METHOD: The meta-analysis included all studies that examined the effect of prebiotic, probiotic, and synbiotic supplements on one or more renal function parameters and had a control group. We searched July 1967 through to March 2016 MEDLINE, Scopus, and Google Scholar databases.
RESULTS: Of 437 studies, 13 were eligible for inclusion in the meta-analysis. GFR levels tended to be reduced; whereas creatinine levels increased in the intervention group compared with the placebo group, both in a non-significant manner. The pooled effect on BUN demonstrated a significant decline compared with the placebo group (MD, -1.72 mmol/L; 95% confidence interval [CI], -2.93 to -0.51; P = 0.005). Urea significantly decreased after intervention (-0.46 mmol/L; 95% CI, -0.60 to -0.32; P <0.0001). The UA levels significantly increased in the intervention group compared with the placebo group (12.28 µmol/L; 95% CI, 0.85-23.71; P = 0.035).
CONCLUSION: This study showed a significant increase in UA and a decrease in urea and BUN. The use of prebiotic, probiotic, and synbiotic supplements among those with compromised renal function or those at risk for renal failure should be limited until large-scale, well-designed randomized controlled trials prove the safety and efficacy of these supplements in improving renal function.
Methods: 2,2-diphenyl-1-picrylhydrazyl (DPPH) and Ferric reducing antioxidant power assay (FRAP) were applied to evaluate the antioxidant activity of carob. In vitro cytotoxicity of carob was conducted on human hepatocytes (WRL68) and rat pancreatic β-cells (RIN-5F). Acute oral toxicity of carob was conducted on a total of 18 male and 18 female Sprague-Dawley (SD) rats, which were subdivided into three groups (n = 6), namely: high and low dose carob-treated (CS5000 and CS2000, respectively) as well as the normal control (NC) receiving a single oral dose of 5,000 mg kg-1 carob, 2,000 mg kg-1 carob and 5 mL kg-1 distilled water for 14 days, respectively. Alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, total bilirubin, creatinine and urea were assessed. Livers and kidneys were harvested for histopathology. In vitro inhibitory effect against α-amylase and α-glucosidase was evaluated. In vivo glycemic activity was conducted on 24 male SD rats which were previously intraperitoneally injected with 55 mg kg-1 streptozotocin (STZ) followed by 210 mg kg-1nicotinamide to induce type 2 diabetes mellitus. An extra non-injected group (n = 6) was added as a normal control (NC). The injected-rats were divided into four groups (n = 6), namely: diabetic control (D0), 5 mg kg-1glibenclamide-treated diabetic (GD), 500 mg kg-1 carob-treated diabetic (CS500) and 1,000 mg kg-1 carob-treated diabetic (CS1000). All groups received a single oral daily dose of their treatment for 4 weeks. Body weight, fasting blood glucose (FBG), oral glucose tolerance test, biochemistry, insulin and hemostatic model assessment were assessed. Pancreases was harvested for histopathology.
Results: Carob demonstrated a FRAP value of 3191.67 ± 54.34 µmoL Fe++ and IC50 of DPPH of 11.23 ± 0.47 µg mL-1. In vitro, carob was non-toxic on hepatocytes and pancreatic β-cells. In acute oral toxicity, liver and kidney functions and their histological sections showed no abnormalities. Carob exerted an in vitro inhibitory effect against α-amylase and α-glucosidase with IC50 of 92.99 ± 0.22 and 97.13 ± 4.11 µg mL-1, respectively. In diabetic induced rats, FBG of CS1000 was significantly less than diabetic control. Histological pancreatic sections of CS1000 showed less destruction of β-cells than CS500 and diabetic control.
Conclusion: Carob pod did not cause acute systemic toxicity and showed in vitro antioxidant effects. On the other hand, inhibiting α-amylase and α-glucosidase was evident. Interestingly, a high dose of carob exhibits an in vivo antihyperglycemic activity and warrants further in-depth study to identify the potential carob extract composition.
METHODOLOGY: A total of 89 patients with gouty arthritis and 100 normal subjects who consented and were recruited in this study. The serum urate and creatinine were measured. The SNP genotyping was performed using PCR-RFLP method for rs3733591 and BST 1236 was used as a restriction enzyme to cut the targeted amplicons.
RESULT: SLC2A9 variant was associated with gout, p-value of 0.007, OR=4.713 [95%CI 1.530-14.513], however this association was not significant after adjustment for age and gender with p=0.465 (OR=1.950; 95%CI[0.325-11.718]).
CONCLUSION: Our data suggest that the genetic variant of SLC2A9 may contribute to the susceptibility of gout among Malays in Malaysia.
Methods: A prospective observational study including 223 patients receiving the branded medicine Exjade® and 101 patients receiving the copy Osveral® was carried out. Data were assessed for a 1-year period and included clinical symptoms, serum ferritin (SF), serum creatinine (SC), and alanine aminotransferase (ALT). Data were analyzed with SPSS version 22 software (SPSS, Chicago, IL, USA).
Results: The median age of the sample was 8 years. There was no significant difference in gender distribution between the two groups (p = 0.625). Nausea was the most frequently reported adverse effect followed by diarrhea and abdominal pain in both groups. Patients receiving Exjade® had a higher relative reduction of SF at the end of the study compared with the Osveral® group (19.9% versus 9.93%, p = 0.028). SC was found to be significantly higher in the Osveral® group than in the Exjade® group throughout the study period. The mean platelet count was higher in the Exjade® group. ALT was significantly higher among patients receiving Osveral® over the last three months of the study.
Conclusions: Exjade® showed a better ability to reduce SF, with less liver toxicity, and better hemostasis profile. No congenital anomalies associated with short-term use of both drugs during pregnancy were observed or reported.
Methods: We conducted a single-arm intervention study at the Clinical Lab of Community Medicine, Universiti Sains Malaysia, and included 31 healthy individuals aged between 30 and 60 years old. Wet cupping therapy was performed at five treatment points at the beginning of the study and repeated after three months. Health outcomes at baseline, one, three, and four months were assessed for FBS, renal function parameters (urea, creatinine, and uric acid), systolic blood pressure (SBP), and von Willebrand factor (vWF).
Results: Forty-five percent of participants were female, and the mean age of study participants was 44.9±6.4 years. Wet cupping therapy significantly reduced FBS, serum urea, and serum creatinine at one, three, and four months compared with baseline values. Serum uric acid and SBP showed a significant reduction at one and four months compared with baseline. The vWF (a measure of endothelial function) had a 4.0% reduction at four months compared to baseline, with a mean difference of 5.3 (95% confidence interval (CI): 2.20 = 8.55; p = 0.002).
Conclusions: This study provides preliminary support that repeated wet cupping therapy enhances body health status; thus, it could be an effective complementary medicine in disease prevention.
METHODS: This cross-sectional study was performed at Hue Central Hospital from 2012-2016 on 176 CKD and 64 control subjects. ADMA levels were measured by using the enzyme linked immunosorbent assay (ELISA) method.
RESULTS: Mean ADMA level was markedly higher (p<0.001) in all patients combined (0.73±0.24μmol/L) than in control subjects (0.47±0.13μmol/L). Mean ADMA levels in advanced kidney disease were higher than control subjects. ADMA levels correlated inversely and relatively strictly to estimated glomerular filtration rate (eGFR) (r = -0.689; p<0.001), haemoglobin (r = -0.525; p<0.001) and haematocrit (r = - 0.491; p<0.001); correlated favourably and relatively strictly to serum creatinine (r = 0.569; p<0.001) and serum urea (r = 0.642; p<0.001). ADMA elevation was predicted simultaneously by eGFR<60 mL/min/1.73m2 (p<0.001), anaemia (p=0.002), body mass index (BMI) (p=0.011) and high sensitivity C-reactive protein (hs-CRP) (p=0.041). Cutoff of ≥0.68μmol/L, ADMA levels predict reduction of eGFR<60 mL/min/1.73m2, sensitivity of 86.9 %, specificity of 82.6%, area under ROC 92.4% (95%CI: 88.6-96.1%).