Cold snare versus cold forceps polypectomy for endoscopic resection of diminutive polyps: meta-analysis of randomized controlled trials.

BACKGROUND AND AIMS: The practices for resection of diminutive colon polyps vary among endoscopists, and U.S. Multi-Society Task force guidelines recommend use of cold snare polypectomy (CSP) for this purpose. In this meta-analysis, we compared CSP and cold forceps polypectomy (CFP) for resection of diminutive polyps. METHODS: Several databases were reviewed to identify randomized controlled trials that compared CSP and CFP for resection of diminutive polyps. The study outcomes of interest were complete resection of all diminutive polyps, complete resection of polyps ≤3 mm in size, failure of tissue retrieval, and polypectomy time. For categorical variables, pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated; for continuous variables, mean differences (MDs) with 95% CIs were calculated. Data were analyzed by using a random-effects model, and heterogeneity was assessed by using the I2 statistic. RESULTS: We included 9 studies with 1037 patients. Rate of complete resection of all diminutive polyps was significantly higher in the CSP group (OR, 1.68; 95% CI, 1.09-2.58). Subgroup analysis, including jumbo or large-capacity forceps, found no significant difference in complete resection between groups (OR, 1.43; 95% CI, .80-2.56). We found no significant between-groups in the rates of complete resection of polyps ≤3 mm in size (OR, .83; 95% CI, .30-2.31). Rate of failure of tissue retrieval was significantly higher in the CSP group (OR, 10.13; 95% CI, 2.29-44.74). No significant between-group difference was noted in polypectomy time. CONCLUSIONS: CFP using large-capacity or jumbo biopsy forceps is noninferior to CSP for complete resection of diminutive polyps.

Blockage of the Na-K-ATPase signaling-mediated oxidant amplification loop elongates red blood cell half-life and ameliorates uremic anemia induced by 5/6th PNx in C57BL/6 mice.

We have previously demonstrated that the Na-K-ATPase signaling-mediated oxidant amplification loop contributes to experimental uremic cardiomyopathy and anemia induced by 5/6th partial nephrectomy (PNx). This process can be ameliorated by systemic administration of the peptide pNaKtide, which was designed to block this oxidant amplification loop. The present study demonstrated that the PNx-induced anemia is characterized by marked decreases in red blood cell (RBC) survival as assessed by biotinylated RBC clearance and eryptosis as assessed by annexin V binding. No significant change in iron homeostasis was observed. Examination of plasma samples demonstrated that PNx induced significant increases in systemic oxidant stress as assessed by protein carbonylation, plasma erythropoietin concentration, and blood urea nitrogen. Systemic administration of pNaKtide, but not NaKtide (pNaKtide without the TAT leader sequence) and a scramble "pNaKtide" (sc-pNaKtide), led to the normalization of hematocrit, RBC survival, and plasma protein carbonylation. Administration of the three peptides had no significant effect on PNx-induced increases in plasma erythropoietin and blood urea nitrogen without notable changes in iron metabolism. These data indicate that blockage of the Na-K-ATPase signaling-mediated oxidant amplification loop ameliorates the anemia of experimental renal failure by increasing RBC survival.NEW & NOTEWORTHY The anemia of CKD is multifactorial, and the current treatment based primarily on stimulating bone marrow production of RBCs with erythropoietin or erythropoietin analogs is unsatisfactory. In a murine model of CKD that is complicated by anemia, blockade of Na-K-ATPase signaling with a specific peptide (pNaKtide) ameliorated the anemia primarily by increasing RBC survival. Should these results be confirmed in patients, this strategy may allow for novel and potentially additive strategies to treat the anemia of CKD.

Correlation of Autoimmune Pancreatitis and Malignancy: Systematic Review and Meta-Analysis.

BACKGROUND: There is conflicting evidence regarding autoimmune pancreatitis (AIP) association with pancreatic and non-pancreatic cancers. Literature lacks data on overall prevalence of malignancies in autoimmune pancreatitis. AIM: Given the lack of definite evidence, we aimed to pool and summarize data from available literature regarding prevalence of different malignancies in AIP. METHODS: We conducted a systematic search of MEDLINE, EMBASE, Cochrane Register of Controlled Trials, and Web of Science through February 16, 2021, to include observational studies assessing the incidence of cancer in AIP. We used the DerSimonian-Laird method with random effects for meta-analysis. Pooled prevalence, 95% confidence interval (CI), and I2 statistic are reported. RESULTS: A total of 17 studies with 2746 patients were included assessing the prevalence of cancer in AIP. The overall prevalence of cancer in AIP was 9.6% [95% confidence interval (CI), 5.7-13.5%]. The cancers with the highest prevalence in AIP population were gastric and colorectal cancer, with prevalence of 1.3% (95% CI, 0.5-2.1%) and 1.2% (95% CI, 0.6-1.8%), respectively. CONCLUSION: We demonstrate the prevalence of different cancers in AIP. Inflammatory surge in AIP and subsequent carcinogenesis is one explanation for this association. Moreover, AIP can be a paraneoplastic syndrome manifestation of malignancies.

The potential role of Na-K-ATPase and its signaling in the development of anemia in chronic kidney disease.

Chronic kidney disease (CKD) is one of the most prominent diseases affecting our population today. According to the Factsheet published by Centers for Disease Control and Prevention (CDC), it effects approximately 15% of the total population in the United States in some way, shape, or form. Within the myriad of symptomatology associated with CKD, one of the most prevalent factors in terms of affecting quality of life is anemia. Anemia of CKD cannot be completely attributed to one mechanism or cause, but rather has a multifactorial origin in the pathophysiology of CKD. While briefly summarizing well-documented risk factors, this review, as a hypothesis, aims to explore the possible role of Na-K-ATPase and its signaling function [especially recent identified reactive oxygen species (ROS) amplification function] in the interwoven mechanisms of development of the anemia of CKD.

The Redox-Sensitive Na/K-ATPase Signaling in Uremic Cardiomyopathy.

In recent years, Na/K-ATPase signaling has been implicated in different physiological and pathophysiological conditions, including cardiac hypertrophy and uremic cardiomyopathy. Cardiotonic steroids (CTS), specific ligands of Na/K-ATPase, regulate its enzymatic activity (at higher concentrations) and signaling function (at lower concentrations without significantly affecting its enzymatic activity) and increase reactive oxygen species (ROS) generation. On the other hand, an increase in ROS alone also regulates the Na/K-ATPase enzymatic activity and signaling function. We termed this phenomenon the Na/K-ATPase-mediated oxidant-amplification loop, in which oxidative stress regulates both the Na/K-ATPase activity and signaling. Most recently, we also demonstrated that this amplification loop is involved in the development of uremic cardiomyopathy. This review aims to evaluate the redox-sensitive Na/K-ATPase-mediated oxidant amplification loop and uremic cardiomyopathy.

Fatal Venous Gas Embolism During Endoscopic Retrograde Cholangiopancreatography After Simultaneous Deployment of 2 Self-Expandable Metallic Stents.

Gas embolisms are a rare complication of endoscopic retrograde cholangiopancreatography (ERCP). While there have been multiple reports of ERCP-associated air embolisms, only 2 case reports using oral cholangioscopy and CO2 insufflation have been reported in the literature. We present a unique case of a fatal CO2 venous air embolism during ERCP without using cholangioscopy and with no intentional CO2 insufflation of the biliary tree.

Eosinophilic Esophagitis After an Allegra-D Bolus: A Case Report.

Eosinophilic esophagitis (EoE) is an immune-mediated disorder that may be related to exposure to additive chemicals in crops, air pollutants, or supplements found within livestock. Co-occurring allergic or atopic diseases including atopic dermatitis, food allergies, and asthma are also commonly seen in 70% of cases and help guide diagnosis. Diagnosis of EoE requires eosinophilic infiltration greater than 15 eosinophils per high power field (HPF) with endoscopic evidence of abnormal esophageal changes. Here, we discuss a rare presentation of food bolus impaction secondary to EoE after ingestion of a nasal decongestant and antihistamine pill that has previously never been described in the literature. A 22-year-old male with no significant past medical history presented to the emergency department (ED) with a chief complaint of a sudden onset respiratory distress, regurgitation of clear oral secretions, and globus sensation post ingestion of a fexofenadine-pseudoephedrine tablet. Prior to intake of the capsule, the patient was consuming liquids and solids appropriately. The patient was afebrile, hypertensive at 172/114, and found to have a normal heart rate of 88 bpm and a respiration rate of 18 breaths per minute. An esophagogastroduodenoscopy (EGD) was performed, which revealed a fexofenadine-pseudoephedrine capsule at 23 cm from the incisors along with a superficial ulceration at the corresponding level in the esophagus. The foreign body was successfully removed using raptor forceps. Further visualization demonstrated trachealization of the esophagus and furrowing and severe narrowing (< 10mm), which raised suspicion for EoE. Proximal biopsy indicated 16 intraepithelial eosinophils per HPF within the squamous epithelium, likely compatible with EoE. The patient tolerated the procedure well and was discharged on an eight-week course of proton-pump inhibitors. EoE is defined as an immune-mediated esophageal disease characterized histologically by eosinophil-predominant inflammation. Our patient was reported to have up to 30 eosinophils per HPF from the proximal esophageal biopsy, which satisfies the requirements for an EoE diagnosis. Based on the current literature review, there have been no other reported cases of symptomatic food bolus impaction secondary to EoE after ingestion of antihistamines.