Correlation of serum interleukin-6 levels and neutrophil-lymphocyte ratio in the severity of COVID-19.

Background: Interleukin-6 (IL-6) is a pro-inflammatory cytokine that is produced at varying levels in patients with coronavirus disease 2019 (COVID-19). The neutrophil-lymphocyte ratio (NLR) is one of the new inflammatory markers of COVID-19. This study aimed to evaluate the differences in IL-6 level and the NLR in mild and severe COVID-19 and assess their correlation with COVID-19 severity and the correlation of IL-6 and NLR in COVID-19. Methods: A total of 91 patients with COVID-19 were divided into mild (n = 57) and severe (n = 34) COVID-19 groups. IL-6 levels were measured using the electrochemiluminescence immunoassay method on Roche Cobas e411. The NLR was the ratio of the total neutrophil and lymphocyte counts from complete haematology on the Sysmex XS-800i. Data were analysed using the Kolmogorov-Smirnov, Mann-Whitney, receiver operating characteristic curve, chi-square and Spearman correlation tests. The statistical test was significant at p <0.05. Results: Serum IL-6 levels and NLR significantly differed in mild and severe COVID-19. The median (min-max) IL-6 levels for mild and severe COVID-19 were 3.59 (1.50-638.30) pg/mL and 28.82 (5.52-926.30) pg/mL, respectively (p <0.001). The median (min-max) NLR in mild and moderate COVID-19 was 2.18 (0.69-15.58) and 8.13 (2.24-30.90), respectively (p <0.001). The obtained cut-off values for IL-6 and NLR were >6.99 pg/mL and >4.18, with odds ratios of 29.29 and 26.19, respectively. A positive correlation was found between IL-6 and NLR and COVID-19 severity (r = 0.612; p <0.001). Conclusions: The results indicated that serum IL-6 levels and NLR are higher in severe COVID-19 than in mild COVID-19. Patients with IL-6 levels >6.99 pg/mL and NLR >4.18 are 29 and 26 times more likely to suffer from severe COVID-19, respectively. Serum IL-6 levels and NLR are strongly correlated with COVID-19 severity. Serum IL-6 levels correlate with NLR in COVID-19.

Glycemic control as the main determinant factor of serum VEGF levels in type 2 diabetes mellitus patients.

Introduction. Diabetes mellitus (DM) is a main endocrine disorder that may cause vascular complications as the disease progresses. Vascular endothelial growth factor (VEGF) has been linked to the development of micro and macrovascular diabetic complications. This study aimed to assess several factors including blood pressure, body mass index, lipid profile, kidney function, and glycemic control that may provide the rise of serum VEGF levels in type 2 DM subjects. Methods. This cross-sectional study was carried out among 65 type 2 DM subjects. Systole, diastole, mean arterial pressure (MAP), and body mass index (BMI) were measured. The levels of serum VEGF were measured by Enzyme-linked immunosorbent assay (ELISA), Hemoglobin A1c (HbA1c) levels were measured by latex agglutination inhibition test, while serum glucose, lipid profiles, urea, and creatinine levels were tested by enzymatic photometric method. Results. The levels of serum VEGF had a significant correlation with BMI (p = 0.001, r = 0.397), fasting plasma glucose (FPG) (p = 0.001, r = 0.418), HbA1c (p < 0.001, r = 0.600), systole (p = 0.001), r = 0.397), diastole (p = 0.021, r = 0.286), and MAP (p = 0.001, r = 0.001). Further multivariate linear regression analysis revealed that HbA1c logarithm (log) was the determinant factor of VEGF levels (p < 0.001, ß = 0.631, Adjusted R2 = 38.9%) Conclusion. HbA1c is the main determinant factor of serum VEGF levels among type 2 DM patients.

Anthropometric features in predicting insulin resistance among non-menopausal Indonesian adult females.

INTRODUCTION: The prevalence of obesity is increasing worldwide in high, low, and middle-income countries such as Indonesia. Obesity rate is higher in females in Indonesia. Obesity has important contribution in the occurrence of insulin resistance (IR) and type 2 diabetes mellitus. Several anthropometric measurements such as waist circumference (WC), body mass index (BMI), body mass (BM), total body fat percentage (Fat%) and visceral fat (VF) are related to IR. This study aimed to investigate which of those measurements could be used as a better predictor of IR in non-menopausal Indonesian adult females. METHODS: Total of 80 non-menopausal Indonesian adult females ranging from 21 to 40 years were recruited in this study. Insulin resistance was measured by using Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) equation. Subjects with HOMA-IR index >75th percentile with cut-off 2.74 were defined as IR. Waist circumference, BMI and BM were measured, while TF and VF were measured by bioelectrical impedance analysis (BIA). RESULTS: HOMA-IR had significant correlation with WC (r = 0.563, p < 0.001), BMI (r = 0.537, p < 0.001), BM (r = 0.515, p < 0.001), VF (r = 0.515, p < 0.001), Fat% (r = 0.490, p < 0.001). The area under curve of VF (0.809), BMI (0.807), WC (0.805), and BM (0.799) are slightly larger than and Fat% (0.766). CONCLUSION: Insulin resistance had strong correlation with all anthropometric measurements, but the correlation was less significant with Fat%.

OPA1 gene mutations in Japanese patients with bilateral optic atrophy unassociated with mitochondrial DNA mutations at nt 11778, 3460, and 14484.

PURPOSE: To report mutations in the OPA1 gene in Japanese patients with bilateral optic atrophy unassociated with mitochondrial DNA mutations at nt 11778, 3460, and 14484. METHODS: Twelve unrelated patients with bilateral optic atrophy and 100 healthy controls were examined. Each exon of the OPA1 gene was amplified by polymerase chain reaction (PCR). All PCR products were sequenced. RESULTS: Of the 12 patients, 2 had nonsense mutations of the OPA1 gene (nt 1039G --> T and nt 1096C --> T, leading to Glu347Stop and Arg366Stop, respectively). These nonsense mutations were not found in the 100 healthy controls. Two of the patients had silent mutations of OPA1 gene (nt 1177T --> G and nt 1923G --> A causing no amino acid change). CONCLUSIONS: The mutations (Glu347Stop and Arg366Stop) of the OPA1 gene are involved in the pathogenesis of bilateral optic atrophy in Japanese patients.