In patients undergoing knee arthroscopy, prophylactic LMWH for 1 week reduced a composite end point of asymptomatic proximal deep venous thrombosis, symptomatic venous thromboembolism, and all-cause mortality more than did graduated compression stockings.

Antithrombin and protein C and S defects, factor V Leiden mutation, and G20210A prothrombin gene mutation are well-recognized risk factors for venous thromboembolism (VTE) in adults, especially during circumstantial situations such as trauma, immobilization, surgery, or oral contraceptive treatment. The relevance of these defects in predisposing children to VTE is still undefined. In a prospective cohort study we assessed the incidence of spontaneous and risk period-related VTE in asymptomatic children (aged 1-14 years), who were family members of a proband with an objectively diagnosed venous thromboembolic event and a documented single thrombophilic abnormality. We enrolled 143 children from 63 families. Of them, 81 (56.6%) were carriers of an inherited defect, whereas the remaining 62 were free from known genetic or acquired causes of thrombophilia. The mean observation period was 5 years (range, 1-8 years) in each group. Thirty-one risk periods occurred in the carriers group and 20 in noncarriers. Neither spontaneous nor risk period-related VTE occurred in either group during 395 and 296 observation years, respectively. However, circumstances where most of the pediatric thromboses occur (insertion of central venous lines, cancer, and cardiovascular surgery) were not encountered. In conclusion, the thrombotic risk in otherwise healthy children with a single identified thrombophilic defect appears to be very low. Common triggering conditions for VTE in thrombophilic adults do not seem to increase the thrombotic risk in children carrying the same inherited defect. Accordingly, screening for thrombophilia in otherwise healthy children younger than 15 years who belong to families with inherited defects predisposing to thrombosis seems unjustified.

The preventive method of intrasac "thrombization" using fibrin glue injection with or without the insertion of coils proves to be a simple, low cost, safe, and effective technique to significantly reduce the risk of type II endoleaks irrespective of the endograft used.

Maintenance of iron balance is essential for humans and requires the coordinate regulation of iron transport into plasma from dietary sources in the duodenum, from recycled senescent red cells in macrophages, and from storage in hepatocytes. Hepcidin, a recently identified antimicrobial peptide produced in the liver, has been shown to play a central role in the homeostatic regulation of iron absorption and distribution [1]. It is a negative regulator of iron absorption in the small intestine and of iron release from macrophages engaged in the recycling of iron senescent erythrocytes [2]. The human hepcidin gene contains three exons that encode a 72-aa precursor (pro-hepcidin) with a characteristic furin cleavage site immediately N-terminal to the 25-aa major hepcidin species found in plasma and urine [3]. Recently, hepcidin has been shown to regulate iron homeostasis by interaction with ferroportin, an iron cellular exporter highly expressed in absorptive enterocytes, macrophages, hepatocytes, and placental cells [4].Hepcidin binds ferroportin, inducing its internalization and lysosomal degradation, and therefore decreases export of cellular iron to the plasma [5]. Hepcidin and ferroportin dysregulation, resulting from mutations in the genes encoding these proteins, is implicated in the pathogenesis of several iron disorders [6]. This study analyzed hepcidin and ferroportin genes in blood donors with increased iron load hereditary hemochromatosis gene (HFE) negative to clarify their possible role as primary genes responsible for iron load in individuals with a normal HFE genotype. Two-hundred voluntary blood donors originating from different areas of Italy were previously tested for hematological and iron parameters [7]. Twenty subjects (17 males and 3 females, 18-57 years) with increased transferrin saturation (%TS > 50%; normal values <45%) or serum ferritin (SF > 300 ng/mL; normal values <250 ng/mL) were submitted to genetic screening for hepcidin and ferroportin genes. Factors possibly responsible for the abnormalities in iron status such as HFE and TfR2 mutations, inflammation, or liver disease were excluded in all the 20 subjects. Moreover, none of them had unusual dietary habits or abnormal ethanol consumption that could explain their iron overload. The control cohort (n 5 50; 30 males and 20 females, 20-60 years) included individuals with the same geographical origin, normal hematological and iron parameters, and negative results from viral and autoimmune screening studies.Serum iron (SI), %TS, SF, aspartate transaminase (AST), and alanine transaminase (ALT) were obtained from routine clinical laboratory procedures. Red blood cells (RBC), hematocrit (Ht), hemoglobin (Hb), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), platelet count, and leukocytes were determined by standard methods. The genes of hepcidin and ferroportin were analyzed by PCR amplifications of single exons followed by mutations screening with direct sequencing and restr...

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