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To evaluate whether the presence of antiphospholipid antibodies in lymphoma patients influences their response to treatment, and their rate of thromboembolic complications, we followed up 100 consecutive patients with different lymphomas, who underwent measurement of lupus anticoagulants and anticardiolipin antibodies at diagnosis. In all, 27 patients had lupus anticoagulants and/or anticardiolipin antibodies. This prevalence was significantly higher than in a group of 100 age- and sex-matched normal control subjects (8%; P=0.0008, odds ratio 4.25, 95% confidence interval, 1.82-9.92). At diagnosis, antiphospholipid-positive and -negative patients were similar with respect to age, sex, type and staging of lymphomas. During follow-up, the rate of thrombosis was significantly higher in patients with (5.1% patients/year) than without (0.75% patients/year) antiphospholipid antibodies. The two groups were similar with respect to relapse and death rate. In conclusion, antiphospholipid antibodies are associated with lymphomas. Their determination is useful to identify patients at high risk to develop thrombotic complications, but not to predict treatment outcome or disease prognosis.

SummaryWe performed a case-control study to assess whether anti-β2-glycoprotein I and anti-prothrombin antibodies are independent risk factors of thrombosis. Cases were 79 patients with arterial and/or venous thrombosis without lupus anticoagulants, anticardiolipin antibodies and systemic lupus erythematosus; controls were 85 normal subjects. The prevalences and titers of IgG and IgM anti-β2-glycoprotein I and antiprothrombin antibodies were similar in both groups. Cases were analyzed with respect to the arterial or venous type of thrombosis and to the presence of congenital or acquired risk factors for thrombosis: no statistically significant relationships with the presence of anti-β2glycoprotein I and anti-prothrombin antibodies were found. Our data indicate that anti- β2-glycoprotein I and anti-prothrombin antibodies are not risk factors for thrombosis independent of lupus anticoagulants and anticardiolipin antibodies. Their measurement, therefore, is not warranted in the laboratory screening of patients with arterial and/or venous thrombosis.

The recent discovery of hepcidin, the key iron regulatory hormone, has changed our view of iron metabolism, which in turn is long known to be linked with insulin resistant states, including type 2 diabetes mellitus and the Metabolic Syndrome (MetS). Serum ferritin levels are often elevated in MetS (Dysmetabolic hyperferritinemia - DHF), and are sometimes associated with a true mild-to-moderate hepatic iron overload (dysmetabolic iron overload syndrome - DIOS). However, the pathophysiological link between iron and MetS remains unclear. This study was aimed to investigate, for the first time, the relationship between MetS and hepcidin at population level. We measured serum hepcidin levels by Mass Spectrometry in 1,391 subjects from the Val Borbera population, and evaluated their relationship with classical MetS features. Hepcidin levels increased significantly and linearly with increasing number of MetS features, paralleling the trend of serum ferritin. In multivariate models adjusted for relevant variables including age, C-Reactive Protein, and the HFE C282Y mutation, ferritin was the only significant independent predictor of hepcidin in males, while in females MetS was also independently associated with hepcidin. Overall, these data indicate that the fundamental iron regulatory feedback is preserved in MetS, i.e. that hepcidin tends to progressively increase in response to the increase of iron stores. Due to recently discovered pleiotropic effects of hepcidin, this may worsen insulin resistance and contribute to the cardiovascular complications of MetS.

There is an error in the affiliation list for author Ginevra Biino. The following are the correct affiliations for this author: 1) Institute of Molecular Genetics, National Research Council of Italy, Pavia, Italy 2) Institute of Population Genetics, National Research Council of Italy, Sassari, Italy

We performed a case-control study to assess whether anti-beta2-glycoprotein I and anti-prothrombin antibodies are independent risk factors of thrombosis. Cases were 79 patients with arterial and/or venous thrombosis without lupus anticoagulants, anticardiolipin antibodies and systemic lupus erythematosus; controls were 85 normal subjects. The prevalences and titers of IgG and IgM anti-beta2-glycoprotein I and anti-prothrombin antibodies were similar in both groups. Cases were analyzed with respect to the arterial or venous type of thrombosis and to the presence of congenital or acquired risk factors for thrombosis: no statistically significant relationships with the presence of anti-beta2-glycoprotein I and anti-prothrombin antibodies were found. Our data indicate that anti-beta2-glycoprotein I and anti-prothrombin antibodies are not risk factors for thrombosis independent of lupus anticoagulants and anticardiolipin antibodies. Their measurement, therefore, is not warranted in the laboratory screening of patients with arterial and/or venous thrombosis.

Abstract 348 Background and Aims: Hepcidin is a 25 amino acid hormone mainly produced by the liver in response to increased plasma or tissue iron to homeostatically down-regulate absorption and recycling of the metal from duodenum and macrophages, respectively. Hepcidin expression is also upregulated by inflammation. Dysmetabolic hyperferritinemia is among the commonest causes of increased serum ferritin levels encountered in clinical practice, but its pathophysiology remains unclear. Indeed, the Metabolic Syndrome (MS) that affects near 20–25% of western adults, is characterized by subclinical inflammation, which hampers the interpretation of serum ferritin as a marker of body iron stores. We recently measured serum hepcidin levels in the large Val Borbera (VB) population to evaluate their genetic determinants (Traglia et al. J Med Genet 2011). Taking advantage of this survey, we investigated for the first time the relationships between hepcidin, ferritin, C-Reactive Protein (CRP) and MS phenotypes at population level. Subjects and Methods: Serum hepcidin-25 levels measured by Mass Spectrometry were analyzed in 941 subjects for whom complete data allowing classification of MS according to NLHBI criteria (fasting glucose ≥100 mg/dl or antidiabetes medication; blood pressure ≥135/85 mmHg or antihypertensive medication; triglycerides ≥150 mg/dl; HDL cholesterol Main Results: Serum hepcidin-25 levels increased linearly with the increasing number of MS traits in males (ANOVA: F=6.8, P=0.009) and, even more strongly, in females (ANOVA: F=35.2, P Conclusions: Hepcidin levels are strongly associated with MS features at population level, independently of subclinical inflammation. This association appears to reflect a response to increasing iron stores in males, while in females some MS traits may directly influence hepcidin levels. Disclosures: No relevant conflicts of interest to declare.