Cortisol dynamics and endothelin-1/nitric oxide ratio are associated with clinical vasospasme.

Background: Cortisol dynamics in serum might be related to clinical vasospasm, also known as delayed ischemic neurological deficits (DIND). Two vasoactive substances that play a role in pathophysiology of DIND are endothelin-1 (ET1) and nitric oxide (NO), both are proved associated with cortisol. This study aimed to know how cortisol plays a role on ET1/NO ratio and its relationship to DIND. Methods: This was a prospective cohort study for the first 14 days after aneurysmal subarachnoid hemorrhage (SAH). Patients with inclusion criteria will be enrolled for blood test before surgery, and post-operative day 2, 4, 7, and 10 (between 8:00-9:00 AM). The blood tests were performed for cortisol, ACTH, CBG, NO, and ET1. Free cortisol is calculated with Coolens equation. Logistic regression was used to see the interaction model and its scale. Bivariate analysis (corelation) was used to see the relationship between total cortisol, free cortisol, NO, ET1, and clinical vasospasm (DIND). Results: Forty-four patients were enrolled into this study (20 males; 24 females). Mean age was 52.02 ± 11.23 years. There were 29 patients (66%) within DIND group and 15 patients non-DIND as the control group. The mean of cortisol level shown was significantly higher in DIND group (35.99 ± 14.24) μg/dL compared to non-DIND group (19.57 ± 6.19) μg/dL, p < 0.001. The mean of free cortisol level was significantly higher in DIND group (2.06 ± 1.094) μg/dL compared to non-DIND group (0.838 ± 0.365 μg/dL; p < 0.001). The scatter plot graph showed that correlation of cortisol with ET1/NO ratio started increasing on day 4 and became stronger on day 10. Conclusion: Cortisol is associated with DIND following aneurysmal SAH, probably through its role in keeping the balance between ET1 and NO level.

Association between multimeric adiponectin and free leptin index with atherogenic dyslipidemia in non-diabetic obese men.

Background: To analyze the role of various adiponectin and free leptin index on the occurrence of atherogenic dislipidemia in non-diabetic central obese men. Methods: This is a cross-sectional study on 120 non-diabetic central obese men that was done in Jakarta. The measured indicators were total adiponectin, high molecular weight adiponectin (HMW adiponectin), medium molecular weight adiponectin (MMW adiponectin), low molecular weight adiponectin (LMW adiponectin), leptin, soluble leptin receptor, triglycerides, high-density lipoprotein cholesterol (HDL cholesterol), low density lipoprotein cholesterol (LDL cholesterol) and apolipoprotein B (Apo B). Atherogenic dyslipidemia was characterized by reduced level of HDL cholesterol, and high levels of triglyceride and small dense LDL (sdLDL). Ratio of LDL cholesterol and Apo B were calculated to get sdLDL. Free Leptin Index (FLI) was the ratio between total leptin and soluble leptin receptor (sOB-R), and median values were used as cut off to defi ne high and low values of each parameter. Cross tabulation were done on categorical data. Relationships between multimeric adiponectin and free leptin index with atherogenic lipids were analyzed by using Spearman analysis. Further, the interaction of all indicators with the occurence of atherogenic dyslipidemia was analyzed using binary logistic regression. Results: A negative correlation of HMW adiponectin with atherogenic dyslipidemia (p < 0.05), whereas there were no correlation between MMW adiponectin and LMW adiponectin with atherogenic dyslipidemia (p > 0.05). Free Leptin Index was associated positively with atherogenic dyslipidemia (p < 0.05). Odds Ratio (OR) of HMW adiponectin for the occurrence of atherogenic dyslipidemia was 3.62 (p < 0.05), where as OR of FLI with atherogenic dyslipidemia was 4.57 (p < 0.05). Conclusion: HMW Adiponectin and FLI might contribute to atherogenic dyslipidemia in central obese non-diabetic males.

Angiopoietin like protein 3 (Angptl3), fatty acid binding protein 4 (FABP4) and homeostasis model assessment of insulin resistance (HOMA-IR) among Indonesian obese non diabetic males.

Aim To reveal the correlation between Angptl3, FABP4 and HOMA-IR among Indonesian obese non diabetic males. Methods This is a cross sectional study with 133 obese non diabetic males volunteers (characterized by waist circumference > 90 cm; fasting blood glucose < 126 mg/dL; and no diabetic specific symptoms) age between 30-60 years which was done in Jakarta, Indonesia. We measured biochemical markers such as Angptl3, FABP4, FFA, fasting insulin and fasting glucose. We also measured weight, height, waist circumference (WC), systolic blood pressure (SBP) and diastolic blood pressure (DBP). Correlation between each marker was measured using Pearson and Spearman’s analysis. Results Pearson and Spearman’s correlation analysis showed significant positive correlation between Angptl3 and FABP4 (r = 0.319; P = 0.000), Angptl3 and FFA (r = 0.171; r = 0.049), FABP4 and HOMA-IR (r = 0.202; P = 0.019), FFA and FABP4 (r = 0.506; P = 0.000), WC and HOMA-IR (r = 0.323; P = 0.000), WC and FABP4 (r = 0.387; P = 0.000), Body Mass Index (BMI) and HOMA-IR (r = 0.270; P = 0.002), BMI and FABP4 (r = 0.362; P = 0.000). Conclusion This study showed positive significant correlations between Angptl3-FABP4, Angptl3-FFA, FFA-FABP4 and FABP4-HOMA-IR. We suggest that Angptl3 can activate lipolysis in adipose tissue (through its correlation with FABP4), and Angptl3 concentration is related to insulin resistance risk among Indonesian obese non diabetic males.

The Relationship Between Retinol/Retinol Binding Protein 4 ratio, resistin and inflammation in non diabetic obese Indonesian men.

Aim To verify the correlation between Retinol/RBP4 Ratio, and resistin with inflammation (represented by hsCRP) in non-diabetic obese Indonesian men Methods This was a cross sectional study using 125 subjects. Measured parameters were retinol, RBP4, resistin, and hsCRP. Correlation between retinol, RBP4, resistin, hsCRP and Retinol/RBP4 Ratio was calculated. Cut off point of hsCRP were classiied as follows: <1 mg/l for low risk of inflammation, 1-3 mg/l for moderate risk, and 3-10 mg/l for high risk (according to CVD risk). The Retinol/RBP4 ratio was dichotomized into high (>0.9) and low ratio (≤0.9). The cross tabulation test was performed to predict the inflammation trends described by Retinol/RBP4 Ratio and resistin. Results Retinol was found strongly correlated with RBP4 and resistin (r=0.53; p<0.01). A positive but not significant correlation was found between resistin and Retinol/RBP4 Ratio with hsCRP. In high ratio group, 17.6% subjects were found with low risk inflammation, 26.4% with moderate risk, and 20.8% with high risk, in low ratio group, 8% subjects were low risk inflammation, 20% moderate risk, and 7.2% high risk. Combination between ratio and resistin showed that in “high ratio and low resistin” group, 12% subjects have low risk of inflammation and 8% have high risk. Meanwhile in “low ratio and high resistin” group, 3.2% subjects were found having low risk and 13.6% high risk of inflammation. Conclusions Combination between Retinol/RBP4 Ratio and resistin showed better description about the inflammation risk in non-diabetic obese subjects compare to the ratio itself.

Negative impact of imflammation and insulin resistance on the biogenesis of HDL-c in Indonesian men with metabolic syndrome.

Aim To find out the relationship between inflammation and insulin resistance with impaired HDL biogenesis that cause low HDL-c concentration Methods Using a cross-sectional design, this study involved 163 adult men, aged 25-60 years old with metabolic syndrome (IDF criteria, 2005), without liver and kidney dysfunction. This study was undertaken in Jakarta in the year 2007-2009. Measured indicators were serum apolipoprotein A-1 (apoA-1), prebeta-1 HDL, cholesteryl ester transfer protein (CETP), HDL cholesterol (HDL-c), body weight, height, waist circumference (WC), systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG), and triglyceride. The apoA-1/HDL-c ratios were taken as indicator of HDL maturation, whereas CETP/HDL-c and CETP/TG ratios were indicated HDL catabolism. high-sensitivity CRP (hsCRP) and HOMA-IR were taken as indicator of inflammation and insulin resistance, respectively. Data were analyzed by using univariate, bivariate, and multivariate analysis. Results Positive correlations were found between hsCRP and CETP (rs= 0.200, p= 0.042), and CETP/HDL-c ratios (rs= 0.188, p= 0.013). HOMA-IR positively correlated with apoA-1/HDL-c ratios (rs= 0.190, p= 0.016) and negatively correlated with the CETP/TG ratios (rs= -0.162, p= 0.04). Results of general linear model analysis showed that serum hsCRP concentration had the highest contribution to CETP/HDL-c ratios, apoA-1, dan CETP (p= 0.009; 0.016; 0.054, respectively). Conclusions Inflammation and insulin resistance related to dysfunction of HDL biogenesis in men with metabolic syndrome. The inflammation correlated with increased HDL catabolism, whereas the insulin resistance correlated with decreased HDL maturation and increased HDL catabolism. These may lead to low HDL-c concentration. Inflammation had higher contribution to HDL biogenesis factors than insulin resistance.

The effects of zinc supplementation on the TNF-α profile and diarrhea in severely malnourished children of low income family.

Zinc deficiency has a great impact on growth and development, especially in malnourished children. Zinc is important in both local and systemic immunity. The aim of this study was to assess the impact of zinc supplementation on the cytokine, tumor necrosis factor α (TNF-α), and diarrhea in severely undernourished under-five children of low-income families. A randomized double blind pre-test post-test controlled design was selected. A group of 12-59 month-old children were given local food, and treated as control group (n=60), and another group (n=60) were given local food with 15 mg/5 ml zinc as intervention group. Zinc concentration was measured by atomic absorption spectrophotometer (AAS), and TNF-α concentration was determined by ELISA. Data on nutrient intakes were collected using 24-hour food recall method. The result of the study showed that after zinc intervention, zinc serum increased significantly, and TNF-α concentration decreased along with reduction of the duration and frequency of diarrhea. Zinc concentration increased 87.0% in the intervention group, while in the control group the increase was only 19.6%. There was a significant reduction of both serum and fecal TNF-α concentration after intervention (p<0.05). Severity and duration of diarrhea were reduced significantly in the intervention group compared to the control group (p<0.001). It was concluded that zinc intervention reduced the duration and severity of diarrhea through improvement of immunity, especially local immunity with TNF-α as biomarker.