Increased detection of human immunodeficiency virus antigen carriers by simultaneous assay of plasma and extracts from resting and phytohaemagglutinin-stimulated peripheral blood mononuclear cells.

Antigenaemia due to human immunodeficiency virus (HIV) is thought to be significant either before the appearance of a specific antibody response, or after its decline during terminal stages. In order to increase the rate of detection of HIV antigen carriers, regardless of the stage or despite the presence of specific serum antibodies, we assayed, simultaneously, plasma samples and extracts from resting and phytohaemagglutinin-stimulated mononuclear cells from 25 infected, anti-body-positive individuals and 10 healthy, antibody-negative female volunteer blood donors. We detected the presence of HIV antigen in at least one of the three types of specimens obtained from all the 25 infected subjects but in none of the 10 healthy blood donors. This approach might prove most useful for the study of patients with controversial or equivocal antibody test results.

Congenital Acute Megakaryoblastic Leukaemia in Down's Syndrome.

The case of a newborn with Down's syndrome and congenital leukaemia is reported. The malignant white blood cells displayed the CD41 antigen (glycoprotein Ilb/IIIa) identified by monoclonal antibodies HP1-ld and FMC24 and the CD9/p24 antigen identified by monoclonal antibody FMC27. The number of cells in S-phase was 14%, as assessed by the incorporation of 5-bromo 2-deoxyuridine. No other chromosomal abnormalities were identified in addition to 47 XY + 21. The patient died 15 days after the diagnosis, due to Pneumocystis Carinii pneumonia. Post-mortem examination showed heavy leukaemic infiltration and cardiac abnormalities including inter-atrial septal defect and a patent Ductus arteriosus. This patient appears to be the first identified case of congenital leukaemia with megakaryocytic differentiation, although previous instances of transient abnormal myelopoiesis with megakaryocytic differentiation have been recorded in Down's syndrome.

Infusion of anti-CD10 monoclonal antibody (J5) following ablative chemotherapy in a patient with refractory pre-B acute lymphoblastic leukemia.

The case of a 9-year old girl with end-stage refractory pre-B CD10/CALLA positive acute lymphoblastic leukaemia is described. The patient was treated with high doses of cytarabine followed by intravenous anti-CD10 monoclonal antibody (J5) in an effort to prevent the recovery of the leukemic CD10 positive clone following the bone marrow hypoplasia resulting from the chemotherapy. The number of CD10 positive cells dissapeared both in the peripheral blood as well as in the bone marrow, but when granulocytic recovery ensued, the patient died from respiratory infection. No evidence of antigenic modulation of the CD10 antigen was observed in the blast cells.

Demonstration of a cross-reactive idiotype (IdRQ) in rheumatoid factors from patients with rheumatoid arthritis but not in rheumatoid factors from healthy, aged subjects.

A human monoclonal IgM kappa paraprotein with rheumatoid factor (RF) activity was used to elicit antiidiotypic antibodies in rabbits. The antiidiotypic antiserum thus obtained reacted with samples from 40% of 72 rheumatoid arthritis patients, but not with any of the samples from 22 aged control subjects having serum RF. Our findings suggest that, despite the similarities between RF from rheumatoid arthritis patients and that from healthy individuals, the expression of V region genes may be different in healthy subjects and those with the disease.

Natural anticoagulants in systemic lupus erythematosus. Deficiency of protein S bound to C4bp associates with recent history of venous thromboses, antiphospholipid antibodies, and the antiphospholipid syndrome.

The association of thrombosis with antiphospholipid antibodies (aPL) in patients with systemic lupus erythematosus (SLE) could be due to their interference with natural phospholipid dependent anticoagulant mechanisms. We studied antigenic protein C (APC), functional protein C (FPC), free protein S (FPS), protein S bound to C4 binding protein (C4bp-S), antithrombin III (ATIII), as well as IgG and IgM anticardiolipin antibodies (aCL) in 38 patients with SLE with a history of thromboses and 70 patients with SLE without such history. We found a high frequency of deficiencies of natural anticoagulants in both groups of patients with SLE but, because of patient selection, we could not determine the actual prevalence of these defects. Patients having had a venous thrombosis in the previous year had low C4bp-S more frequently than patients with older or no thromboses. When we divided our patients with SLE into those who had a definite, probable, questionable or no antiphospholipid syndrome (aPS) we found the frequency of C4bp-S deficiency to be significantly higher in those with definite aPS than in those without aPS. Intermediate proportions were found in patients with probable and questionable aPS. The levels of C4bp-S decreased as the levels of aCL, particularly IgG, increased. Stepwise discriminant analysis of natural anticoagulants selected deficiencies of C4bp-S and FPC with increased ATIII as a set of variables with highest predictive power for classification of patients with and without aPS. Thus, deficiencies of natural anticoagulants may occur frequently in patients with SLE.(ABSTRACT TRUNCATED AT 250 WORDS)