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2.
Dig Dis Sci ; 67(8): 4161-4169, 2022 08.
Article in English | MEDLINE | ID: mdl-34796411

ABSTRACT

BACKGROUND: Clinical guidelines recommend continuing antiplatelet monotherapy with aspirin and, in certain situations, other antiplatelet agents in patients undergoing endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy. AIMS: Given the scant evidence supporting this recommendation, our primary objective was to determine if the risk of post-sphincterotomy bleeding was increased in patients on antiplatelet monotherapy. METHODS: We performed a systematic search of Cochrane Library, Ovid Embase, Ovid Medline, Pubmed, Scopus, and Web of Science Core Collection databases. Inclusion criteria were adult patients undergoing ERCP and sphincterotomy on antiplatelet monotherapy with the comparator of no antithrombotic therapy. Our primary outcome was post-sphincterotomy bleeding. Methodological quality was assessed with the ROBINS-I tool and the Newcastle-Ottawa Scale. Meta-analysis with random-effects model was performed. RESULTS: The search identified 4676 unique citations, with six cohort studies meeting our inclusion criteria. Post-sphincterotomy bleeding was increased in patients on antiplatelet monotherapy: OR = 1.53 (95% CI 1.03-2.28) without substantial heterogeneity (I2 = 0%). The number needed to harm (the number of patients who would have to receive antiplatelet monotherapy for one additional patient to have a post-sphincterotomy bleeding episode) was 185(95% CI 80-2272). All included studies had methodological shortcomings. CONCLUSION: Antiplatelet monotherapy was associated with a modestly increased risk of post-sphincterotomy bleeding in our systematic review and meta-analysis. More high-quality studies are needed to improve certainty regarding the estimated effect size. REGISTRATION: PROSPERO CRD42020153019.


Subject(s)
Hemorrhage , Platelet Aggregation Inhibitors , Sphincterotomy, Endoscopic , Adult , Aspirin/adverse effects , Cholangiopancreatography, Endoscopic Retrograde , Hemorrhage/chemically induced , Humans , Platelet Aggregation Inhibitors/adverse effects
3.
Dis Mon ; 67(7): 101130, 2021 Jul.
Article in English | MEDLINE | ID: mdl-33478678

ABSTRACT

Gallbladder disorders encompass a wide breadth of diseases that vary in severity. We present a comprehensive review of literature for the clinical presentation, pathophysiology, diagnostic evaluation, and management of cholelithiasis-related disease, acute acalculous cholecystitis, functional gallbladder disorder, gallbladder polyps, gallbladder hydrops, porcelain gallbladder, and gallbladder cancer.


Subject(s)
Gallbladder Diseases , Gallbladder/pathology , Cholecystitis/diagnosis , Cholecystitis/therapy , Cholelithiasis/diagnosis , Cholelithiasis/therapy , Gallbladder Diseases/diagnosis , Gallbladder Diseases/therapy , Gallbladder Neoplasms/diagnosis , Gallbladder Neoplasms/therapy , Humans
5.
Gastroenterol Hepatol Bed Bench ; 11(2): 153-158, 2018.
Article in English | MEDLINE | ID: mdl-29910857

ABSTRACT

AIM: To determine the impact of obesity on development of portal vein thrombosis in cirrhotic patients. BACKGROUND: Cirrhosis is a known risk factor for portal vein thrombosis (PVT). Evidence also points to obesity as being a risk factor for venous thromboembolism. Limited information is available on how obesity impacts the development of PVT in cirrhotic patients. METHODS: This was a retrospective cohort study using the 2013 National Inpatient Sample. Patients older than 18 years with an ICD-9 CM code for any diagnosis of liver cirrhosis were included. There was no exclusion criteria. The primary outcome was the impact of obesity on development of PVT. Obesity was also sub-classified according to body-mass index (BMI). Secondary outcomes were in-hospital mortality, ICU admission, shock, TPN use, and resource utilization. Odds ratios (OR) and means were adjusted for age, gender, and ethnicity. RESULTS: We included 69,934 obese cirrhotics of which, 1,125 developed PVT (mean age 59 years, 35% female). Overall in-hospital mortality rates were 9% (11% with PVT vs 5% without PVT). On multivariate analysis, obesity was not associated with a significantly different adjusted OR for development of PVT compared to non-obese. When stratifying by obesity subtype, class 1 obesity was associated with increased odds of PVT (OR: 1.45, 95%CI: 1.06-1.96, p=0.02), while class 3 obesity was associated with a decreased odds of PVT (OR: 0.72, 95%CI: 0.58-0.88, p<0.01) compared to non-obese. CONCLUSION: Obesity is not associated with increased odds of PVT.

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