The hepatitis C virus (HCV) is a recently described and important cause of acute and chronic liver disease. A hallmark of HCV is its propensity to become chronic, some patients with chronic HCV progressing to cirrhosis and hepatocellular carcinoma (HCC). HCV is also lymphotrophic and we report 2 patients with HCV cirrhosis who developed non-Hodgkins lymphoma (NHL). These cases raise the possibility that chronic HCV infection of lymphocytes plays an aetiological role in this malignancy. However screening of a further 63 consecutive patients over the age of 50 years with NHL for HCV antibody by second generation enzyme linked immunoassay (ELISA) failed to identify any patients with evidence of HCV infection. This suggests that HCV is an uncommon contributory factor for the development of non-Hodgkins lymphoma in the United Kingdom.

Summary. Post-transplant lymphoproliferative disorder (PTLD) is a well-recognized complication of organ transplant and has been associated with high mortality using conventional chemotherapy. We have investigated 11 cases of PTLD for alterations to the interferon alpha (IFNA) and p16 genes on chromosome 9p using archival material. 4/9 (44%) cases had deletions of the IFNA genes, in contrast to 1/59 (1 . 7%) cases of intermediate/high-grade de novo NHL drawn from the same geographical region. PTLD may therefore represent a distinct NHL subgroup exhibiting distinct gene pathology.

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4452 Introduction Glycoprotein IIb/IIIa inhibitors (GPI) improve outcomes in patients following percutaneous coronary intervention (PCI) and troponin positive acute coronary syndrome. However, GPI's can result in severe but transient thrombocytopenia (platelet count <50×109 cells/l). Guidelines on management of this complication are lacking. Minimal data exist on clinical outcomes of this cohort of patients and routine prophylactic use of blood products for these patients is controversial. Aim We aimed to study the clinical course and outcomes of patients with coronary artery disease who were admitted for coronary revascularisation and developed severe thrombocytopenia in coronary care unit of our tertiary cardiac centre. Methods We undertook review of 50 consecutive patients who had severe thrombocytopenia. Patients were divided in to two groups, severe thrombocytopenia following GPI usage and severe thrombocytopenia without exposure to GPI (control group). Severe thrombocytopenia in control group was due to co-existent sepsis (4), drugs other than GPI (4), myelodysplasia (4) and unknown aetiology (7). Patients with heparin induced thrombocytopenia, pseudo thrombocytopenia and bypass surgery associated thrombocytopenia and who died within 48 hours were excluded (one in each group). We chose in-hospital mortality, 30-day mortality, repeat coronary intervention and major bleeding as defined by TIMI criteria, as our combined primary endpoint. Results Data from 27 patients with severe thrombocytopenia following GPI administration and 19 age-matched controls were included for analysis. The GPI group had more males (92.6% vs.78.9%), smokers (29.6% vs.3.7%) and patients with a history of hypertension (59.3% vs.57.9%) and dyslipidaemia (66.7% vs.57.9%). Baseline platelet counts were higher in GPI group (in X109 Cells/l, mean, (SD), 201.63 (78.69) vs. 92.2 (8.02), p<0.05). More number of patients in the GPI group had PCI procedures and coronary stents. Patients in GPI group had major fluctuations and quicker recovery of platelet counts (Figure 1). This group had more patients with minor bleeding without any increase in major bleeding (Table 1). GPI group received fewer blood product transfusions (mean units, blood: 0.07 vs.1.32, p<0.05, platelets: 0.22 vs.1.05, p<0.05). GPI group had significant favourable outcomes such as, lower combined primary end point (3.7% vs.42.1%, p<0.05), lower in hospital mortality (3.7% vs.26.3%, p<0.05) and shorter duration of hospital stay (mean days 3.92 vs.25.08, p<0.05) compared to no-GPI group. Conclusion GPI related severe thrombocytopenia was not associated with an increase in bleeding complications or adverse cardiovascular events. A conservative approach with minimal blood product replacement was safe in this group of patients. These findings may have implications in minimising blood product support in this cohort of patients. Disclosures: Zaman: British Heart Foundation/FS/07/033: Research Funding.