CD36 autoantibodies and thrombotic diathesis, thrombocytopenia and repeated early fetal losses.

BACKGROUND AND OBJECTIVES: Autoantibodies to CD36, a platelet glycoprotein, have been found in patients with thrombotic thrombocytopenic purpura, and in those with lupus-like anticoagulant with thrombotic complications. MATERIALS AND METHODS: Conventional hematologic and laboratory methods were used. The patient was a pregnant woman, who had had two early fetal losses separated by a normal offspring. Despite severe thrombocytopenia, she was asymptomatic. RESULTS: Serological investigations were strongly suggestive of CD36 autoantibodies. Neither clinical nor laboratory data were typical of those usually associated with cd36 autoantibodies, namely thrombotic thrombocytopenic purpura (TTP), systemic lupus erythematosis (SLE), or prothrombotic compliance. Prophylaxis with salicylates and prednisone was started at the 8th week of gestation, and an offspring with mild thrombocytopenia was delivered by cesarean section at the 32nd week of gestation because of abruptio placentae. CONCLUSIONS: There may be a cause-and-effect relationship between early fetal losses and CD36 autoantibodies.

Association of the alpha-adducin locus with essential hypertension.

Previous studies on genetic rat hypertension have shown that polymorphism within the alpha-adducin gene may regulate blood pressure. Adducin is a cytoskeletal protein that may be involved in cellular signal transduction and interacts with other membrane-skeleton proteins that affect ion transport across the cell membrane. There is a high homology between rat and human adducin and pathophysiological similarities between the Milan hypertensive rat strain and a subgroup of patients with essential hypertension. Thus, we designed a case-control study to test the possible association between the alpha-adducin locus and hypertension. One hundred ninety primary hypertensive patients were compared with 126 control subjects. All subjects were white and unrelated. Four multiallelic markers surrounding the alpha-adducin locus located in 4p16.3 were selected: D4S125 and D4S95 mapping at 680 and 20 kb centromeric, and D4S43 and D4S228/E24 mapping at 660 and 2500 kb telomeric. Alleles for each marker were pooled into groups. Comparisons between control subjects and hypertensive patients were carried out by testing the allele-disease association relative to the marker genotype. The maximal association occurred for D4S95 (chi 2(1) 13.33), which maps closest to alpha-adducin. These data suggest that a polymorphism within the alpha-adducin gene may affect blood pressure in humans.

Immune-complexes in malignant skin melanoma: quantitation by three methods, purification, and characterization of their non-tumor related constituents.

Circulating immune-complexes (ICs) and complement system (C) were studied in sera from 10 patients with malignant skin melanoma. The presence of ICs was demonstrated in all of them by three distinct methods. Moreover, ICs were purified in all the patient sera. The fact that ICs were detected in each serum and that the results of the analysis obtained by the different methods were not overlapping is discussed. It is stressed that the differences among the intrinsic characteristic of each technique are responsible for these discrepancies. The C profile was altered if compared with normal values, but it was not strictly characteristic for an ICs disease. In the purified ICs C3, C4, IgM, IgC1, and IgG3 were demonstrated; C1q, C1s, IgA, IgG2, and IgG4 never. It is noteworthy that a rheumatoid activity was found in the purified material and that this activity was significantly correlated with serum immuno-conglutinins (IKs) titre.

[Behavior of some parameters of humoral immunity in renal transplants after more than 3 years]. / Comportamento di alcuni parametri dell'immunita' umorale nei trapiantati renali da piu' di tre anni.

This paper evaluates the humoral immune response of 15 cadaver kidney transplant recipients more than three years after transplantation. The study was performed by determining immunoglobulin levels, complement fractions and circulating antigen-antibody complexes. The data obtained suggest that humoral immunity is impaired in patients who have undergone kidney transplant, even after more than three years later. The impairment of immunocompetence may be ascribed both to the immunosuppressive therapy (corticosteroids and azathioprine) and to the transplanted organ itself which represents a chronic antigenic stimulus.