Risk factors of emerging multidrug resistant Acinetobacter baumannii in burn patients at burn Unit of Dr. Soetomo Hospital.

INTRODUCTION: Burn injury patients are at high risk of infection as a result of the nature of the burn injury itself, including prolonged hospital stays, antibiotics use, treatment procedures, etc. In this era, nosocomial infections caused by Acinetobacter baumannii (A.ba) have increased significantly. This study was conducted to investigate the micro-organism pattern and the risk factors for burn patients with multi-drug resistant (MDR) Acinetobacter baumannii (A.ba) in the Burn Unit at Dr. Soetomo Hospital. MATERIALS AND METHODS: We conducted a retrospective, observational study among burn patients with A.ba admitted to the Burn Unit at Dr. Soetomo Hospital from January 2020 to December 2021. Potential risk factors for MDR-A.ba were analysed by univariate and multivariate analysis. The patients diagnosed with MDR-A.ba wound infection were included in the case group. The patients diagnosed with non MDR, these are: (1) the patients isolated micro-organisms other than A.ba, (2) sterile isolates, and (3) the patients isolated as A.ba but not MDR, were included in the control group. RESULTS: A total of 120 burn patients were included in this study. During this study, 24% burn patients were found to have Acinetobacter baumannii and 79% (from 24% of Acinetobacter baumannii) had MDR-A.ba. According to univariate analysis, risk factors that significant were: Abbreviated Burn Severity Index (ABSI) (p = 0,002; OR: 6.10; CI: 1,68 - 21,57); hospital Length Of Stay (LOS) (p < 0,000; OR: 6.95; CI: 2,56 - 18,91) and comorbid (p = 0,006; OR: 3,72; CI: 1,44 - 9,58). But, after analysed by multivariate analysis, only ABSI was the significant factor (p = 0,010; OR: 1,70; CI: 1,23 - 2,36). CONCLUSION: Based on univariate analysis, the significant risk factors for MDR-A.ba were: ABSI, hospital length of stay and comorbid. But after adjusted by multivariate analysis, only ABSI was the significant factor.

Adverse bone health and abnormal bone turnover among perinatally HIV-infected Asian adolescents with virological suppression.

OBJECTIVES: This study aimed to determine the prevalence of low bone mass and assess its relationship with abnormal bone turnover among HIV-infected Asian adolescents. METHODS: A multicentre, cross-sectional study was conducted at four paediatric HIV centres in Thailand and Indonesia. Perinatally HIV-infected adolescents aged 10-18 years receiving antiretroviral therapy (ART) with virological suppression (HIV RNA < 400 copies/mL) were enrolled. Study assessments included lumbar spine (L2-L4) dual-energy X-ray absorptiometry and measurement of bone turnover markers. Bone mineral density (BMD) and bone mineral apparent density (BMAD) Z-scores were calculated based on Thai normative age- and sex-matched references. Low bone mass was defined as BMD or BMAD Z-scores ≤ -2. RESULTS: Of 396 participants, 57% were female. The median age was 15.0 [interquartile range (IQR) 13.3-16.9] years, and 73% were in Tanner stage 3-5. At enrolment, the median CD4 T-cell count was 734 (IQR 581-907) cells/µL, and 37% were on protease inhibitor (PI)-based regimens. The overall prevalence of lumbar spine BMD and BMAD Z-scores ≤ -2 were 16.4% and 8.3%, respectively. Z-scores were lower with older age, female sex, body mass index (BMI) <5th percentile, boosted PI exposure and CD4 T-cell percentage < 15% before ART initiation. Increased bone turnover markers were inversely associated with BMD and BMAD Z-scores. CONCLUSIONS: Low bone mass was linked to older age, female sex, low BMI, boosted PI exposure, and poor immunological status before ART commencement in our cohort of perinatally HIV-infected Asian adolescents. Dysregulation of bone turnover was associated with bone demineralization. Screening for low bone mass should be implemented to identify individuals who might benefit from interventions to preserve bone health.

MicroRNA-126 contributes to renal microvascular heterogeneity of VCAM-1 protein expression in acute inflammation.

Endothelial cells in different microvascular segments of the kidney have diverse functions and exhibit differential responsiveness to disease stimuli. The responsible molecular mechanisms are largely unknown. We previously showed that during hemorrhagic shock, VCAM-1 protein was expressed primarily in extraglomerular compartments of the kidney, while E-selectin protein was highly induced in glomeruli only (van Meurs M, Wulfert FM, Knol AJ, de Haes A, Houwertjes M, Aarts LPHJ, Molema G. Shock 29: 291-299, 2008). Here, we investigated the molecular control of expression of these endothelial cell adhesion molecules in mouse models of renal inflammation. Microvascular segment-specific responses to the induction of anti-glomerular basement membrane (anti-GBM), glomerulonephritis and systemic TNF-α treatment showed that E-selectin expression was transcriptionally regulated, with high E-selectin mRNA and protein levels preferentially expressed in the glomerular compartment. In contrast, VCAM-1 mRNA expression was increased in both arterioles and glomeruli, while VCAM-1 protein expression was limited in the glomeruli. These high VCAM-1 mRNA/low VCAM-1 protein levels were accompanied by high local microRNA (miR)-126 and Egfl7 levels, as well as higher Ets1 levels compared with arteriolar expression levels. Using miR-reporter constructs, the functional activity of miR-126 in glomerular endothelial cells could be demonstrated. Moreover, in vivo knockdown of miR-126 function unleashed VCAM-1 protein expression in the glomeruli upon inflammatory challenge. These data imply that miR-126 has a major role in the segmental, heterogenic response of renal microvascular endothelial cells to systemic inflammatory stimuli.