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Biomedical subjects

J Shorey

Publications and source records attributed to J Shorey.

8 recordsLinked to original sources
PubMed1979

Nodular regenerative hyperplasia of the liver in a case of myelofibrosis with extramedullary hematopoiesis and secondary portal venous hypertension.

Nodular regenerative hyperplasia of the liver was identified at autopsy in a patient with myelofibrosis with extramedulary hematopoiesis, an association not previously reported. Portal venous hypertension, documented during the patient's terminal hospitalization, was ascribed, in part, to a high rate of blood flow through the enlarged spleen. Possible mechanisms accounting for the development of nodular regenerative hyperplasia of the liver, and evidence provided by this case pertinent to these mechanisms, are discussed.

Autopsy↗
PubMed1979

Etiology of liver disease in renal-transplant patients.

The etiology of 72 episodes of liver disease that developed in 62 of 162 renal-transplant recipients was evaluated. Infection with hepatitis B virus was a minor problem, and none of our patients had evidence of infection with hepatitis A. Cytomegalovirus infection was ubiquitous in the population and probably accounted for many episodes of acute liver disease. This agent's role in causing chronic hepatitis is less secure. Infections with other viruses including Epstein-Barr virus, adenovirus, and the herpes viruses were only rarely associated with hepatic disease. Azathioprine was responsible for some episodes of acute cholestasis but could not be incriminated as a direct cause of chronic disease. A cause could be identified for the majority of episodes of acute hepatic dysfunction, but the cause of most of the chronic hepatitis remains undetermined. It is likely that infection with non-A, non-B hepatitis virus accounts for much of this serious, often fatal, complication of renal transplantation.

Antibodies, Viral↗
PubMed1977

Hepatitis and pregnancy.

The maternal and fetal outcomes of 50 pregnancies complicated by acute viral hepatitis were examined. Twenty (40%) cases were due to type B hepatitis virus. The clinical course of the maternal hepatitis was unaffected by the pregnant state. Maternal hepatitis (type B or nontype B) had no effect on the incidence of congenital malformations, stillbirths, abortions, or intrauterine malnutrition; it did increase the incidence of prematurity (type B 31.6%; nontype B 25%; overall 27.6%) over that seen in the general delivery population (10 to 11%). Eight mothers acquired acute type B hepatitis during the third trimester; two of their infants (25%) were found to be chronic asymptomatic carriers of hepatitis B surface antigen and to have mild, persistent elevations of SGOT for up to 45 months.

Carrier State↗
PubMed1976

A new hepatitis B virus surface antigen.

A new determinant of hepatitis B surface antigen (HBs Ag), g, which is distinct from the previously identified determinants a, d, y, w, and r, was studied. This new antigen tended to be associated with the d antigen; it was found in 97% of ad specimens and in 15% of ay specimens. With few exceptions, the atypical subtypes, adg- and ayg+, were identified in sera from blood donors, but not in sera from patients with acute viral hepatitis; this finding possibly reflects a reduced tendency of these viral strains to evoke a host immune response. The ability to identify g represents a refinement of HBs Ag serotyping that may be of value in the study of the epidemiology of hepatitis B virus.

Cell Membrane↗