Showing papers by "Alfred Sommer published in 2011"
TL;DR: Use of weekly vitamin A or beta carotene in pregnant women in Bangladesh, compared with placebo, did not reduce all-cause maternal, fetal, or infant mortality.
Abstract: Context Maternal vitamin A deficiency is a public health concern in the developing world. Its prevention may improve maternal and infant survival. Objective To assess efficacy of maternal vitamin A or beta carotene supplementation in reducing pregnancy-related and infant mortality. Design, Setting, and Participants Cluster randomized, double-masked, placebo-controlled trial among pregnant women 13 to 45 years of age and their live-born infants to 12 weeks (84 days) postpartum in rural northern Bangladesh between 2001 and 2007. Interventions Five hundred ninety-six community clusters (study sectors) were randomized for pregnant women to receive weekly, from the first trimester through 12 weeks postpartum, 7000 μg of retinol equivalents as retinyl palmitate, 42 mg of all -trans beta carotene, or placebo. Married women (n = 125 257) underwent 5-week surveillance for pregnancy, ascertained by a history of amenorrhea and confirmed by urine test. Blood samples were obtained from participants in 32 sectors (5%) for biochemical studies. Main Outcome Measures All-cause mortality of women related to pregnancy, stillbirth, and infant mortality to 12 weeks (84 days) following pregnancy outcome. Results Groups were comparable across risk factors. For the mortality outcomes, neither of the supplement group outcomes was significantly different from the placebo group outcomes. The numbers of deaths and all-cause, pregnancy-related mortality rates (per 100 000 pregnancies) were 41 and 206 (95% confidence interval [CI], 140-273) in the placebo group, 47 and 237 (95% CI, 166-309) in the vitamin A group, and 50 and 250 (95% CI, 177-323) in the beta carotene group. Relative risks for mortality in the vitamin A and beta carotene groups were 1.15 (95% CI, 0.75-1.76) and 1.21 (95% CI, 0.81-1.81), respectively. In the placebo, vitamin A, and beta carotene groups the rates of stillbirth and infant mortality were 47.9 (95% CI, 44.3-51.5), 45.6 (95% CI, 42.1-49.2), and 51.8 (95% CI, 48.0-55.6) per 1000 births and 68.1 (95% CI, 63.7-72.5), 65.0 (95% CI, 60.7-69.4), and 69.8 (95% CI, 65.4-72.3) per 1000 live births, respectively. Vitamin A compared with either placebo or beta carotene supplementation increased plasma retinol concentrations by end of study (1.46 [95% CI, 1.42-1.50] μmol/L vs 1.13 [95% CI, 1.09-1.17] μmol/L and 1.18 [95% CI, 1.14-1.22] μmol/L, respectively; P Conclusion Use of weekly vitamin A or beta carotene in pregnant women in Bangladesh, compared with placebo, did not reduce all-cause maternal, fetal, or infant mortality. Trial Registration clinicaltrials.gov Identifier: NCT00198822
133 citations
TL;DR: Vitamin A supplementation early in life was not associated with a decreased risk of asthma in an area with chronic vitamin A deficiency, and being born to mothers who received vitamin A, &bgr;-carotene or placebo before, during and after pregnancy was found to be normal.
Abstract: Animal models suggest that vitamin A deficiency affects lung development adversely and promotes airway hyperresponsiveness, and may predispose to an increased risk of asthma. We examined the long-term effects of vitamin A supplementation early in life on later asthma risk. In 2006-2008, we revisited participants from two cohorts in rural Nepal who were enrolled in randomised trials of vitamin A supplementation. The first cohort received vitamin A or placebo for <16 months during their pre-school years (1989-1991). The second cohort was born to mothers who received vitamin A, β-carotene or placebo before, during and after pregnancy (1994-1997). At follow-up, we asked about asthma symptoms and performed spirometry. Out of 6,421 subjects eligible to participate, 5,430 (85%) responded to our respiratory survey. Wheezing prevalence during the previous year was 4.8% in participants aged 9-13 yrs and 6.6% in participants aged 14-23 yrs. We found no differences between the vitamin A supplemented and placebo groups from either trial in the prevalence of lifetime or current asthma and wheeze or in spirometric indices of obstruction (p ≥ 0.12 for all comparisons). Vitamin A supplementation early in life was not associated with a decreased risk of asthma in an area with chronic vitamin A deficiency.
57 citations
TL;DR: Ocular hypertension and low-/ normal-tension glaucoma are not clinical entities; they are meaningless statistical constructs that have done more to confuse the diagnosis and management of primary open-angle glAUcoma (POAG) than they ever did to enhance it.
Abstract: L ET ME BEGIN WITH A SIMPLE, DECLARATIVE conclusion: ocular hypertension and low-/ normal-tension glaucoma are not clinical entities. They are meaningless statistical constructs that have done more to confuse the diagnosis and management of primary open-angle glaucoma (POAG) than they ever did to enhance it. It is time these terms were put to permanent rest. How did these terms come about? Von Graefe concluded that all glaucomatous optic disc “excavation” was associated with high intraocular pressure (IOP), based on the only instrument then available for measuring IOP, digital palpation. Not until nearly a century later were reliable instruments used to measure the IOP of patients with characteristic glaucomatous optic nerve damage and of representative samples of older, Europeanderived populations. These early pioneers debated statistical analyses in an attempt to identify an IOP that would differentiate patients with “chronic simple glaucoma” from the rest of the population. Since the IOP among subjects without glaucoma had a mean of 15 mm Hg to 16 mm Hg and an SD of 2.5 mm Hg, less than 2% of the general population was expected to have an IOP greater than 21 or 22 mm Hg (the ū±2 SD). It was assumed that those who did either had POAG or were bound to develop it; because they were “uncommon” in the general population, they were unlikely to be “normal.” “Uncommon” had become “abnormal.” Perkins, referring to a consensus among “a number of English ophthalmologists engaged in glaucoma research,” recommended “for clarity” that people with an IOP of 22 mm Hg or higher on 2 or more occasions without glaucomatous discs or visual field abnormality, be termed ocular hypertension. Leydhecker concurred. This would distinguish them from patients with “elevated” pressure and clear evidence of optic nerve damage (“chronic simple glaucoma”). Thus, ocular hypertension became a distinct clinical entity. Since the definition of “chronic simple glaucoma” required an “abnormally elevated” (eg, uncommon) IOP, confusion soon multiplied. Once population surveys found that a substantial number of subjects with otherwise typical POAG had pressures that did not exceed 21 mm Hg, low-/normal-tension glaucoma entered our lexicon, as yet another distinct clinical entity. Primary openangle glaucoma had been divided, purely on the basis of having an IOP higher or lower than 21 (or 22) mm Hg, into 3 purportedly distinct ophthalmic entities: ocular hypertension, normal-tension glaucoma, and POAG. Surveys over the past 30 years, using more sensitive and specific diagnostic techniques and criteria that largely excluded IOP from the definition (and to a lesser degree, case finding), emphasize how arbitrary and meaningless these IOP-based distinctions are. Every wellexecuted survey indicates that the risk of open-angle glaucoma increases with the height of the IOP, but in none is there is an IOP that neatly distinguishes between patients with and without open-angle glaucoma or the risk of one day developing it. The relationship between IOP and POAG is continuous, not dichotomous. Because the distribution of IOP in subjects without glaucoma of European extraction is not “normal” but has an extended tail to the right, roughly 5% to 7% of older subjects without glaucoma, not 1% to 2%, have an IOP greater than 21 mm Hg. When the diagnosis of POAG is based solely on the presence of typical glaucomatous optic nerve damage, irrespective of IOP, one-third to more than one-half of all subjects with POAG have an IOP lower than 22 mm Hg (Table 1). There is obviously nothing distinctive about an IOP of 21 or 22 mm Hg. If the prevalence (“risk”) of POAG increases in subjects with higher IOP, how can half the patients with POAG have a screening IOP lower than 22 mm Hg? Because the vast majority of the population has low IOP! In the Baltimore Eye Survey, subjects with pressures greater than 21 mm Hg were 10 times as likely to have POAG as subjects with lower IOP (relative risk=10). But there were 12 times as many subjects with lower IOP. Hence, the group of survey subjects with an IOP lower than 22 mm Hg contained 40% more cases of POAG than the group with higher IOP (attributable risk = 1.4) (Table 2). Indeed, more than half the subjects with POAG in the Baltimore Eye Survey had an IOP lower than 20 mm Hg. Non-European–derived populations may have different underlying distributions of IOP, but these are entirely consistent with this same principle. The mean IOP Table 1. Percentage of Eyes (or Subjects) With POAG and Screening IOP Lower Than 22 mm Hg
39 citations
2 citations
TL;DR: The primary problem at present is that most low- and middle-income countries have yet to grapple with the difficult task of providing high-quality cataract surgical services to those who need them, particularly those residing in poor, rural communities.
2 citations