Practices and attitudes of providers towards continuity of care with patients using prescription contraceptives.

The aim of this study was to explore provider practices and attitudes towards routine follow-up counselling after prescription of contraceptives. An anonymous 16-item survey was pilot-tested and sent to providers of the Internal Medicine, Family Medicine, Pediatrics, and OBGYN departments of Thomas Jefferson University Hospitals (TJUH), an urban academic medical centre in Philadelphia, PA, USA. Frequency and descriptive statistics were used to analyse quantitative data while a framework analysis approach was applied to open-ended questions. Fifty percent of providers said they typically follow up with patients regarding a newly prescribed contraceptive. Only 15.3% said they do for an existing prescription. Eighty-three percent reported that it is important though only 30% believed follow-up guidelines were clear. Ultimately, there is a gap between providers' interest in delivering follow-up care and established direction on how to do so.Impact StatementWhat is already known on the subject? Prescription contraceptive adherence is suboptimal. However, it is known that proactive follow-up has positive effects on prescription contraceptive adherence.What do the results of the study add? Most respondents believe that patients take their prescription contraception as prescribed. In light of this finding, providers are less likely to follow up with an existing prescription contraceptive. Interestingly, most respondents do believe that follow-up is important for patients using prescribed contraception but endorse that guidelines about follow-up are neither established nor clear.What are the implications of these findings for clinical practice and/or further research? Patient adherence to prescription contraceptives can be improved through optimised routine patient follow-up after initial prescription. This must be done in ways that minimise burdens to both patients and providers. Providers could benefit from clear guidelines regarding best practices. Future research is needed to understand how providers can best support patients on their contraceptive journey.

Coronary artery dilatation and aortic outflow tract enlargement in children with unicommissural aortic valves.

We evaluated the aortic outflow tract (AOT) and coronary artery dimensions in pediatric patients with unicommissural aortic valves. A retrospective review of an echocardiographic database identified 37 patients with unicommissural aortic valves. A total of 115 echocardiograms were reviewed, and the right coronary artery (RCA), left main coronary artery (LM), left anterior descending coronary artery aortic valve annulus, aortic root, sinotubular junction (STJ), and ascending aorta were measured and z scores determined. The aortic stenosis peak gradient and the amount of aortic regurgitation (AR) were also measured. The RCA diameter (z score, 1.85 +/- 1.8, p = 0.03) and LM diameter (z score, 1.74 +/- 1.47, p = 0.04) are significantly dilated, as are all the AOT measurements: aortic annulus (2.02 +/- 1.9, p = 0.02), aortic root (2.25 +/- 1.9, p = 0.02), STJ (2.22 +/- 1.74, p = 0.01), and ascending aorta (4.38 +/- 2.03, p < 0.001). Longitudinal follow-up showed that there was no significant variation over time in any variable. The AOT measurements were significantly correlated with each other. A trend was found in which an increasing amount of AR gave an increase in AOT measurements. The aortic gradient was not significantly associated with any measurement. Our study population demonstrated significant dilatation of the RCA and LM as well as the AOT. The dilatation of the AOT structures is likely caused by the same mechanism that accounts for the AOT dilatation in patients with bicommissural aortic valves. Dilatation of the coronary arteries may represent an intrinsic abnormality in the vessel wall. Further studies are needed to define possible changes.

Testing candidate genes for non-syndromic oral clefts using a case-parent trio design.

Markers in five candidate genes were examined on 269 case-parent trios ascertained through a child with an isolated, non-syndromic oral cleft (cleft lip, CL; cleft palate, CP; or cleft lip and palate, CLP). Cases and their parents were ascertained through treatment centers in Maryland. Markers at two of the five candidate genes, transforming growth factor beta3 (TGFbeta3) and MSX1, showed consistent evidence of linkage and disequilibrium due to linkage using several statistical tests (e.g., the global chi-square for TGFbeta3 was 21.1 with 12 df, P = 0.03; that for MSX1 was 8.7 with 3 df, P = 0.03). There was little evidence of heterogeneity in the role of TGFbeta3 between different types of oral clefts, but MSX1 did yield marginal evidence for such heterogeneity. MSX1 also showed evidence for interaction between infant's genotype and maternal smoking, giving a likelihood ratio test for heterogeneity between smoker and non-smoker mothers of 7.16 (2 df, P = 0.03). Using a conditional logistic model to test for gene-gene interaction showed no evidence of interaction between TGFbeta3 and MSX1, with both seeming to contribute independently to risk of isolated, non-syndromic oral clefts.

A case-control study of nonsyndromic oral clefts in Maryland.

PURPOSE: Isolated, nonsyndromic oral clefts cases (n = 171) and unaffected controls (n = 182) were used to identify both genetic and environmental risk factors. METHODS: Infants born in Maryland between 1992 to 1998 with an isolated, nonsyndromic oral cleft [cleft lip (CL), cleft lip and palate (CLP), or cleft palate (CP)] were recruited and exposure plus family history data were collected. Controls were unaffected infants. DNA was collected from all cases and their parents, plus controls. RESULTS: No statistically significant association was found between any of the following: maternal smoking, vitamin use, urinary tract infection, or recreational drug use in either univariate analysis or after adjusting for maternal age and education. More control mothers reported alcohol use during the critical time period of pregnancy (one month before conception through the first trimester) as compared to case mothers. There was a 10-fold increase in risk to siblings of cases as compared to siblings of controls. Markers at four candidate genes were examined: transforming growth factor alpha (TGF alpha), transforming growth factor beta 3 (TGF beta 3), MSX1, and BCL3. Only MSX1 showed significant differences in allele frequencies between CP cases and controls. MSX1 also showed significant evidence of linkage disequilibrium with a susceptibility gene controlling risk for CP. CONCLUSION: Most environmental risk factors examined here gave little evidence of association with risk to isolated, nonsyndromic oral clefts, although any alcohol consumption seemed protective. MSX1 showed evidence of linkage disequilibrium in both case-control and case-parent trio analysis.

Testing for interaction between maternal smoking and TGFA genotype among oral cleft cases born in Maryland 1992-1996.

OBJECTIVE: Infants born in Maryland between June 1992 and June 1996 were used in a case-control study of nonsyndromic oral clefts to test for effects of maternal smoking and a polymorphic genetic marker at the transforming growth factor alpha (TGFA) locus, both of which have been reported to be risk factors for these common birth defects. DESIGN AND SETTING: Cases were infants with an oral cleft ascertained through three comprehensive treatment centers, with additional ascertainment through a registry of birth defects maintained by the Maryland Health Department. Controls were healthy infants. Medical history information on infants and mothers were collected, along with DNA samples. PATIENTS, PARTICIPANTS: Among 286 cases contacted (72% ascertainment), there were 192 nonsyndromic isolated oral clefts (106 M; 86 F) available for this case-control study. MAIN OUTCOME MEASURES: The largest group of 149 Caucasian nonsyndromic cases and 86 controls was used to test for association with maternal smoking and genotype at the Taq1 polymorphism in TGFA. RESULTS: While this modest sample had limited statistical power to detect gene-environment interaction, there was a significant marginal increase in risk of having an oral cleft if the mother smoked (odds ratio = 1.75, 95% CI = 1.01 to 3.02). We could not demonstrate statistical interaction between maternal smoking and TGFA genotype in this study, however, and the observed increase in the C2 allele among cases was not statistically significant. CONCLUSIONS: We could not confirm either the reported association between oral clefts and TGFA genotype or its interaction with maternal smoking. However, these data do show an increased risk if the mother smoked during pregnancy, and this effect was greatest among infants with a bilateral cleft and no close family history of clefts.