Effect of morphine use on oral P2Y12 platelet inhibitors in acute myocardial infarction: Meta-analysis

Background Morphine is the recommended analgesic in acute myocardial infarction (AMI). This recommendation has come under scrutiny because of possible slow uptake of oral antiplatelet agents. Objective We performed a meta-analysis of all available studies in AMI patients treated with prasugrel or ticagrelor (P2Y12 inhibitors) that reported use of morphine prior to loading the antiplatelet agents to critically assess the safety of co-administration of morphine and the newer P2Y12 inhibitors. Methods Several sources were searched from inception to December 2017 with inclusion of eight studies, largely observational. Mean difference (MD) was calculated for continuous variables, and standardized mean difference (SMD) for platelet function was assessed by the various platelet assays, 2 h after the loading dose of oral P2Y12 inhibitors. Results Higher platelet activity was noted among morphine group [SMD = 0.8, 95% confidence interval (CI) = 0.4–1.1, p < 0.01]. Morphine use caused higher odds of “high residual platelet reactivity” at 2 h (odds = 3.3, 95 %CI = 2.2–5.1, p < 0.01). Ticagrelor reached a lower plasma concentration in morphine group (MD = −481.8 ng/ml, 95% CI = −841.2 to −122.4 ng/ml, p < 0.01) with a higher vomiting rate (odds = 5.3, 95% CI = 2.5–11.1, p < 0.01). However, the composite of in-hospital mortality, stroke, and re-infarction was not significantly different between the groups (p = 0.83). Conclusion Co-administration of morphine with P2Y12 inhibitors possibly decreases their efficacy in platelet inhibition. However, this did not translate into higher adverse outcomes because of low event rates, inadequate for analysis. A large randomized study is needed to evaluate the narcotic-P2Y12 interaction.

Draft genome sequence of a caprolactam degrader bacterium: Pseudomonas taiwanensis strain SJ9

Abstract Pseudomonas taiwanensis strain SJ9 is a caprolactam degrader, isolated from industrial wastewater in South Korea and considered to have the potential for caprolactam bioremediation. The genome of this strain is approximately 6.2 Mb (G + C content, 61.75%) with 6,010 protein-coding sequences (CDS), of which 46% are assigned to recognized functional genes. This draft genome of strain SJ9 will provide insights into the genetic basis of its caprolactam-degradation ability.

Assessment of hearing loss in multi-drug resistant tuberculosis (MDR-TB) patients undergoing Aminoglycoside treatment.

Background: Incomplete treatments and treatment failures has led to Multi-drug resistant tuberculosis, which has emerged as a significant problem in treating tuberculosis and thus the second line drugs are used with the concomitant increase in the incidence of adverse effects. Methods: This prospective study was carried out from June 2009 to May 2014 in the department of ENT in collaboration with TB & Chest at Teerthanker Mahaveer Medical College & Research Centre. Out of 104, only 84 patients were included in our study. Patients were divided into three groups: group I (n=27) patients using Amikacin, group II (n=40) patients using kanamycin and group III (n=17) patients using streptomycin. Baseline pre-treatment pure tone audiometry was performed on all the patients and repeated every three months until completion of therapy. Results: Patients included were 15 to 55 years age with higher number of males (65%, n=55) than females (35%, n =29). Only 22.7% (n=19) of patients were found to be suffered from Hearing Loss. At the end of the study (at 12 month), Overall incidence of HFL was 58.0% (n=11) while incidence of Dead ear was 31.5% (n=6) and LFL was 10.5% (n=2). Amikacin was found to be more Ototoxic than Kanamycin and streptomycin. Conclusion: Aminoglycosides in MDR-TB patients may cause irreversible hearing loss involving higher frequencies and can become a hearing handicap as speech frequencies are too implied in more or less of the patients, thus underlining the need for regular audiologic evaluation in patients of MDR-TB during the treatment.