Asymptomatic Helicobacter pylori infection increases asymmetric dimethylarginine levels in healthy subjects.

BACKGROUND: Chronic infections have been demonstrated to be early factors of atherosclerosis and cardiovascular diseases, and their relevance increases when they are caused by agents with extremely broad spectrum of disease outcome such as Helicobacter pylori. The consequent endothelial impairment leads to a reduced bioavailability of nitric oxide. Increasing evidences have pointed out that the endogenous inhibitor of nitric oxide synthase, asymmetric dimethylarginine, defined as a risk factor for cardiovascular disease, may increase in infections and plays an important role impairing the vascular functions of the endothelium. Starting from these findings, we aim to investigate whether H. pylori may affect asymmetric dimethylarginine levels. MATERIALS AND METHODS: The study was carried out on a group of 186 subjects (age 46.2 +/- 14.9 years). We evaluated asymmetric dimethylarginine, symmetric dimethylarginine, L-arginine, presence of H. pylori by 13C-urea breath test, and the main parameters of glyco and lipo metabolic balance. RESULTS: Increased levels of asymmetric dimethylarginine were found in H. pylori-positive subjects with respect to H. pylori-negative subjects (0.46 x/ / 1.13 versus 0.42 x/ / 1.23 mol/l, p < .001, respectively). No differences were detected in L-arginine levels between the two groups. Multiple regression analysis performed in H. pylori-positive subjects and H. pylori-negative subjects showed profound differences in the variables related to asymmetric dimethylarginine (R2 = 66.9%, p < .01 versus 34.3%, p < .01, respectively) and symmetric dimethylarginine (R2 = 39.2%, p < .01 versus 20.6%, p = .09, respectively) levels. CONCLUSIONS: Our data clearly demonstrate that H. pylori infection increases asymmetric dimethylarginine levels. Moreover, this infection causes a profound metabolic modification that alters the role of the known determinants of asymmetric dimethylarginine levels. We conclude that H. pylori infection must be taken into account as a cause of increased asymmetric dimethylarginine levels and that the eradication of H. pylori may therefore lead to a decrease in asymmetric dimethylarginine levels, which is a further reason for the reduction of the risk for cardiovascular disease in this large portion of population.

A novel succinate dehydrogenase subunit B gene mutation, H132P, causes familial malignant sympathetic extraadrenal paragangliomas.

We report a family with malignant sympathetic paragangliomas (PGL) exhibiting a new type of germline mutation in the succinate dehydrogenase subunit B (SDHB) gene. Two affected brothers, presenting with symptoms at the ages of 25 and 52 yr, suffered from malignant abdominal extraadrenal sympathetic PGL. They died of their disease at ages 43 and 61 yr. Their mother had the same history of signs and symptoms, suggesting a catecholamine-producing tumor at the age of 55 yr. Analysis of the germline DNA from these three patients revealed a novel mutation in exon 4 (H132P) of the SDHB gene. This mutation was absent in 160 control chromosomes. Loss of heterozygosity analysis of the tumors showed a loss of one SDHB allele, and RT-PCR-based expression analysis confirmed the exclusive expression of the mutated allele in both tumors. A review of the published PGL families revealed malignant tumors in seven of 12 well-documented families with SDHB mutation-associated extraadrenal PGL. These findings, as well as findings of the family reported here, suggest a strong causal relationship of SDHB germline mutations with malignant extraadrenal abdominal PGL and imply the necessity of a close follow-up of affected individuals and family members.

Great saphenous vein stripping with liberal use of subfascial endoscopic perforator vein surgery (SEPS).

This study is based on a unique registry of 632 patients who underwent great saphenous vein (GSV) stripping and liberal use of subfascial endoscopic perforator vein surgery (SEPS) for minimal to severe lower limb venous insufficiency. Clinical examinations and color-coded duplex scanning were performed on a randomly selected, manageable sample of 170 limbs to assess the affect of early SEPS on junctional (saphenofemoral [SFJ] and/or saphenopopliteal [SPJ]) and perforator vein (PV) insufficiencies and superficial varicosities at a median of 6.5 years. PV incompetence was present in 68 legs (40%), as the sole transfascial insufficiency in 28 limbs and combined with SFJ or SPJ incompetence in 40 limbs. Junction incompetence alone characterized an additional 38 limbs, bringing the total transfascial insufficiency prevalence to 62%. Superficial varicosities affected 46% of limbs. Overall CEAP clinical class was unimproved beyond preoperative values. PV incompetence was associated with higher CEAP and clinical venous severity scores than were junctional insufficiencies alone. We concluded that PV incompetence alone or combined with junctional insufficiency is associated with increased symptoms and disease progression. The prevalence of SFJ, SPJ, and PV incompetence (62%) and recurrent varicosities (46%) suggests that early use of SEPS does not prevent disease progression and offers no benefit over GSV stripping in the absence of deep vein insufficiency or threatened ulceration.