Quality of Diabetes Care in Blended Fee-for-Service and Blended Capitation Payment Systems.

OBJECTIVES: In the middle to late 2000s, many family physicians switched from a Family Health Group (FHG; a blended fee-for-service model) to a Family Health Organization (FHO; a blended capitation model) in Ontario, Canada. The evidence on the link between physician remuneration schemes and quality of diabetes care is mixed in the literature. We examined whether physicians who switched from the FHG to FHO model provided better care for individuals living with diabetes relative to those who remained in the FHG model. METHODS: Using longitudinal health administrative data from 2006 to 2016, we investigated the impact of physicians switching from FHG to FHO on 8 quality indicators related to diabetes care. Because FHO physicians are likely to be systematically different from FHGs, we employed propensity-score-based inverse probability-weighted fixed-effects regression models. All analyses were conducted at the physician level. RESULTS: We found that FHO physicians were more likely to provide glycated hemoglobin testing by 2.75% (95% confidence interval [CI], 1.89% to 3.60%), lipid assessment by 2.76% (CI, 1.95% to 3.57%), nephropathy screening by 1.08% (95% CI, 0.51% to 1.66%) and statin prescription by 1.08% (95% CI, 0.51% to 1.66%). Patients under FHOs had a lower estimated risk of mortality by 0.0124% (95% CI, 0.0123% to 0.0126%) per physician per year. However, FHG and FHO physicians were similar for annual eye examination, prescription of angiotensin-converting enzyme inhibitors (or angiotensin II receptor blockers) and patients' risk of avoidable diabetes-related hospitalizations. CONCLUSIONS: Compared with blended fee-for-service, blended capitation payment is associated with a small, but statistically significant, improvement in some aspects of diabetes care.

Familial hypercholesterolemia mutations in the Middle Eastern and North African region: a need for a national registry.

BACKGROUND: Familial hypercholesterolemia (FH) is a well-understood Mendelian disorder that increases the risk of cardiovascular disease (CVD), a leading cause of mortality in Middle Eastern and North African (MENA) countries. OBJECTIVE: Review the reporting status of FH mutations across MENA and propose a systemic and strategic method for building a MENA FH registry. METHODS: Systematic literature search for statistics pertaining to CVD and comparison of number of FH mutations reported in MENA countries and countries with established FH registries. RESULTS: Only 57 mutations were reported in 17 MENA countries, whereas more than 500 mutations reported in 3 Western countries. Mortality rates due to CVD were significantly higher in MENA countries compared with Western countries. CONCLUSIONS: The relatively low reporting of FH mutations in the consanguineous MENA communities with higher prevalence of CVD indicates poor awareness of CVD genetic risk and warrants a registry to prevent premature CVD due to FH. This registry will help in identifying novel and reported FH mutations, all of which will have clinical and research benefits in MENA countries.

APOE p.Leu167del mutation in familial hypercholesterolemia.

BACKGROUND: Autosomal dominant hypercholesterolemia (ADH) is caused by mutations in the low density lipoprotein receptor (LDLR), its ligand apoB (APOB) or proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. Yet DNA sequencing does not identify mutations in these genes in a significant number of cases, suggesting that ADH has multiple genetic etiologies. METHODS: Through a combination of clinical examination, biochemical analysis, candidate gene approach and next-generation exome sequencing we investigated the genetic basis of an ADH phenotype in a proband of an Italian origin. RESULTS: The proband presented with an acute myocardial infarction at age 43. He had tendinous xanthomas, xanthelasmas and elevated levels of total and LDL cholesterol, at 11.2 and 9.69 mmol/L, respectively, with normal levels of HDL cholesterol and triglycerides at 1.62 and 1.13 mmol/L, respectively. HPLC lipoprotein profile showed selective increase in LDL-C. DNA sequencing did not identify any mutation in the LDLR, PCSK9, LDLRAP1 and APOB gene. We then performed exome sequencing on three individuals from the family. The strongest evidence of association was found for the previously identified apolipoprotein E mutation (APOE, chromosome 19:45412053-55) known as APOE Leu167del, an in-frame three base-pair deletion. Computational biology confirmed the deleterious nature of this mutation. The Leu167del mutation is predicted to alter the protein structure of apoE near the α-helix within the receptor binding domain. CONCLUSIONS: This report confirms a previous report that ADH can be caused by mutations within the APOE gene and represents the 4th loci causing ADH. Standard screening for ADH should include APOE gene.