Visceral fat index: a novel predictor for coronary collateral circulation.

Objective This study was designed to investigate the role of visceral adiposity along with other clinical parameters in predicting poor coronary collateral circulation (CCC) among patients with severe obstructive coronary artery disease (CAD). Subjects and methods A total of 135 patients with severe obstructive CAD and good (n = 70) or poor (n = 65) CCC were included. Data on angiographically detected CCC, the quality criteria for CCC (Rentrop scores) and visceral fat index (VFI) obtained via bioelectrical impedance were compared between good and poor CCC groups. Independent predictors of poor CCC, the correlation between VFI and Rentrop score and the role of VFI in the identification of CCC were analyzed. Results A significant negative correlation was noted between VFI and Rentrop scores (r = -0.668, < 0.001). The presence of hypertension (OR 4.244, 95% CI 1.184 to 15.211, p = 0.026) and higher VFI (OR 1.955, 95% CI 1.342 to 2.848, p < 0.001) were shown to be independent predictors of an increased risk for poor CCC. ROC analysis revealed a VFI > 9 (AUC [area under the curve] (95% CI): 0.898 (0.834-0.943), p < 0.0001) to be a potential predictor of poor CCC with a sensitivity of 95.38% and specificity of 85.71%. Conclusion In conclusion, our findings revealed comorbid hypertension and higher VFI to significantly predict the risk of poor CCC in patients with severe obstructive CAD.

Visceral fat index: a novel predictor for coronary collateral circulation

ABSTRACT Objective This study was designed to investigate the role of visceral adiposity along with other clinical parameters in predicting poor coronary collateral circulation (CCC) among patients with severe obstructive coronary artery disease (CAD). Subjects and methods A total of 135 patients with severe obstructive CAD and good (n = 70) or poor (n = 65) CCC were included. Data on angiographically detected CCC, the quality criteria for CCC (Rentrop scores) and visceral fat index (VFI) obtained via bioelectrical impedance were compared between good and poor CCC groups. Independent predictors of poor CCC, the correlation between VFI and Rentrop score and the role of VFI in the identification of CCC were analyzed. Results A significant negative correlation was noted between VFI and Rentrop scores (r = -0.668, < 0.001). The presence of hypertension (OR 4.244, 95% CI 1.184 to 15.211, p = 0.026) and higher VFI (OR 1.955, 95% CI 1.342 to 2.848, p < 0.001) were shown to be independent predictors of an increased risk for poor CCC. ROC analysis revealed a VFI > 9 (AUC [area under the curve] (95% CI): 0.898 (0.834-0.943), p < 0.0001) to be a potential predictor of poor CCC with a sensitivity of 95.38% and specificity of 85.71%. Conclusion In conclusion, our findings revealed comorbid hypertension and higher VFI to significantly predict the risk of poor CCC in patients with severe obstructive CAD.

Identification of two novel PNPLA1 mutations in Turkish families with autosomal recessive congenital ichthyosis.

Dökmeci-Emre S, Taskiran ZE, Yüzbasioglu A, Önal G, Akarsu AN, Karaduman A, Özgüç M. Identification of two novel PNPLA1 mutations in Turkish families with autosomal recessive congenital ichthyosis. Turk J Pediatr 2017; 59: 475-482. Autosomal recessive congenital ichthyosis (ARCI) is a group of inherited keratinization disorders that are characterized by abnormal epidermal keratinization. ARCI patients generally represent serious symptoms including collodion baby phenotype accompanied by dehydration, heat loss, electrolytic imbalance, and sepsis. ARCI shows high degree of clinical and genetic heterogeneity. To date, nine genes were shown to be responsible for ARCI phenotype. One of these genes, patatin-like phospholipase domain containing protein-1 (PNPLA1) was suggested to be involved in the synthesis of ω-O-acylceramides related to epidermal cornified lipid envelope organization. In addition to previously reported PNPLA1 mutations, we report two novel PNPLA1 mutations including one novel missense mutation c.335C > A (p.Ser112Tyr) and one novel deletion mutation c.733_735delTAC (p.Tyr245del) in Turkish ARCI patients from unrelated consanguineous families. We also report previously reported missense mutation c.514G > A (p.Asp172Asn) in Turkish ARCI patients. Novel PNPLA1 mutations were shown to be located in the catalytic patatin domain of PNPLA1 gene. Identification of novel mutations in PNPLA1 gene expands the mutational spectrum in the causative gene. Increase in the total number of cases has high diagnostic value in terms of genotype-phenotype correlation in ARCI patients.