St Thomas' Hospital

About: St Thomas' Hospital is a healthcare organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Pregnancy. The organization has 12105 authors who have published 15596 publications receiving 624309 citations. The organization is also known as: St Thomas's Hospital & St. Thomas's.

Early response to immunosuppressive therapy predicts good renal outcome in lupus nephritis: Lessons from long-term followup of patients in the Euro-Lupus Nephritis Trial

Abstract: OBJECTIVE: In the Euro-Lupus Nephritis Trial (ELNT), 90 patients with lupus nephritis were randomly assigned to a high-dose intravenous cyclophosphamide (IV CYC) regimen (6 monthly pulses and 2 quarterly pulses with escalating doses) or a low-dose IV CYC regimen (6 pulses of 500 mg given at intervals of 2 weeks), each of which was followed by azathioprine (AZA). After a median followup of 41 months, a difference in efficacy between the 2 regimens was not observed. The present analysis was undertaken to extend the followup and to identify prognostic factors. METHODS: Renal function was prospectively assessed quarterly in all 90 patients except 5 who were lost to followup. Survival curves were derived using the Kaplan-Meier method. RESULTS: After a median followup of 73 months, there was no significant difference in the cumulative probability of end-stage renal disease or doubling of the serum creatinine level in patients who received the low-dose IV CYC regimen versus those who received the high-dose regimen. At long-term followup, 18 patients (8 receiving low-dose and 10 receiving high-dose treatment) had developed permanent renal impairment and were classified as having poor long-term renal outcome. We demonstrated by multivariate analysis that early response to therapy at 6 months (defined as a decrease in serum creatinine level and proteinuria <1 g/24 hours) was the best predictor of good long-term renal outcome. CONCLUSION: Long-term followup of patients from the ELNT confirms that, in lupus nephritis, a remission-inducing regimen of low-dose IV CYC followed by AZA achieves clinical results comparable with those obtained with a high-dose regimen. Early response to therapy is predictive of good long-term renal outcome.

Does the efficacy of BCG decline with time since vaccination

Abstract: OBJECTIF: Evaluer dans quelle mesure l'efficacite protectrice du bacille Calmette-Guerin (BCG) contre la tuberculose diminue avec le temps ecoule apres la vaccination. SCHEMA: Revue quantitative de tous les 10 essais randomises du BCG contre la tuberculose avec des donnees pour des periodes judicieuses chez des individus tuberculino-negatifs. Pour chaque essai, nous avons derive le logarithme du rapport des incidences pour apprecier la modification annuelle de l'efficacite du BCG. Nous avons egalement compare l'efficacite au cours des deux premieres annees, et des dix premieres annees a celle du reste de l'essai. RESULTATS : On a note une heterogeneite considerable entre les essais en ce qui concerne les modifications annuelles de l'efficacite du BCG. Dans sept d'entre eux, l'efficacite diminue avec le temps, alors que dans trois elle augmente. La modification annuelle moyenne d'efficacite est sans relation avec l'efficacite globale. l'efficacite varie egalement entre les essais au cours des deux premieres annees apres la vaccination, plus de deux ans apres la vaccination et dans les dix premieres annees apres la vaccination. Toutefois, la variation d'efficacite entre les essais, plus de dix ans apres la vaccination, n'a pas de valeur significative (P = 0,26). C'est pour cette raison que nous avons calcule l'efficacite moyenne plus de dix ans apres la vaccination : celle-ci est de 14% (intervalle de confiance a 95% de - 9% a 32%). CONCLUSION : La protection due au BCG peut s'effacer avec le temps apres la vaccination. Il n'y a pas de preuve solide que le BCG assure une protection plus de dix ans apres la vaccination.

Role of arterial stiffness in cardiovascular disease

Abstract: Propagation of the pressure wave along the arterial tree (pulse wave velocity [PWV]) is related to the intrinsic elasticity of the arterial wall. PWV is increased in stiffer arteries and, when measured over the aorta, is an independent predictor of cardiovascular morbidity and mortality. Given the predictive power of PWV, identifying strategies that prevent or reduce stiffening may be important in prevention of cardiovascular events. One view is that aortic stiffness occurs as a result of atherosclerosis along the aorta. However, there is little or no association between PWV and classical risk factors for atherosclerosis, other than age and blood pressure. Furthermore, PWV does not increase during early stages of atherosclerosis, as measured by intima-media thickness and non-calcified atheroma, but it does increase in the presence of aortic calcification that occurs within advanced atherosclerotic plaque. Age-related widening of pulse pressure is the major cause of age-related increase in prevalence of hypertension and has been attributed to arterial stiffening. This review summarizes the methods of measuring aortic stiffness in humans, the pathophysiological mechanisms leading to aortic stiffness, including its association with atherosclerosis, and the haemodynamic consequences of increased aortic stiffness.

Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors

Abstract: Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.