Pugh's classification A, and all had only unilateral PV involvement. The main tumors were treated by transcatheter arterial embolization. The PVI was irradiated with a dose of 3000-5000 cGY using a linear accelerator under localization by real-time ultrasound. All ten patients responded to the external irradiation, with complete disappearance of the PVI occurring in five and partial shrinkage, in the other five. However, the HCC extended to the contralateral PV in two patients, although the irradiated lesion had shrunk. Both patients had shown involvement of the main PV in the initial study. Six patients died after 3, 6, 7, 7, 8, and 10 months, respectively, due to advance of the HCC, rupture, liver failure, and respiratory failure. The others survived for longer than 6 months and remain under follow-up. The branch of PVI at discovery might have an important bearing on the effect of the radiotherapy. No postirradiation hepatitis or other complication was observed.
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PMID:The effect of external radiotherapy in treatment of portal vein invasion in hepatocellular carcinoma. 813 72

Indications for liver transplant in acute fulminating hepatitis (AFH) are predominantly affected by the high mortality of this spontaneous evolution (80-100%). At present patients with AFH have priority for transplant since they form part of the 0 emergency group according to the National Transplant Organisation. During the period between 1986 and the end of February 1992, a total of 254 liver transplants were performed in 202 patients (52 retransplants). In 26 patients (12.8%) (16 females and 10 males) the indication was fulminating acute hepatitis. Etiology was unknown in 20 patients, secondary to hepatitis B in 4 and to hepatitis A in 1, and was caused by isonazide ingestion in 1 case. The age limits were 3-60 years (X = 31.5 years). An isogroup graft was performed in 16 patients (61.5%), compatible in 3 (11.6%) and incompatible in 7 (26.9%). Due to anthropometric differences, a partial graft was used in 7 patients (26.9%); in 2 of the latter the graft was taken from the same donor ("split-liver"). Placement was always orthotopic with resection of the retrohepatic vena cava in 25 patients and its preservation in 1 (left lobe of split-liver). Peroperative (30 days) mortality was 23% (6/26); 2 due to cerebral death, 2 due to sepsis, 1 due to multisystemic insufficiency (MSI) and 1 due to acute pancreatitis. Four patients (15.3%) died some time after transplant; 1 after 5 months due to broncho-pulmonary complications, 1 after 7 months due to subacute hepatitis, 1 after 3 months due to respiratory failure and the last after 5 months due to anoxic encephalopathy and lung infection. Ten patients (39.4%) were re-transplanted; 4 following chronic rejection, 4 due to primary graft no function, 1 due to arterial thrombosis and 1 due to recurrent hepatitis (with cirrhosis). Two of the latter patients died intraoperatively due to coagulopathy and hemorrhage, and 3 following surgery (1 due to sepsis, 1 due to respiratory complications and 1 due to respiratory insufficiency). Two patients underwent a second re-transplant (1 due to chronic rejection and 1 due to recurrent hepatitis) and of these 1 died peroperatively due to sepsis and MSF. Overall mortality was therefore 61.5% (16/26) and the actuarial survival rate of 17 patients (10 living + 7 postoperative deaths) was 68% at 12 months and 52.9% at 36 months. Even if peroperative mortality is relatively high, liver transplant is currently the elective treatment for fulminating acute hepatitis.
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PMID:[The treatment of acute liver failure due to fulminating hepatitis by total or partial orthotopic liver transplantation. The clinical results]. 832 33

We studied four patients who presented a striking elevation of blood transaminases suggesting acute hepatitis. The post mortem histological examination of the liver revealed centrolobular necrosis that is commonly diagnosed as ischaemic hepatitis. The liver necrosis arose from heart failure which was worsened by an acute anaemia in one patient and by a severe hypoxemia, due to respiratory failure, in another. In three subjects there was evidence of disseminated intravascular coagulation that may be responsible for aggravating the condition of liver hypoxia. The authors also review the literature on the various aspects of ischaemic hepatitis.
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PMID:[Ischemic hepatitis. Description of 4 cases and review of the literature]. 836 7

Adult respiratory distress syndrome or ARDS as coined by Ashbaugh et al in 1967, has been a great challenge in the field of critical care since then. It is a clinical entity which can be caused by various insults at any age. There have been several case reports of ARDS involving infants and children in the past 10 years, but pediatric ARDS is still not well recognized in Taiwan. A review of admissions to the pediatric intensive care unit in the past 2 years shows that 11 of the cases were included as pediatric ARDS combined with the expanded definition of Murray et al, and that each patient had an acute lung injury score greater than 2.5. Clinical manifestations also presented acute pulmonary distress indicating ARDS. The distribution of age ranged from 13 months to 11 years. The predisposing insults included sepsis, gastrointestinal bleeding with shock and massive blood transfusion, central nervous system infection, major trauma, near drowning, fulminant hepatitis and chemotherapy for acute leukemia. All received mechanical ventilatory support. The average peak inspiratory pressure was 46.7 +/- 6.4 cmH2O and the mean value of maximal PEEP used was 11.9 +/- 4.4 cmH2 O. Three patients developed barotrauma. Two patients survived and nine expired, a mortality rate of 82%. It is important for physicians caring for infants and children with respiratory failure to consider the diagnosis and initiate adequate ventilatory support and other resuscitation management.
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PMID:Adult respiratory distress syndrome in children. 838 48

In conclusion, the availability of liver transplantation has dramatically advanced the management of fulminant hepatic failure. A major responsibility of the gastroenterologist/hepatologist involved in the care of patients with liver failure is early decision making regarding likelihood of spontaneous recovery and consideration toward referral to a transplantation center. In particular, patients with exposure to drugs or toxins (other than acetaminophen); patients with presumed non-A, non-B hepatitis; children or older patients; patients with prolonged jaundice; profoundly jaundiced patients; or patients with severe coagulopathy should be given the highest consideration for urgent transplantation. Supportive care should take into account the potential complications of bleeding, sepsis, cerebral edema, renal failure, and respiratory failure. Such complications are the major limiting factors that prevent patients with fulminant hepatic failure from undergoing liver transplantation and contribute to the majority of postoperative deaths among patients who undergo transplantation. If these issues are heeded, and in light of emerging therapeutic modalities and surgical innovations, it is anticipated that ongoing improvement of the overall outcome of patients with fulminant hepatic failure will continue to be seen.
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PMID:Liver transplantation for fulminant hepatic failure. 850 70

A 27-year-old male suffered from Epstein-Barr virus (EBV)-related liver dysfunction with persistent hypogammaglobulinemia. IgG titers to EBV antigens were significantly high, while other hepatitis markers were negative. Liver biopsy disclosed active intralobular inflammation. Two years later, he manifested persistent fever, leukopenia, effusions and hypoproteinemia, and his general condition worsened progressively. The peripheral blood small lymphocytes predominantly expressed natural killer (NK)-like phenotypes (CD2+, CD7+, CD16+, CD56+). Hepatosplenomegaly and marked elevation of serum lactic dehydrogenase were observed. He died of respiratory failure at the age of 29. At autopsy, the liver (2190 g), spleen (860 g), small bowel and mesenteric lymph nodes showed massive infiltration of large atypical lymphoid cells in close association with hemophagocytic histiocytes. Involvement was mildly noted also in the bone marrow, lungs, gall-bladder and kidneys. The atypical cells belonged to CD30+ activated NK-type cells expressing CD2, cytoplasmic CD3 epsilon, CD7, CD45RO, CD56, HLA-DR and HLA-DQ. T cell receptors (TCR), surface CD3, CD4, CD5 and CD8 were not expressed. Epstein-Barr virus-related small nuclear RNA (EBER1) and Epstein-Barr virus-associated nuclear antigen 1 were detected in the nuclei of a significant number of atypical cells, while EBV-related latent membrane protein-1 was negative. EBER1 was also identified in the nuclei of non-neoplastic small lymphocytes at both biopsy and autopsy. Monoclonal integration of the EBV genome into the lymphoma cells was shown by Southern blot analysis. Clonal rearrangement of TCR was undetectable. Roles of chronic active EBV infection in the development of NK cell-type malignancy resembling malignant histiocytosis are discussed.
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PMID:Epstein-Barr virus (EBV)-induced CD30+ natural killer cell-type malignancy resembling malignant histiocytosis: malignant transformation in chronic active EBV infection associating hypogammaglobulinemia. 921 26

Cardiac and circulatory failure are the main causes of hypoxic hepatitis. In a prospective study of 142 cases of hypoxic hepatitis collected during a 10-year period, we encountered two cases resulting from extreme arterial hypoxemia without congestive heart failure, cor pulmonale, or circulatory failure. Both patients were morbidly obese women admitted to the intensive care unit for carbonarcosis. Oxygen arterial saturation was very low, less than 35% in both patients, but there was no history of cardiac or respiratory failure and no clinical evidence of circulatory failure. Cardiac function, evaluated by isotopic scintigraphy, was normal. After the episode of hypoxic hepatitis, a diagnosis of obstructive sleep apnea was made clinically and confirmed by performing nocturnal oximetry, which showed multiple episodes of oxygen desaturation in both patients. Polysonography could be performed in one case and was typical of obstructive sleep apnea. Liver ischemia is the main mechanism leading to hypoxic hepatitis. More recently, the role of passive congestion of the liver has been emphasized. Arterial hypoxemia, however, is generally considered to be a minor factor. Our two cases support the hypothesis that severe arterial hypoxemia may lead to hypoxic hepatitis even in the absence of cardiac and circulatory failure.
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PMID:Hypoxic hepatitis caused by severe hypoxemia from obstructive sleep apnea. 925 50

Ischemic hepatitis, a relatively infrequent disorder occurring in 0.16% to 0.50% of patients admitted to medical intensive care units, often follows episodes of hypotension or acute heart failure. Investigating the clinical characteristics of patients with ischemic hepatitis may add to our understanding of the pathogenesis and significance of this syndrome. We therefore conducted a retrospective analysis of 34 patients to examine the possible contribution of the various baseline characteristics to the severity of the hepatic damage. In all patients liver disease was unexpected and in some, liver dysfunction dominated the clinical picture. All patients had high serum glutamic pyruvic transaminase (SGPT) and lactic dehydrogenase (LDH) levels (mean +/- SE, 2073 +/- 255 international units and 6085 +/- 748 international units, respectively). The mean SGPT/LDH ratio was 0.34. Most patients had coagulopathy with a prolonged prothrombin time (mean +/- SE, 5.86 +/- 1.37 international normalized ratio [INR]). The most common diagnosis on admission was respiratory distress secondary to various causes. Before the development of the hepatic dysfunction, respiratory failure and hypoxemia were observed in 68% of the patients, whereas hypotension was observed in only 38%. More than 90% of the patients had three or more associated comorbid conditions. The most frequent of these were left heart failure (88.2%), right heart failure (67.6%), chronic obstructive lung disease (58.8%), and chronic renal failure (55.9%). During the acute episode, more than 90% of the patients had transient deterioration of their renal functions. Hypoglycemia was noted in 11 patients (32.4%), and the glucose level was inversely correlated with the SGPT level (r = -0.43, p = 0.01). Stepwise multiple regression analysis showed that left heart failure, systolic blood pressure lower than 90 mm Hg, and female gender, together, accounted for 34% of the variance of the peak SGPT levels (p = 0.002). Fourteen (41.2%) patients died during the 3-month follow-up period, but none from the hepatic injury. None of the clinical or laboratory parameters measured predicted mortality. Clearly, ischemic hepatitis is associated with a high risk of death. The characteristic patients are those with multiple underlying systemic diseases and conditions, especially those with left heart failure. Liver function test results and levels of liver enzymes should be monitored in these patients, particularly when they are admitted for respiratory deterioration and episodes of hypotension.
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PMID:Ischemic hepatitis: clinical and laboratory observations of 34 patients. 960 Mar 66

Out of a prospective series of 142 consecutive episodes of hypoxic (ischemic) hepatitis (HH), we identified 17 episodes associated with an acute exacerbation of chronic respiratory failure (CRF) without left cardiac failure. In the aim to evaluate the role of arterial hypoxemia in the pathogenesis of HH associated with respiratory failure, these 17 episodes of HH (study group) were hemodynamically compared with a control group of 17 episodes of HH associated with congestive heart failure (CHF) (control group 1) and a group of 16 episodes of acute respiratory failure (ARF) not complicated by HH (control group 2). Arterial hypoxemia was significantly more severe in the study group (arterial blood tension in O2 [PaO2], 34 mm Hg) than in control group 1 (PaO2, 70 mm Hg; P <.0001) and control group 2 (PaO2, 45.5 mm Hg; P =.002). The role of arterial hypoxemia, however, appeared weakened by comparable degrees of systemic hypotension and liver passive congestion in episodes of HH associated with CRF and episodes of HH associated with CHF. Finally, the causative role of arterial hypoxemia emerged from hemodynamic measurements of cardiac index (CI), systemic vascular resistances (SVR), and oxygen transport: systemic hypotension in HH associated with CHF (control group 1) was the result of a fall in CI (median, 2. 33 L/min. m2; range, 1.21-3.14 L/min. m2) associated with high SVR (median, 2,492 dyn. s/cm5. m2; range, 1,382-4,053 dyn. s/cm5. m2), whereas in HH associated with respiratory failure (study group), systemic hypotension was the result of a fall in SVR (median, 1,053 dyn. s/cm5. m2; range, 646-3,148 dyn. s/cm5. m2), resulting in high CI (median, 4.23 L/min. m2; range, 1.9-5.32 L/min. m2) (P =.0087 and. 0038 for cardiac index and SVR, respectively). Moreover, measurements of oxygen transport in patients with HH associated with respiratory failure showed low values of O2 delivery (DO2) (median, 376 mL/min. m2; range, 253-427 mL/min. m2) as a result of extreme arterial hypoxemia despite high CI. In conclusion, these hemodynamic results and additional measurements of hepatic blood flow (HBF) by the method of galactose clearance at a low concentration suggest that in the setting of HH associated with respiratory failure, the liver is not "ischemic," despite hypotension, but rather "hypoxic" as a result of the combination of severe arterial hypoxemia and elevated central venous pressure (CVP).
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PMID:Hypoxic hepatitis caused by acute exacerbation of chronic respiratory failure: a case-controlled, hemodynamic study of 17 consecutive cases. 991 19


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