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High incidence of heparin-induced thrombocytopaenia (HIT) in splanchnic vein thrombosis treated with low molecular weight heparin (LMWH)
Abstracts / Digestive and Liver Disease 39 (2007) A29–A47 Aims. To evaluate the influence of pre-treatment parameters on 1-year dropout for HCC progression in a cohort of transplant candidate HCC patients. Methods. Out of all patients submitted to OLTx evaluation for HCC, 80 patients with at least 1-year follow-up from diagnosis were selected: 41 listed and 39 not listed for comorbidity/alcohol consumption/refusal (median age 57 years, range 35–65; M:F = 5:1). Diagnosis of HCC was histological in 75% of cases, according to the EASL criteria in the remaining cases. All patients (except one for refusal) were submitted to treatment (17 surgical resections, 50 percutaneous therapies, 12 chemoembolizations) and 40 of them were eventually transplanted. At 1 year from diagnosis, 36 patients did not show disease progressions (group A) and 44 showed disease progression, 31 patients within (group B) and 13 patients outside (group C) Milan criteria. No differences were present in natural MELD score among groups. Qualitative and quantitative variables were first analysed with the likelihood Mantel-Haenszel 2 -test and ANOVA one-way model, respectively, and then analysed with a multivariate analysis with stepwise method. Results. At univariate analysis, TNM (p = 0.038), CLIP (0/1/≥2, p = 0.004), overall tumour burden (p = 0.003) and number of nodules (p = 0.032) were significantly different among groups. After multivariate analysis, only CLIP score (odds ratio: 1vs. 0 = 1.452, 95%CI 0.503–4.192; OR ≥ 2 vs. 0 = 6.595, 95% CI 1.963–22.155) resulted to be significant independent predictor of HCC progression. The predictive power of CLIP stage system, expressed by c-statistic value, resulted 0.637. Conclusion. CLIP stage system seems a helpful instrument for a preliminary assessment of HCC patients evaluated for liver transplantation according to their estimated risk of dropout from waiting list for disease progression. Further analyses on larger series of patients are needed to confirm the role of this prognostic model in decision making and organ allocation. doi:10.1016/j.dld.2007.07.048 HIGH INCIDENCE OF HEPARIN-INDUCED THROMBOCYTOPAENIA (HIT) IN SPLANCHNIC VEIN THROMBOSIS TREATED WITH LOW MOLECULAR WEIGHT HEPARIN (LMWH) F.M. Fabris, R. Reati, A. Dell’Era, A. Artoni, F. Morelati, M. Primignani Dipartimento di Medicina e delle Specialit`a Mediche, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli, Regina Elena, Milan, Italy Background. HIT is an immune-mediated complication in patients receiving heparin, and represents a strong risk factor for thromboembolic disease associated with high morbidity and mortality. Its occurrence is low (around 3%) in patients on unfractioned heparin (UFH) and extremely low
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(less than 1:1000) in patients on low molecular weight heparin (LMWH). In Budd-Chiari Syndrome (BCS) or primary extrahepatic portal vein obstruction (EHPVO), often caused by occult myeloproliferative disorders, anticoagulant therapy is recommended and heparin is currently the preferred choice in the early management, when invasive diagnostic and/or therapeutic procedures are needed. Recently a high incidence of HIT in BCS patients treated with UFH has been reported [1], suggesting that LMWH should be used instead of UFH. In the last several years the standard policy at our Institution has been the use of LMWH in the early management of anticoagulant therapy. Aim. To assess the incidence of HIT, its risk factors and the associated clinical events in patients with BCS or EHPVO seen at our Institution from 2000 to 2007. Methods. All 51 consecutive patients with newly diagnosed BCS (n = 20) or EHPVO (n = 31) started therapy with LWMH. Platelet count was monitored weekly and patients with a severe reduction of platelet count were suspected for HIT. Diagnosis of HIT was based on the association of a drop in platelet count >50% to a count <150 × 109 /l and a positive HIT antibody test (PF4-dependant EIA). Patients with HIT were switched to danaparoid sulfate or lepirudin. Results. Seven patients developed thrombocytopaenia; HIT was confirmed by EIA in 4 (8% of all patients) within a median delay of 14 days from initiation of LMWH therapy (range 6–16 days). HIT occurred in 3 of 29 (10%) patients with myeloproliferative disorders as compared to 1 of 22 (4%) patients without. Clinically, HIT was not associated with new or worsening thromboses in three patients, but caused a delay in radiological (TIPS) or surgical (portocaval or splenectomy plus mesocaval shunt) procedures. In the remaining patient (with BCS) partial portal vein thrombosis occurred and exacerbated liver failure, leading to an emergency liver transplantation. Conclusions. We observed an unexpected high number of cases of HIT in patients with splanchnic vein thrombosis receiving LMWH, especially in patients with an underlying myeloproliferative disorder. Based on these findings we suggest that heparin (either UFH or LMWH) should not be used and danaparoid sulphate should be preferred for the initiation of anticoagulant therapy in patients with primary splanchnic vein thrombosis.
Reference [1] Plessier A, et al. Budd-Chiari syndrome (BCS) and heparin induced thrombocytopenia (HIT). J Hepatol 2006;44:S92. doi:10.1016/j.dld.2007.07.049
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(less than 1:1000) in patients on low molecular weight heparin (LMWH). In Budd-Chiari Syndrome (BCS) or primary extrahepatic portal vein obstruction (EHPVO), often caused by occult myeloproliferative disorders, anticoagulant therapy is recommended and heparin is currently the preferred choice in the early management, when invasive diagnostic and/or therapeutic procedures are needed. Recently a high incidence of HIT in BCS patients treated with UFH has been reported [1], suggesting that LMWH should be used instead of UFH. In the last several years the standard policy at our Institution has been the use of LMWH in the early management of anticoagulant therapy. Aim. To assess the incidence of HIT, its risk factors and the associated clinical events in patients with BCS or EHPVO seen at our Institution from 2000 to 2007. Methods. All 51 consecutive patients with newly diagnosed BCS (n = 20) or EHPVO (n = 31) started therapy with LWMH. Platelet count was monitored weekly and patients with a severe reduction of platelet count were suspected for HIT. Diagnosis of HIT was based on the association of a drop in platelet count >50% to a count <150 × 109 /l and a positive HIT antibody test (PF4-dependant EIA). Patients with HIT were switched to danaparoid sulfate or lepirudin. Results. Seven patients developed thrombocytopaenia; HIT was confirmed by EIA in 4 (8% of all patients) within a median delay of 14 days from initiation of LMWH therapy (range 6–16 days). HIT occurred in 3 of 29 (10%) patients with myeloproliferative disorders as compared to 1 of 22 (4%) patients without. Clinically, HIT was not associated with new or worsening thromboses in three patients, but caused a delay in radiological (TIPS) or surgical (portocaval or splenectomy plus mesocaval shunt) procedures. In the remaining patient (with BCS) partial portal vein thrombosis occurred and exacerbated liver failure, leading to an emergency liver transplantation. Conclusions. We observed an unexpected high number of cases of HIT in patients with splanchnic vein thrombosis receiving LMWH, especially in patients with an underlying myeloproliferative disorder. Based on these findings we suggest that heparin (either UFH or LMWH) should not be used and danaparoid sulphate should be preferred for the initiation of anticoagulant therapy in patients with primary splanchnic vein thrombosis.
Reference [1] Plessier A, et al. Budd-Chiari syndrome (BCS) and heparin induced thrombocytopenia (HIT). J Hepatol 2006;44:S92. doi:10.1016/j.dld.2007.07.049