Transfusion of packed RBCs may significantly increase intravascular levels of IL-6 and IL-8 in patients with FNHTRs.

In an attempt to investigate the incidence and clinical course of non-A, non-B (NANB) hepatitis following blood transfusion in Taiwan, 288 patients who underwent cardiovascular surgery and received blood transfusion were followed prospectively with serum liver aminotransferase levels and viral hepatitis markers for at least six months. None had any past history of liver disease or drug abuse. All blood donors were tested for serum hepatitis B surface antigen and alanine aminotransferase (ALT) (greater than 45 U/L). Thirty-seven (12.8%) patients developed PTH. 34 (91.9%) were considered to be cases of NANB hepatitis, 2 (5.4%) were cytomegalovirus hepatitis, and one (2.7%) was caused by Epstein-Barr virus. No one developed hepatitis B post-transfusion hepatitis (PTH). Of the 34 NANB PTH patients, 15 (44.1%) were asymptomatic, 16 (47.1%) had clinical symptoms, and 9 (26.5%) had serum total bilirubin levels higher than 2 mg/dl. There was no case of fulminant hepatic failure. Of 26 NANB PTH patients who were followed up for more than one year, 15 (57.7%) still had abnormal serum ALT levels. The incubation period of NANB PTH ranged from 2 to 16 (mean 6.1 +/- 3.2) weeks. Of the 37 PTH patients, 32 (86.5%) were found to have anti-HCV seroconversion during one year follow-up period. NANB PTH is as common in Taiwan as in the United States and Japan, and is demonstrated by this study to be due mostly to HCV.

A male, full-term baby with thrombocytopenia was born by a G3P2A1 mother who was not associated with autoimmune disease. Platelet antibody screening was positive by using lymphocytotoxicity test, platelet suspension immunofluorescence test and solid-phase red cell adherence test. The identified HLA antibody was of A2 specificity. It was confirmed by testing the mother’s and the baby’s sera against the lymphocytes and platelets of 10 HLA-A2-positive donors. The possibility of platelet-specific antibody as the cause of neonatal alloimmune thrombocytopenia was ruled out by testing against platelets of 10 HLA-A2-negative donors and the known platelet-specific antigens utilizing immobilized, purified platelet glycoprotein as targets. The mother’s serum reacted strongly with both the father’s and the baby’s platelets and lymphocytes. This neonatal thrombocytopenia was most likely due to the maternal HLA antibody, which was induced by her antecedent gestations.

We examined the iron status of 23 adult patients with hemoglobin H (Hb H) disease. None of them had received multiple blood transfusions or prolonged iron therapy. Studies included serum iron and ferritin concentrations, transferrin saturation, a desferrioxamine test, computed tomography (CT) scan of the liver, and liver biopsy. Iron overload was found in 17 patients (73.9%), especially in males and in patients with splenomegaly (92.9% and 100%, respectively). Four patients with excessive alcohol consumption had clinical manifestations of severe iron overload. Idiopathic hemochromatosis associated HLA antigens, i.e., HLA-A3, -B7, or -B14, were not found in any of the 15 patients tested. These findings indicate that iron overload is common in adult patients with Hb H disease; such patients should abstain from alcohol and be considered for treatment with an iron chelating agent before irreversible organ damage occurs.

No abstract