Background: The feasibility of liver transplantation (LT) in elderly recipients remains a topic of debate. Methods: This cohort study evaluated the impact of recipient's age on LT outcome between January 2007 and May 2016 covered by the Korean National Health Insurance system (n = 9415). Multilevel regression models were used to determine the impact of recipient's age on in-hospital and long-term mortality after LT. Results: All patients had a first LT, with 2473 transplanted with liver from deceased donors (DD) and 6942 from living donors. The mean age was 52.2 ± 9.0 years. Most LT were performed on patients in their 50s (n = 4290, 45.6%) and 0.9% (n = 84) of the LT was performed on patients older 70 years. The overall in-hospital mortality was 6.3%, and the 3-year mortality was 11.3%. The in-hospital mortality included, 13.5% associated with DDLT and 3.7% involved living donor LT. When compared with that for patients aged 51 to 55 years, the risk of death among recipients older than 70 years was about fourfold higher after adjusting for baseline liver disease (odds ratio, 4.1; 95% confidence interval, 2.21-7.58), and was nearly threefold higher after adjusting for baseline liver disease and perioperative complications (odds ratio, 2.92; 95% confidence interval, 1.37-6.24). Also, the cost of LT increased significantly with age. Conclusions: The data show that age remains an important risk factor for LT, suggesting that LT should be considered with caution in elderly recipients.

Acute respiratory distress syndrome (ARDS) is potentially underrecognized by clinicians. Early recognition and subsequent optimal treatment of patients with ARDS may be facilitated by usage of biomarkers. Surfactant protein D (SP-D), a marker of alveolar epithelial injury, has been proposed as a potentially useful biomarker for diagnosis of ARDS in a few studies. We tried to validate the performance of plasma SP-D levels for diagnosis of ARDS. We conducted a retrospective analysis using data from three (two in USA and one in Korea) prospective biobank cohorts involving 407 critically ill patients admitted to medical intensive care unit (ICU). A propensity score matched analysis (patients with versus without ARDS, matched 1:1) was carried out using significant variables from multiple logistic regression. The diagnostic accuracy of plasma SP-D as a diagnostic marker of ARDS was assessed by receiver operating characteristic curve analysis. Out of the 407 subjects included in this study, 39 (10%) patients fulfilled ARDS criteria. Patients with ARDS had higher SP-D levels in plasma (p < 0.01) and higher hospital-mortality (p < 0.001) than those without ARDS. Thirty eight subjects with ARDS (cases) were successfully matched for propensity for ARDS with 38 subjects without ARDS (controls). Plasma levels of SP-D were higher in cases with ARDS compared to their matched controls without ARDS [median 20.8 ng/mL (interquartile range, 12.7–38.4) versus 7.9 (4.1–17.0); p = 0.001]. The area under the receiver operating characteristic curve for SP-D for the diagnosis of ARDS was 0.71 (95% confidence intervals, 0.60–0.83). A cut-off point of 12.7 ng/mL for SP-D yielded sensitivity of 74% and specificity of 63%. High levels of SP-D within 48 h after ICU admission might serve as a diagnostic marker for ARDS in patients hospitalized in medical ICU. Further prospective trials are required to validate the diagnostic role of SP-D in ARDS, and if its usefulness is greater in direct than in indirect ARDS, as well as across different strata of severity of ARDS.

Oh MD, et al. J Korean Med Sci. 2015 Nov;30(11):1701-1705. https://doi.org/10.3346/jkms.2015.30.11.1701

Joo H, et al. J Korean Med Sci. 2012 Aug;27(8):901-906. http://dx.doi.org/10.3346/jkms.2012.27.8.901

Low levels of serum vitamin D is associated with several lung diseases. The production and activation of matrix metalloproteinases (MMPs) may play an important role in the pathogenesis of emphysema. The aim of the current study therefore is to investigate if vitamin D modulates the expression and activation of MMP-2 and MMP-9 in human lung fibroblasts (HFL-1) cells. HFL-1 cells were cast into three-dimensional collagen gels and stimulated with or without interleukin-1β (IL-1β) in the presence or absence of 100 nM 25-hydroxyvitamin D (25(OH)D) or 1,25-dihydroxyvitamin D (1,25(OH)2D) for 48 hours. Trypsin was then added into the culture medium in order to activate MMPs. To investigate the activity of MMP-2 and MMP-9, gelatin zymography was performed. The expression of the tissue inhibitor of metalloproteinase (TIMP-1, TIMP-2) was measured by enzyme-linked immunosorbent assay. Expression of MMP-9 mRNA and TIMP-1, TIMP-2 mRNA was quantified by real time reverse transcription polymerase chain reaction. IL-1β significantly stimulated MMP-9 production and mRNA expression. Trypsin converted latent MMP-2 and MMP-9 into their active forms of MMP-2 (66 kDa) and MMP-9 (82 kDa) within 24 hours. This conversion was significantly inhibited by 25(OH)D (100 nM) and 1,25(OH)2D (100 nM). The expression of MMP-9 mRNA was also significantly inhibited by 25(OH)D and 1,25(OH)2D. Vitamin D, 25(OH)D, and 1,25(OH)2D play a role in regulating human lung fibroblast functions in wound repair and tissue remodeling through not only inhibiting IL-1β stimulated MMP-9 production and conversion to its active form but also inhibiting IL-1β inhibition on TIMP-1 and TIMP-2 production.