Maternal thrombophilia and adverse pregnancy outcome: a case-control study.

OBJECTIVE: To assess the risk of adverse pregnancy outcomes in patients with acquired and/or congenital thrombophilia factors. PATIENTS AND METHODS: A cohort of 130 women with a history of pregnancy loss and no successful gestation were investigated for the presence of congenital and acquired thrombophilia factors, and then compared with a control group of 130 healthy women who had had at least one successful gestation and no pregnancy loss, and were screened for congenital and acquired thrombophilia factors. RESULTS: Acquired and congenital thrombophilia factors were found in 30 (23%) patients and in 14 (10.8%) controls (p < 0.015). The presence of ≥1 congenital thrombophilia factor was associated with pregnancy loss with an odds ratio of 2.46 (p = 0.040). Moreover, women who had had >1 early fetal loss had a 2.85-fold risk of being carriers of congenital thrombophilia factors, compared to the controls. CONCLUSION: Our study showed the increased risk of miscarriage in patients with congenital thrombophilia factors and >1 early fetal loss.

Immunoadsorption apheresis and immunosuppressive drug therapy in the treatment of complicated HCV-related cryoglobulinemia.

The immunosuppressive drug therapy (IDT) is not always effective to avoid the development of complications in hepatitis C virus-related cryoglobulinemia (HCV-Cr). Removal of cryoglobulins by therapeutic plasmapheresis is currently accepted. In this randomized, parallel group study, 17 male and female patients aged 43-79 years, with complicated HCV-Cr, were submitted for 12 weeks (initial immunosuppressive therapy) to IDT (alpha-interferon, pegylated-interferon alpha-2a, cyclophosphamide, methylprednisolone, prednisone, cyclosporine, ribavirin, and melphalan). Then, they were randomly assigned to two parallel groups: A # 9 patients treated by immunoadsorption apheresis (Selesorb((R))) (IA) plus IDT, and B # 8 patients submitted to IDT only, for further 12 weeks. # 187 IA aphereses were performed. No adverse reactions or complications were observed. A Clinical Score (CS) was adapted from a pre-existing scoring model to evaluate signs and symptoms inherent to the underlying immunologic disorder. The CS was calculated at baseline (CS0), after the initial immunosuppressive therapy (CS1 = 12 weeks) when patients were treated only with IDT, and at the end of the study (24 weeks) in the group A (CSA; IA plus IDT) and B (CSB; IDT only). The score did not change significantly from CS0 to CS1. However, statistically significant differences were observed between CS1 and CSA (P < 0.001), and CSA versus CSB (P = 0.03), respectively. The changes observed were favorable to the patients assigned to the IA plus IDT group (A): in most case relief of symptoms and complications have been obtained.

Autoantibodies in patients with monoclonal gammopathies.

Although autoantibody activities are rather often associated to monoclonal gammopathies, only monoclonal immunoglobulins of the IgM isotype are really directed against autoantigens that are often polysaccharides or are formed by highly repetitive structures. This strict association is frequently revealed also by clinical manifestations of the autoimmune response generated by the monoclonal macroglobulin. Most monoclonal immunoglobulins of non-IgM isotype are instead totally inactive toward self-antigens, the autoantibody activity being instead associated, if present, to polyclonal immunoglobulins. Although the same BAFF/APRIL system is involved in perpetuation of humoral autoimmunity as well as in stimulation of clonal B-cell expansion, the autoimmune commitment of B cells of a non-IgM isotype is hardly compatible with their possible involvement in an uncontrolled proliferation pathway, whose prerequisite is the homing of these B cells to the bone marrow compartment. The IgM-secreting cells appear instead to possess a much lower tendency, and/or a looser requirement, for their homing in the bone marrow prior to their actual proliferation. This may explain the quite different consequences, in terms of autoimmunity, between IgM and non-IgM paraproteinemias.