Assessing Pancreatic Morphology via Endosonography in Alcohol-Induced Chronic Liver Disease.
1/5 보강
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
28 patients (39.
I · Intervention 중재 / 시술
추출되지 않음
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
[CONCLUSION] EUS proves valuable for assessing pancreatic changes in alcoholic cirrhosis, illuminating the complex relationship between alcohol consumption and pancreatic morphology.
[OBJECTIVES] Alcohol consumption is a major risk factor for liver cirrhosis and chronic pancreatitis (CP).
APA
Vatansever S, Isik E, et al. (2025). Assessing Pancreatic Morphology via Endosonography in Alcohol-Induced Chronic Liver Disease.. Sisli Etfal Hastanesi tip bulteni, 59(2), 212-217. https://doi.org/10.14744/SEMB.2025.15975
MLA
Vatansever S, et al.. "Assessing Pancreatic Morphology via Endosonography in Alcohol-Induced Chronic Liver Disease.." Sisli Etfal Hastanesi tip bulteni, vol. 59, no. 2, 2025, pp. 212-217.
PMID
40756291 ↗
Abstract 한글 요약
[OBJECTIVES] Alcohol consumption is a major risk factor for liver cirrhosis and chronic pancreatitis (CP). The interplay between pancreatic changes and alcoholic cirrhosis remains poorly understood due to limited diagnostic tools. Endosonography (EUS) offers high sensitivity for detecting pancreatic morphological changes, even in early fibrosis stages.
[METHODS] Between February 2010 and February 2017, 71 male patients diagnosed with alcoholic cirrhosis based on clinical, biochemical, and imaging findings were enrolled. Cirrhosis and pancreatitis from other causes were excluded. EUS, performed under midazolam and propofol sedation using a radial probe, classified pancreatic morphology per Rosemont criteria: normal, indeterminate for CP, suggestive of CP, or consistent with CP. Clinical data, including alcohol and smoking history, liver function, and portal hypertension markers, were recorded.
[RESULTS] EUS identified normal pancreatic morphology in 28 patients (39.4%), indeterminate findings in 18 (25.4%), and CP-consistent or suggestive changes in 25 (35.2%). Logistic regression revealed no significant association between pancreatic changes and age, smoking, alcohol intake, BMI, spleen size, INR, platelet count, diabetes mellitus (DM), or compensated cirrhosis. Kaplan-Meier analysis revealed no significant survival difference between patients with normal pancreatic morphology (median 3.9 years) and those with abnormal morphology (median 3.1 years; p=0.792). One patient (1.4%) with normal morphology developed pancreatic cancer after 3.3 years. Hepatic and extrahepatic malignancy incidence reached 18% over five years, with hepatocellular carcinoma (HCC) at 4.3%, yet no statistically significant association was found between pancreatic changes and malignancy development (p=0.639). Portal hypertension severity and mortality showed no correlation with pancreatic findings.
[CONCLUSION] EUS proves valuable for assessing pancreatic changes in alcoholic cirrhosis, illuminating the complex relationship between alcohol consumption and pancreatic morphology.
[METHODS] Between February 2010 and February 2017, 71 male patients diagnosed with alcoholic cirrhosis based on clinical, biochemical, and imaging findings were enrolled. Cirrhosis and pancreatitis from other causes were excluded. EUS, performed under midazolam and propofol sedation using a radial probe, classified pancreatic morphology per Rosemont criteria: normal, indeterminate for CP, suggestive of CP, or consistent with CP. Clinical data, including alcohol and smoking history, liver function, and portal hypertension markers, were recorded.
[RESULTS] EUS identified normal pancreatic morphology in 28 patients (39.4%), indeterminate findings in 18 (25.4%), and CP-consistent or suggestive changes in 25 (35.2%). Logistic regression revealed no significant association between pancreatic changes and age, smoking, alcohol intake, BMI, spleen size, INR, platelet count, diabetes mellitus (DM), or compensated cirrhosis. Kaplan-Meier analysis revealed no significant survival difference between patients with normal pancreatic morphology (median 3.9 years) and those with abnormal morphology (median 3.1 years; p=0.792). One patient (1.4%) with normal morphology developed pancreatic cancer after 3.3 years. Hepatic and extrahepatic malignancy incidence reached 18% over five years, with hepatocellular carcinoma (HCC) at 4.3%, yet no statistically significant association was found between pancreatic changes and malignancy development (p=0.639). Portal hypertension severity and mortality showed no correlation with pancreatic findings.
[CONCLUSION] EUS proves valuable for assessing pancreatic changes in alcoholic cirrhosis, illuminating the complex relationship between alcohol consumption and pancreatic morphology.
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