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Query: UMLS:C0019158 (
hepatitis
)
30,205
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The clinical profile of antituberculosis treatment (ATT)-induced hepatotoxicity is variable, and the reintroduction of ATT in patients who have developed such injury is controversial. We conducted a prospective study to determine the clinical profile in patients with ATT-induced hepatotoxicity and to test a predefined strategy of reintroduction of ATT. Seventy-two consecutive patients with clinical evidence of ATT-induced hepatotoxicity were included. Jaundice was the presenting symptom in 44 (61%) patients; prodromal symptoms were present in 28 (39%). Serious complications developed in 12 (16.6%) patients (fulminant hepatic failure in seven, subacute hepatic failure in four,
hepatic encephalopathy
in one). Nine patients (three males, six females) died from these complications. The mean duration of treatment before the onset of
hepatitis
was significantly longer in the group that died (53.22 +/- 36.22 days) than in the rest of the patients (31.07 +/- 30.30 days; p < 0.01). Malnutrition was present in 37 of the 72 patients. After resolution of drug induced
hepatitis
, reintroduction of isoniazid and rifampicin was possible in 41 of 44 patients. Thus, our results showed that ATT-induced
hepatitis
carried significant morbidity and mortality, that malnutrition was common in patients with ATT-related
hepatitis
, and that potentially hepatotoxic antituberculosis agents could be safely reintroduced after recovery from
hepatitis
.
...
PMID:Hepatotoxicity due to antituberculosis therapy. Clinical profile and reintroduction of therapy. 872 60
We describe nine asymptomatic chronic carriers of hepatitis B virus, four males and five females, with a mean age of forty-six years and all were Chinese, who developed exacerbation of
hepatitis
following chemotherapy for haematological malignancies. Seven patients had non-Hodgkin's lymphoma of whom three were treated with MACOP-B, two with BCEPP, one with PROMACE-CYTABOM and one with CHOP. Two patients had acute myeloid leukaemia and were treated with daunorubicin and cytosine arabinoside. Exacerbation of
hepatitis
occurred between one to four weeks following the last course of chemotherapy in eight patients. Two patients developed exacerbation of
hepatitis
when the dosage of prednisolone was reduced after they had ten weeks of high dose prednisolone. The outcome was fatal in six patients; all of whom developed
hepatic encephalopathy
. In four of these patients, alanine transaminase levels exceeded 1000 iu/l. Cytotoxic and immunosuppressive therapy permit enhanced viral replication. Withdrawal of the drugs results in partial restoration of immunocompetence and leads to rapid destruction of hepatocytes with consequent hepatic necrosis. Hence, patients who are hepatitis B virus carriers undergoing chemotherapy should be closely monitored. The fatal outcome of reactivation of chronic hepatitis B virus warrants prospective trials addressing preventive measures.
...
PMID:Exacerbation of hepatitis in hepatitis B carriers following chemotherapy for haematological malignancies. 889 18
Hepatotoxicity by antituberculous drugs is well known. Nonetheless, severe liver involvement is infrequent. Several series of fulminant
hepatitis
by antituberculous drugs have recently been reported with a much greater frequency than previously reported. The present study describes the authors' experience which, similar to other groups, has shown a marked increase with respect to previous experience. During 1994 5 patients with acute severe
hepatitis
associated to antituberculous drugs were admitted to the authors' unit. The mean age of the patients was 43 years (range: 25-62). Two patients were healthy HBsAg carriers, one undergoing enzymatic inducer treatment and was anti-HIV positive. Another patient presented compensated liver cirrhosis by HCV. The 5 cases received combined isoniazid and rifampicin and four had also received pyrazinamide. Four patients presented
hepatic encephalopathy
. Of these cases, three could not undergo emergency liver transplantation because of contraindications and died due to complications of acute severe liver failure. Another patient evolved favorably following emergency liver transplantation. The only patient who presented good evolution with conservative treatment and who did not present
hepatic encephalopathy
had discontinued isoniazid because of the finding of slight hypertransaminasemia during a routine analytical control. Several risk factors have been reported for the appearance of hepatotoxicity by antituberculous drugs. The factor of greatest clinical importance for the development of severe hepatotoxicity is probably continuation of the treatment once hepatic dysfunction has initiated. The important increase in cases of severe toxicity urges the need for strict analytical monitoring following initiation of treatment.
...
PMID:[Severe hepatotoxicity of tuberculostatic agents. Increase in the incidence]. 899 67
Evoked responses have not been studied in patients with acute severe
hepatitis
(ASH) with or without
hepatic encephalopathy
. This prospective study was undertaken to find out diagnostic as well as prognostic value of visual evoked responses (VER), and brain stem auditory evoked responses (BAER) in patients with ASH with or without encephalopathy. Visual evoked responses and BAER were studied in 20 patients (14 males and six females) with ASH. The patients were diagnosed as having severe
hepatitis
if acute hepatitis was associated with raised serum bilirubin and serum transaminases, and if they had a prothrombin time index of < 50%. After a detailed neuropsychiatric examination of each patient, the study sample was divided into two groups of 10 patients: ASH without encephalopathy (ASH-WOE), and ASH with encephalopathy (fulminant hepatic failure, FHF). The median P100 latencies of FHF patients were significantly increased compared with controls and patients in the ASH-WOE group. Abnormal P100 latencies, exceeding 95th percentile values of the controls, were present in one patient in the ASH-WOE group and six patients in the FHF group. The median interpeak latencies I-III, III-V and I-V were significantly prolonged in the FHF group. Interpeak latencies III-V were also increased significantly in patients in the ASH-WOE group. While abnormal BAER were seen frequently in both groups, VER abnormalities were largely confined to patients in the FHF group. In the FHF group, six out of 10 patients survived and exhibited clinical improvement in the status of
hepatic encephalopathy
. Evoked responses were repeated after 2-3 weeks of recovery in these patients and VER abnormalities showed a tendency to normalize, thereby suggesting a prognostic implication. The incidence of abnormal VER in
hepatic encephalopathy
complicating ASH far exceeded that of abnormal BAER. Markedly prolonged P100 latencies in FHF patients indicate poor prognosis.
...
PMID:Visual and auditory evoked responses in acute severe hepatitis. 925 51
The aim of this study was to select prognostic factors from information available on admission in order to list patients for liver transplantation before the onset of
hepatic encephalopathy
in patients with fatal
hepatitis
type non-A, non-B. Information regarding patient profile and biochemical data obtained on admission was analyzed by multiple stepwise logistic regression, and independent prognostic factors related to death were selected. Four parameters were selected as independent prognostic factors. Patient age (over 50 years), serum total bilirubin level (over 10 mg/dl), peripheral leukocyte count, and prothrombin time were independently related to death. Positive predictive value, negative predictive value, and predictive accuracy were 0.86, 0.79, and 0.84, respectively. Our model is able to predict a patient's fatal outcome much earlier than other currently used models. It will be helpful for early referral to a transplant center.
...
PMID:Selection of prognostic factors of acute hepatitis type non-A, non-B for patient listing for liver transplantation. 927 6
Four cases of typhoid fever complicated by both acute oliguric renal failure and
hepatitis
are presented. Two patients had type II
hepatitis
according to criteria proposed by Khosla et al. (30) with hepatomegaly, hyperbilirubinaemia and markedly elevated asparate transaminase (AST); the others had type III
hepatitis
, characterized clinically and biochemically by profound jaundice, hepatomegaly,
hepatic encephalopathy
(one case only), hyperbilirubinemia and markedly elevated serum AST. Renal biopsy was not performed in any of our patients. However, a combination of proteinuria and abnormal urinary sediments containing red cell casts and granular casts, as noted in these patients, is considered highly suggestive of glomerulonephritis. Although isolated renal failure and
hepatitis
with hepatomegaly and deranged liver enzyme values have been reported previously in typhoid fever, their occurrence simultaneously in the same patient in distinctly rare, having been reported only twice in the English language literature.
...
PMID:Typhoid fever complicated by acute renal failure and hepatitis: case reports and review. 964 38
Typhoid fever is often associated with abnormal liver biochemical tests, but severe hepatic involvement with a clinical feature of acute hepatitis is a rare complication. There have been more than 150 cases of salmonella
hepatitis
reported from both developed and developing countries. The documented incidence varies widely from less than 1% to 26% patients with enteric fever. The possible associated factors for development of salmonella
hepatitis
are virulence of the organisms, delayed treatment and poor general health of the patients. The pathogenesis of severe hepatic involvement in salmonella infection may be multifactorial and includes endotoxin, local inflammatory and/or host immune reactions. Clinical jaundice in salmonella
hepatitis
usually occurs within the first 2 weeks of the febrile illness. Hepatomegaly and moderate elevation of transaminase levels are common findings. Extreme hepatic dysfunction with
hepatic encephalopathy
is a rare coexisting complication in salmonella
hepatitis
. A positive culture for salmonella from blood or stool is essential to differentiate salmonella
hepatitis
from other causes of acute hepatitis. Hepatic pathology is characterized by the presence of typhoid nodules with marked hyperplasia of reticuloendothelial cells. The prognosis is usually good as salmonella
hepatitis
responds well to a specific antibiotic therapy and juandice resolves with clinical improvement. The clinical course can be severe with a mortality rate as high as 20%, particularly with delayed treatment or in patients with other complications of salmonella infection. As enteric fever is a common infection, the recognition of salmonella
hepatitis
is of clinical importance.
...
PMID:Salmonella hepatitis. 971 30
Liver failure with
hepatic encephalopathy
during an acute viral hepatitis carries a very high mortality. Liver transplantation is the usual treatment, but for poor candidates for transplantation only supportive therapy is available. Two patients with HIV infection developed an acute B
hepatitis
with liver insufficiency and
hepatic encephalopathy
. After an alprostadil infusion was begun they improved quickly and made a full recovery. This drug merits further investigation.
...
PMID:Can alprostadil improve liver failure in HIV-infected patients with severe acute viral hepatitis? 973 93
Although exacerbations of previously quiescent HBV infection, associated with chemotherapy, have been attributed to enhanced immunological responses to hepatocytes harboring reactivated HBV, the recommended treatment, prednisolone, is often unsuccessful. A young HBsAg-positive, anti-HBe-positive carrier, who received chemotherapy for choriocarcinoma, developed icteric
hepatitis
. The serum HBV DNA level was 34,000 x 10(6) genomic equivalents per milliliter serum. Treatment with prednisolone alone did not prevent progression to overt hepatic failure. By three days after initiating lamivudine therapy, however, there was reversal of stage III
hepatic encephalopathy
. With further lamivudine treatment, substantial further improvement in hepatocellular function occurred and HBV-DNA levels became undetectable. When an immunocompromised patient develops an exacerbation of hepatitis B associated with high HBV DNA levels, treatment with prednisolone seems inappropriate, as hepatocytotoxic HBV replication may be stimulated further. In this situation inhibition of HBV replication, eg, by administering lamivudine, may be life-saving.
...
PMID:Recovery from life-threatening, corticosteroid-unresponsive, chemotherapy-related reactivation of hepatitis B associated with lamivudine therapy. 979 Apr 64
Childhood liver disorders have, in general, mode of presentations which are distinct from that in adult population. It is due to varying etiology and natural history of the liver diseases in childhood. Chronic hepatitis B and C can be managed with alpha interferon. Remission rates in children have been reported to be between 20-58%. Recently available lamuvidine has also been used in combination with interferon therapy. Oral chelation therapy and liver transplantation have radically affected the outcome of patients with Wilson's disease. Corticosteroids and immunosuppressive therapy are effective in reducing both morbidity and mortality due to auto-immune
hepatitis
. Offending carbohydrates are eliminated from the diet of patients with galactosemia and hereditary fructose intolerance. The most important and often neglected component of management of chronic liver diseases in childhood are nutritional management and prompt interventions for ascites, spontaneous bacterial peritonitis, portal hypertension and
hepatic encephalopathy
. With definitive etiological and histological assessment and institution of specific as well as supportive therapy, children with chronic liver disease can have a prolonged survival with improved quality of life. Several of them can potentially receive the liver transplant as and when it becomes available.
...
PMID:Management of chronic liver disease. 1113 57
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