Summary. Sixty-one consecutive patients undergoing splenectomy for chronic immune thrombocytopenia were retrospectively evaluated. Platelet response was considered as complete (CR) when platelet count rose to . 100 Â 10 9 / l, partial (PR) when 30±100 Â 10 9 /l or absent (NR) if otherwise. Follow-up (mean time 7´6 years) was possible in 54 patients. Forty-eight patients (88%) had an immediate response to splenectomy (39 CR, 9 PR) whereas six (12%) were NR. Thirty-six responders (67%) had sustained remission (31 CR; 5 PR) without further treatment; thrombocytopenia recurred in 12 patients (33%). The probability curve of continued remission showed a constant relapse-rate during the first 36 months; a further step of relapse was observed beginning 70 months after surgery. The only positive predictive factor for the long-term response to splenectomy was age , 40 (P , 0´005). Neither duration of thrombocytopenia nor previous response to medical treatment (steroids and/or intravenous immunoglobulins) were related to splenectomy response.

Abstract. Fabris F, Luzzatto G, Soini B, Ramon R, Scandellari R, Randi ML, Girolami A (University of Padua Medical School, Padova, Italy). Risk factors for thrombosis in patients with immune mediated heparin-induced thrombocytopenia. J Intern Med 2002; 252: 149-154.Background. As reported by major clinical series in the literature, about 2% of patients receiving unfractionated heparin (UFH) develop immunemediated (type II) heparin-induced thrombocytopenia (HIT) that may be complicated in 30-75% of cases by a paradoxical thrombotic syndrome (HITTS), either arterial or venous. HITTS carries relevant rates of mortality and morbidity, amongst which cerebral and/or myocardial infarction and limb amputations. It is unclear as yet why some patients suffer from isolated thrombocytopenia (HIT), whilst others have HITTS. The aim of the present study was to look for clinical and laboratory features related to the occurrence of HITTS. Patients and methods. We retrospectively analysed the clinical records of 56 patients with proven HIT, as diagnosed on clinical grounds and by in vitro demonstration of immunoglobulin (IgG)/ IgM against the PF4/heparin complex. Thirty-four patients (61%) had HITTS (19 venous thrombosis, seven arterial thrombosis, five arterial and venous thrombosis, two skin necrosis, one diffuse intravascular coagulation), whereas 22 had uncomplicated HIT. Amongst HITTS patients, two had limb amputation, five had recurrent thrombosis and seven died.Amongst HIT patients three died from causes unrelated to HIT. Results. No significant difference in sex, age, previous exposure to heparin, UFH route of administration or dose, duration of therapy, time of onset of thrombocytopenia and platelet count recovery, nor antiheparin/PF4 antibodies subtype (IgG or IgM) was detected when comparing HIT and HITTS. In contrast, in the HITTS group a higher prevalence of orthopaedic surgery (15 of 34 vs. 2/22; P ¼ 0.01), a significantly lower platelet count nadir (43 ± 32 vs. 75 ± 63 · 10 9 /L; P ¼ 0.01) and a significantly higher titre of antiheparin/PF4 antibodies, expressed as optical density of enzyme-linked immunosorbent assay (ELISA); (1989 ± 1024 vs. 1277 ± 858; P ¼ 0.009), were observed in comparison with the HIT group. Amongst HITTS patients, the prevalence of venous thrombosis was significantly higher in orthopaedic patients and in those being treated for venous thromboembolism (18/24 vs. 1/9 patients, v 2 8.4, P ¼ 0.004), whilst arterial thrombosis (ART) occurred more often in heparin treatment for arterial disease (3/4 vs. 4/29 patients, v 2 4.6, P ¼ 0.03). Conclusions. Orthopaedic surgery, the severity of thrombocytopenia and high antiheparin/PF4 antibodies titre are adverse prognostic or concurrent factors in the development of HITTS.

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There were 50 consecutive idiopathic thrombocytopenic purpura (ITP) adult patients (platelet count < 100 x 10(9)/L) grouped according to positivity or negativity of a solid-phase modified antigen capture enzyme-linked immunosorbent assay (ELISA) test (MACE) against glycoprotein IIb/IIIa (GPIIb/IIIa), Ib/IX, and IIa/IIIa. Observation started on the day of MACE assay and lasted at least 6 months. Clinical worsening was defined as the need for starting or modifying therapy because of thrombocytopenia lower than 20 x 10(9)/L or patient admission due to bleeding symptoms. MACE-positive patients had a higher probability of clinical worsening than MACE-negatives (P <.004). The proportion of patients worsening was 18 (72%) of 25 among MACE-positives and 8 (32%) of 25 among MACE-negatives. The median time to clinical worsening was 2.1 months for MACE-positive patients and 27.7 months for MACE-negatives. The assay of specific platelet autoantibodies may be a useful prognostic tool for the clinical course of ITP.