GiT Updates and More
Post_Banding_Ulcer_Bleeding_After_Endoscopic_Ligation_Incidence.pdf
SUMMARY: Post-banding ulcer bleeding (PBUB) is a significant but understudied complication of endoscopic band ligation (EBL), a primary treatment for esophageal variceal bleeding in cirrhosis. This study aimed to investigate the incidence, mortality, and risk factors for PBUB.
Study Design & Population
A retrospective cohort study was conducted at Bern University Hospital, Switzerland (Jan 2018–Dec 2022). It included 206 patients with cirrhosis who underwent a total of 630 EBL sessions (for primary/secondary prophylaxis or urgent treatment).
Key Findings
Incidence of PBUB:
17.5% of patients experienced PBUB.
6.8% of all EBL procedures resulted in PBUB.
Incidence was higher after urgent EBL (13.1%) vs. prophylactic EBL (3.6%).
Independent Risk Factors (Multivariate Analysis):
Urgent EBL: SHR 2.78 (95% CI: 1.29–6.00, p=0.009).
Elevated Creatinine: SHR 1.04 per 10 µmol/L increase (95% CI: 1.01–1.07, p=0.024).
Clinical Outcomes & Management:
High Resource Use: PBUB required blood transfusions in 88.1% of cases and ICU admission in 74.4%.
High Mortality:
Short-term (in-hospital): 19% for patients with PBUB.
Long-term (52 weeks): 64% for patients with PBUB vs. 54% without.
Survival: Significantly lower in PBUB patients (HR=3.86, p<0.001), with a sharp decline within 4 months post-EBL.
Management: Involved a combination of endoscopic (repeat EBL, clips, spray, TIPS) and medical therapy (antibiotics, vasoactive drugs, PPIs).
Other Notable Results:
Post-banding ulcers (PBU) were common (37.9% per patient), but only a subset progressed to bleeding.
NSBB use was associated with a lower risk of PBUB in univariate analysis, but not in multivariate analysis.
PPI use, anticoagulant/antiplatelet therapy, and endoscopic factors (e.g., number of bands) were not independently associated with PBUB risk.
Patients who developed PBUB had more severe liver disease (higher MELD and Child-Pugh scores) and more frequent decompensation events.
Key Timing:
The median time between the EBL procedure and the occurrence of PBUB was 12 days.
The interquartile range (IQR) was 6–19 days, meaning most cases occurred within this window after the band ligation.
Clinical Context:
PBUB arises from ulcers that develop at the sites where the ligation bands were applied.
It was diagnosed when one or more ulcers at the ligation site were identified as the source of upper gastrointestinal bleeding, with no other bleeding source found.
Endoscopic Classification (Jamwal & Sarin):
The ulcers leading to PBUB were classified as:
Type A: Ulcer with active spurting (17% of PBUB cases)
Type B: Ulcer with oozing (2.4%)
Type C: Ulcer with a clot or pigmented base (56%)
Type D: Ulcer with a clean base (less commonly associated with bleeding)
Independent Risk Factors (Multivariate Analysis)
These factors remained statistically significant after adjusting for other variables:
Urgent EBL (performed for acute variceal bleeding within 24 hours of admission)
Sub-distribution Hazard Ratio (SHR): 2.78 (95% CI: 1.29–6.00, p=0.009)
Elevated Serum Creatinine (a marker of renal impairment)
SHR: 1.04 per 10 µmol/L increase (95% CI: 1.01–1.07, p=0.024)
Factors Associated in Univariate Analysis (but not independent)
These were significant in initial analysis but did not remain independent in the final multivariate model:
Higher MELD Score (SHR: 1.06, p=0.012)
Presence of Infection at the time of EBL (SHR: 4.42, p=0.003)
Elevated INR (SHR: 1.85, p=0.007)
Elevated Total Bilirubin (SHR: 1.03, p=0.018)
Lower Use of Non-Selective Beta Blockers (NSBB) was protective (SHR: 0.47, p=0.017)
Clinical & Demographic Factors Linked to Higher Risk (from cohort description)
More Severe Liver Disease: Patients who developed PBUB had significantly higher Child-Pugh scores and more frequent decompensation events (e.g., ascites, encephalopathy).
Indication for EBL: The incidence was over 3.5 times higher in urgent EBL (13.1%) compared to prophylactic EBL (3.6%).
Study Design & Population
A retrospective cohort study was conducted at Bern University Hospital, Switzerland (Jan 2018–Dec 2022). It included 206 patients with cirrhosis who underwent a total of 630 EBL sessions (for primary/secondary prophylaxis or urgent treatment).
Key Findings
Incidence of PBUB:
17.5% of patients experienced PBUB.
6.8% of all EBL procedures resulted in PBUB.
Incidence was higher after urgent EBL (13.1%) vs. prophylactic EBL (3.6%).
Independent Risk Factors (Multivariate Analysis):
Urgent EBL: SHR 2.78 (95% CI: 1.29–6.00, p=0.009).
Elevated Creatinine: SHR 1.04 per 10 µmol/L increase (95% CI: 1.01–1.07, p=0.024).
Clinical Outcomes & Management:
High Resource Use: PBUB required blood transfusions in 88.1% of cases and ICU admission in 74.4%.
High Mortality:
Short-term (in-hospital): 19% for patients with PBUB.
Long-term (52 weeks): 64% for patients with PBUB vs. 54% without.
Survival: Significantly lower in PBUB patients (HR=3.86, p<0.001), with a sharp decline within 4 months post-EBL.
Management: Involved a combination of endoscopic (repeat EBL, clips, spray, TIPS) and medical therapy (antibiotics, vasoactive drugs, PPIs).
Other Notable Results:
Post-banding ulcers (PBU) were common (37.9% per patient), but only a subset progressed to bleeding.
NSBB use was associated with a lower risk of PBUB in univariate analysis, but not in multivariate analysis.
PPI use, anticoagulant/antiplatelet therapy, and endoscopic factors (e.g., number of bands) were not independently associated with PBUB risk.
Patients who developed PBUB had more severe liver disease (higher MELD and Child-Pugh scores) and more frequent decompensation events.
Key Timing:
The median time between the EBL procedure and the occurrence of PBUB was 12 days.
The interquartile range (IQR) was 6–19 days, meaning most cases occurred within this window after the band ligation.
Clinical Context:
PBUB arises from ulcers that develop at the sites where the ligation bands were applied.
It was diagnosed when one or more ulcers at the ligation site were identified as the source of upper gastrointestinal bleeding, with no other bleeding source found.
Endoscopic Classification (Jamwal & Sarin):
The ulcers leading to PBUB were classified as:
Type A: Ulcer with active spurting (17% of PBUB cases)
Type B: Ulcer with oozing (2.4%)
Type C: Ulcer with a clot or pigmented base (56%)
Type D: Ulcer with a clean base (less commonly associated with bleeding)
Independent Risk Factors (Multivariate Analysis)
These factors remained statistically significant after adjusting for other variables:
Urgent EBL (performed for acute variceal bleeding within 24 hours of admission)
Sub-distribution Hazard Ratio (SHR): 2.78 (95% CI: 1.29–6.00, p=0.009)
Elevated Serum Creatinine (a marker of renal impairment)
SHR: 1.04 per 10 µmol/L increase (95% CI: 1.01–1.07, p=0.024)
Factors Associated in Univariate Analysis (but not independent)
These were significant in initial analysis but did not remain independent in the final multivariate model:
Higher MELD Score (SHR: 1.06, p=0.012)
Presence of Infection at the time of EBL (SHR: 4.42, p=0.003)
Elevated INR (SHR: 1.85, p=0.007)
Elevated Total Bilirubin (SHR: 1.03, p=0.018)
Lower Use of Non-Selective Beta Blockers (NSBB) was protective (SHR: 0.47, p=0.017)
Clinical & Demographic Factors Linked to Higher Risk (from cohort description)
More Severe Liver Disease: Patients who developed PBUB had significantly higher Child-Pugh scores and more frequent decompensation events (e.g., ascites, encephalopathy).
Indication for EBL: The incidence was over 3.5 times higher in urgent EBL (13.1%) compared to prophylactic EBL (3.6%).
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GiT Updates and More
Post_Banding_Ulcer_Bleeding_After_Endoscopic_Ligation_Incidence.pdf
Procedure Context: Urgent EBLs, often performed in actively bleeding or unstable patients, carried a higher inherent risk.
Factors NOT Associated with Increased PBUB Risk
The study found no significant association between PBUB and:
Proton Pump Inhibitor (PPI) use
Anticoagulant or antiplatelet therapy
Endoscopic technical factors (e.g., number of bands placed, variceal size, endoscopist experience)
Presence of hiatal hernia or gastroesophageal reflux disease (GERD)
Factors NOT Associated with Increased PBUB Risk
The study found no significant association between PBUB and:
Proton Pump Inhibitor (PPI) use
Anticoagulant or antiplatelet therapy
Endoscopic technical factors (e.g., number of bands placed, variceal size, endoscopist experience)
Presence of hiatal hernia or gastroesophageal reflux disease (GERD)
An ascitic fluid neutrophil count above 250 cells/mm³ confirms the diagnosis of SBP. Empiric treatment with intravenous third-generation cephalosporins is appropriate, as these antibiotics effectively target the common gram-negative bacteria responsible for SBP and achieve therapeutic levels in ascitic fluid. Prompt antibiotic initiation is crucial to prevent complications such as renal impairment and increased mortality.
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Diabetes and cirrhosis: Current concepts on diagnosis and management.
AASLD 2023
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Diabetes_and_cirrhosis_Current_concepts_on_diagnosis_and_management.pdf
909.5 KB
Diabetes and cirrhosis: Current concepts on diagnosis and management.
AASLD 2023
Toxic megacolon is a life-threatening complication of inflammatory conditions affecting the intestines like ulcerative colitis, with a history of bloody diarrhea and abdominal pain. To diagnose toxic megacolon, there must be radiographic evidence of colonic dilation (transverse colon diameter > 6 cm) and three of the following features must be present: fever, tachycardia (> 120/min), leukocytosis (> 10,500/mm3), and anemia. Furthermore, one of the following must be present: dehydration, hypotension, altered mental status, or electrolyte disturbance (e.g., hypokalemia). The initial treatment is conservative (including IV antibiotics, fluid resuscitation, complete bowel rest, nasogastric decompression, and IV steroids for inflammatory bowel disease), but surgery may be required if there is no response to medical management within 24–72 hours.
Toxic megacolon is also a potential complication of infectious colitis due to bacteria (e.g., C. difficile, Salmonella) or parasites (e.g., E. histolytica).
Toxic megacolon is also a potential complication of infectious colitis due to bacteria (e.g., C. difficile, Salmonella) or parasites (e.g., E. histolytica).
In pregnant women with heartburn, lifestyle modifications are the first-line management strategy before considering pharmacological interventions.
During pregnancy, increased progesterone levels relax the lower esophageal sphincter, and the enlarging uterus raises intra-abdominal pressure, contributing to gastroesophageal reflux. Dietary modifications, such as smaller, frequent meals and avoiding trigger foods, reduce gastric distension and reflux events. Positional changes, like elevating the head of the bed and not lying down after meals, use gravity to minimize reflux. These nonpharmacologic strategies address the underlying pathophysiology with minimal fetal risk, making them the most appropriate initial management for heartburn in pregnancy.
During pregnancy, increased progesterone levels relax the lower esophageal sphincter, and the enlarging uterus raises intra-abdominal pressure, contributing to gastroesophageal reflux. Dietary modifications, such as smaller, frequent meals and avoiding trigger foods, reduce gastric distension and reflux events. Positional changes, like elevating the head of the bed and not lying down after meals, use gravity to minimize reflux. These nonpharmacologic strategies address the underlying pathophysiology with minimal fetal risk, making them the most appropriate initial management for heartburn in pregnancy.
Global_Prevalence_of_Celiac_Disease_in_Patients_With_Rome_III_and.pdf
1.6 MB
Global Prevalence of Celiac Disease in Patients With Rome III and Rome IV Irritable Bowel Syndrome: A Systematic Review and Meta-Analysis.
AJG December 2025
flgastro-2025-103183.full.pdf
1.2 MB
Nutrition in MASLD: a patient focused, evidence-based clinician’s guide.
BMJ, November 2025
jessica-r-biesiekierski-non-coeliac-gluten-sensitivity.pdf
547.9 KB
Non-coeliac gluten sensitivity
The Lancet,, November 2025
✳️ Interpretation of Hepatitis B serological markers and the new advanced markers
Hepatitis B virus (HBV) infection is diagnosed and characterized through a panel of serological markers, each providing specific information about infection status, disease phase, and immunity. Understanding these markers is essential for proper diagnosis, management, and treatment decisions.
✳️Core Serological Markers
▫️HBsAg (Hepatitis B surface antigen): Indicates active HBV infection, either acute or chronic. Persistence beyond 6 months defines chronic infection. HBsAg can be translated from both covalently closed circular DNA (cccDNA) and integrated HBV DNA in the host genome.
▫️Anti-HBs (Antibody to HBsAg): Protective antibody indicating recovery from infection or successful vaccination. Levels ≥10 mIU/mL at 1-2 months after completing vaccination indicate immunity. Among vaccine responders, anti-HBs can decline below 10 mIU/mL over time, but most remain immune and mount an anamnestic response upon re-exposure.
▫️Anti-HBc (Antibody to core antigen): Develops in all HBV infections and typically persists for life. Total anti-HBc detects both IgM and IgG antibodies. Persons immune through vaccination do not develop anti-HBc.
▫️Anti-HBc IgM: Indicates acute infection or acute exacerbation of chronic hepatitis B. During chronic infection, IgM anti-HBc typically disappears while total anti-HBc persists.
▫️HBeAg (Hepatitis B e antigen): Marker of high viral replication and infectivity. Its presence correlates with elevated HBV DNA levels.
Anti-HBe (Antibody to HBeAg): Appears after HBeAg clearance, indicating lower viral replication. Loss of HBeAg with appearance of anti-HBe is a favorable marker during acute infection.
▫️HBV DNA: Primary marker of viral replication measured by quantitative real-time PCR. Results should be expressed in IU/mL using standardized assays. HBV DNA levels guide treatment decisions and monitor therapeutic response.
✳️ Common Serological Patterns
▫️Acute infection: HBsAg positive, anti-HBc IgM positive, anti-HBs negative.
▫️Chronic infection: HBsAg positive, anti-HBc (total) positive, anti-HBs negative, anti-HBc IgM negative.
▫️Resolved infection: HBsAg negative, anti-HBc positive, anti-HBs positive.
▫️Immune due to vaccination: HBsAg negative, anti-HBc negative, anti-HBs positive.
▫️Susceptible (never infected): All markers negative.
✳️ Isolated Anti-HBc Pattern
The isolated anti-HBc pattern (anti-HBc positive, HBsAg negative, anti-HBs negative) has several potential interpretations.
Resolved infection with waning anti-HBs (most common): Previous HBV infection where anti-HBs has declined to undetectable levels. Studies show this pattern can fluctuate, with anti-HBs becoming intermittently detectable, supporting resolved infection rather than occult viremia.
Occult HBV infection: Low-level viremia with HBV DNA detectable by PCR, often due to mutant HBsAg not detected by standard assays. This occurs less commonly than waning immunity.
Window period of acute infection: Transient phase where HBsAg has cleared but anti-HBs has not yet appeared. This pattern evolves over time.
False positive: Particularly in low-prevalence populations or with older, less specific assays.
For isolated anti-HBc in intermediate- to high-risk populations, the most common explanation is previous HBV exposure with waning anti-HBs. HBV DNA testing should be considered in immunocompromised patients to exclude occult infection.
✳️ Advanced Biomarkers
Quantitative HBsAg (qHBsAg): Reflects cccDNA transcriptional activity and integrated HBV DNA. Levels are higher in HBeAg-positive than HBeAg-negative patients. In HBeAg-positive patients, lower HBsAg levels correlate with higher rates of significant fibrosis and cirrhosis. qHBsAg <1,000 IU/mL combined with HBV DNA ≤2,000 IU/mL suggests inactive chronic hepatitis B, while qHBsAg <1,000 IU/mL predicts spontaneous HBsAg clearance in HBeAg-negative patients with low viral load.
HBV core-related antigen (HBcrAg): Composite marker comprising HBcAg, HBeAg, and p22cr precursor protein.
Hepatitis B virus (HBV) infection is diagnosed and characterized through a panel of serological markers, each providing specific information about infection status, disease phase, and immunity. Understanding these markers is essential for proper diagnosis, management, and treatment decisions.
✳️Core Serological Markers
▫️HBsAg (Hepatitis B surface antigen): Indicates active HBV infection, either acute or chronic. Persistence beyond 6 months defines chronic infection. HBsAg can be translated from both covalently closed circular DNA (cccDNA) and integrated HBV DNA in the host genome.
▫️Anti-HBs (Antibody to HBsAg): Protective antibody indicating recovery from infection or successful vaccination. Levels ≥10 mIU/mL at 1-2 months after completing vaccination indicate immunity. Among vaccine responders, anti-HBs can decline below 10 mIU/mL over time, but most remain immune and mount an anamnestic response upon re-exposure.
▫️Anti-HBc (Antibody to core antigen): Develops in all HBV infections and typically persists for life. Total anti-HBc detects both IgM and IgG antibodies. Persons immune through vaccination do not develop anti-HBc.
▫️Anti-HBc IgM: Indicates acute infection or acute exacerbation of chronic hepatitis B. During chronic infection, IgM anti-HBc typically disappears while total anti-HBc persists.
▫️HBeAg (Hepatitis B e antigen): Marker of high viral replication and infectivity. Its presence correlates with elevated HBV DNA levels.
Anti-HBe (Antibody to HBeAg): Appears after HBeAg clearance, indicating lower viral replication. Loss of HBeAg with appearance of anti-HBe is a favorable marker during acute infection.
▫️HBV DNA: Primary marker of viral replication measured by quantitative real-time PCR. Results should be expressed in IU/mL using standardized assays. HBV DNA levels guide treatment decisions and monitor therapeutic response.
✳️ Common Serological Patterns
▫️Acute infection: HBsAg positive, anti-HBc IgM positive, anti-HBs negative.
▫️Chronic infection: HBsAg positive, anti-HBc (total) positive, anti-HBs negative, anti-HBc IgM negative.
▫️Resolved infection: HBsAg negative, anti-HBc positive, anti-HBs positive.
▫️Immune due to vaccination: HBsAg negative, anti-HBc negative, anti-HBs positive.
▫️Susceptible (never infected): All markers negative.
✳️ Isolated Anti-HBc Pattern
The isolated anti-HBc pattern (anti-HBc positive, HBsAg negative, anti-HBs negative) has several potential interpretations.
Resolved infection with waning anti-HBs (most common): Previous HBV infection where anti-HBs has declined to undetectable levels. Studies show this pattern can fluctuate, with anti-HBs becoming intermittently detectable, supporting resolved infection rather than occult viremia.
Occult HBV infection: Low-level viremia with HBV DNA detectable by PCR, often due to mutant HBsAg not detected by standard assays. This occurs less commonly than waning immunity.
Window period of acute infection: Transient phase where HBsAg has cleared but anti-HBs has not yet appeared. This pattern evolves over time.
False positive: Particularly in low-prevalence populations or with older, less specific assays.
For isolated anti-HBc in intermediate- to high-risk populations, the most common explanation is previous HBV exposure with waning anti-HBs. HBV DNA testing should be considered in immunocompromised patients to exclude occult infection.
✳️ Advanced Biomarkers
Quantitative HBsAg (qHBsAg): Reflects cccDNA transcriptional activity and integrated HBV DNA. Levels are higher in HBeAg-positive than HBeAg-negative patients. In HBeAg-positive patients, lower HBsAg levels correlate with higher rates of significant fibrosis and cirrhosis. qHBsAg <1,000 IU/mL combined with HBV DNA ≤2,000 IU/mL suggests inactive chronic hepatitis B, while qHBsAg <1,000 IU/mL predicts spontaneous HBsAg clearance in HBeAg-negative patients with low viral load.
HBV core-related antigen (HBcrAg): Composite marker comprising HBcAg, HBeAg, and p22cr precursor protein.
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May reflect intrahepatic cccDNA levels, particularly in HBeAg-positive patients, and help define disease phase and predict treatment response. Total anti-HBc levels correlate with disease activity and decline with successful antiviral therapy.
HBV RNA: Marker of cccDNA transcriptional activity. Correlates with HBeAg loss during treatment and may predict viral rebound after nucleos(t)ide analog discontinuation.
✳️ Clinical Assessment
Initial evaluation of HBsAg-positive patients should include a comprehensive history focusing on risk factors, family history of HBV and hepatocellular carcinoma, and alcohol use.
Laboratory assessment should include complete blood count with platelets, liver function tests (AST, ALT, bilirubin, alkaline phosphatase, albumin), coagulation studies (PT/INR), HBeAg/anti-HBe, quantitative HBV DNA, and testing for coinfections (anti-HAV, anti-HCV, anti-HDV, anti-HIV in at-risk individuals).
Imaging with abdominal ultrasound and assessment of fibrosis stage using transient elastography or serum fibrosis panels (APRI, FIB-4) should be performed. Liver biopsy may be indicated when treatment decisions are unclear or to assess for other causes of liver disease.
HBV genotype determination can inform prognosis and treatment response, particularly for interferon-based therapy. Genotype A shows higher rates of HBeAg and HBsAg loss with interferon compared to genotypes B-D.
HBV RNA: Marker of cccDNA transcriptional activity. Correlates with HBeAg loss during treatment and may predict viral rebound after nucleos(t)ide analog discontinuation.
✳️ Clinical Assessment
Initial evaluation of HBsAg-positive patients should include a comprehensive history focusing on risk factors, family history of HBV and hepatocellular carcinoma, and alcohol use.
Laboratory assessment should include complete blood count with platelets, liver function tests (AST, ALT, bilirubin, alkaline phosphatase, albumin), coagulation studies (PT/INR), HBeAg/anti-HBe, quantitative HBV DNA, and testing for coinfections (anti-HAV, anti-HCV, anti-HDV, anti-HIV in at-risk individuals).
Imaging with abdominal ultrasound and assessment of fibrosis stage using transient elastography or serum fibrosis panels (APRI, FIB-4) should be performed. Liver biopsy may be indicated when treatment decisions are unclear or to assess for other causes of liver disease.
HBV genotype determination can inform prognosis and treatment response, particularly for interferon-based therapy. Genotype A shows higher rates of HBeAg and HBsAg loss with interferon compared to genotypes B-D.
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Indications for ERCP During Pregnancy (Adapted From American Society for Gastrointestinal Endoscopy Guidelines )