BackgroundHypertriglyceridemia is the third most common cause of acute pancreatitis, but whether the level of triglyceride (TG) is related to severity of pancreatitis is unclear.AimTo evaluate the effect of TG level on the severity of hypertriglyceridemic pancreatitis (HTGP).DesignRetrospective cohort study.MethodsWe reviewed the records of 144 patients with HTGP from 1999 to 2013 at Tri-Service General Hospital. Patients with possible etiology of pancreatitis, such as gallstones, those consuming alcohol or drugs, or those with infections were excluded. The classification of severity of pancreatitis was based on the revised Atlanta classification. We allocated the patients into high-TG and low-TG groups based on the optimal cut-off value (2648 mg/dL), which was derived from the receiver operating characteristic (ROC) curve between TG level and severity of HTGP. We then compared the clinical characteristics, pancreatitis severity, and mortality rates of the groups.ResultsThere were 66 patients in the low-TG group and 78 patients in the high-TG group. There was no significant difference in the age, sex ratio, body mass index, and comorbidity between the 2 groups. The high-TG group had significantly higher levels of glucose (P = 0.022), total cholesterol (P = 0.002), and blood urea nitrogen (P = 0.037), and lower levels of sodium (P = 0.003) and bicarbonate (P = 0.002) than the low-TG group. The incidences of local complication (P = 0.002) and severe and moderate form of pancreatitis (P = 0.004) were significantly higher in the high-TG group than in the low-TG group. The mortality rate was higher in the high-TG group than in the low-TG group (P = 0.07).ConclusionsHigher TG level in patients with HTGP may be associated with adverse prognosis, but randomized and prospective studies are needed in the future verify this relationship.

Tobacco smoking has been found associated with lower cardiorespiratory fitness in white and black males; however, few studies have not been conducted to clarify such relationship in Asian males. We performed a cross-sectional study to investigate the association between tobacco smoking status and physical fitness in 3,669 military males, averaged 29.4 years of age, from the cardiorespiratory fitness and hospitalization events in armed forces (CHIEF) study in Taiwan during 2014. There were 1,376 current smokers, and the others were noncurrent smokers. The effective sample size estimated was 1,230 participants, as the margin of error was ±3% at the 99% confidence level. Physical fitness was evaluated by time for a 3000-meter run test (aerobic fitness) and repetitive numbers of 2-minute sit-ups and 2-minute push-ups (anaerobic fitness) where all procedures were standardized by using computerized scoring systems. A multiple linear analysis adjusting for age, service specialty, body mass index, heart rate, alcohol intake, and training frequency was used to determine the relationship. As compared with noncurrent smoking, current smoking was inversely correlated with longer time for a 3000-meter run (β = 15.66 (95% confidence intervals (CI): 10.62, 20.70)) and fewer repetitive numbers of 2-minute sit-ups and 2-minute push-ups (β = −1.53 (95% CI: −2.08, −0.97) and −1.31 (95% CI: −2.12, −0.50), respectively). Our finding reconfirms the concept that tobacco smoking might reduce both aerobic and anaerobic fitness among young Asian males.

Aims: Obstructive sleep apnea (OSA) and insomnia commonly coexist; hypnotics are broadly prescribed for insomnia therapy. However, the safety of hypnotics use in OSA patients is unclear. We conducted a retrospective case-control study to investigate the risk of adverse respiratory events in hypnotics-using OSA patients.Methods: We obtained data from the Taiwan National Health Insurance Database from 1996 to 2013. The case group included 216 OSA patients with newly diagnosed adverse respiratory events, including pneumonia and acute respiratory failure. The control group included OSA patients without adverse respiratory events, which was randomly frequency-matched to the case group at a 1:1 ratio according to age, gender, and index year. Hypnotics exposure included benzodiazepines (BZD) and non-benzodiazepines (non-BZD). A recent user was defined as a patient who had taken hypnotics for 1–30 days, while a long-term user was one who had taken hypnotics for 31–365 days.Results: Multivariable adjusted analysis showed recent BZD use is an independent risk for adverse respiratory events (OR = 2.70; 95% CI = 1.15–6.33; P < 0.001). Subgroup analysis showed both recent and long-term BZD use increased the risk of acute respiratory failure compared to never BZD use (OR = 28.6; 95% CI = 5.24–156; P < 0.001, OR = 10.1; 95% CI = 1.51–67.7; P < 0.05, respectively). Neither BZD nor non-BZD use increased the risk of pneumonia in OSA patients.Conclusion: BZD use might increase the risk of acute respiratory failure in OSA patients.

Background and objective: Tuberculosis (TB) and sarcoidosis are both granulomatous diseases with potential interassociations. However, much uncertainty remains; thus, the present study aimed to clarify the association between these diseases. Methods: We established two cohorts in this retrospective longitudinal cohort study using data obtained from the Taiwan National Health Insurance Database from 2000 to 2015. One cohort, which comprised 31 221 patients with TB and 62 442 age-, sex-and index yearmatched controls, was used to analyse the risk of sarcoidosis; the other cohort comprised 2442 patients with sarcoidosis and 9688 controls and was used to assess the risk of TB. A Cox proportional hazards model adjusted for potential confounders was used in each cohort. Results: Patients with TB showed an 8.09-fold higher risk of developing sarcoidosis than non-TB subjects (95% CI = 3.66-17.90), whereas patients with sarcoidosis showed a 1.85-fold higher risk of developing TB than non-sarcoidosis subjects (95% CI = 1.36-2.50). The TB subtype analysis revealed the highest risk of developing sarcoidosis in patients with extrapulmonary TB, and the highest risk of developing extrapulmonary TB was observed in patients with sarcoidosis compared with nonsarcoidosis subjects. Patients with TB showed a higher risk of developing sarcoidosis throughout the follow-up period, but patients with sarcoidosis only showed a higher risk of developing TB within the first year. Conclusion: TB is a risk factor for developing sarcoidosis. The results of this bidirectional cohort study also highlight the clinical difficulty of diagnosing sarcoidosis and TB.This bidirectional cohort study strengthens the evidence that tuberculosis (TB) is a risk factor for sarcoidosis. Patients with sarcoidosis showed a higher risk of developing TB within the first year after diagnosis of sarcoidosis.

Background and objective: According to several studies, tuberculosis (TB) may be involved in the pathogenesis of cardiovascular disease. However, the relationship between TB and peripheral arterial disease (PAD) has not been studied. The aim of this study was to investigate whether patients with TB exhibit an increased risk of developing PAD. Methods: The data assessed in this national population-based cohort study were obtained from the Taiwan National Health Insurance Database from 2000 to 2010. Patients with newly diagnosed TB were selected using the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes. The non-TB cohort was randomly frequency-matched to the TB cohort at a ratio of 2:1 according to age, sex and index year. Cox's proportional hazards regression models were used to analyse the risk of PAD. Results: We enrolled 14 350 patients with TB and 28 700 controls in this study. The risk of PAD was 3.93-fold higher in the patients with TB than in the non-TB controls after adjusting for age, sex, co-morbidities and socio-economic status. Based on the subgroup analysis, the TB cohort exhibited an increased risk of developing PAD compared with the non-TB cohort, regardless of age, sex, co-morbidities and socio-economic status. Patients with TB had a higher risk of developing PAD than healthy control subjects after 1 year of follow-up. Conclusion: Patients with TB have a significantly higher risk of developing PAD than patients without TB. TB should be considered when evaluating a patient's risk of developing PAD.

COVID-19, caused by SARS-CoV-2, has rapidly spread to more than 160 countries worldwide since 2020. Despite tremendous efforts and resources spent worldwide trying to explore antiviral drugs, there is still no effective clinical treatment for COVID-19 to date. Approximately 15% of COVID-19 cases progress to pneumonia, and patients with severe pneumonia may die from acute respiratory distress syndrome (ARDS). It is believed that pulmonary fibrosis from SARS-CoV-2 infection further leads to ARDS, often resulting in irreversible impairment of lung function. If the mechanisms by which SARS-CoV-2 infection primarily causes an immune response or immune cell infiltration can be identified, it may be possible to mitigate excessive immune responses by modulating the infiltration and activation of specific targets, thereby reducing or preventing severe lung damage. However, the extent to which immune cell subsets are significantly altered in the lung tissues of COVID-19 patients remains to be elucidated. This study applied the CIBERSORT-X method to comprehensively evaluate the transcriptional estimated immune infiltration landscape in the lung tissues of COVID-19 patients and further compare it with the lung tissues of patients with idiopathic pulmonary fibrosis (IPF). We found a variety of immune cell subtypes in the COVID-19 group, especially naïve B cells were highly infiltrated. Comparison of functional transcriptomic analyses revealed that non-differentiated naïve B cells may be the main cause of the over-active humoral immune response. Using several publicly available single-cell RNA sequencing data to validate the genetic differences in B-cell populations, it was found that the B-cells collected from COVID-19 patients were inclined towards naïve B-cells, whereas those collected from IPF patients were inclined towards memory B-cells. Further differentiation of B cells between COVID-19 mild and severe patients showed that B cells from severe patients tended to be antibody-secreting cells, and gene expression showed that B cells from severe patients were similar to DN2 B cells that trigger extrafollicular response. Moreover, a higher percentage of B-cell infiltration seems associated with poorer clinical outcome. Finally, a comparison of several specific COVID-19 cases treated with targeted B-cell therapy suggests that appropriate suppression of naïve B cells might potentially be a novel strategy to alleviate the severe symptoms of COVID-19.

Objectives: To investigate the association between adjunctive nebulized colistin and treatment outcomes in critically ill patients with nosocomial carbapenem-resistant Gram-negative bacterial (CR-GNB) pneumonia. Methods: This retrospective, multi-centre, cohort study included individuals admitted to the intensive care unit with nosocomial pneumonia caused by colistin-susceptible CR-GNB. Enrolled patients were divided into groups with/without nebulized colistin as adjunct to at least one effective intravenous antibiotic. Propensity score matching was performed in the original cohort (model 1) and a time-window bias-adjusted cohort (model 2). The association between adjunctive nebulized colistin and treatment outcomes was analysed. Results: In total, 181 and 326 patients treated with and without nebulized colistin, respectively, were enrolled for analysis. The day 14 clinical failure rate and mortality rate were 41.4% (75/181) versus 46% (150/326), and 14.9% (27/181) versus 21.8% (71/326), respectively. In the propensity score-matching analysis, patients with nebulized colistin had lower day 14 clinical failure rates (model 1: 41% (68/ 166) versus 54.2% (90/166), p 0.016; model 2: 35.3% (41/116) versus 56.9% (66/116), p 0.001). On multivariate analysis, nebulized colistin was an independent factor associated with fewer day 14 clinical failures (model 1: adjusted odds ratio (aOR) 0.59, 95% CI 0.37e0.92; model 2: aOR 0.37, 95% CI 0.21 e0.65). Nebulized colistin was not associated independently with a lower 14-day mortality rate in the time-dependent analysis in both models 1 and 2.

Background The importance or necessity of a loading dose when prescribing intravenous colistin has not been well established in clinical practice, and approximate one-third to half of patients with carbapenem-resistant gram-negative bacteria (CRGNB) infection did not receive the administration of a loading dose. The aim of this study is to investigate the efficacy and risk of acute kidney injury when prescribing intravenous colistin for critically ill patients with nosocomial pneumonia caused by CRGNB. Methods This was a multicenter, retrospective study that recruited ICU-admitted patients who had CRGNB-associated nosocomial pneumonia and were treated with intravenous colistin. Then, we classified the patients into colistin loading dose (N = 85) and nonloading dose groups (N = 127). After propensity-score matching for important covariates, we compared the mortality rate, clinical outcome and microbiological eradication rates between the groups (N = 67). Results The loading group had higher percentages of patients with favorable clinical outcomes (55.2% and 35.8%, p = 0.037) and microbiological eradication rates (50% and 27.3%, p = 0.042) at day 14 than the nonloading group. The mortality rates at days 7, 14 and 28 and overall in-hospital mortality were not different between the two groups, but the Kaplan–Meier analysis showed that the loading group had a longer survival time than the nonloading group. Furthermore, the loading group had a shorter length of hospital stay than the nonloading group (52 and 60, p = 0.037). Regarding nephrotoxicity, there was no significant difference in the risk of developing acute kidney injury between the groups. Conclusions The administration of a loading dose is recommended when prescribing intravenous colistin for critically ill patients with nosocomial pneumonia caused by CRGNB.