Obesity Paradox in Patients with Acute Coronary Syndrome: Is Malnutrition the Answer?

BACKGROUND: Obesity paradox has been reported in patients with cardiovascular disease, showing an inverse association between obesity as defined by BMI (in kg/m2) and prognosis. Nutritional status is associated with systemic inflammatory response and affects cardiovascular disease outcomes. OBJECTIVES: This study sought to examine the influence of obesity and malnutrition on the prognosis of patients with acute coronary syndrome (ACS). METHODS: This study included consecutive patients diagnosed with ACS and underwent coronary angiogram between January 2009 and February 2023. At baseline, patients were categorized according to their BMI as follows: underweight (<18), normal weight (18-24.9), overweight (25.0-29.9), and obese (>30.0). We assessed the nutritional status by Prognostic Nutritional Index (PNI). Malnutrition was defined as a PNI value of <38. RESULTS: Of the 21,651 patients with ACS, 582 (2.7%) deaths from any cause were observed over 28.7 months. Compared with the patient's state of normal weight, overweight, and obesity were associated with decreased risk of all-cause mortality. Malnutrition was independently associated with poor survival (hazards ratio: 2.64; 95% CI: 2.24, 3.12; P < 0.001). In malnourished patients, overweight and obesity showed a 39% and 72% reduction in the incidence of all-cause mortality, respectively. However, in nourished patients, no significant reduction in the incidence of all-cause mortality was observed (all P > 0.05). CONCLUSIONS: Obesity paradox appears to occur in patients with ACS. Malnutrition may be a significant independent risk factor for prognosis in patients with ACS. The obesity paradox is influenced by the status of malnutrition.

Serum bile acid profiles are associated with heart failure with preserved ejection fraction in patients with metabolic dysfunction-associated fatty liver disease: An exploratory study.

AIM: To analyse the association between serum bile acid (BA) profile and heart failure (HF) with preserved ejection fraction (HFpEF) in patients with metabolic dysfunction-associated fatty liver disease (MAFLD). METHODS: We enrolled 163 individuals with biopsy-proven MAFLD undergoing transthoracic echocardiography for any indication. HFpEF was defined as left ventricular ejection fraction >50% with at least one echocardiographic feature of HF (left ventricular diastolic dysfunction, abnormal left atrial size) and at least one HF sign or symptom. Serum levels of 38 BAs were analysed using ultra-performance liquid chromatography coupled with tandem mass spectrometry. RESULTS: Among the 163 patients enrolled (mean age 47.0 ± 12.8 years, 39.3% female), 52 (31.9%) and 43 (26.4%) met the HFpEF and pre-HFpEF criteria, and 38 serum BAs were detected. Serum ursodeoxycholic acid (UDCA) and hyocholic acid (HCA) species were lower in patients with HFpEF and achieved statistical significance after correction for multiple comparisons. Furthermore, decreases in glycoursodeoxycholic acid and tauroursodeoxycholic acid were associated with HF status. CONCLUSIONS: In this exploratory study, specific UDCA and HCA species were associated with HFpEF status in adults with biopsy-confirmed MAFLD.

High-Sensitivity C-Reactive Protein Is Associated With Heart Failure Hospitalization in Patients With Metabolic Dysfunction-Associated Fatty Liver Disease and Normal Left Ventricular Ejection Fraction Undergoing Coronary Angiography.

BACKGROUND: Systemic chronic inflammation plays a role in the pathophysiology of both heart failure with preserved ejection fraction (HFpEF) and metabolic dysfunction-associated fatty liver disease. This study aimed to investigate whether serum hs-CRP (high-sensitivity C-reactive protein) levels were associated with the future risk of heart failure (HF) hospitalization in patients with metabolic dysfunction-associated fatty liver disease and a normal left ventricular ejection fraction. METHODS AND RESULTS: The study enrolled consecutive individuals with metabolic dysfunction-associated fatty liver disease and normal left ventricular ejection fraction who underwent coronary angiography for suspected coronary heart disease. The study population was subdivided into non-HF, pre-HFpEF, and HFpEF groups at baseline. The study outcome was time to the first hospitalization for HF. In 10 019 middle-aged individuals (mean age, 63.3±10.6 years; 38.5% women), the prevalence rates of HFpEF and pre-HFpEF were 34.2% and 34.5%, with a median serum hs-CRP level of 4.5 mg/L (interquartile range, 1.9-10 mg/L) and 5.0 mg/L (interquartile range, 2.1-10.1 mg/L), respectively. Serum hs-CRP levels were significantly higher in the pre-HFpEF and HFpEF groups than in the non-HF group. HF hospitalizations occurred in 1942 (19.4%) patients over a median of 3.2 years, with rates of 3.7% in non-HF, 20.8% in pre-HFpEF, and 32.1% in HFpEF, respectively. Cox regression analyses showed that patients in the highest hs-CRP quartile had a ≈4.5-fold increased risk of being hospitalized for HF compared with those in the lowest hs-CRP quartile (adjusted-hazard ratio, 4.42 [95% CI, 3.72-5.25]). CONCLUSIONS: There was a high prevalence of baseline pre-HFpEF and HFpEF in patients with metabolic dysfunction-associated fatty liver disease and suspected coronary heart disease. There was an increased risk of HF hospitalization in those with elevated hs-CRP levels.

Clinical characteristics and prognosis of patients with hypertrophic cardiomyopathy and heart failure with preserved ejection fraction.

BACKGROUND: Whether heart failure with preserved ejection fraction (HFpEF) is associated with an increased risk of developing systolic dysfunction and a poor prognosis in hypertrophic cardiomyopathy (HCM) patients is unknown. OBJECTIVE: We aimed to assess risk factors for the development of end-stage (ES) heart failure (HF) (ejection fraction < 50%) and compare the prognosis of different HF phenotypes. METHODS: This retrospective study was conducted on patients with HCM in China between January 2009 and February 2023. Patients were stratified into three different groups: HCM-non-HF, HCM-HFpEF and HCM-heart failure with reduced ejection fraction (HCM-HFrEF). The primary outcome was a composite of major adverse cardiac events (MACEs), including all-cause deaths, HF hospitalization, sudden cardiac death and ventricular tachycardia. RESULTS: Of 3,620 HCM patients enrolled, 1,553 (42.9%) had non-HF, 1,666 (46.0%) had HFpEF, and 579 patients (11.1%) had HFrEF at baseline. During the median follow-up period of 4.0 years (IQR 1.4-9.4 years), patients with HCM-HFpEF exhibited a higher incidence of ES-HF than those with HCM-non-HF (12.4% vs. 2.7%, P < 0.001). HFpEF was an independent risk factor for ES-HF development (HR 3.84, 2.54-5.80, P < 0.001). MACEs occurred in 26.9% with a higher incidence in HCM-HFpEF than HCM-non-HF (36.6% vs 12.2%, P < 0.001). HFpEF was an independent predictor of MACEs (HR 2.13, 1.75-2.59, P < 0.001). CONCLUSIONS: HFpEF is common in HCM. Compared to non-HF, it increases the risk of LVEF decline and poor prognosis. It may aid in risk stratification and need close echocardiography follow-up.

Reduced- or Half-Dose Rivaroxaban Following Left Atrial Appendage Closure: A Feasible Antithrombotic Therapy in Patients at High Risk of Bleeding?

The optimal antithrombotic strategy after percutaneous left atrial appendage closure (LAAC) has not yet been established. The advisability of administering low-dose direct oral anticoagulation after LAAC to patients at high risk of bleeding is uncertain. Thus, in the present study, we evaluated the safety and effectiveness of reduced-(15 mg) or half-dose rivaroxaban (10 mg) versus warfarin regarding real-world risks of thromboembolism, bleeding, and device-related thrombosis (DRT) after LAAC. Patients with non-valvular atrial fibrillation and HASBLED ≥ 3 who had undergone successful LAAC device implantation from October 2014 to April 2020 were screened and those who had received 10 mg or 15 mg rivaroxaban or warfarin therapy were enrolled. The patients were followed up 45 days and 6 months after LAAC to evaluate outcomes, including death, thromboembolism, major bleeding, and DRT. Of 457 patients with HASBLED ≥ 3 who had undergone LAAC, 115 had received warfarin and 342 rivaroxaban (15 mg: N = 164; 10 mg: N = 178). There were no significant differences in the incidence of thromboembolism or DRT between the warfarin and both doses of rivaroxaban groups (all p > 0.05). The incidence of major bleeding was significantly higher in the warfarin group than in either the reduced- or half-dose rivaroxaban groups (warfarin vs. rivaroxaban 15 mg: 2.6% vs. 0%, p = 0.030; warfarin vs. rivaroxaban 10 mg: 2.6% vs. 0%, p = 0.038). Either reduced- or half-dose rivaroxaban may be an effective and safe alternative to warfarin therapy in patients with LAAC and who are at high risk of bleeding, the risk of thromboembolism being similar and of major bleeding lower for both doses of rivaroxaban.

Clinical Outcome After Left Ventricular Thrombus Resolution: Who Needs Long-Term or Lifetime Use of Anticoagulants?

Background Patients with left ventricular thrombus (LVT) resolution can have LVT recurrence and risk for thromboembolism. However, these outcomes after LVT resolution are not well known. We aimed to assess the prevalence, risk factors, and clinical outcomes for LVT recurrence in patients with LVT resolution to inform follow-up and treatment. Methods and Results Patients with LVT resolution were identified retrospectively from a large echocardiography database between January 2009 and May 2022. Participants had echocardiograms at 3 time points, including baseline at LVT diagnosis, at LVT resolution, and a follow-up for identification of LVT recurrence. The cumulative LVT recurrence rate was estimated by the Kaplan-Meier method, and predictors of LVT recurrence were evaluated using Cox regression analysis. Among 115 patients with LVT resolution, 28 (24.3%) had LVT recurrence at a median follow-up of 1.2 (0.5-2.8) years. LV aneurysm (hazard ratio [HR], 2.59 [95% CI, 1.20-5.58], P=0.015) and anticoagulant use (HR, 0.12 [95% CI, 0.04-0.41], P=0.001) were predictors of LVT recurrence on multivariable analysis. Patients with an LV aneurysm who did not receive any anticoagulation demonstrated an LVT recurrence rate of 69.5%, whereas those without an LV aneurysm who received anticoagulation had a recurrence rate of 0%. Patients with LVT recurrence had a higher incidence of an embolic event (10.7% versus 1.1%, P=0.016). Conclusions LVT recurrence after LVT resolution is common, especially in those with an LV aneurysm, and is associated with a higher embolic risk. Continued anticoagulation is protective against LVT recurrence, although bleeding risk needs to be considered. These findings can inform follow-up and treatment of patients with documented LVT resolution.

Helicobacter pylori infection with atrophic gastritis: An independent risk factor for colorectal adenomas.

BACKGROUND: The significance of Helicobacter pylori (H. pylori) infection and atrophic gastritis (AG) in the prevalence of colorectal adenomas has been examined in a limited number of studies. However, these studies reported disputed conclusions. AIM: To investigate whether H. pylori infection, AG, and H. pylori-related AG increase the risk of colorectal adenomas. METHODS: This retrospective cross-sectional study included 6018 health-check individuals. The relevant data for physical examination, laboratory testing, 13C-urea breath testing, gastroscopy, colonoscopy and histopathological examination of gastric and colorectal biopsies were recorded. Univariate and multivariate logistic regression analyses were performed to determine the association between H. pylori-related AG and colorectal adenomas. RESULTS: Overall, 1012 subjects (16.8%) were diagnosed with colorectal adenomas, of whom 143 (2.4%) had advanced adenomas. Among the enrolled patients, the prevalence of H. pylori infection and AG was observed as 49.5% (2981/6018) and 10.0% (602/6018), respectively. Subjects with H. pylori infection had an elevated risk of colorectal adenomas (adjusted odds ratio [OR] of 1.220, 95% confidence interval (CI): 1.053-1.413, P = 0.008) but no increased risk of advance adenomas (adjusted OR = 1.303, 95%CI: 0.922-1.842, P = 0.134). AG was significantly correlated to an increased risk of colorectal adenomas (unadjusted OR = 1.668, 95%CI: 1.352-2.059, P < 0.001; adjusted OR = 1.237, 95%CI: 0.988-1.549, P = 0.064). H. pylori infection accompanied by AG was significantly associated with an increased risk of adenomas (adjusted OR = 1.491, 95%CI: 1.103-2.015, P = 0.009) and advanced adenomas (adjusted OR = 1.910, 95%CI: 1.022-3.572, P = 0.043). CONCLUSION: H. pylori-related AG was associated with a high risk of colorectal adenomas and advanced adenomas in Chinese individuals.

Association between Hemoglobin Glycation Index and NAFLD in Chinese Nondiabetic Individuals.

Purpose: Limited studies have preliminarily identified a positive association between nonalcoholic fatty liver disease (NAFLD) and hemoglobin glycation index (HGI). However, this association has not been fully established. We aim to investigate the association between NAFLD and HGI in Chinese nondiabetic individuals and to construct a risk score based on HGI to predict a person's risk of NAFLD. Methods: After strict exclusion criteria, 5,903 individuals were included in this retrospective cross-sectional study. We randomly selected 1,967 subjects in the enrollment to obtain an equation of linear regression, which was used to calculate predicted HbA1c and drive HGI. The other subjects were classified into four categories according to HGI level (≤-0.22, -0.21∼0.02, 0.03∼0.28, and ≥0.29). All subjects retrospectively reviewed the baseline characteristics, laboratory examinations, and abdominal ultrasonography. Results: The prevalence of NAFLD in this population was 20.7%, which increases along with the growth of HGI levels (P < 0.001). Adjusted to multiple factors, this trend still remained significant (OR: 1.172 (95% CI, 1.074-1.279)). The combined NAFLD risk score based on HGI resulted in an area under the receiver operator characteristic curve (AUROC) of 0.85 provided sensitivity, specificity, positive predictive value, and a negative predictive value for NAFLD of 84.4%, 71.3%, 65.0%, and 88.0%, respectively. Conclusions: NAFLD is independently associated with HGI levels in Chinese nondiabetic individuals. And, NAFLD risk score may be used as one of the risk predictors of NAFLD in nondiabetic population.

Peripheral Arterial Disease in Type 2 Diabetes Is Associated with an Increase in Fibrinogen Levels.

BACKGROUND: The present study is undertaken to investigate the fibrinogen levels in type 2 diabetes mellitus (T2DM) and its relation to peripheral artery disease (PAD) based on a more accurate and applied noninvasive measurements of duplex ultrasonography. METHODS: We performed a cross-sectional study including 1096 T2DM patients (474 males and 622 females). The odds ratios (ORs) and 95% confidence intervals (CIs) were presented to show the association between PAD and fibrinogen in the subjects divided by fibrinogen levels quarterly. Furthermore, the univariate and multiple logistic analyses were performed to explore the correlation between PAD and fibrinogen levels, individual components in the cross-sectional study. RESULTS: Finally, 887 (80.9%) T2DM patients meet the diagnostic criteria of PAD and these patients had considerably higher serum fibrinogen concentration than non-PAD group (P < 0.001). Multiple logistic analyses revealed that higher fibrinogen quartiles were positively related with the development of PAD in the adjusted model. After adjusting for known confounding parameters, the ORs for PAD were 1.993 (95% CI: 1.322-3.005, P < 0.001), 2.469 (95% CI: 1.591-3.831, P < 0.001), and 2.942 (95% CI, 1.838-4.711, P < 0.001) for Q2, Q3, and Q4, respectively (all P values <0.05). CONCLUSIONS: Our results suggest that serum fibrinogen concentration can be considered as an independent risk factor for PAD in T2DM patients.

Role of sLOX-1 in intracranial artery stenosis and in predicting long-term prognosis of acute ischemic stroke.

Objective: The role of sLOX-1 in acute ischemic stroke still remains unclear. This study aims to demonstrate the value of sLOX-1 in evaluating degrees of intracranial artery stenosis and to predict prognosis in stroke. Methods: Two hundred and seventy-two patients were included in this study and basic data were collected within 72 hr on admission. We assessed the association between sLOX-1 levels and stroke conditions in one-year duration. After adjusting for potential confounders, regression analyses were performed. Results: We found that sLOX-1 levels were increased significantly in severe patients compared to the mild stroke group (p = .011). After adjusting confounders, sLOX-1 was associated with a poor functional outcome in patients with an adjusted OR of 2. 946 (95% CI, 1.788-4.856, p < .001). There was also positive correlation between sLOX-1 levels and the degrees of intracranial artery stenosis in the different groups (p = .029). Conclusions: Our study demonstrated that sLOX-1 levels could be used to evaluate the severity of stroke and the degrees of intracranial artery stenosis. Furthermore, sLOX-1 could be exploited to predict the long-term functional outcome of stroke.

Impact of non-alcoholic fatty liver disease and smoking on colorectal polyps.

OBJECTIVES: Non-alcoholic fatty liver disease (NAFLD) and smoking have similar mechanisms of promoting colorectal polyps. The potential link between NAFLD and smoking in men and colorectal polyps has not been adequately evaluated. The aim is to investigate this association. METHODS: A retrospective cross-sectional study was conducted on 2409 individuals undergoing a health check. Univariate and multivariate logistic regression were performed for analyzing the association between risk factors and colorectal polyps. Individuals were divided into four groups: Q1: NAFLD (-)/smoking (-); Q2: NAFLD (+)/smoking (-); Q3: NAFLD (-)/smoking (+); Q4: NAFLD (+)/smoking (+). Logistic analyses were used to explore associations for the whole study population and stratified groups. RESULTS: The prevalence of colorectal polyps was 38.8% in males, and that of colorectal polyps in smokers and individuals with NAFLD were 47.0% (428/911) and 42.9% (267/622), respectively. With Q1 as reference, subjects with NAFLD (+) and smoking habits (+) had the highest ORs for colorectal polyps (OR = 2.64, 95% CI: 1.91 - 3.64, P < 0.001), adenomatous polyps (OR = 2.06, 95% CI: 1.38 - 3.05, P < 0.05), non-adenomatous polyps (OR = 1.97, 95% CI: 1.39 - 2.80, P < 0.05), ≥ 3 polyps (OR = 2.05, 95% CI: 1.31 - 3.22, P < 0.05) and proximal polyps (OR = 1.58, 95% CI: 1.02 - 2.45, P < 0.05) after adjusting for confounding variables. CONCLUSIONS: Men with NAFLD and smoking habits have an increasing risk of colorectal polyps.

Acute circulatory failure-chronic liver failure-sequential organ failure assessment score: a novel scoring model for mortality risk prediction in critically ill cirrhotic patients with acute circulatory failure.

BACKGROUND AND AIM: Acute circulatory failure (ACF) is associated with high mortality rates in critically ill cirrhotic patients. Only a few accurate scoring models exist specific to critically ill cirrhotic patients with acute circulatory failure (CICCF) for mortality risk assessment. The aim was to develop and evaluate a novel model specific to CICCF. PATIENTS AND METHODS: This study collected and analyzed the data on CICCF from the Multiparameter Intelligent Monitoring in Intensive Care-III database. The acute circulatory failure-chronic liver failure-sequential organ failure assessment (ACF-CLIF-SOFA) score was derived by Cox's proportional hazards regression. Performance analysis of ACF-CLIF-SOFA against CLIF-SOFA and model for end-stage liver disease systems was completed using area under the receiver operating characteristic curve. RESULTS: ACF-CLIF-SOFA identified six independent factors: mean arterial pressure [hazard ratio (HR)=0.984, 95% confidence interval (CI): 0.978-0.990, P<0.001], vasopressin (HR=1.548, 95% CI: 1.273-1.883, P<0.001), temperature (HR=0.764, 95% CI: 0.694-0.840, P<0.001), bilirubin (HR=1.031, 95% CI: 1.022-1.041, P<0.001), lactate (HR=1.113, 95% CI: 1.084-1.142, P<0.001), and urine output (HR=0.854, 95% CI: 0.767-0.951, P=0.004). ACF-CLIF-SOFA showed a better predictive performance than CLIF-SOFA and model for end-stage liver disease in terms of predicting mortality (0.769 vs. 0.729 vs. 0.713 at 30 days, 0.757 vs. 0.707 vs. 0.698 at 90 days, 0.733 vs. 0.685 vs. 0.691 at 1 year, respectively, all P<0.05). CONCLUSION: ACF-CLIF-SOFA, as the first model specific to CICCF, enables a more accurate prediction at 30-day, 90-day, and 1-year follow-up periods than other existing scoring systems.

Sex-influenced association of non-alcoholic fatty liver disease with colorectal adenomatous and hyperplastic polyps.

AIM: To investigate the relationship between non-alcoholic fatty liver disease (NAFLD) and colorectal adenomatous and hyperplastic polyps. METHODS: A retrospective cross-sectional study was conducted on 3686 individuals undergoing health checkups (2430 males and 1256 females). All subjects underwent laboratory testing, abdominal ultrasonography, colonoscopy, and an interview to ascertain the baseline characteristics and general state of health. Multinomial logistic regression analysis was performed to examine the association between NAFLD and the prevalence of colorectal adenomatous and hyperplastic polyps. Furthermore, the relationship was analyzed in different sex groups. Subgroup analysis was performed based on number, size, and location of colorectal polyps. RESULTS: The prevalence of colorectal polyps was 38.8% in males (16.2% for adenomatous polyps and 9.8% for hyperplastic polyps) and 19.3% in females (8.4% for adenomatous polyps and 3.9% for hyperplastic polyps). When adjusting for confounding variables, NAFLD was significantly associated with the prevalence of adenomatous polyps (OR = 1.28, 95%CI: 1.05-1.51, P < 0.05) and hyperplastic polyps (OR = 1.35, 95%CI: 1.01-1.82, P < 0.05). However, upon analyzing adenomatous and hyperplastic polyps in different sex groups, the significant association remained in males (OR = 1.53, 95%CI: 1.18-2.00, P < 0.05; OR = 1.42, 95%CI: 1.04-1.95, P < 0.05) but not in females (OR = 0.44, 95%CI: 0.18-1.04, P > 0.05; OR = 1.18, 95%CI: 0.50-2.78, P > 0.05). CONCLUSION: NAFLD is specifically associated with an increased risk of colorectal adenomatous and hyperplastic polyps in men. However, NAFLD may not be a significant factor in the prevalence of colorectal polyps in women.

Scoring model to predict outcome in critically ill cirrhotic patients with acute respiratory failure: comparison with MELD scoring models and CLIF-SOFA score.

BACKGROUND: Critically ill cirrhotic patients have a high mortality, particularly with concomitant respiratory failure on admission. There are no specific models in use for mortality risk assessment in critically ill cirrhotic patients with acute respiratory failure (CICRF). The aim is to develop a risk prediction model specific to CICRF in order to quantify the severity of illness. METHODS: We analyzed 949 CICRF patients extracted from the MIMIC-III database. The novel model (ARF-CLIF-SOFA) was developed from the CLIF-SOFA score. Cox regression analysis and AUROC were implemented to test the predictive accuracy, compared with existing scores including the CLIF-SOFA score and MELD-related scores. RESULTS: ARF-CLIF-SOFA contains PaO2/FiO2 ratio, lactate, MAP, vasopressor therapy, bilirubin and creatinine (1 point each; score range: 0-6). Based on our patient cohort, the ARF-CLIF-SOFA score had good predictive accuracy for predicting the 30-, 90-day and 1-year mortality (AUROC = 0.767 at 30-day, 0.768 at 90-day, 0.765 at 1-year, respectively). Additionally, the performance of the ARF-CLIF-SOFA is superior to existing scores (all P < 0.001). CONCLUSION: The ARF-CLIF-SOFA score can be considered a CICRF specific score with a better predictive accuracy compared to the existing scores.

Remodeling the model for end-stage liver disease for predicting mortality risk in critically ill patients with cirrhosis and acute kidney injury.

Serum creatinine measurement demonstrates a poor specificity and sensitivity for the early diagnosis of acute kidney injury (AKI) in patients with cirrhosis. The existing model for end-stage liver disease (MELD) score reveals multiple pitfalls in critically ill patients with cirrhosis and acute kidney injury (CAKI). The aim of this study was to re-evaluate the role of creatinine values in the existing MELD score and to develop a novel score for CAKI, named the "acute kidney injury-model for end-stage liver disease score" (AKI-MELD score). We extracted 651 CAKI from the Multiparameter Intelligent Monitoring in Intensive Care database. A time-dependent Cox regression analysis was performed for developing remodeled MELD scores (Reweight-MELD score, Del-Cr-MELD score, and AKI-MELD score). The area under the receiver operating characteristic curve provided the discriminative power of scoring models related to outcome. The hazard ratio of creatinine was 1.104 (95% confidence interval [CI], 0.945-1.290; P = 0.211). Reweight-MELD score and Del-Cr-MELD score (decreasing the weight of creatinine) were superior to the original MELD score (all P < 0.001). The new AKI-MELD score consists of bilirubin, the international normalized ratio, and the ratio of creatinine in 48 hours to creatinine at admission. It had competitive discriminative ability for predicting mortality (area under the receiver operating characteristic curve, 0.720 [95% CI, 0.653-0.762] at 30 days, 0.688 [95% CI, 0.630-0.742] at 90 days, and 0.671 [95% CI, 0.612-0.725] at 1 year). Further, AKI-MELD score had significantly higher predictive ability in comparison with MELD score, MELD-Na score, and Updated MELD score (all P < 0.001). Conclusion: The predictive value of creatinine for CAKI should be re-evaluated. AKI-MELD score is a potentially reliable tool to determine the prognosis for mortality of CAKI. (Hepatology Communications 2017;1:748-756).

Endoplasmic reticulum stress is activated in acute pancreatitis.

Endoplasmic reticulum (ER) is one of the most important cell organelles in the body, regulating protein synthesis, folding and aggregation. Endoplasmic reticulum stress (ERS) is a particular subcellular pathological process involving an imbalance of homeostasis and ER disorder. In the early stage of ERS, cells show a protective unfolded protein response that changes the cellular transcriptional and translational programs to alleviate the process. Therefore, a certain degree of ERS can activate the protective adaptation of cells, whereas sustained severe ERS triggers an apoptotic signal and leads to apoptosis. Acute pancreatitis is a disease caused by trypsin digestion of the pancreas, although the pathogenesis is not completely understood. However, a close association has been suggested between pancreatitis and ERS. This article reviewed relevant research advances and discussed the effect of ERS on the development and progression of acute pancreatitis.

Defective expression and modulation of B7-2/CD86 on B cells in B cell chronic lymphocytic leukemia.

Malignant monoclonal B cells of chronic B cell lymphocytic leukemia (B-CLL) usually fail to be cleared, which indicates important costimulatory molecules may be lacking. Among those costimulatory signals, B7-1/CD80 and B7-2/CD86 caused utmost attention. In this study, B7-1 and B7-2 expression on B cells in chronic B cell lymphocytic leukemia patients were detected. Data showed that B7-2 expression in chronic B cell lymphocytic leukemia patients is significantly lower than in normal people, which suggests defective B7-2 expression may be one of the pathogenic mechanisms of chronic B cell lymphocytic leukemia. Further, we confirmed interferon-gamma could induce B7-2 expression slightly and promote T-cell response against chronic B cell lymphocytic leukemia cells, indicating interferon-gamma has clinical value in chronic leukemia immunotherapy based on modulating B7-2 expression.

[Efficacy of diacetyl hexamethylene diamine in treatment of patients with high risk myelodysplastic syndrome].

The aim of this study was to investigate the efficacy of diacetyl hexamethylene diamine (CAHB) for patients with high risk myelodysplastic syndrome (MDS), and to explore the effect of CAHB on HL-60 cells in vitro and its possible mechanism. 8 patients with high risk MDS were treated with CAHB by continuous intravenous infusion for 10 days, and repeated once after an interval of 28 days. The count of the granulo- and mono-blasts in bone marrow (BM) aspirate was measured before and after treatment. HL-60 cells were treated with different concentrations of CAHB for 72 hours in vitro. The inhibitory effect of CAHB on proliferation of HL-60 cells in vitro was measured by MTT assay. Differentiation of HL-60 cells was detected by the changes of CD11b and CD14 expression on cell surface. Apoptosis of HL-60 cells was detected by double staining of Annexin V and PI. The cell cycle distribution change of HL-60 cells was analyzed by flow-cytometry. The results indicated that the granulo- and mono-blasts in BM decreased in all the 8 patients after CAHB treatment. The main side effect of CAHB on hematological system was thrombocytopenia. After being treated with 1, 2, 3, 4 mmol/L CAHB for 72 hours in vitro, the result of MTT assay showed the inhibitory effect of CAHB on the proliferation of HL-60 cells in dose-dependent manner. After being treated manner 1, 2, 3, 4 mmol/L CAHB for 72 hours, the CD11b positive HL-60 cells were 22.39+/-3.97%, 33.12+/-4.46%, 49.25+/-5.27%, 78.05+/-5.66%, respectively, which were significantly different from the control group (CD11b positive HL-60 cells was 5.89+/-2.94%) (p<0.01). The CD14 expression was negative in all the 5 groups. These results suggested that CAHB could induce HL-60 cells to differentiate into mature granulocytes, and the effect of CAHB appeared in dose-dependent manner. After being treated for 72 hours by 1, 2, 3, 4 mmol/L CAHB, the apoptotic cells (Annexin V(+)/PI(-) cells) increased mildly, which suggested that CAHB only weakly induces HL-60 cells to apoptosis at the concentration of 1 to 4 mmol/L. Along with the concentration increase of CAHB, the ratio of cells in G(0)/G(1) phase increased, and ratio of cells in S phase and G(2)/M phase decreased correspondingly, it indicated that CAHB could arrest HL-60 cells in G(0)/G(1) phase in a dose-dependent manner. It is concluded that induction of cell differentiation may be the primary effect of CAHB on MDS. Cell cycle arrest may be essential to the effect of CAHB as well. Side effect of CAHB on platelet count may correlated with its inhibitory effect on hematopoiesis.