Commentary: Iron metabolism in hepatitis C infection.

Hepatitis C virus (HCV) infections have started to decline, but up to 10,000 deaths each year are the consequence of chronic liver disease, following the infection. Laboratory testing identifies HCV-infected individuals using positive recombinant immunoblot assays to detect the presence of the antibody; the diagnosis is confirmed by detecting HCV RNA in serum. HCV-infected patients who have large accumulations of hepatic iron have not responded well to interferon therapy, compared to patients with normal hepatic iron stores.

Long-term maintenance of immunity in patients with common variable immune deficiency by plasma transfusion.

The AIDS crisis and the fear of blood product contamination stimulated the development of a designated plasma collection and transfusion for patients with common variable immune deficiency. Four patients have been maintained over 1 year; 5 years and 10 months; 8 years and 7 months; and 12 years. A new crisis affecting commercial IgG manufacturing, owing to recalls, has made the life saving product scarce, threatening patients' health maintenance.

Understanding iron absorption and metabolism, aided by studies of hemochromatosis.

Duodenal iron absorption from food is selectively blocked to prevent iron intoxication. The prime example of pathologic increase in intestinal iron absorption is seen in patients with hemochromatosis. They suffer iron damage to the heart, liver, and other tissues resulting in premature death if the iron is not removed by vigorous phlebotomy.

Past and future of providing matched, unrelated donors for marrow transplantation.

Prior to 1979, bone marrow transplants were only performed with histocompatible sibling donors. Once it was established that histocompatible, unrelated donors could donate marrow for transplantation, the recruitment of such donors needed to be standardized. Blood donor centers had already identified the histocompatibility locus antigen (HLA) typing for donors who could be recruited to donate bone marrow.

Do we have to rethink serologic markers used to diagnose hepatitis B infection?

The recent addition of testing volunteer blood donors for antibody to hepatitis B core antigen (anti-HBc) has raised questions not apparent when such testing is applied to hepatitis B (HB) infected patients. The review of published studies, and our own, demonstrates that it is difficult to evaluate false positive results. Some patients appear to lose antibody to hepatitis B surface antigen (anti-HBs) but not antibody to hepatitis B core antigen (anti-HBc), thus raising the possibility of disease transmission.

Posttransfusion hepatitis A in a neonatal intensive care unit.

A single unit of infected blood transfused into 11 neonates resulted in a large multistate outbreak of 55 cases of hepatitis A, 35 of which were symptomatic. The person who donated the blood to the 11 neonates became ill with hepatitis A one week after the donation. Hepatitis A infection was then acquired by nurses and physicians having direct contact with the neonates and by parents and relatives.

Transfusion requirements of patients with enzyme deficient red blood cells.

Red cell enzyme deficiency disease states are reviewed to outline the requirements for transfusion therapy in the neonatal period, during spontaneous crises, drug or infection-induced crises and chronic anemia.

Cutaneous larva migrans, an occupational disease.

Creeping skin eruption is known to follow exposure to canine and feline hookworm larvae found in contaminated soil encountered in humid, tropical and subtropical regions. A little known hazard of similar infections exists among veterinarians and laboratory workers exposed to Strongyloides larvae from horses located in temperate climates. The evolving clinical picture is described in detail.

Thrombocytopenia and its management in the surgical patient needing multiple reconstructive procedures.

Thrombocytopenic patients with surgically correctable lesions such as radial clubhands are too often repeatedly transfused with randomly pooled platelets. This is followed by a clinical rejection of the foreign protein and rapid destruction of the platelets. There may be excessive bleeding episodes.