Glucosamine Enhancement of BDNF Expression and Animal Cognitive Function.

Brain-derived neurotrophic factor (BDNF) is an important factor for memory consolidation and cognitive function. Protein kinase A (PKA) signaling interacts significantly with BDNF-provoked downstream signaling. Glucosamine (GLN), a common dietary supplement, has been demonstrated to perform a variety of beneficial physiological functions. In the current study, an in vivo model of 7-week-old C57BL/6 mice receiving daily intraperitoneal injection of GLN (0, 3, 10 and 30 mg/animal) was subjected to the novel object recognition test in order to determine cognitive performance. GLN significantly increased cognitive function. In the hippocampus GLN elevated tissue cAMP concentrations and CREB phosphorylation, and upregulated the expression of BDNF, CREB5 and the BDNF receptor TrkB, but it reduced PDE4B expression. With the in vitro model in the HT22 hippocampal cell line, GLN exposure significantly increased protein and mRNA levels of BDNF and CREB5 and induced cAMP responsive element (CRE) reporter activity; the GLN-mediated BDNF expression and CRE reporter induction were suppressed by PKA inhibitor H89. Our current findings suggest that GLN can exert a cognition-enhancing function and this may act at least in part by upregulating the BDNF levels via a cAMP/PKA/CREB-dependent pathway.

Regulation of the regulator of G protein signaling 2 expression and cellular localization by PKA and PKC pathways in mouse granulosa cells.

G protein-coupled receptor (GPCR) activation-mediated PKA and PKC pathways have been recognized to be important in ovarian physiology. Expression of regulator of G-protein signaling 2 (RGS2) has been reported in ovarian granulosa cells. The detailed mechanisms in PKA- and PKC-regulated RGS2 expression and cellular translocation in granulosa cells remain mostly unclear. PKA activator 8-bromo-cAMP and PKC activator phorbol-12, 13-didecanoate appeared to rapidly elevate both protein and mRNA levels and promoter activation of RGS2 gene. Two consensus Sp1 elements within the shortest 78 bp fragment of RGS2 promoter sequence were essential for the full responsiveness to PKA and PKC. PKC activation appeared to increase the RGS2 translocation from nucleus to cytosol. PKA- and PKC-mediated RGS2 transcription in a Sp-1-dependent manner and a PKC-mediated RGS2 intracellular translocation were noted in granulosa cells.

The association of non-alcoholic fatty liver disease and metabolic syndrome in a Chinese population.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is associated with features of metabolic syndrome. The aim of this study was to investigate the association between NAFLD and metabolic syndrome in a Chinese population. METHODS: Data from subjects were retrospectively collected from 2006 to 2009. The exclusion criteria included significant consumption of alcohol and chronic hepatitis B and C. The patients were assigned to two groups according to ultrasound findings: normal group and fatty liver group. The liver function of patients was determined by assessing serum alanine aminotransferase (ALT). Metabolic syndrome was diagnosed based on the 2005 International Diabetes Federation criteria. RESULTS: A total of 7568 subjects were enrolled and 5736 (75.8%) and 1832 (24.2%) patients were assigned to the normal and fatty liver groups, respectively. The fatty liver group had significant male predominance (69.7% vs 56.0%), higher body mass index (mean, 26.67 vs 23.55 kg/m2) compared with the normal group. There were 441 (7.7%) and 377 (20.6%) cases with metabolic syndrome in the normal and fatty liver groups, respectively, with significant difference (P=0.001), and the subgroup of 385 cases with fatty liver and elevated ALT had higher prevalence (28.8%) of metabolic syndrome. The strongest association of an individual component of metabolic syndrome with NAFLD was hyperlipidemia (adjusted OR=2.55, 95% CI: 2.22-2.94). CONCLUSION: The individuals with NAFLD had a higher ratio of metabolic syndrome. Hyperlipidemia had the strongest positive association with NAFLD.

Diverticular disease and additional comorbidities associated with increased risk of dementia.

BACKGROUND AND AIM: Colonic diverticular disease may cause a chronic systemic effect, but its role in the development of dementia remains unclear. The purpose of this study was to investigate the potential increased risk for dementia in colonic diverticular disease. METHODS: We conducted a population-based cohort study using data from Taiwan's National Health Insurance Research Database. A total of 66 377 sex-matched, age-matched, and index year-matched (1:4) pairs of patients with colonic diverticular disease and 265 508 patients without colonic diverticular disease, who served as controls, were selected from all potential participants aged 20 years or older in the database. Each subject was individually tracked from 2000 to 2011 to identify incident cases of dementia. Cox proportional hazards regression was employed to calculate the hazard ratios and 95% confidence intervals for the association between colonic diverticular disease and dementia. RESULTS: There were 1057 dementia cases in the diverticular disease cohort during the follow-up period of 315 171 person-years; the overall incidence rate of dementia differed from that of the control group (3.35 vs 2.43 per 1000 person-years, P < 0.001). The adjusted hazard ratio for dementia was 1.24 (95% confidence interval 1.15-1.33) for diverticular disease patients after adjusting for age, sex, and comorbidities. CONCLUSIONS: Colonic diverticular disease may be associated with increased risk for dementia.

Growth Hormone Releasing Peptide-2 Attenuation of Protein Kinase C-Induced Inflammation in Human Ovarian Granulosa Cells.

Cyclooxygenase-2 (COX-2) and interleukin-8 (IL-8) are two important inflammatory mediators in ovulation. Ghrelin may modulate inflammatory signaling via growth hormone secretagogue receptors. We investigated the role of ghrelin in KGN human ovarian granulosa cells using protein kinase C (PKC) activator phorbol 12, 13-didecanoate (PDD) and synthetic ghrelin analog growth hormone releasing peptide-2 (GHRP-2). GHRP-2 attenuated PDD-induced expression of protein and mRNA, the promoter activity of COX-2 and IL-8 genes, and the secretion of prostaglandin E2 (PGE2) and IL-8. GHRP-2 promoted the degradation of PDD-induced COX-2 and IL-8 proteins with the involvement of proteasomal and lysosomal pathways. PDD-mediated COX-2 production acts via the p38, c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways; PDD-mediated IL-8 production acts via the p38, JNK and ERK pathways. GHRP-2 reduced the PDD-induced phosphorylation of p38 and JNK and activator protein 1 (AP-1) reporter activation and PDD-induced NF-κB nuclear translocation and reporter activation. The inhibitors of mitogen-activated protein kinase phosphatase-1 (MKP-1) and protein phosphatase 2 (PP2A) reduced the inhibitory effect of GHRP-2 on PDD-induced COX-2 and IL-8 expression. Our findings demonstrate an anti-inflammatory role for ghrelin (GHRP-2) in PKC-mediated inflammation of granulosa cells, at least in part, due to its inhibitory effect on PKC-induced activation of p38, JNK and NF-κB, possibly by targeting to MKP-1 and PP2A.

Risk of liver cirrhosis in patients with tuberculosis: a nationwide cohort study.

BACKGROUND: Most of the previous reports found cirrhosis patients with a high risk of subsequent tuberculosis (TB). However, data about the risk of developing liver cirrhosis in TB patients are limited. As a hepatitis endemic area, the risk of liver cirrhosis in patients with TB should be elucidated in Taiwan. METHODS: We conducted the study using Taiwan's National Health Insurance Research Database. Patients with TB (n = 9339) were identified as the TB cohort and matched with a control (n = 37 356). Each study participant was followed until diagnosis of liver cirrhosis, loss of follow-up, death, withdrawal from the insurance or until 31 December 2011. RESULTS: A cumulative incidence of liver cirrhosis in the TB cohort had a significantly higher risk for liver cirrhosis compared with the control (log-rank test, P < 0·001). The overall incidence of liver cirrhosis was significantly higher in the TB group than in controls [3·83 vs. 2·02 per 1000 person-year; crude hazard ratio (HR) = 1·88; 95% confidence interval (CI) = 1·59-2·23]. After controlling for age, gender and comorbidities, the risk was 1·79-fold (95% CI = 1·50-2·14) higher in the TB group than in the controls. Analysis by Cox proportional hazard regression revealed that TB increased the risk of cirrhosis in patients with either hepatitis B (adjusted HR = 1·91; 95% CI = 1·05-3·47) or hepatitis C (adjusted HR = 2·56; 95% CI = 1·37-4·78). CONCLUSION: An increased incidence of liver cirrhosis was observed among TB patients in Taiwan.

Statins are associated with a reduced risk of cholangiocarcinoma: a population-based case-control study.

AIMS: Cholangiocarcinoma (CCA) is the second most common primary liver cancer in the world. Due to the lack of effective treatments, the survival rate of CCA is low and it is usually considered difficult to diagnose early. To date, no effective strategies for the prevention of CCA have been developed. Statins are cholesterol-lowering agents which possess pleiotropic properties and the use of statins may reduce cancer risk. The aim of the study was to investigate the effect of statin use on the risk of CCA. METHODS: We used nationwide insurance data to perform a case-control study including 3174 CCA patients diagnosed in 2002-2011 and 3174 propensity score matched controls. Odds ratios (ORs) and 95% confidence intervals (CI) were calculated to assess the association between CCA risk and statin use by type of statin and dose. RESULTS: Patients with CCA were slightly younger than controls with mean ages of 67.4 (SD 12.3) and 68.5 (SD 13.2) years (P = 0.001), respectively, and had less users of statins (22.7 vs. 26.5%, P < 0.001). The overall adjusted OR of statin use associated CCA was 0.80 (95% CI 0.71, 0.90) and lowered for those with longer medications. The OR ranged from 0.65 to 0.77. Stronger dose-response association was seen when using lovastatin. CONCLUSIONS: Statin use is associated with reduced risk of CCA and there is a dose-response relationship between the use of statins and risk of CCA.

Impact of Overlapping Functional Gastrointestinal Disorders on the Presentation and Quality of Life of Patients with Erosive Esophagitis and Nonerosive Reflux Disease.

OBJECTIVE: The aim of this study was to investigate the impact of overlapping functional gastrointestinal disorder (FGID) on the quality of life of patients with nonerosive reflux disease (NERD) and erosive esophagitis (EE). MATERIALS AND METHODS: Data from patients with NERD and EE were collected between January 2009 and March 2010. These cases were further stratified into the subgroups of overlapping NERD-functional dyspepsia (FD), NERD-irritable bowel syndrome (IBS), EE-FD, EE-IBS, and NERD or EE alone according to the symptoms. All patients completed the modified Chinese GERDQ and the SF-36 questionnaires. RESULTS: Of the 222 enrolled patients, 96 (43.2%) had NERD and 126 (56.8%) had EE. Overlap of FGID occurred in 43.8-45.8% of the NERD patients, and in 41.3-44.4% of EE cases. The impact of overlapping FGID on patient quality of life was greater in the patients with overlapping NERD-FD compared to those with NERD alone (mean SF-36 total scores 59 vs. 72, adjusted p = 0.025) and the cases with overlapping EE-FD compared to those with EE alone (mean SF-36 total scores 53.19 vs. 73.11, adjusted p = 0.047). There were no significant differences between the individuals with overlapping NERD/EE-IBS and those with NERD/EE alone. CONCLUSIONS: There was a high prevalence of overlapping FGID, with both FD and IBS, among the GERD patients. The individuals with overlapping GERD and FD had lower quality of life scores than those with GERD alone.

Implications of Serum IgG4 Levels for Pancreatobiliary Disorders and Cancer.

Background/Objectives: Immunoglobulin G4-related disease (IgG4-RD) is an immune-mediated disorder presenting as mass-like lesions with obstructions. An elevated serum IgG4 level is identified in more than half of affected patients and is considered a diagnostic criterion. IgG4-RD is still easily misdiagnosed as neoplastic or infectious disease. We aimed to conduct a hospital-based study to illuminate the association between serum IgG4 levels and pancreatobiliary disorders and cancer. Methods: In this study, serum IgG4 levels were assessed at our hospital's immunology laboratory, utilizing data from the hospital's computer center, and the diagnostic codes used were based on ICD-9-CM. We analyzed IgG4 level data collected between April 2013 and April 2020, including patients' age, gender, and diseases, but excluding the rationale for IgG4 level assessment. Employing propensity score matching (PSM) at a 1:1 ratio to mitigate age and gender confounding, we analyzed 759 patients divided into groups by IgG4 levels (≤140 and >140 mg/dL; and ≤140, 141-280, >280 mg/dL). We explored associations between IgG4 levels and conditions such as pancreatobiliary cancer (the group included cholangiocarcinoma, pancreatic cancer, and ampullary cancer), cholangitis, cholangiocarcinoma, pancreatitis, pancreatic cancer, and ampullary cancer. Results: Our study analyzed the demographics, characteristics, and serum IgG4 levels of participants and found no significant differences in serum IgG4 levels across various pancreatobiliary conditions. Nevertheless, the crude odds ratios (ORs) suggested a nuanced association between a higher IgG4 level > 280 mg/dL and increased risks of cancer and pancreatitis, with crude ORs of 1.52 (p = 0.03) and 1.49 (p = 0.008), respectively. After PSM matching, the further analysis of 759 matched patients showed no significant differences in IgG4 levels > 140 mg/dL between cancerous and non-cancerous groups, nor across other pancreatobiliary conditions. A higher serum IgG4 level > 280 mg/dL was significantly associated with pancreatobiliary cancer and cholangiocarcinoma, with crude ORs of 1.61 (p = 0.026) and 1.62 (p = 0.044), respectively. In addition, IgG4 > 280 mg/dL showed a greater association with pancreatic cancer compared with 141-280 mg/dL, with crude OR of 2.18 (p = 0.038). Conclusions: Our study did not find a clear association between serum IgG4 levels (>140 mg/dL) and pancreatobiliary cancer. We observed that higher IgG4 levels (>280 mg/dL) may be associated with cholangiocarcinoma and pancreatic cancer, as indicated by crude ORs. However, the adjusted analysis did not demonstrate the significant association between IgG4 level > 280 mg/dL and cancer. Considering IgG4-RD as a chronic and persistent inflammatory status, it is more closely associated with inflammatory diseases than with cancer. Therefore, further long-term cohort studies are necessary to evaluate the potential role of IgG4 levels in cancer risk among these patients.

The Impact of Sequential Therapies after First-Line Systemic Therapies in Unresectable Hepatocellular Carcinoma.

Background: The therapeutic options for hepatocellular carcinoma (HCC) have greatly expanded recently, and current first-line therapies include sorafenib, lenvatinib, and atezolizumab-bevacizumab. The aim of this study was to investigate the therapeutic efficacy of sequential systemic treatments after progressing to the first-line agent in patients with unresectable HCC. Methods: Data were collected from subjects with HCC, BCLC stage B or C, who received first-line sorafenib, lenvatinib, or atezolizumab-bevacizumab from September 2020 to December 2022. The patients who progressed after first-line therapy were evaluated according to individual clinical status in order to decide whether or not to accept sequential therapy. The clinical baseline characteristics and overall survival (OS) of enrolled patients were collected and further analyzed. Results: Among the 127 enrolled patients, percentage of sequential therapy was 67.9%, 21.6%, and 37.5% in those with tumor progression after first-line sorafenib, lenvatinib, or atezolizumab-bevacizumab, respectively. Acceptance of sequential therapy (HR 0.46, p = 0.041) and presentation of ALBI grade I (HR 0.36, p = 0.002) had a significantly positive impact on OS. Pre-treatment ALBI grade had a significant impact on the decision to accept sequential therapy in patients with progressed HCC. Conclusions: The patients who were able to undergo sequential therapy had a better survival outcome compared to those who received only one agent, and the pre-treatment ALBI level might be regarded as a cornerstone tool to assess survival outcomes in patients undergoing treatment for HCC.

Ursodeoxycholic Acid Modulates the Interaction of miR-21 and Farnesoid X Receptor and NF-κB Signaling.

(1) Background: This study investigates the effects of Ursodeoxycholic acid (UDCA) on NF-κB signaling, farnesoid X receptor (FXR) singling, and microRNA-21 in HepG2 cells. (2) Methods: HepG2 cells were treated with lipopolysaccharide (LPS) to simulate hepatic inflammation. The investigation focused on the expression of NF-κB activation, which was analyzed using Western blot, confocal microscopy, and Electrophoretic Mobility-shift Assays (EMSA). Additionally, NF-κB and farnesoid X receptor (FXR) singling expressions of micro-RNA-21, COX-2, TNF-α, IL-6, cyp7A1, and shp were assessed by RT-PCR. (3) Results: UDCA effectively downregulated LPS-induced expressions of NF-κB/65, p65 phosphorylation, and also downregulated FXR activity by Western blot. Confocal microscopy and EMSA results confirmed UDCA's role in modulating NF-κB signaling. UDCA reduced the expressions of LPS-induced COX-2, TNF-α, and IL-6, which were related to NF-κB signaling. UDCA downregulated LPS-induced cyp7A1 gene expression and upregulated shp gene expression, demonstrating selective gene regulation via FXR. UDCA also significantly decreased micro-RNA 21 levels. (4) Conclusions: This study demonstrates UDCA's potent anti-inflammatory effects on NF-κB and FXR signaling pathways, and thus its potential to modulate hepatic inflammation and carcinogenesis through interactions with NF-κB and FXR. The decrease in micro-RNA 21 expression further underscores its therapeutic potential.

Attenuation of LPS-induced lung inflammation by glucosamine in rats.

Acute inflammation is often observed during acute lung injury (ALI) and acute respiratory distress syndrome. Glucosamine is known to act as an anti-inflammatory molecule. The effects of glucosamine on acute lung inflammation and its associated mechanisms remain unclear. The present study sought to address how glucosamine plays an anti-inflammatory role in acute lung inflammation in vivo and in vitro. Using the LPS intratracheal instillation-elicited rat lung inflammation model, we found that glucosamine attenuated pulmonary edema and polymorphonuclear leukocyte infiltration, as well as the production of TNF-α, IL-1ß, cytokine-induced neutrophil chemoattractant (CINC)-1, macrophage inflammatory protein (MIP)-2, and nitric oxide (NO) in the bronchoalveolar lavage fluid (BALF) and in the cultured medium of BALF cells. The expression of TNF-α, IL-1ß, IFN-γ, CINC-1, MIP-2, monocyte chemotactic protein-1, and inducible NO synthase (iNOS) in LPS-inflamed lung tissue was also suppressed by glucosamine. Using the rat alveolar epithelial cell line L2, we noted that the cytokine mixture (cytomix)-regulated production and mRNA expression of CINC-1 and MIP-2, NO production, the protein and mRNA expression of iNOS, iNOS mRNA stability, and iNOS promoter activity were all inhibited by glucosamine. Furthermore, glucosamine reduced LPS-mediated NF-κB signaling by decreasing IκB phosphorylation, p65 nuclear translocation, and NF-κB reporter activity. Overexpression of the p65 subunit restored the inhibitory action of glucosamine on cytomix-regulated NO production and iNOS expression. In conclusion, glucosamine appears to act as an anti-inflammatory molecule in LPS-induced lung inflammation, at least in part by targeting the NF-κB signaling pathway.

A miniature ultrasound probe is useful in reducing rebleeding after endoscopic cyanoacrylate injection for hemorrhagic gastric varices.

OBJECTIVE: To better assess the usefulness of miniature ultrasound probe (MUP) sonography in the evaluation of the adequacy of gastric variceal injection with cyanoacrylate to decrease the risk of post injection rebleeding. MATERIAL AND METHODS: Sixty-nine patients with bleeding gastric varices were included in this study. Endoscopic cyanoacrylate injection was performed in the acute phase for variceal hemostasis. After injection, patients (n = 34) included in the MUP group prospectively received endoscopic ultrasonography (EUS) with MUP during each scheduled endoscopic follow-up session. Patients (n = 35) in the control group who were included historically were followed up with the same interval with endoscopy only. RESULTS: Four (11.4%) patients in the control group received reinjection, and there were 10 episodes of rebleeding in 7 (20.0%) patients. Nine (26.5%) patients received reinjection due to inadequate obturation as judged by EUS. There were six episodes of rebleeding in three (8.8%) patients in the MUP group. The free-of-rebleeding rate for the MUP group was significantly higher than that for the control group (p < 0.05). The cumulative survival for the MUP group was slightly better than that for the control group but was not statistically significant. The patients' compliance in both groups was similar. The endosonographers considered the performance of MUP sonography to be convenient. CONCLUSIONS: MUP sonography is useful for the evaluation of the adequacy of tissue adhesive obturation of gastric varices that may reduce the probability of rebleeding.

Comparison the efficacy of intermediate dose argon plasma coagulation versus hemoclip for upper gastrointestinal non-variceal bleeding.

BACKGROUND/AIMS: Endoscopic argon plasma coagulation (APC) and hemoclip were used for the treatment of bleeding peptic ulcers. There are wide ranges of hemostatic doses (power and flow) of APC used in previous studies. The aim of our study was to assess the efficacy and safety of "intermediate dose" APC compared to hemoclips for hemostasis from bleeding peptic ulcer. METHODOLOGY: The present study was designed as a retrospective study using historical controls. One hundred and ninety-four consecutive upper GI bleeding patients with bleeding visible vessel lesions were treated with either APC or hemoclips. There are 110 patients received APC treatment and 84 patients received hemoclip hemostasis. The main outcome measurements were one week rebleeding rate, one month rebleeding rate, surgery, morality, amount of blood transfusion and durations of hospital stay. RESULTS: There were no significant differences between the two groups in 1 week rebleeding rate (1.8% vs. 2.4%, p = 1.0), 1 month rebleeding rate (0% vs. 1.2%, p = 0.433), mortality, surgery and amount of blood transfusion (2.67 +/- 3.27 vs. 3.04 +/- 2.75 units, p = 0.322). However, the hospital stay was longer in hemoclip group (5.38 +/- 6.76 vs. 8.49 +/- 11.19 days p = 0.011). CONCLUSIONS: APC and hemoclip are with different hemostatic mechanisms, but the hemostatic outcomes were not significantly different between the two groups. APC is an effective, safe, and easily applicable endoscopic hemostatic modality as hemoclip for patients with non-variceal bleeding.

Hepatitis Flares or Hepatic Decompensation after Discontinuation of Tenofovir Disoproxil Fumarate and Entecavir in Non-Cirrhotic Hepatitis B e Antigen-Negative Patients.

Hepatic events can occur after discontinuing antiviral therapy. We investigated factors associated with hepatitis flares and hepatic decompensation after discontinuing tenofovir disoproxil fumarate (TDF) and entecavir (ETV). Hepatitis flares within 6 months and hepatic decompensation were compared between non-cirrhotic hepatitis B e antigen-negative patients after discontinuing TDF or ETV by using the Cox proportional hazard model. The cumulative rates of hepatitis flare at 6 months after discontinuing ETV and TDF were 2% and 19%, respectively (p < 0.001). The respective rates of hepatic decompensation at 6 months were 0% and 7% (p = 0.009). Higher alanine aminotransferase (ALT) (AASLD criteria) at the end of treatment (EOT) (HR = 4.93; p = 0.001), an off-therapy dynamic change in HBV DNA (rapid rebound of HBV DNA from the nadir, ≥1 log10 IU/mL per month) (HR = 10.7; p < 0.001), and the discontinuation of TDF (HR = 6.44; p = 0.006) were independently associated with hepatitis flares within 6 months. Older age (HR = 1.06; p < 0.001) and an off-therapy dynamic change in HBV DNA (HR = 3.26; p = 0.028) were independently associated with hepatic decompensation after the discontinuation of antiviral therapy. In summary, we demonstrated several factors associated with hepatitis flares and hepatic decompensation after discontinuing antiviral therapy in non-cirrhotic hepatitis B e antigen-negative patients.

Impact of Helicobacter pylori eradication timing on the risk of thromboembolism events in patients with peptic ulcer disease: a population-based cohort study.

OBJECTIVES: To evaluate the impact of Helicobacter pylori eradication on venous thromboembolism (VTE) events, and the differences between early and late treatment timing. DESIGN: A population-based cohort study. SETTING: Taiwan's National Health Insurance Research Database. PARTICIPANTS: A total of 6736 patients who received H. pylori eradication therapy from 2000 to 2010 were identified. We randomly selected 26 944 subjects matching in gender, age and baseline year as comparison cohort. PRIMARY AND SECONDARY OUTCOME MEASURES: The incidence rate ratios of VTE in the H. pylori eradication cohorts to that of the control cohort were examined. Multivariable Cox proportional hazard regression analysis was used to estimate the relative HRs and 95% CI of VTE development. RESULTS: The total incidence rate of VTE was observed in the late H. pylori eradication cohort, the early H. pylori eradication cohort and the control cohort (15.2, 3.04 and 2.91 per 1000 person-years, respectively). An age-specific trend was found in the late H. pylori eradication cohort, with a greater rate of VTE in the 50-65 years and more than 65 years age groups (adjusted HR 5.44; 95% CI 4.21 to 7.03 and 3.13; 95% CI 2.46 to 3.99). With comorbidities, the late H. pylori eradication cohort seemed to have the highest VTE incidence rate and adjusted HR (4.48, 95% CI 3.78 to 5.30). CONCLUSIONS: Late H. pylori eradication was associated with a significantly increased risk of VTE, and there was a significantly greater risk of VTE in patients with female gender, age more than 50 years and with comorbidities.

Critically-Ill Patients with Biliary Obstruction and Cholangitis: Bedside Fluoroscopic-Free Endoscopic Drainage versus Percutaneous Drainage.

Severe acute cholangitis is a life-threatening medical emergency. Endoscopic biliary drainage (EBD) or percutaneous transhepatic biliary drainage (PTBD) is usually used for biliary decompression. However, it can be risky to transport a critical patient to the radiology unit. We aimed to compare clinical outcomes between bedside, radiation-free EBD and fluoroscopic-guided PTBD in patients under critical care. METHODS: A retrospective study was conducted on critically ill patients admitted to the intensive care unit with biliary obstruction and cholangitis from January 2011 to April 2020. RESULTS: A total of 16 patients receiving EBD and 31 patients receiving PTBD due to severe acute cholangitis were analyzed. In the EBD group, biliary drainage was successfully conducted in 15 (93.8%) patients. Only one patient (6.25%) encountered post-procedure pancreatitis. The 30-day mortality rate was no difference between the 2 groups (32.72% vs. 31.25%, p = 0.96). Based on multivariate analysis, independent prognostic factors for the 30-day mortality were a medical history of malignancy other than pancreatobiliary origin (HR: 5.27, 95% confidence interval [CI]: 1.01-27.57) and emergent dialysis (HR: 7.30, 95% CI: 2.20-24.24). CONCLUSIONS: Bedside EBD is safe and as effective as percutaneous drainage in critically ill patients. It provides lower risks in patient transportation but does require experienced endoscopists to perform the procedure.