Introduction. Intestinal parasitic infections, especially due to helminths, increase anemia in pregnant women. The results of this are low pregnancy weight gain and IUGR, followed by LBW, with its associated greater risks of infection and higher perinatal mortality rates. For these reasons, in the setting of no large previous studies in Venezuela about this problem, a national multicentric study was conducted. Methods. Pregnant women from nine states were studied, a prenatal evaluation with a coproparasitological study. Univariated and multivariated analyses were made to determine risk factors for intestinal parasitosis and related anemia. Results. During 19 months, 1038 pregnant women were included and evaluated. Intestinal parasitosis was evidenced in 73.9%: A lumbricoides 57.0%, T trichiura 36.0%, G lamblia 14.1%, E hystolitica 12.0%, N americanus 8.1%, E vermicularis 6.3%, S stercoralis 3.3%. Relative risk for anemia in those women with intestinal parasitosis was 2.56 (P < .01). Discussion. Intestinal parasitoses could be associated with conditions for development of anemia at pregnancy. These features reflect the need of routine coproparasitological study among pregnant women in rural and endemic zones for intestinal parasites. Further therapeutic and prophylactic protocols are needed. Additional research on pregnant intestinal parasitic infection impact on newborn health is also considered.

HIV-infected patients receiving antiretroviral therapy who have low or mild cardiovascular risk and lipid levels within the normal range have endothelial dysfunction compared with healthy controls.

The objective of the study is to determine the importance of the mode of onset as prognostic factor in systemic sclerosis (SSc). Data were collected from the Spanish Scleroderma Registry (RESCLE), a nationwide retrospective multicenter database created in 2006. As first symptom, we included Raynaud's phenomenon (RP), cutaneous sclerosis, arthralgia/arthritis, puffy hands, interstitial lung disease (ILD), pulmonary arterial hypertension (PAH), and digestive hypomotility. A total of 1625 patients were recruited. One thousand three hundred forty-two patients (83%) presented with RP as first symptom and 283 patients (17%) did not. Survival from first symptom in those patients with RP mode of onset was higher at any time than those with onset as non-Raynaud's phenomenon: 97 vs. 90% at 5 years, 93 vs. 82% at 10 years, 83 vs. 62% at 20 years, and 71 vs. 50% at 30 years (p < 0.001). In multivariate analysis, factors related to mortality were older age at onset, male gender, dcSSc subset, ILD, PAH, scleroderma renal crisis (SRC), heart involvement, and the mode of onset with non-Raynaud's phenomenon, especially in the form of puffy hands or pulmonary involvement. The mode of onset should be considered an independent prognostic factor in systemic sclerosis and, in particular, patients who initially present with non-Raynaud's phenomenon may be considered of poor prognosis.

Abstract-Several studies have demonstrated that endothelial dysfunction is present in patients with essential hypertension.However, the presence of endothelial dysfunction in patients with white coat hypertension has not been studied. We evaluated the variation in the diameter of the brachial artery produced by flow-mediated dilation after a mechanical stimulus in patients with recently diagnosed mild to moderate sustained essential hypertension compared with patients with white coat hypertension. A total of 29 patients fulfilled inclusion criteria; 15 healthy volunteers were also included. After 24-hour ambulatory blood pressure monitoring, 15 patients were classified with sustained essential hypertension; 14 patients with white coat hypertension. Vascular ultrasound scans were performed according to the method described by Celermajer et al, with modification for noninvasive determination of endothelial dysfunction. Basal brachial artery diameter did not differ significantly among the 3 groups. Changes in arterial diameter 60 seconds after cuff deflation were higher in the control group compared with both hypertensive groups, but no significant differences were found between the sustained essential hypertension group and the white coat hypertension group. Flow-mediated dilation was similar in white coat hypertensives and sustained essential hypertensives. The presence of endothelial dysfunction in subjects with white coat hypertension suggests that it should not be considered a harmless trait and that white coat hypertension has common features with sustained essential hypertension. The prevalence of WCH has been estimated by several transversal studies between 20% and 40% among the population of mild hypertensives. 3,4 Whether this group of patients has an increased cardiovascular risk similar to that of sustained essential hypertensives (SEHs), or similar to that of normotensive subjects, is an interesting and still unsolved question that could entail therapeutic implications. 5 Only a few studies have been published about the natural history of WCH; some of them have found a higher frequency of progression to SEH compared with that of normotensive subjects. 6,7 Endothelial dysfunction (ED) is considered an early event in the development of atherosclerosis, 8 and several studies have demonstrated that ED is present in patients with essential hypertension. 9 However, the presence of ED in patients with WCH has not been studied. ED was first studied by measuring the increase of the diameter of coronary arteries after intravenous infusion of acetylcholine; the absence of vasodilation in response to acetylcholine was considered a marker of ED. 10 More recent publications studied ED by measuring vasodilation in response to acetylcholine in brachial or femoral arteries with plethysmography. 11 Nowadays, noninvasive methods based on flow-mediated dilation (FMD) after the compression of the arterial wall with a pneumatic tourniquet have been validated for the study of ED, and they are used in most recent works. 12 Th...

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La homocisteína es un aminoácido que se sintetiza en el organismo a partir de otro: la metionina. La única fuente de metionina es la ingesta, a partir principalmente de proteínas animales. El metabolismo de la homocisteína está muy relacionado con las vitaminas B 6 , B 12 y ácido fólico. La metionina que proviene de la ingesta se metaboliza, principalmente en el hígado, en homocisteína (Figura 1). A partir de aquí, la homocisteína puede seguir dos vías: a) Remetilación: transformarse de nuevo en metionina, mediante un proceso catalizado por la enzima metionina sintasa y dependiente de la vitamina B 12 y del N 5-metil-tetrahidro-folato (que actúan como cofactor y como dador de metilo). b) Transulfuración: unirse a la serina y transformarse en cisteína, que se elimina por la orina. Esta segunda vía depende de la enzima cistationina β-sintasa, que tiene a la vitamina B 6 como cofactor (88). LA HOMOCISTINURIA Las extremidades longilíneas, aracnodactilia, genu valgo, pie plano e hiperlaxitud articular conforman un fenotipo denominado marfanoide. Éste no es exclusivo de la enfermedad de Marfan, sino que se observa también en otra enfermedad hereditaria: la homocistinuria.

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