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Biomedical subjects

A G Redeker

Publications and source records attributed to A G Redeker.

At least 37 records · Page 2Linked to original sources

Treatment of fulminant hepatic failure with insulin and glucagon. A randomized, controlled trial.

Insulin and glucagon are among the therapeutic modalities that have been investigated in the treatment of fulminant hepatic failure (FHF). We have completed a randomized, controlled trial of insulin and glucagon in 38 patients with FHF from either viral or toxin exposure. The control and treatment groups consisted of 21 and 17 patients, respectively, and did not differ significantly in etiology or admission laboratory values. Mortality was not significantly different between control and treatment groups and was 67% and 82%, respectively. Time from randomization to death or discharge was not significantly different between the two groups. Peak levels of alpha-fetoprotein were statistically higher in survivors than in nonsurvivors (P less than 0.01). We conclude that even though a type-2 error may exist, the combination of insulin and glucagon is not useful in the treatment of FHF.

Adult↗

Hepatitis C virus antibodies in acute icteric and chronic non-A, non-B hepatitis.

Hepatitis C virus antibodies were measured in 213 patients who had acute (n = 122) and chronic (n = 91) non-A, non-B hepatitis. In acute infection, anti-hepatitis C virus was detected in 61% of IV drug abusers, in 33% of patients with transfusion-associated hepatitis, and in 22% of patients with sporadic infections (P less than 0.0005, drug abusers vs. sporadic). Mean time to seroconversion was 11.6 weeks (range, 1-80 weeks). Anti-hepatitis C virus was more common in chronic infection (P less than 0.001) and was more often detected in IV drug users (89%; P less than 0.0001) and after transfusion (71%; P less than 0.005) compared with chronic sporadic infection (27%). Antibody persisted for up to 8 years. Six chronic case patients (8.3%) later lost antibody (mean, 24 months; range, 12-48 months).

Acute Disease↗

Human immunodeficiency virus infection does not alter serum transaminases and hepatitis B virus (HBV) DNA in homosexual patients with chronic HBV infection.

The influence of human immunodeficiency virus (HIV) infection on the clinical course of chronic hepatitis B virus (HBV) infection is controversial. We followed a cohort of 64 homosexual men with persistent HBs antigenemia for a median of 24 months in the hepatitis clinic of a large urban public hospital. We divided the patients into three groups according to their immune status. Group 1 (n = 13) consisted of HIV-seropositive men with evidence of immunosuppression; group 2 (n = 17), HIV-positive patients without evidence of immunosuppression; and group 3 (n = 34), HIV-negative patients. We followed serum ALT and HBV DNA determinations. There was no difference in the demographic characteristics of the three groups. Group 1 had significantly lower levels of circulating T4 lymphocytes. We found no differences in the number and severity of episodes of HBV reactivation, serum ALT levels, or HBV DNA scores among the three groups. In each group, the percentage of patients with circulating HBV DNA was the same. We conclude that HIV infection apparently does not influence the markers of liver inflammation or HBV replication in homosexual men.

Adult↗

Acute delta hepatitis: serological diagnosis with particular reference to hepatitis delta virus RNA.

To evaluate serologic diagnosis of hepatitis delta virus, we tested HDV RNA in stored sera from 48 patients with acute delta hepatitis who were identified with anti-HD antibodies. Initial sera were positive for HDV RNA in 27 of 48 (56%) patients. In comparison, isolated IgM anti-HD was present in 18 (38%) patients, although IgM and IgG anti-HD were present concurrently in 16 (33%) additional patients. Overall, either HDV RNA or IgM anti-HD was present in 69% of the initial sera. The HDV infection was self-limiting in all except two patients who died of fulminant hepatitis and nine others in whom chronic delta hepatitis ensued. Patterns of HDV seropositivity during progression to chronicity induced variable persistence, disappearance or recrudescence of either HDV RNA or IgM and IgG anti-HD. Results of HDV RNA and IgM anti-HD tests were concordant in only 40-50% of instances. Our results indicate that serological testing for HDV RNA is direct and will demonstrate HDV replication in a large number of cases with acute delta hepatitis. Testing for IgM anti-HD could provide supplemental evidence for HDV infection. Sequential testing for these markers will facilitate assessment of the outcome of acute HDV infection.

Acute Disease↗

Interactions of HDV, HBV and HIV in chronic B and D infections and in reactivation of chronic D infection.

From this study, we can conclude that there is significant influence of HIV infection on the clinical course of chronic HDV as follows: In these patients, there is simultaneous replication of both HBV and HDV and the suppression of HBV by HDV is modified. There is decreased antibody response to HDV, however, the degree of liver injury is not altered. Although these patients tend to have "reactivation episodes" as frequently as the HIV negative group, no correlation of serum ALT to HDV-RNA could be found. The possibility of these episodes resulting from injury due to other viruses such as non-A, non-B cannot be excluded.

Alanine Transaminase↗

Spontaneous reactivation in chronic hepatitis B: patterns and natural history.

We identified spontaneous reactivation of hepatitis B virus (HBV) retrospectively by utilizing serum alanine aminotransferase and HBV DNA in 19 men (79% homosexual), with an estimated annual incidence of 7.3%. In 11 patients, spontaneous reactivation occurred as a single episode and in eight patients, reactivation was recurrent, with two to five episodes each. The mean serum alanine aminotransferase level was elevated over 10-fold at the peak of reactivation. Serum anti-HBc IgM was detected during 73% of the reactivation episodes. Actuarial analysis revealed that reactivation was long lasting with 45% and nearly 20% of episodes continued after 6 and 24 months, respectively. The course of 24 chronic HBV carriers with a negative serum HBV DNA test and normal alanine aminotransferase levels at initial appearance was unremarkable. We could not identify clinical features predictive of reactivation or its resolution. Severe reactivation hepatitis occurred in three patients (10%), with two deaths (6%). None of the patients lost HBsAg. Spontaneous reactivation in chronic hepatitis B can appear variably, persist long term, recur, and be fatal. Therefore, accurate classification of chronic HBV infection requires prolonged observation, and spontaneous reactivation should be considered a variable in therapeutic trials for chronic hepatitis B.

Adult↗

An assay for circulating antibodies to a major etiologic virus of human non-A, non-B hepatitis.

A specific assay has been developed for a blood-borne non-A, non-B hepatitis (NANBH) virus in which a polypeptide synthesized in recombinant yeast clones of the hepatitis C virus (HCV) is used to capture circulating viral antibodies. HCV antibodies were detected in six of seven human sera that were shown previously to transmit NANBH to chimpanzees. Assays of ten blood transfusions in the United States that resulted in chronic NANBH revealed that there was at least one positive blood donor in nine of these cases and that all ten recipients seroconverted during their illnesses. About 80 percent of chronic, post-transfusion NANBH (PT-NANBH) patients from Italy and Japan had circulating HCV antibody; a much lower frequency (15 percent) was observed in acute, resolving infections. In addition, 58 percent of NANBH patients from the United States with no identifiable source of parenteral exposure to the virus were also positive for HCV antibody. These data indicate that HCV is a major cause of NANBH throughout the world.

Antibodies, Viral↗

Correlation of IgM anti-hepatitis D virus (HDV) to HDV RNA in sera of chronic HDV.

One hundred forty-four serum samples from 52 patients with chronic hepatitis D virus infection were analyzed for hepatitis D virus RNA by dot-blot hybridization using hepatitis D virus cDNA probe labeled with 32P. The results were correlated with the presence of serum IgM anti-hepatitis D virus and hepatitis D antigen in liver biopsy specimens when available. Although there was a trend of positive correlation between serum hepatitis D virus RNA and IgM anti-hepatitis D virus, no statistical significance could be found. In the serum samples with hepatitis D virus RNA, 32% were found to be negative for IgM anti-hepatitis D virus. Therefore, in chronic hepatitis D virus, absence of IgM anti-hepatitis D virus does not rule out active viral infection, as suggested by previous studies. There was a strong correlation between serum hepatitis D virus RNA and hepatic hepatitis D virus antigen. These data indicate that detection of hepatitis D virus RNA in serum samples is a reliable noninvasive marker of active viral infection.

Antibodies, Viral↗

Spontaneous rupture of nonparasitic cyst of the liver.

A case of spontaneous rupture of a nonparasitic liver cyst, documented by serial computed tomography scans, is reported. The patient was closely followed clinically after the rupture of the cyst and was treated conservatively, without surgical intervention. No peritonitis developed. This unusual complication of nonparasitic simple liver cysts may not always require surgery.

Cysts↗

Study of reactivation of chronic hepatitis delta infection.

Five patients with chronic hepatitis delta virus (HDV) infection suffered spontaneous episodes of liver enzyme elevation on a background of otherwise biochemically stable liver disease. In all five patients these episodes were accompanied by a rise in serum levels of anti-HDV IgM, HDV antigen and HDV RNA. These episodes of increased HDV replication accompanied by biochemical evidence of liver injury are reminiscent of reactivation in chronic hepatitis B. Surges of increased HDV replication may be important in the progression of liver disease in chronic HDV infection.

Adult↗

Twenty isoniazid-associated deaths in one state.

Twenty deaths from isoniazid-associated hepatitis are known to have occurred in California over a 14-yr period in persons ranging in age from 5 to 73 yr. Because no comprehensive survey was carried out, more such deaths probably occurred. With one exception, the patients were not seen or contacted monthly throughout the course of treatment. However, in 16 patients where the information was known, eight were seen by a member of the group giving the isoniazid (INH) within 30 days prior to the patients presenting with hepatitis. In 12 of 17 cases, symptoms were present for 7 days or more before the patient presented for medical care. In at least 35% of cases where the information was known, a management error occurred, usually failing to immediately stop INH when the patient presented with symptoms. The duration of treatment before hepatitis developed varied from 9 to 53 wk. Four of the 20 patients had cholelithiasis or a history of cholelithiasis. With one possible exception, no excessive alcohol use was noted. Concomitant acetaminophen, barbiturate, and tetracycline use occurred in several cases. There were no deaths in Orientals. Sixteen of the 20 deaths occurred in women who had started to receive INH between the ages of 15 and 55. Four of these women began receiving INH during pregnancy and continued it postpartum. Eight deaths occurred in persons starting INH before 35 yr of age. The continued occurrence of INH-associated deaths suggests that indications and precautions for INH preventive treatment be carefully reconsidered.

Adolescent↗

Permanent HBsAg clearance in chronic hepatitis B viral infection following acute delta superinfection.

Three patients are described with chronic hepatitis B virus infection for three to six years before hepatitis delta virus superinfection occurred. Liver biopsy performed in two patients prior to their delta illness revealed chronic persistent hepatitis and chronic active hepatitis, respectively. Within one to seven months of the acute delta event, all three patients lost their circulating hepatitis B surface antigen. Subsequently, delta antibody also cleared. Clinical well-being and normal transaminases were documented over 10-44 months of follow-up. Although most cases of delta infection in chronic hepatitis B result in severe or progressive disease, a small number of patients may develop clearance of the HBsAg with clearance of both B and delta infections.

Adult↗

Markers of viral replication in patients with chronic hepatitis B virus infection.

Serum samples from 56 patients with biopsy-proven chronic B viral hepatitis without superimposed delta hepatitis were analyzed for the various markers of viral replication, including serum hepatitis B e Ag (HBeAg), hepatitis B virus deoxyribonucleic acid (HBV-DNA), and hepatitis B core antigen (HBcAg) in the liver tissues. Twenty-seven patients had persistent viral hepatitis (PH) and 29 patients had chronic active hepatitis (CAH) with or without cirrhosis. HBV-DNA was identified in the sera of 81% of patients with PH and 60% of patients with CAH. Significantly higher levels of HBV-DNA were found in patients with PH than in those with CAH. Both HBeAg in serum and HBcAg in liver correlated positively with serum HBV-DNA. Nine patients had serum HBV-DNA in the absence of HBeAg (four had anti-HBe), and seven of these nine patients had stainable HBcAg in the liver (two did not have staining). None of these patients had hepatic HBcAg in the absence of serum HBV-DNA. When these patients were stratified according to their epidemiologic background, serum HBV-DNA was present in a significantly higher number of male homosexuals than in any other groups. This was unrelated to their status of human immunodeficiency viral serology.

Chronic Disease↗

Experience with human immunodeficiency virus infection in patients with hepatitis B virus and hepatitis delta virus infections in Los Angeles, 1977-1985.

Stored serum specimens from 723 patients with acute hepatitis B and 228 patients with chronic hepatitis B seen between 1977 and 1985 in the Hepatitis Clinic of the Los Angeles County-University of Southern California Medical Center, Los Angeles, CA, were tested for antibody to human immunodeficiency virus (anti-HIV). Risk factors were ordered hierarchically; cases with multiple risk factors were tabulated only in the risk group listed first on the clinic records. Anti-HIV was first detected in 1979, and by 1983 was found in about half of all homosexual men with chronic hepatitis B. The prevalence was significantly lower in patients with acute hepatitis B than in patients with chronic hepatitis B, and in nonhomosexual subjects compared with homosexual subjects. By 1985, 30 per cent of intravenous drug users with chronic hepatitis B were anti-HIV-positive. The highest annual seroconversion rate for anti-HIV, 21 per cent, was found in homosexual men in 1983. A significant association existed between anti-HIV positivity and hepatitis delta virus infection in homosexual men but not in drug abusers. This study provides data on the natural history of the human immunodeficiency virus epidemic in Los Angeles. Further study on the interaction of these different viruses is warranted.

Acute Disease↗