Management_of_colorectal_polyps_update_and_future_directions 2025.pdf
7.6 MB
Management of colorectal polyps: update and future directions.
BMJ December 2025
✳️ Low molecular weight heparin (LMWH) is the preferred anticoagulant for treating acute deep vein thrombosis in patients with decompensated cirrhosis, regardless of the elevated INR.
▶️ The elevated INR should not be considered an absolute contraindication to anticoagulation, as it reflects impaired hepatic synthetic function rather than true anticoagulation status in cirrhosis.
✳️ Direct oral anticoagulants (DOACs) are contraindicated in decompensated cirrhosis, particularly in Child-Pugh class C patients and critically ill individuals, due to hepatic metabolism and unpredictable drug levels.
▶️ While DOACs may be considered in compensated cirrhosis (Child-Pugh class A or B), they should be avoided in decompensated disease.
▶️ LMWH has demonstrated superior outcomes in cirrhotic patients with venous thromboembolism, achieving higher recanalization rates (71% vs 42% without treatment) and lower variceal bleeding risk compared to no anticoagulation. Meta-analyses confirm that LMWH produces more complete recanalization than warfarin and reduces all-cause mortality.
✳️ Warfarin may be considered as an alternative if LMWH is contraindicated, though INR monitoring is problematic in cirrhosis due to baseline coagulopathy and uncertain target ranges. Historical studies have used INR targets of 2-3, but this approach requires careful individualization.
▶️ The decision to anticoagulate should be individualized based on extent of thrombosis, bleeding risk, platelet count (generally safe if >50,000/μL), and fall risk rather than INR alone.
▶️ Active bleeding would be a contraindication, but thrombocytopenia and prolonged INR should not automatically preclude treatment.
▶️ The elevated INR should not be considered an absolute contraindication to anticoagulation, as it reflects impaired hepatic synthetic function rather than true anticoagulation status in cirrhosis.
✳️ Direct oral anticoagulants (DOACs) are contraindicated in decompensated cirrhosis, particularly in Child-Pugh class C patients and critically ill individuals, due to hepatic metabolism and unpredictable drug levels.
▶️ While DOACs may be considered in compensated cirrhosis (Child-Pugh class A or B), they should be avoided in decompensated disease.
▶️ LMWH has demonstrated superior outcomes in cirrhotic patients with venous thromboembolism, achieving higher recanalization rates (71% vs 42% without treatment) and lower variceal bleeding risk compared to no anticoagulation. Meta-analyses confirm that LMWH produces more complete recanalization than warfarin and reduces all-cause mortality.
✳️ Warfarin may be considered as an alternative if LMWH is contraindicated, though INR monitoring is problematic in cirrhosis due to baseline coagulopathy and uncertain target ranges. Historical studies have used INR targets of 2-3, but this approach requires careful individualization.
▶️ The decision to anticoagulate should be individualized based on extent of thrombosis, bleeding risk, platelet count (generally safe if >50,000/μL), and fall risk rather than INR alone.
▶️ Active bleeding would be a contraindication, but thrombocytopenia and prolonged INR should not automatically preclude treatment.
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✳️ Navigating the Maze of Functional Dyspepsia: Emergence of a New Entity, Postprandial Epigastric Pain Syndrome.
▶️ Conclusion: In contrast to earlier characterization of EPS symptoms as purely meal-unrelated, we identied a relevant patient cohort with postprandial epigastric pain in the absence of PDS symptoms in 4 different cohorts. Further research is needed to determine the underlying pathophysiology and the response to different treatment approaches in these newly de ned patient cohorts.
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▶️ Conclusion: In contrast to earlier characterization of EPS symptoms as purely meal-unrelated, we identied a relevant patient cohort with postprandial epigastric pain in the absence of PDS symptoms in 4 different cohorts. Further research is needed to determine the underlying pathophysiology and the response to different treatment approaches in these newly de ned patient cohorts.
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CGH 2025
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✳️ Prevalence and Prognosis of Mild Inflammatory Bowel Disease: A Population-based Cohort Study, 1997–2020.
▶️ Conclusions : Approximately one-fourth of individuals with mild UC within 1 year after diagnosis and one-half of those with mild CD progressed to moderate-severe disease over time. Young age at diagnosis increased the probability of progression, whereas increasing duration of mild disease decreased the probability.
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▶️ Conclusions : Approximately one-fourth of individuals with mild UC within 1 year after diagnosis and one-half of those with mild CD progressed to moderate-severe disease over time. Young age at diagnosis increased the probability of progression, whereas increasing duration of mild disease decreased the probability.
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CGH December 2025
✳️ Effect of glucagon-like peptide-1 receptor agonists on histologic MASH: A meta-analysis of randomized controlled trials.
▶️ Conclusions:
In patients with noncirrhotic MASH, GLP-1RAs appear to be associated with both MASH resolution without fibrosis worsening and ≥1-stage fibrosis regression without MASH worsening.
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▶️ Conclusions:
In patients with noncirrhotic MASH, GLP-1RAs appear to be associated with both MASH resolution without fibrosis worsening and ≥1-stage fibrosis regression without MASH worsening.
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AASLD February 2026
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✳️ Clinically significant portal hypertension (CSPH) can be diagnosed without elastography by identifying gastroesophageal varices on endoscopy, portosystemic collaterals or hepatofugal flow on imaging, or clinical decompensation (ascites, variceal bleeding). These findings are sufficient to establish the diagnosis of CSPH, which is defined as hepatic venous pressure gradient (HVPG) ≥10 mm Hg.
▶️ Conventional imaging modalities including ultrasound, CT, and MRI can identify surrogate markers of CSPH such as portosystemic collaterals (periesophageal varices, recanalized umbilical vein, splenorenal shunt), dilated portal vein (>12 mm), splenomegaly (≥13 cm), and ascites. Doppler ultrasound demonstrating hepatofugal flow within the portal system is also considered adequate to diagnose CSPH.
▶️ Thrombocytopenia , platelet count alone has insufficient accuracy to exclude CSPH and cannot eliminate the need for endoscopic assessment to detect varices requiring treatment.
▶️ Blood-based scores such as APRI and FIB-4 have limited diagnostic accuracy for CSPH, with sensitivities of 56% and 54% and specificities of 68% and 73%, respectively. The liver stiffness-spleen size-to-platelet ratio (values >2.65 corresponding to >80% risk of CSPH) has shown promise but requires further validation.
▶️ In the absence of elastography, combining clinical findings, laboratory markers (particularly platelet count), and imaging evidence provides the best available approach to assess for CSPH, though many patients will remain in a diagnostic "gray zone" requiring further evaluation.
▶️ Conventional imaging modalities including ultrasound, CT, and MRI can identify surrogate markers of CSPH such as portosystemic collaterals (periesophageal varices, recanalized umbilical vein, splenorenal shunt), dilated portal vein (>12 mm), splenomegaly (≥13 cm), and ascites. Doppler ultrasound demonstrating hepatofugal flow within the portal system is also considered adequate to diagnose CSPH.
▶️ Thrombocytopenia , platelet count alone has insufficient accuracy to exclude CSPH and cannot eliminate the need for endoscopic assessment to detect varices requiring treatment.
▶️ Blood-based scores such as APRI and FIB-4 have limited diagnostic accuracy for CSPH, with sensitivities of 56% and 54% and specificities of 68% and 73%, respectively. The liver stiffness-spleen size-to-platelet ratio (values >2.65 corresponding to >80% risk of CSPH) has shown promise but requires further validation.
▶️ In the absence of elastography, combining clinical findings, laboratory markers (particularly platelet count), and imaging evidence provides the best available approach to assess for CSPH, though many patients will remain in a diagnostic "gray zone" requiring further evaluation.
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Barrett s Esophagus- J of Gastro and Hepatol - 2025.pdf
445.1 KB
REVIEW ARTICLE -Barrett's Esophagus
Journal of Gastroenterology and Hepatology November 2025
Target Trial Emulation of Beta‐Blockers After Diagnosis ofColorectal Polyps—Beneficial in Women 2025
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✳️Associations between demographic, clinical and dietary factors and flares in inflammatory bowel disease: the PRognostic effect of Environmental factors in Crohn’s and Colitis (PREdiCCt) prospective cohort study
▶️ Conclusion: Higher habitual meat intake was associated with increased risk of objective flare in UC, suggesting diet may contribute to flare susceptibility in specific patient groups.
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▶️ Conclusion: Higher habitual meat intake was associated with increased risk of objective flare in UC, suggesting diet may contribute to flare susceptibility in specific patient groups.
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BMJ Jan 2025
Acute-on-chronic liver failure (ACLF): pathophysiological mechanisms and clinical management.
Nature 2025
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