1.Reference range of random urinary calcium creatinine ratio in North Indian children and adolescents
Raman Kumar MARWAHA ; Mahendra Kumar GARG ; Navin DANG ; Ambrish MITHAL ; Archna NARANG ; Aditi CHADHA ; Nandita GUPTA ; Manchanda Raj KUMAR
Annals of Pediatric Endocrinology & Metabolism 2019;24(1):34-40
PURPOSE: Urinary calcium creatinine ratio (UCaCrR) is a reliable indicator for monitoring hypercalciuria following vitamin D supplementation. However, the reference range varies from region to region. Previous studies did not take vitamin D and parathyroid hormone status into account while evaluating UCaCrR. Hence, we undertook this study to establish the 95th percentile of UCaCrR as an indicator of hypercalciuria in North Indian children and adolescents. METHODS: Four hundred seventy-three participants (boys 62.2%, girls 37.8%) with adequate dietary calcium intake, normal serum levels of 25-hydroxy-vitamin D (>20 ng/mL), and without secondary hyperparathyroidism following supplementation were selected for evaluation of UCaCrR. RESULTS: The mean age and body mass index of subjects were 11.2±2.6 years and 18.0±3.6 kg/m2, respectively. The 95th percentile of UCaCrR in the study population was 0.126. The mean, median, and 95th percentile of UCaCrR was significantly higher in prepubertal children (age ≤10 years) (0.0586±0.0374, median=0.0548, 95th percentile=0.136) compared to those >10 years old (0.0503±0.0363, median=0.0407, 95th percentile=0.123, P=0.02). No significant difference in UCaCrR was observed between genders and different weight categories. CONCLUSIONS: UCaCrR of 0.13 defines the cutoff value for hypercalciuria in North Indian children and adolescents with adequate dietary intake of calcium and sufficient serum vitamin D levels.
Adolescent
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Body Mass Index
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Calcium
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Calcium, Dietary
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Child
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Creatinine
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Female
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Humans
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Hypercalciuria
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Hyperparathyroidism, Secondary
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Parathyroid Hormone
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Reference Values
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Vitamin D
2.Calcarea carbonica treatment rescues lipopolysaccharide-induced inflammatory response in human mononuclear cells via downregulation of inducible cyclooxygenase pathway.
Swatantra KUMAR ; Vimal K MAURYA ; Debadatta NAYAK ; Anil KHURANA ; Raj K MANCHANDA ; Srinivasulu GADUGU ; Madan L B BHATT ; Shailendra K SAXENA
Journal of Integrative Medicine 2020;18(5):441-449
OBJECTIVE:
Prolonged use of nonsteroidal anti-inflammatory drugs is associated with severe side effects and toxicity. Therefore, we studied the anti-inflammatory role of Calcarea carbonica which had minimal toxicity at the low doses.
METHODS:
THP-1 human mononuclear cells were treated with C. carbonica to evaluate the 50% cytotoxicity concentration (CC) and 50% effective concentration (EC). Cell survival was evaluated in lipopolysaccharide-stimulated C. carbonica-treated cells. Nitric oxide (NO) and tumor necrosis factor-α (TNF-α) were measured to evaluate the anti-inflammatory activity of C. carbonica. Cyclooxygenase-2 (COX-2) protein expression was determined by Western blotting analysis, and the interaction of C. carbonica with the COX-2 protein was evaluated using molecular docking simulation.
RESULTS:
The CC and EC of C. carbonica were found to be 43.26 and 11.99 µg/mL, respectively. The cell survival assay showed a 1.192-fold (P = 0.0129), 1.443-fold (P = 0.0009) and 1.605-fold (P = 0.0004) increase in cell survival at 24, 48 and 72 h after initiating C. carbonica treatment, respectively. C. carbonica-treated cells showed a reduction in NO levels by 2.355 folds (P = 0.0001), 2.181 folds (P = 0.0001) and 2.071 folds (P = 0.0001) at 24, 48 and 72 h, respectively. The treated cells also showed a reduction in TNF-α levels by 1.395 folds (P = 0.0013), 1.541 folds (P = 0.0005) and 1.550 folds (P = 0.0005) at 24, 48 and 72 h, respectively. In addition, a 1.193-fold reduction (P = 0.0126) in COX-2 protein expression was found in C. carbonica-treated cells. The molecular docking showed interaction of C. carbonica with the phenylalanine 367 residue present in active site of Cox-2.
CONCLUSION
C. carbonica exhibited anti-inflammatory properties in lipopolysaccharide-stimulated cells by significantly reducing NO production and TNF-α level through downregulation of the COX-2 protein. This effect is probably mediated through interaction of C. carbonica with the phenylalanine 367 residue present in active site of Cox-2.