Racial and Ethnic Differences in Psychotropic Prescription Receipt Among Pediatric Patients Enrolled in North Carolina Medicaid.

OBJECTIVE: The authors aimed to examine racial-ethnic differences in filled psychotropic prescriptions among a pediatric Medicaid population. METHODS: This retrospective cohort study included patients ages 0-21 with at least one North Carolina Medicaid claim from October 1, 2017, through September 30, 2018 (N=983,886). The primary outcome was a filled psychotropic prescription. Separate multivariable modified Poisson regression models generated adjusted risk ratios (ARRs) and 95% confidence intervals (CIs), adjusted for patient demographic characteristics. RESULTS: Black and Hispanic patients were significantly less likely to receive any filled psychotropic prescription (ARR=0.61, 95% CI=0.60-0.62; ARR=0.29, 95% CI=0.28-0.29, respectively) compared with White and non-Hispanic patients. Furthermore, Black and Hispanic patients were less likely to receive filled prescriptions in the four included drug classes compared with White and non-Hispanic patients. CONCLUSIONS: Future studies should focus on understanding the factors contributing to racial and ethnic differences among pediatric patients receiving filled psychotropic prescriptions.

Use of North Carolina Medicaid Collaborative Care Billing Codes After Statewide Approval for Reimbursement.

Effective October 2018, North Carolina Medicaid approved reimbursement for collaborative care model (CoCM) billing codes. From October 2018 through December 2019, only 915 of the estimated two million eligible Medicaid beneficiaries had at least one CoCM claim, and the median number of claims per patient was two. Availability of reimbursement for CoCM Medicaid billing codes in North Carolina did not immediately result in robust utilization of CoCM. Furthermore, the low median number of claims per patient suggests lack of fidelity to CoCM. A better understanding of barriers to CoCM implementation is necessary to expand utilization of this evidence-based model.

Brief Report: Classifying Rates of Students with Autism and Intellectual Disability in North Carolina: Roles of Race and Economic Disadvantage.

We examined special education classifications among students aged 3-21 in North Carolina public schools, highlighting autism spectrum disorder (ASD) and intellectual disability (ID). Results revealed variability by county in ASD and ID prevalence, and in county-level ratios of ID vs. ASD classifications. Sociodemographic characteristics predicted proportion of ASD or ID within a county; correlations showed an association between race and ID, but not ASD. County's median household income predicted proportion of students classified as ASD and ID (opposite directions), controlling for number of students and gender. Variability was unlikely related to biological incidence, and more likely related to district/school practices, or differences in resources. Disparities warrant further examination to ensure that North Carolina's youth with disabilities access necessary, appropriate resources.

Correction to: De novo CACNA1D Ca2+ channelopathies: clinical phenotypes and molecular mechanism.

The above article was published online with an error in Article title. Author mispronounced the name of a gene (CACNA1D instead of CACAN1D). The correct gene is presented above.

De novo CACNA1D Ca2+ channelopathies: clinical phenotypes and molecular mechanism.

The identification of rare disease-causing variants in humans by large-scale next-generation sequencing (NGS) studies has also provided us with new insights into the pathophysiological role of de novo missense variants in the CACNA1D gene that encodes the pore-forming α1-subunit of voltage-gated Cav1.3 L-type Ca2+ channels. These CACNA1D variants have been identified somatically in aldosterone-producing adenomas as well as germline in patients with neurodevelopmental and in some cases endocrine symptoms. In vitro studies in heterologous expression systems have revealed typical gating changes that indicate enhanced Ca2+ influx through Cav1.3 channels as the underlying disease-causing mechanism. Here we summarize the clinical findings of 12 well-characterized individuals with a total of 9 high-risk pathogenic CACNA1D variants. Moreover, we propose how information from somatic mutations in aldosterone-producing adenomas could be used to predict the potential pathogenicity of novel germline variants. Since these pathogenic de novo variants can cause a channel-gain-of function, we also discuss the use of L-type Ca2+ channel blockers as a potential therapeutic option.

Suggestive linkage at 9p22 in bipolar disorder weighted by alcohol abuse.

Bipolar disorder (BP) is a highly heritable disorder, however attempts to map genetic risk factors are challenging. One possible reason for these difficulties is the genetic heterogeneity of BP. Hence, focusing on clinically homogeneous families to create a genetically more homogeneous sample may increase the power of finding a specific variant. Alcohol abuse (AA) and alcohol dependence (AD) are familial in BP families, and these families may carry a specific risk variant for BP. We tested this hypothesis by performing a genome-wide linkage scan in 638 pedigrees (1,835 individuals) from the National Institute of Mental Health Genetics Initiative for BP, weighting the evidence for linkage according to the family's frequency of AA or AD. Using AA weighting, we identified a linkage region on 9p22.2 with an NPL score of 3.23. The region had previously been identified in a meta-analysis of linkage in bipolar disorder. We used permutation analysis to assess if weighting by AA increased the linkage signal more than expected by chance and observed a significant P-value (P = 0.048). Therefore, the genetic risk factor for BP on 9p22.2 has an increased effect in families with high levels of AA. In summary, we present an example of using covariates such as AA and AD to define subtypes of BP, demonstrate how using such subtypes can improve the power of a linkage scan, and demonstrate statistical approaches to validate the suggested interaction.