Anomalous union of the pancreaticobiliary duct (AUPBD) is a congenital malformation in which the pancreatic and biliary ducts join outside the duodenal wall, forming an elongated common channel. Because sphincter action does not directly affect this junction, reciprocal reflux of pancreatic juice and bile occurs, increasing the risk of biliary tract cancer. AUPBD is frequently associated with choledochal cysts and is a known risk factor for biliary malignancies. We report a case of a 70-year-old woman diagnosed with gallbladder cancer with liver metastases, accompanied by AUPBD without choledochal cysts. She presented with upper abdominal pain, obstructive jaundice, and a large hepatic mass on imaging. Endoscopic retrograde cholangiopancreatography confirmed pancreatobiliary-type AUPBD. Despite biliary drainage, her condition rapidly deteriorated and she died soon after. This case underscores the role of AUPBD in carcinogenesis and the need for early recognition and management.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Background: Mycobacterium avium complex (MAC) is a major cause of pulmonary nontuberculous mycobacterial disease; however, treatment outcomes remain suboptimal.Phenotypic drug susceptibility testing (DST) is conditionally recommended; however, conventional broth microdilution is labor-intensive. The Sensititre SLOMYCO® panel offers a standardized platform for DST of slowly growing mycobacteria. Methods: Eighty-six clinical MAC isolates (48 M. avium and 38 M. intracellulare) from respiratory specimens were tested for 13 antimicrobials using the SLOMYCO panel and reference Clinical and Laboratory Standards Institute (CLSI) broth microdilution methods at the Korean Institute of Tuberculosis. Essential agreement (EA) was defined as minimum inhibitory concentrations within ± 1 dilution, and categorical agreement (CA) was based on CLSI 2018 breakpoints for clarithromycin, amikacin, moxifloxacin, and linezolid. Results: The EA was high for amikacin (90%), moxifloxacin (92%), linezolid (92%), and ethambutol (98%). Moderate EA was observed for clarithromycin (79%), ciprofloxacin (67%), and doxycycline (63%), and low EA was observed for trimethoprim-sulfamethoxazole (34%).The CA values were 100%, 77.9%, 69.8%, and 47.7% for clarithromycin, amikacin, moxifloxacin, and linezolid, respectively. All isolates were clarithromycin-susceptible according to both methods, and no clarithromycin- or amikacin-resistant isolates were detected. Conclusion The SLOMYCO DST system demonstrated high agreement with the reference methods for clarithromycin and amikacin in the tested susceptible population. The variability in the results for moxifloxacin and linezolid highlights the need for refined breakpoints. The validation of resistant isolates is essential before the SLOMYCO system can be recommended for comprehensive clinical applications.