Impact of contrast-enhanced versus non-contrast computed tomography on acute kidney injury in acute necrotizing pancreatitis: A randomized controlled trial.

BACKGROUND: The data evaluating contrast-induced-acute kidney injury (AKI) in patients with acute pancreatitis is scarce. This study aimed to compare the frequency of AKI in patients with acute necrotizing pancreatitis undergoing non-contrast computed tomography (NCCT) with those undergoing contrast-enhanced computed tomography (CECT) during hospitalization. METHODS: This prospective randomized controlled trial (CTRI/2019/12/022206) screened consecutive patients with acute pancreatitis for eligibility and randomly allocated patients with acute necrotizing pancreatitis (based on CECT in the first week of illness) and normal renal functions to receive either NCCT or CECT during hospitalization. The incidence of development of new AKI and clinical outcomes was compared between the two groups. Post-hoc analysis was done to adjust for disease severity. RESULTS: As many as 105 patients completed the study as per protocol (NCCT = 45 and CECT = 60). AKI occurred in 36 (34.3%) patients, nine (20%) in the NCCT and 27 (45%) in the CECT group. Contrast induced-AKI occurred in 11 (18.3%) patients, while 25 had AKI secondary to acute pancreatitis. The relative risk (RR) of AKI in the CECT group was 2.25 (95% CI 1.17-4.30, p = .0142). The frequency of intensive care unit (ICU) admission (RR = 2.1, 95% CI 1.34-3.27, p = .0001) and need for drainage of collections (RR = 1.39, 95% CI 1.1-1.7, p = .005) was significantly higher and the length of hospitalization (p = .001) and ICU admission (p = 0.001) were significantly longer in the CECT group. However, when adjusted for the severity of acute pancreatitis, there was no difference in AKI and clinical outcomes between the NCCT and CECT groups. The duration of AKI was significantly longer and the need for dialysis was significantly higher in patients who had AKI secondary to acute pancreatitis compared to those with contrast induced-AKI (p = .003). CONCLUSION: CECT is not significantly associated with AKI in acute necrotizing pancreatitis.

Comparative Analysis of the Genetic Variants in Haematopoietic Stem/Progenitor and Mesenchymal Stem Cell Compartments in de novo Myelodysplastic Syndromes.

Myelodysplastic Syndromes (MDS) are hematological clonal disorders. Bone marrow (BM) mesenchymal stem cells (MSCs) interact with the haematopoietic stem and progenitor cells (HSPCs) to regulate haematopoiesis. We studied the genetic variation profiles of BM derived CD34+ HSPCs and MSCs of same patient in a South Asian de novo MDS cohort with 20 patients. A total of 42 genes (variants 471) and 38 genes (variants 232) were mutated in HSPCs and MSCs respectively and majority (97%) were distinct variants. Variants included both known and novel, with variants predicted as pathogenic. In both cell types, most frequently mutated genes were TET2, KDM6A, BCOR, EZH2 and ASXL. DNA methylation and chromatin remodeling were shown to be affected in both cell types with a high frequency. RNA splicing was affected more in HSPCs. Gene variants in the cohesion complex and epigenetic mechanisms were shown to co-exist. We report variant profile of MSCs and CD34+ HSPCs from a South Asian cohort, with novel variants with potential for further study as biomarkers in MDS. Distinct variants confined to each cellular compartment indicate that the genetic variations occur following lineage commitment.

Evaluation of the Indian TrueNAT micro RT-PCR device with GeneXpert for case detection of pulmonary tuberculosis.

To evaluate the performance of TrueNAT (RT Micro PCR device) assay in comparison with GeneXpert on sputum samples from pulmonary cases of tuberculosis. 274 samples were processed to detect MTB by ZN smear examination, MGIT culture and molecular methods that included RT-PCR (ABI 7500 & TrueNAT) and GeneXpert for case detection of TB. The overall performance of the test with MGIT(Mycobacterium Growth Indicator Tube) culture as gold standard, sensitivity of smear, RT PCR/TrueNAT and Genexpert was 61.5% (CI:53.3-69.3%), 94.7% (CI:89.8-97.6%) & 96.0% (CI: 91.5-98.5%), respectively. Amongst the S+ (108) samples, RT-PCR/TrueNAT and GeneXpert showed a sensitivity of 99% (CI:94.9%-99.8%) and 100% (98.6%-100.0%), respectively. High concordance was observed between GeneXpert and TrueNAT for case detection of TB. The GeneXpert MTB/RIF test was independent on the user's skills. It has a short turn-around time and simultaneously detects RIF resistance with M. tuberculosis in less than 3h. The TrueNAT MTB has good sensitivity and specificity in case detection with hands on time of less than 3h as well as fits the requirements in resourcelimited health care settings. Larger, multi-site studies are required to obtain better estimates of the performance of TrueNAT MTB.

Anti-cell proliferative efficacy of ferulic acid against 7, 12-dimethylbenz(a) anthracene induced hamster buccal pouch carcinogenesis.

The present study was designed to explore the anti-cell proliferative efficacy of ferulic acid by analysing the expression pattern of cell proliferative markers, proliferating cellular nuclear antigen (PCNA) and cyclin D1, in the buccal mucosa of golden Syrian hamsters treated with 7,12-dimethylbenz(a)anthracene (DMBA). Oral squamous cell carcinomas developed in the buccal pouch of hamsters using topical application of 0.5% DMBA three times a week for 14 weeks. Immunohistochemical (PCNA) and RT-PCR (Cyclin D1) analysis revealed over expression of PCNA and cyclin D1 in the buccal mucosa of hamsters treated with DMBA alone (tumor bearing hamsters). Oral administration of ferulic acid at a dose of 40 mg/kg bw to hamsters treated with DMBA not only completely prevented the tumor formation but also down regulated the expression of PCNA and cyclin D1. The results of the present study thus suggests that ferulic acid might have inhibited tumor formation in the buccal mucosa of hamsters treated with DMBA through its anti-cell proliferative potential as evidenced by decreased expression of PCNA and cyclin D1.