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Dive into the research topics where John A. Payne is active.

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Featured researches published by John A. Payne.


The New England Journal of Medicine | 1990

A Randomized, Controlled Trial of Interferon Alfa-2b Alone and after Prednisone Withdrawal for the Treatment of Chronic Hepatitis B

Robert P. Perrillo; Eugene R. Schiff; Gary L. Davis; Henry C. Bodenheimer; Karen L. Lindsay; John A. Payne; Jules L. Dienstag; Christopher B. O'Brien; Carlo H. Tamburro; Ira M. Jacobson; Sampliner Re; David Feit; Jay H. Lefkowitch; Mary C. Kuhns; Carlton Meschievitz; Bharati Sanghvi; Janice K. Albrecht; Alexandra L. Gibas

Abstract Background and Methods. Chronic hepatitis B is a common and often progressive liver disorder for which there is no accepted therapy. To assess the efficacy of treatment with interferon, we randomly assigned patients with chronic hepatitis B to one of the following regimens: prednisone for 6 weeks followed by 5 million units of recombinant interferon alfa-2b daily for 16 weeks; placebo followed by 5 million units of interferon daily for 16 weeks; placebo followed by 1 million units of interferon daily for 16 weeks; or observation with no treatment. Results. Hepatitis B e antigen and hepatitis B viral DNA disappeared from serum significantly more often in the patients given prednisone plus interferon (16 of 44 patients, or 36 percent) or 5 million units of interferon alone (15 of 41; 37 percent) than in the untreated controls (3 of 43; 7 percent; P<0.001); the difference between those given 1 million units of interferon (7 of 41; 17 percent) and the controls was not significant. The strongest indep...


Gastroenterology | 1993

Pathological diagnosis of chronic hepatitis C: A multicenter comparative study with chronic hepatitis B

Jay H. Lefkowitch; Eugene R. Schiff; Gary L. Davis; Robert P. Perrillo; Karen L. Lindsay; Henry C. Bodenheimer; Luis A. Balart; Terryl J. Ortego; John A. Payne; Jules L. Dienstag; Alexandra L. Gibas; Ira M. Jacobson; Carlo H. Tamburro; William D. Carey; Christopher B. O'Brien; Sampliner Re; David H. Van Thiel; David Feit; Janice K. Albrecht; Carlton Meschievitz; Bharati Sanghvi; Roger D. Vaughan

BACKGROUND Hepatic histological responses described in hepatitis C virus (HCV) infection include bile duct damage, lymphoid follicles and/or aggregates in portal tracts, large- and small-droplet fat, Mallory body-like material in hepatocytes, liver cell dysplasia and multinucleation, and activation of sinusoidal inflammatory cells. The specificity of these lesions for HCV infection is uncertain. METHODS In two multicenter trials of recombinant interferon alfa therapy for chronic hepatitis C and B, the frequency of these eight lesions in pretherapy and posttherapy liver biopsy specimens was examined to determine the set of features, if any, that distinguishes HCV from hepatitis B virus (HBV) infection. The lesions were scored in 317 HCV biopsy specimens and 299 HBV specimens. RESULTS Stepwise logistic regression determined a set of three features more likely to be seen in HCV than in HBV infection: bile duct damage [odds ratio (OR), 4.7; 95% confidence interval (Cl), 1.8-12.3], lymphoid follicles and/or aggregates (OR, 2.4; 95% Cl, 1.2-4.7), and large-droplet fat (OR, 2.4; 95% Cl, 1.4-4.1). A fourth lesion, Mallory body-like material, was seen only in HCV biopsy specimens (OR, 71.6; 95% Cl, 4.4-996.1). CONCLUSIONS These four histological lesions are useful pathological parameters in the diagnosis of liver disease caused by HCV.


Journal of Clinical Gastroenterology | 1985

Enhanced toxicity of acetaminophen in alcoholics: report of three cases

Michael H. Leist; Lawrence E. Gluskin; John A. Payne

Severe intoxication from excessive acetaminophen without suicidal intent occurred in three patients, all alcohol abusers, one with evidence of underlying cirrhosis. Apparently, acetaminophen toxicity may be enhanced by alcohol.


Gastroenterology | 1984

Congenital Hepatic Fibrosis and Asymptomatic Familial Adult-Type Polycystic Kidney Disease in a 19-Year-Old Woman

Henry D. Tazelaar; John A. Payne; Nargis S. Patel

Congenital hepatic fibrosis has been associated with a variety of renal malformations, but rarely adult-type polycystic kidneys. The case of a 19-yr-old woman with congenital hepatic fibrosis associated with asymptomatic familial adult-type (autosomal dominant) polycystic kidney disease is described. A literature review revealed seven other reports of this association. Our patient differs because the association between congenital hepatic fibrosis and adult-type polycystic kidney disease is clear, and because her asymptomatic kidney disease accords with the later onset of symptomatic polycystic kidney disease in her family.


The American Journal of the Medical Sciences | 1982

Case Report Amanita Virosa Acute Hepatic Necrosis: Treatment with Thioctic Acid

Richard Plotzker; Donald M. Jensen; John A. Payne

A 55-year-old woman suffered acute hepatic necorsis following ingestion of Amanita virosa mushrooms. Successful treatment included the use of thioctic acid. A discussion of Amanita poisoning an the therapeutic modalities available is presented.


Journal of Clinical Gastroenterology | 1985

Hepatocellular carcinoma in a patient with precirrhotic primary biliary cirrhosis

Lawrence E. Gluskin; Perry Guariglia; John A. Payne; Barbara F. Banner; Peter Economou

Hepatocellular carcinoma is generally associated with long-standing chronic liver disease of diverse etiology, most commonly HBsAg-positive chronic active hepatitis, hemochromatosis, or alcoholic liver disease. Patients with primary biliary cirrhosis have only rarely developed a subsequent hepatocellular carcinoma. We report such a patient, a 77-year-old woman with an early, precirrhotic stage of primary biliary cirrhosis who developed a hepatoma.


Journal of Clinical Gastroenterology | 1982

Acute hepatitis B: a further serological characterization.

John A. Payne; Donald M. Jensen; Rose G. Codini; Isa K. Mushahwar; David A. Peterson

Sequential determinations of HBsAg, anti-HBs, HBeAg, anti-HBe, and anti-HBc in thirteen patients with acute hepatitis B have shown that the viral antigens and their respective antibodies may be simultaneously absent (9/13 with serologic window) or present (6/13 with presumed immune complex formation) in the early convalescent period. These data emphasize the usefulness of sequential determinations of antigen and antibody in the unequivocal assessment of etiology and potential for chronicity and contagion) in resolving acute hepatitis B. The transient appearance of an antibody to liver specific protein (anti-LSP) in eleven out of thirteen patients was documented; we found no correlation of anti-LSP titers with viral antigens or host antibody titers.


Journal of Intensive Care Medicine | 1986

Causes and Complications of Fulminant Hepatic Failure

John A. Payne

Fulminant hepatic failure can be caused by a number of viral, metabolic, toxic, and vascular factors. Identification of the cause can lead to specific intervention in some conditions. Care of the patient with fulminant hepatic failure resulting from diverse causes requires intensive monitoring to prevent death from a variety of complications. Cerebral edema, gastrointestinal hemorrhage, sepsis, coagulopathy, and hypoglycemia are potentially catastrophic complications that must be anticipated and preempted whenever possible. Liver transplantation has emerged as a reasonable therapeutic option; survival rates in small series are approximately 50%.


Journal of Clinical Gastroenterology | 1983

Primary pulmonary hypertension after portocaval shunt

Allen C. Bernthal; Carl E. Eybel; John A. Payne


Gastroenterology | 1979

Hemorrhage from esophageal varices after placement of the LeVeen shunt.

William Markey; John A. Payne; Albert Straus

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Gary L. Davis

Baylor University Medical Center

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Ira M. Jacobson

Beth Israel Medical Center

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Karen L. Lindsay

University of Southern California

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Robert P. Perrillo

Baylor University Medical Center

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