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Judy S Cohain, Researcher
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judyslome{at}hotmail.com Judy S Cohain
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Dear Editor, I am writing to express concern about several potential confounding factors apparently not considered by Merewood et al. (1). First, the non-randomly selected sample was not done at the time of delivery as the conclusions of the study misleadingly state; the sample was selected postpartum after the outcome variable was known. Second, their study patients included a disproportionate number of obese women: 40% obese (BMI 25-35) and another 8% extremely obese women (BMI > 35); and for 10 women (4%) of the sample of 253 women the BMI is missing. This is the known obesity rate for the US as a whole, but atypical of primiparous women. Third, since 29% of Boston Medical Center births are attended by Nurse-Midwives who are known to have lower cesarean section rates, it would have been revealing to evaluate the cesarean section outcomes of midwife births vs. non-midwife births. Fourth, the sample includes diabetics, alcohol users, users of drugs during labor, postpartum hemorrhages and postpartum infections, none of which were evaluated as variables, but are all known to adversely affect vitamin D content of blood. In addition to these concerns, the authors only studied vitamin D levels both pre- and postpartum , but failed to establish a baseline for normal postpartum vitamin D levels, measuring these before and after surgery in only five women. The only previous article which studied serum 25-hydroxyvitamin D in American primiparous pregnancy, found an average serum level in women reportedly taking daily vitamin D supplements and 2 cups of milk/day to be 73 ng/mL for nulliparous white women and 40 ng/mL for nulliparous black women at 4-21 weeks of pregnancy (2). In a postpartum study of 40 mostly black mothers, the average level was 30 nmol/L at 24–48 h postpartum, and black women had significantly lower vitamin D levels but a much higher vaginal birth rate (3). Therefore, we believe that the authors’ suggested association between hypovitaminosis D and cesarean section frequency is highly dubious. The authors’ theory that muscle weakness is responsible fail to consider that paraplegic women restricted to wheelchairs deliver babies just fine vaginally, and that epidural anesthesia knocks the muscle tone out of women, often causing the baby to turn posterior because of lack of pelvic muscle tone. References 1. Merewood A, Mehta SD, Chen TC, Bauchner H, Holick MF. 2009. Association between vitamin D deficiency and primary cesarean section. J Clin Endocrinol Metab 94:940-945 2. Bodnar LM, Simhan HN, Powers RW, Frank MP, Cooperstein E, Roberts JM. 2007. High prevalence of vitamin D insufficiency in black and white pregnant women residing in the northern United States and their neonates. J Nutr 137:447-452 3. Lee JM, Smith JR, Philipp BL, Chen TC, Mathieu J, Holick MF. 2007. Vitamin D deficiency in a healthy group of mothers and newborn infants. Clin Pediatr 46:42-44 |
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Daniel S Hirsch, Assistant Professor of Pediatrics Division of Neonatology, Robert Wood Johnson Medical School- UMDNJ, Carol L. Wagner and Donna D. Johnson
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danieldphoto{at}gmail.com Daniel S Hirsch, et al.
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Merewood et al. (1). are to be commended for their detailed description and analysis of a significant association between the prevalence of maternal vitamin D deficiency at birth and delivery via primary cesarean section (PCS) at term. The authors concluded that “A randomized clinical trial is now needed to determine if adequate vitamin D supplementation during pregnancy to raise blood levels of 25(OH)D above at least 37.5 nmol/L can reduce the cesarean section rate and whether increasing it above 75 nmol/L provides any additional reduction ...” (1). Caution is appropriate before drawing any conclusions from this study. The biological plausibility for the association of vitamin D deficiency and PCS secondary to failure to progress or cephalopelvic disproportion might be that vitamin D deficient women have a rachitic-type pelvis or muscle weakness that prevents normal uterine contractions and/or maternal expulsion forces during labor. Although a grossly abnormal pelvis may be detected via clinical pelvimetry, use of this technique was not reported. The strength of uterine contractions can be measured using an intrauterine pressure catheter and reported in Montevideo units, which would have added more credence to the study. Moreover, failure to progress is an imprecise and over-utilized clinical description for labor dystocia. The remaining 53% of the PCS’s included in this analysis were performed for a condition unrelated to maternal vitamin D status (“non-reassuring fetal tracing,” “fetal malpresentation”, “variable fetal heart rate” and “other”). The study would have been strengthened by excluding these patients from the analysis. Another significant shortcoming of this paper concerns the failure to account and control for numerous factors which have been shown to impact the route of delivery including, spontaneous or medical induction of labor, method and administration of pitocin and birth weight. In light of these considerations, we speculate that the statistically significant association between maternal vitamin D status and delivery via PCS noted by Merewood et al. may be merely an incidental finding. Before conducting a randomized clinical trial on the use of vitamin D supplementation to reduce the rate of PCS, additional retrospective and prospective observational studies that include more precise definitions and inclusion of variables that impact the reason for a PCS are needed. Reference 1. Merewood A, Mehta SD, Chen TC, Bauchner H, Holick HF. 2008. Association Between Vitamin D Deficiency and Primary Cesarean Section. J Clin Endocrinol Metab jc.2008-1217v1 |
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