Antibody to hepatitis C virus among cardiac surgery patients, homosexual men, and intravenous drug users in Baltimore, Maryland.

In order to define the risk factors for infection with hepatitis C virus, the authors determined the prevalence and incidence of antibodies to hepatitis C in three cohorts in Baltimore, Maryland, enrolled in prospective studies of human immunodeficiency virus (HIV-1) infection. Among 500 multi-transfused patients who underwent cardiac surgery in 1985 and 1986, 12 (2.4%) were hepatitis C seropositive before surgery while 19 (3.9%) developed antibodies in the 8-12 months after surgery. The seroprevalence of hepatitis C virus among 225 intravenous drug users followed since 1988 was 85%, which did not vary by HIV-1 status. Longer duration of intravenous drug use was significantly associated with hepatitis C seropositivity. Among 926 homosexual/bisexual men followed since 1984, 15 (1.6%) were hepatitis C seropositive; only intravenous drug use and a history of hepatitis A were marginally associated with hepatitis C in this population. No association was found between hepatitis C virus and HIV-1 or sexual behavior variables in this population. These data suggest that hepatitis C is readily transmitted by blood exposure, but is transmitted inefficiently by sexual means.

Mediators, initiating the inflammatory response, released in organ culture by full-thickness human skin explants exposed to the irritant, sulfur mustard.

Mediators released from injured human skin that initiate the inflammatory response have not been adequately identified. Organ culture of full-thickness skin explants enables us to do so, because injury to the skin can be made in vitro, eliminating the rapid leakage of serum and infiltration of leukocytes that occur in vivo. In our studies, the military vesicant sulfur mustard (SM) (10 microliters of a 0.01 to 1.0% dilution) was topically applied to injure the epidermis of the explant. Then, the explants were cultured in small Petri dishes, usually for 18 h at 36 degrees C, and the organ-culture fluids were assayed for various inflammatory mediators. We found that the culture fluids from SM-exposed and control explants contained similar amounts of angiotensin-converting enzyme, trypsin-like and chymotrypsin-like proteases, acid phosphatase, beta-glucuronidase, beta-galactosidase, lysozyme, deoxyribonuclease, ribonuclease, interleukin 1, and lactic dehydrogenase. However, the culture fluids from SM-exposed explants contained increased amounts of histamine and plasminogen-activating activity, and often prostaglandin E2, when compared to culture fluids from control explants. After 3 to 4 d in culture, full-thickness human skin explants, when exposed to 0.2% SM (but not when exposed to 1.0% SM), sometimes showed separation of the epidermis and increased collagenase activity (i.e., hydroxyproline release). Thus, histamine (from local mast cells), and prostaglandin E2 and plasminogen-activating activity (probably from both mast cells and epidermal cells) are apparently involved in early mediation of the inflammatory response.