Correction of vitamin E deficiency in children with chronic cholestasis. II. Effect on gastrointestinal and hepatic function

Ronald J. Sokol, James E. Heubi, Catherine McGraw, William F. Balistreri – 1 November 1986 – Although secondary vitamin E deficiency causes a reversible neurologic disorder in children with chronic cholestasis, the effect of this deficiency state on other organ systems is unknown. We studied the effects of vitamin E therapy on selected gastrointestinal and hepatic functions in five children with chronic cholestasis and well‐documented biochemical and neurologic evidence of vitamin E deficiency.

Epidemiologic aspects of Santa Marta hepatitis over a 40‐year period

Bernardo Buitrago, Stephen C. Hadler, Hans Popper, Swan N. Thung, Michael A. Gerber, Robert H. Purcell, James E. Maynard – 1 November 1986 – “Santa Marta” hepatitis has been recognized as an unusual type of severe hepatitis occurring in northern Colombia since 1930. Liver specimens from a historic viscerotomy series, used by Gast‐Galvis to identify cases and describe epidemiologic features of this disease, were available for review and histopathologic staining for δ‐virus.

A histological study of hepatitis delta virus liver disease

Giorgio Verme, Pietro Amoroso, Gennaro Lettieri, Paola Pierri, Ezio David, Fausto Sessa, Roberto Rizzi, Ferruccio Bonino, Serafino Recchia, Mario Rizzetto – 1 November 1986 – The histopathology of hepatitis delta virus disease was studied in carriers of HBsAg with chronic hepatitis delta antigen‐positive hepatitis and in serial biopsies of patients with acute hepatitis delta virus hepatitis that progressed to chronicity.

Cell‐mediated cytotoxicity in hepatitis A virus infection

Angelika Vallbracht, Peter Gabriel, Katharina Maier, Franz Hartmann, Hans Jörg Steinhardt, Claudia Müller, Alexis Wolf, Klaus Herbert Manncke, Bertram Flehmig – 1 November 1986 – We studied cell‐mediated cytotoxicity to hepatitis A virus‐infected cells in seven patients with acute type A hepatitis and two controls. Skin fibroblast cultures obtained from the skin biopsies of seven patients after acute hepatitis A virus infection and from two persons without history of current or past hepatitis A virus infection were inoculated with hepatitis A virus.

Demonstration of pre‐S polypeptides of hepatitis B virus in infected livers

Swan N. Thung, Michael A. Gerber, Efthimios J. Kasambalides, Bal K. Gilja, William Keh, Wolfram H. Gerlich – 1 November 1986 – The large (pre‐S1), middle (pre‐S2) and major (P24) polypeptides of HBsAg have been defined in detail, but their role in hepatitis B virus infection is not known. Therefore, we studied the expression of pre‐S1, pre‐S2 and P24 in the liver of 15 patients with acute or chronic hepatitis B virus infection using monoclonal and polyclonal antibodies in a double staining immunofluorescence method.

Liver and biliary disease: Pathophysiology, diagnosis, management. Edited by Ralph Wright, G. H. Millward‐Sadler, K. G. M. M. Alberti and Stephen Karran, second edition. 1608 pp. London/Philadelphia: Ballière Tindall/W. B. Saunders Company, 1985. $125.00

Medium‐chain and long‐chain acyl CoA dehydrogenase deficiency: Clinical, pathologic and ultrastructural differentiation from Reye's syndrome

William R. Treem, Camillus A. Witzleben, David A. Piccoli, Charles A. Stanley, Daniel E. Hale, Paul M. Coates, John B. Watkins – 1 November 1986 – The clinical and pathologic findings in 12 patients with medium‐chain acyl CoA dehydrogenase deficiency and three patients with long‐chain acyl CoA dehydrogenase deficiency are summarized. Although these inborn errors of intramitochondrial β‐oxidation of fatty acids present with similar findings to Reye's syndrome, there are clinical, laboratory and hepatic histologic differences.

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