Attention deficit/hyperactivity disorder medication and dental caries in children.

PURPOSE: Few studies have been conducted to investigate the effects, if any, of specific medication used to manage the symptoms of attention deficit/hyperactivity disorder (ADHD) as a risk factor for dental caries. A reported side-effect of the medication is a reduction in saliva. Healthy saliva has been shown to play many important functions in the prevention of dental caries. The focus of this review is to determine if any evidence exists to confirm that stimulant medication used to treat the symptoms of ADHD in children increases the risk of dental caries by virtue of its effect on the reduction of salivary flow. METHODS: A MEDLINE search was conducted for relevant studies. Search terms used were dental caries, attention deficit/hyperactivity disorder, ADHD, pharmacologic treatment of ADHD, stimulant medication, xerostomia, dry-mouth and saliva flow. Publication dates ranged from 2002 to 2012. RESULTS: Although dental caries prevalence has been found to be higher in children with ADHD, decreased salivary flow as a side-effect of pharmacological treatment does not appear to be responsible. CONCLUSION: Dental caries is a multi-factorial disease process. The most effective method of reducing dental caries in ADHD children is more frequent recare visits focusing on home plaque removal practices along with dietary counseling to reduce the consumption of cariogenic foods and drinks. This can only be accomplished with inclusion of the parent/guardian in the process.

Comparison of 3 school-based influenza surveillance indicators: lessons learned from 2009 pandemic influenza A (H1N1)--Denver Metropolitan Region, Colorado.

CONTEXT: Early in the 2009 pandemic influenza A (H1N1) experience, children aged 5 to 17 years were determined to be disproportionately affected compared with recent influenza seasons. OBJECTIVE: To characterize the pandemic among school-aged children, to enable timely influenza outbreak identification, and to determine which school-based influenza surveillance indicator correlated most closely with a laboratory-based standard influenza indicator (standard) and, therefore, might be most useful for future school-based influenza surveillance. DESIGN: : During the 2009-2010 school year, we monitored students using 3 different surveillance indicators: (1) all-cause absenteeism, (2) influenza-like illness (ILI)-related absenteeism, (3) and ILI-related school health office visits. Thresholds were set for each indicator to identify individual school outbreaks. Each surveillance indicator was compared with the standard, confirmed influenza cases among hospitalized patients. SETTING: Tri-County (Denver metropolitan area), Colorado. PARTICIPANTS: Prekindergarten through 12th-grade students in public schools. MAIN OUTCOME MEASURES: Correlation coefficients comparing each influenza surveillance indicator with the standard and graphs comparing weekly rates for each influenza surveillance indicator or weekly outbreak counts with the standard. RESULTS: Correlation between the surveillance indicators and the standard varied greatly. All-cause absenteeism correlated most poorly with the standard (Pearson's r = 0.33) and ILI-related health office visits correlated moderately well (r = 0.63). Influenza-like illness-related absenteeism correlated best (r = 0.92) and could be improved (r = 0.97) by shifting ILI-absenteeism data later by 1 week. Graphs of weekly rates or weekly outbreak counts also illustrated that ILI-related absenteeism correlated best with the standard. CONCLUSIONS: For influenza surveillance among school-aged children, when feasible, we recommend using ILI-related absenteeism, which correlated best and its rate peaked more than 1 week sooner than the standard. The other 2 surveillance indicators might be useful in certain situations, such as when resources are limited.

Needlestick injury surveillance during mass vaccination clinics: lessons learned and why more is needed--Tri-County (Denver Metropolitan) region, Colorado, 2009.

Tri-County Health Department studied needlestick injury (NSI) risks in pandemic influenza A (H1N1) mass vaccination clinics through incident reports and an Internet-based vaccinator survey. The mass vaccination clinic NSI rate was 4.9 times the mean rate observed during Tri-County Health Department's 2003 to 2009 routine vaccination clinics. There was also a trend of increased risk for NSI with vaccination inexperience. These findings can be used to improve future mass vaccination clinic safety.

Utah clinical guidelines on prescribing opioids for treatment of pain.

Utah Clinical Guidelines on Prescribing Opioids for Treatment of Pain were produced and made available to medical providers in March 2009. These guidelines were developed by a multidisciplinary consensus panel after a review of existing evidence-based guidelines. Common recommendations were compiled and presented to the panel for review. The guidelines consist of a set of recommendations for both acute and chronic pain. A second panel reviewed existing tools for providers and determined the need for any new tools. The final guidelines include 20 tools for providers to use in their practice. The complete version of the guidelines and the accompanying tools are available at: www.useonlyasdirected.org or www.health.utah.gov/prescription.

A genomewide search finds major susceptibility loci for nicotine dependence on chromosome 10 in African Americans.

Epidemiological studies have demonstrated that genetic factors account for at least 50% of the liability for nicotine dependence (ND). Although several linkage studies have been conducted, all samples to date were primarily of European origin. In this study, we conducted a genomewide scan of 1,261 individuals, representing 402 nuclear families, of African American (AA) origin. We examined 385 autosomal microsatellite markers for ND, which was assessed by smoking quantity (SQ), the Heaviness of Smoking Index (HSI), and the Fagerstrom Test for ND (FTND). After performing linkage analyses using various methods implemented in the GENEHUNTER and S.A.G.E. programs, we found a region near marker D10S1432 on chromosome 10q22 that showed a significant linkage to indexed SQ, with a maximum LOD score of 4.17 at 92 cM and suggestive linkage to HSI, SQ, and log-transformed SQ. Additionally, we identified three regions that met the criteria for suggestive linkage to at least one ND measure: on chromosomes 9q31 at marker D9S1825, 11p11 between markers D11S1993 and D11S1344, and 13q13 between markers D13S325 and D13S788. Other locations on chromosomes 15p11, 17q25, and 18q12 exhibited some evidence of linkage for ND (LOD >1.44). The four regions with significant or suggestive linkage were positive for multiple ND measures by multiple statistical methods. Some of these regions have been linked to smoking behavior at nominally significant levels in other studies, which provides independent replication of the regions for ND in different cohorts. In summary, we found significant linkage on chromosome 10q22 and suggestive linkage on chromosomes 9, 11, and 13 for major genetic determinants of ND in an AA sample. Further analysis of these positive regions by fine mapping and/or association analysis is thus warranted. To our knowledge, this study represents the first genomewide linkage scan of ND in an AA sample.

Single- and multilocus allelic variants within the GABA(B) receptor subunit 2 (GABAB2) gene are significantly associated with nicotine dependence.

Twelve single-nucleotide polymorphisms (SNPs) in the human gamma-aminobutyric acid type B (GABA(B)) receptor subunit 2 gene (GABAB2) were tested for association with nicotine dependence (ND) in an extensively phenotyped cohort of 1,276 smokers and nonsmokers, representing approximately 404 nuclear families of African American (AA) or European American (EA) origin. The GABAB2 gene encodes a subunit of the GABA(B) receptor for GABA, an inhibitory neurotransmitter involved in the regulation of many physiological and psychological processes in the brain. The gene is located within a region of chromosome 9q22 that showed a "suggestive" linkage to ND. Individual SNP analysis performed using the PBAT-GEE program indicated that two SNPs in the AAs and four SNPs in the EAs were significantly associated with ND. Haplotype analysis using the Family-Based Association Test revealed that, even after Bonferroni correction, the haplotype C-C-G of rs2491397-rs2184026-rs3750344 had a significant positive association with ND in both the pooled and the AA samples. In the EAs, we identified two haplotypes, C-A-C-A and T-A-T-A, formed by SNPs rs1435252-rs378042-rs2779562-rs3750344, that showed a highly significant negative and positive association with ND, respectively. In summary, our findings provide evidence of a significant association of GABAB2 variants with ND, implying that this gene plays an important role in the etiology of this drug addiction.

A genome-wide scan to identify loci for smoking rate in the Framingham Heart Study population.

BACKGROUND: Although many years of genetic epidemiological studies have demonstrated that genetics plays a significant role in determining smoking behavior, little information is available on genomic loci or genes affecting nicotine dependence. Several susceptibility chromosomal regions for nicotine dependence have been reported, but few have received independent confirmation. To identify susceptibility loci for nicotine dependence, 313 extended pedigrees selected from the Framingham Heart Study population were analyzed by both the GENEHUNTER and S.A.G.E. programs. RESULTS: After performing linkage analyses on the 313 extended Framingham Heart Study families, the EM Haseman-Elston method implemented in GENEHUNTER provided evidence for significant linkage of smoking rate to chromosome 11 and suggestive linkage to chromosomes 9, 14, and 17. Multipoint sib-pair regression analysis using the SIBPAL program of S.A.G.E. on 1389 sib pairs that were split from the 313 extended families identified suggestive linkage of smoking rate to chromosomes 4, 7, and 17. Of these identified positive regions for nicotine dependence, loci on chromosomes 7, 11, and 17 were identified by both GENEHUNTER and S.A.G.E. programs. CONCLUSION: Our genome-wide scan results on the Framingham Heart Study data provide evidence for significant linkage of smoking rate to chromosome 11 and suggestive linkage to chromosomes 4, 7, 9, 14, and 17. These findings suggest that some of these regions may harbor susceptibility loci for nicotine dependence, and warrant further investigation in this and other populations.