Thrombose veineuse profonde et foramen ovale perméable (à propos de quatre cas)

BORDEAUX2-BU Santé (330632101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

De la vérité historique à la validité médicale du syndrome de Münchausen

BORDEAUX2-BU Santé (330632101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

A clinical prediction score for upper extremity deep venous thrombosis.

It was the objective of this study to design a clinical prediction score for the diagnosis of upper extremity deep venous thrombosis (UEDVT). A score was built by multivariate logistic regression in a sample of patients hospitalized for suspicion of UEDVT (derivation sample). It was validated in a second sample in the same university hospital, then in a sample from the multicenter OPTIMEV study that included both outpatients and inpatients. In these three samples, UEDVT diagnosis was objectively confirmed by ultrasound. The derivation sample included 140 patients among whom 50 had confirmed UEDVT, the validation sample included 103 patients among whom 46 had UEDVT, and the OPTIMEV sample included 214 patients among whom 65 had UEDVT. The clinical score identified a combination of four items (venous material, localized pain, unilateral pitting edema and other diagnosis as plausible). One point was attributed to each item (positive for the first 3 and negative for the other diagnosis). A score of -1 or 0 characterized low probability patients, a score of 1 identified intermediate probability patients, and a score of 2 or 3 identified patients with high probability. Low probability score identified a prevalence of UEDVT of 12, 9 and 13%, respectively, in the derivation, validation and OPTIMEV samples. High probability score identified a prevalence of UEDVT of 70, 64 and 69% respectively. In conclusion we propose a simple score to calculate clinical probability of UEDVT. This score might be a useful test in clinical trials as well as in clinical practice

Novel risk factors for premature peripheral arterial occlusive disease in non-diabetic patients: a case-control study.

BACKGROUND: This study aimed to determine the prevalence of genetic and environmental vascular risk factors in non diabetic patients with premature peripheral arterial disease, either peripheral arterial occlusive disease or thromboangiitis obliterans, the two main entities of peripheral arterial disease, and to established whether some of them are specifically associated with one or another of the premature peripheral arterial disease subgroups. METHODS AND RESULTS: This study included 113 non diabetic patients with premature peripheral arterial disease (diagnosis <45-year old) presenting either a peripheral arterial occlusive disease (N = 64) or a thromboangiitis obliterans (N = 49), and 241 controls matched for age and gender. Both patient groups demonstrated common traits including cigarette smoking, low physical activity, decreased levels of HDL-cholesterol, apolipoprotein A-I, pyridoxal 5'-phosphate (active form of B6 vitamin) and zinc. Premature peripheral arterial occlusive disease was characterized by the presence of a family history of peripheral arterial and carotid artery diseases (OR 2.3 and 5.8 respectively, 95% CI), high lipoprotein (a) levels above 300 mg/L (OR 2.3, 95% CI), the presence of the factor V Leiden (OR 5.1, 95% CI) and the glycoprotein Ia(807T,837T,873A) allele (OR 2.3, 95% CI). In thromboangiitis obliterans group, more patients were regular consumers of cannabis (OR 3.5, 95% CI) and higher levels in plasma copper has been shown (OR 6.5, 95% CI). CONCLUSIONS: According to our results from a non exhaustive list of study parameters, we might hypothesize for 1) a genetic basis for premature peripheral arterial occlusive disease development and 2) the prevalence of environmental factors in the development of thromboangiitis obliterans (tobacco and cannabis). Moreover, for the first time, we demonstrated that the 807T/837T/873A allele of platelet glycoprotein Ia may confer an additional risk for development of peripheral atherosclerosis in premature peripheral arterial occlusive disease

Risk Factors for PAOD Patients and TAO.

*<p>p<0.001, †p<0.01, ‡ p<0.05, ns: no significant different when p>0.05.</p><p>(PAOD, peripheral arterial occlusive disease; TAO, thromboangiitis obliterans).</p

PCR analysis of genomic DNA encoding the glycoprotein Ia gene surrounding the 807, 837 and 873 polymorphisms.

<p><i>(A)</i> Amplified products (1332 bp) were resolved by 1% agarose gel electrophoresis and stained with ethidium bromide. Lane 1: molecular weight marker; lane 2: blank; lanes 3 to 11: different genotyped individuals. <i>(B)</i> Analysis of <i>ITGA2^{807C/T, 837C/T, 873 G/A}</i> polymorphisms by PCR-RFLP using <i>Bgl II</i> and <i>Asn I</i> endonucleases on 1.5% agarose gel. Lane 7: molecular weight marker; other lanes: different genotypes according to reference 29 (lanes 1, 4, 5: 2/2, lanes 2, 3, 6: 1/2, lane 7: 1/3, lane 8: 2/3, lane 9: 1/1).</p

Clinical Characteristics of the Study Sample.

<p>Results as mean ± SD; ns: no significant different when p>0.05.</p><p>(PPAD, premature peripheral arterial diseases; PAOD, peripheral arterial occlusive disease; TAO, thromboangiitis obliterans).</p

Cardiovascular Risk Factors in the Study Sample.

<p> <b>Results as mean ± SD; ns: no significant different when p>0.05.</b></p>*<p>THC: tetrahydrocannabinol, † Lp(a): lipoprotein(a), ‡ hsCRP: ultrasensible C-reactive protein.</p><p>(PPAD, premature peripheral arterial diseases; PAOD, peripheral arterial occlusive disease; TAO, thromboangiitis obliterans).</p