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 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 134 patients with chronic active liver disease, selected by identical clinical, biochemical and morphologic criteria, assigned to standard treatment programs and followed at regular intervals, 21 of 105 failed treatment with standard regimens containing steroids. Treatment failure was more common in patients whose serum contained hepatitis B surface antigen, those with more severe liver disease as judged by liver function tests (prothrombin time) and hepatic morphology (subacute hepatitis or cirrhosis). Early diagnosis of treatment failure, based on changes in liver function tests rather than on clinical features of deterioration, coupled with the immediate administration of higher doses of prednisone with or without higher doses of azathioprine, resulted in disappearance of clinical and biochemical features of disease activity in the majority of patients. These results were greatly superior to those earlier reported by us from patients chosen by identical criteria but treated by conventional measures. However, when endogenous encephalopathy developed the outlook was grave, regardless of previous or subsequent therapy. We recommend that patients at risk for failing conventional treatment be identified early, followed carefully with serial liver function tests, and be treated promptly with higher doses of medication when deterioration occurs.
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PMID:Failure of customary treatment in chronic active liver disease: causes and management. 79 99

Twenty patients with acute fulminant hepatic failure and stage II, III, or IV hepatic encephalopathy attributable to viral hepatitis were studied to assess the risk factors, as well as the affects of vigorous medical management. These patients were treated according to a protocol that directed aggressive medical management of fluid balance with electrolyte solutions, plasma, and blood; acid-base balance; coagulation defects with fresh frozen plasma; blood replacement as needed; dietary protein elimination; and orally administered neomycin sulfate. Among the 20 patients there were eight survivors (40%). Seven of the 13 patients who were positive for the hepatitis B surface antigen (HB-Ag) survived (54%), while one of the seven patients whoe were negative for HB-Ag survived (14%). The stage of encephalopathy on admission did not correlate with survival. Patients under the age of 40 years had a 43% survival rate, while those over 40 years had a 33% survival rate. Conservative but vigorous medical management may improve survival in fulminant hepatic failure.
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PMID:Vigorous medical management of acute fulminant hepatitis. 85 88

To evaluate indications for new therapies such as liver transplantation and antiviral therapy, survival of histologically proven hepatitis B surface antigen (HBsAg)-positive cirrhosis of the liver was assessed in a cohort of 98 patients followed up for a mean of 4.3 years. The overall survival probability was 92% at 1 year, 79% at 3 years, and 71% at 5 years. Variables significantly associated with the duration of survival were age, serum aspartate aminotransferase levels, presence of esophageal varices, and all five components of the Child-Pugh index (bilirubin, albumin, coagulation factors, ascites, encephalopathy). Multivariate analysis showed that only age, bilirubin, and ascites were independently related to survival. Survival of patients with decompensated cirrhosis (determined by the presence of ascites, jaundice, encephalopathy, and/or a history of variceal bleeding) and those with compensated cirrhosis at 5 years was 14% and 84%, respectively. For patients with compensated liver cirrhosis, hepatitis B e antigen (HBeAg) positivity was also a prognostic factor with a 5-year survival of 72% for HBeAg-positive cirrhosis and 97% for HBeAg-negative cirrhosis; the risk of death was decreased by a factor of 2.2 when HBeAg seroconversion occurred during follow-up. It is concluded that liver transplantation should be considered for patients with decompensated HBsAg-positive liver cirrhosis and antiviral therapy for patients with HBeAg-positive compensated cirrhosis.
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PMID:Survival and prognostic indicators in hepatitis B surface antigen-positive cirrhosis of the liver. 142 89

Brain biopsy is justified in patients suspected of having encephalitis or viral encephalopathy because those patients are most likely to be helped if a diagnosis is made rapidly and with the greatest certainty possible. Neurosurgeons are occasionally reluctant to undertake brain biopsy because the procedure is diagnostic rather than therapeutic in intent. However, using currently available techniques a 1 cm3 sample of brain tissue can be taken with very low risk of morbidity or mortality. We recommend that the sample be taken from the anterior portion of the inferior temporal gyrus on the more affected side in patients with herpes simplex encephalitis, and from an area of maximum demonstrated involvement in other situations, using stereotactic techniques and intraoperative ultrasound as necessary. The risk to the operating surgeon and to the other members of the operating team appears very low in all of the situations discussed in this chapter. However, the authors feel that every patient should be approached as if he carries the hepatitis B virus. As indicated, the incidence of contracting hepatitis B after sustaining needle stick exposure to blood from persons positive for hepatitis B surface antigen is 10-15%. Conjunctival contamination by splash from the wound is a known method of inoculation of surgeons with hepatitis B virus and is a possible means for transmission of other viral diseases. We recommend that every patient be approached as if he has hepatitis B, not because the agent diseases discussed are known to be as infectious as hepatitis B, but because constant vigilance and careful technique offer the best protection to the surgeon and the members of the operating team in most situations, and because one can never be certain what agent diseases a given patient may harbor. With the exception of the Creutzfeldt-Jakob virus, the agents responsible for all of the viral diseases discussed are inactivated by standard procedures for sterilization of operating room instruments. Procedures necessary to inactivate the Creutzfeldt-Jakob disease virus have been presented. In the report documenting transmission of Creutzfeldt-Jakob disease through human growth hormone preparations the authors state, "We are once again dramatically reminded that human tissues are a source of infectious disease, and that any therapeutic transfer of tissue from one person to another carries an unavoidable risk of transferring the infection.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Brain biopsy for encephalitis. 353 42

A 12-week-old female infant died from acute encephalopathy mimicking Reye syndrome. Because of positive serum hepatitis B surface antigen (HBs Ag) and perivascular inflammatory cell infiltration in the liver, she was diagnosed as having acute hepatitis. The most striking finding in the present case was extremely excessive lipid accumulation in the striated muscles including biceps brachii, tongue and cardiac muscles. The levels of serum, liver and muscle carnitine were within normal limits, though liver carnitine palmityl transferase (CPT) was markedly decreased in activity. Although the primary metabolic defect has yet to be elucidated, it is assumed that the fulminant hepatic failure induced lipid accumulation in the skeletal muscle by a certain abnormal lipid metabolism.
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PMID:Fatal lipid storage disorder. 648 84

To determine the frequency and prognosis of histologic cirrhosis developing during or after corticosteroid therapy of hepatitis B surface antigen-negative chronic active hepatitis, we followed 83 patients for 90 +/- 5 mo after administration of corticosteroids. Thirty-three patients satisfied histologic criteria for cirrhosis after 30 +/- 5 mo. In 25 patients, cirrhosis developed during treatment; in 8 patients, cirrhosis eventuated after remission and cessation of therapy. The probability of developing histologic findings of cirrhosis was 59% if remission had not been achieved after 3 yr of continuous therapy. Longer requirements for treatment and deterioration during therapy characterized these patients. Once remission was achieved, the mean annual incidence of cirrhosis was only 2.6%. Patients who manifested evidence of cirrhosis in their biopsy specimens could not be distinguished by initial clinical, biochemical, or histologic findings. Ascites, encephalopathy, and esophageal varices developed infrequently; 5-yr survival after documentation of cirrhosis was 93%. We conclude that histologic features of cirrhosis develop commonly during therapy, especially if remission is not achieved quickly. After remission, cirrhosis develops infrequently. The development of histologic cirrhosis does not influence immediate morbidity and 5-yr life expectancy.
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PMID:Development and prognosis of histologic cirrhosis in corticosteroid-treated hepatitis B surface antigen-negative chronic active hepatitis. 648 94

Reactivation of chronic hepatitis B viral (HBV) infection, defined as conversion from the low level replicative phase (HBV-DNA negative) to the high level replicative phase (HBV-DNA positive) with continued hepatitis B surface antigen positivity, occurs after immunosuppressive therapy, chemotherapy, and rarely spontaneously. Development of hepatic failure after spontaneous reactivation of chronic HBV is rare. We report two patients with chronic HBV infection and stable cirrhosis in whom spontaneous reactivation lead to hepatic failure. In one, spontaneous reactivation lead to severe jaundice, ascites, and encephalopathy. Treatment with alpha-interferon resulted in transient improvement, but the patient ultimately died with hepatorenal syndrome. In the second, severe liver failure required orthotopic liver transplantation. Spontaneous reactivation is an unusual cause of hepatic decompensation in patients with chronic HBV infection and may lead to fulminant hepatic failure. The role of interferon or liver transplantation in the management of spontaneous reactivation remains to be clarified.
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PMID:Spontaneous reactivation of chronic hepatitis B infection leading to fulminant hepatic failure. Report of two cases and review of the literature. 822 85

One hundred and sixteen cirrhotic patients were prospectively studied over a ten year period. Hepatitis B surface antigen was positive in 70% of tested patients. The cirrhotic liver was mainly macronodular and primary hepatocellullar carcinoma was associated with 63% of the patients. Half of the patients were critically ill with high incidences of ascites, jaundice and encephalopathy. Cirrhotic patients had significantly lower body temperature onycholysis and hyperpigmented palmo-plantar macular areas. The mean survival time was three years from onset of the initial symptoms to death. Patients with concomitant liver cancer were usually dead within six months after onset of the illness. Gender did not substantially affect the course of the disease. The major causes of death were tumour development (63%), gastrointestinal bleeding (40%), haemoperitoneum (28%) and hepatic failure (25%).
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PMID:Natural history of liver cirrhosis in 116 Nigerians. 870 5

Five cases that were referred to the Division of Transplantation at NYU School of Medicine for consideration for liver transplantation were discussed among a panel of hepatitis B and liver transplant experts. Opinions were obtained on the management at every stage of treatment of patients with the following initial information: Case one: young Asian woman in stage IV hepatic coma; intubated; prothrombin time (PT): 30 s; serum glutamic oxaloacetic transaminase (SGOT): 8,000 IU; total bilirubin: 25 mg/dL; hepatitis B surface antigen (HBsAg) positive. Case two: 70-yr-old woman, native of Greece; decompensated cirrhosis with encephalopathy; Child-Pugh Class C; HBsAg positive; hepatitis B surface antibody (HBsAb) negative; hepatitis B e antigen (HBeAg) positive; hepatitis B e antibody (HBeAb) negative; hepatitis B virus (HBV) DNA titer: 10,000. Case three: Muscular detective working full-time; cirrhosis; Child Pugh Class B; ascites controlled with spironolactone and furosemide; PT: 19s; HBsAg positive; HBsAb negative; HBV DNA titer: 50,000; low platelet count. Case four: 45-yr-old baker; cirrhosis and resectable 4-cm hepatoma; Child-Pugh Class B; PT: 16 s; Blood type O; United Network for Organ Sharing (UNOS) 2B; HBV DNA titer: 3,000. Case five: 40-yr-old Indian man; 300 pounds with massive ascites; Child Pugh Class C; PT: 17 s; HBsAg positive; HBV DNA titer: 22,000; transplanted with intra-operative hypotension; tacrolimus; graft functioning; HBIg 10,000 IU intra-operative and around the clock during the first post-operative week; required huge doses of hepatitis B immune globulin (HBIg) to maintain adequate HBsAb level; daily loss of 5 6 L of ascites fluid; post-operative day 8: anuric, blood urea nitrogen (BUN) 127, creatinine 3, mental status changes.
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PMID:Case studies in orthotopic liver transplantation for hepatitis B: a panel discussion. 1096 64

Lamivudine is effective in inhibiting hepatitis B virus (HBV) replication, and its clinical use in patients with chronic hepatitis B is associated with improvements in serum aminotransferase levels and liver histopathologic characteristics. Few data are available on its use in patients with advanced liver disease. We report on the outcomes of 5 patients with hepatic decompensation caused by chronic hepatitis B treated long term with lamivudine. All patients were adult white men seropositive for hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) before therapy. All 5 patients had biopsy-proven cirrhosis with clinical and biochemical evidence of hepatic decompensation. Two patients had Child's class C cirrhosis; 2 patients, class B; and 1 patient, class A (although this patient had persistent portasystemic encephalopathy and developed variceal bleeding). HBV DNA became undetectable in all patients and remained so throughout the study. Both patients with Child's class C and 1 patient with class B cirrhosis had significant clinical improvement. Child-Pugh scores improved from 12 to 7 and 11 to 7 in the 2 patients with Child's class C cirrhosis, and the patient with class B cirrhosis had complete resolution of troublesome encephalopathy. Serum aminotransferase, albumin, and total bilirubin levels improved significantly in 3 of 5 patients. One patient with Child's class B cirrhosis underwent orthotopic liver transplantation at week 13 after dramatic increases in liver tests and clinical worsening. The patient subsequently cleared HBeAg and HBsAg from serum posttransplantation. In conclusion, prolonged therapy with lamivudine resulted in improved serum biochemical values and loss of HBV DNA in patients with decompensated cirrhosis. Clinical improvements, reflected in Child-Pugh classification and functional status, may also occur, particularly among those with Child's class C disease initially.
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PMID:Clinical improvement in patients with decompensated liver disease caused by hepatitis B after treatment with lamivudine. 1108 57


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