Mortality data from high-income group countries are frequently used in developing countries for healthcare planning. This study was planned to explore the mortality pattern of cirrhosis in India in terms of survival after diagnosis of cirrhosis, predictors of death and aetiology specific effect on mortality.
Methods
This observational study enrolled newly diagnosed patients with liver disease (n = 3193) attending a tertiary care hospital in Kolkata, India between April 2010 and October 2012 and were followed up to September 2015.
Results
Patients with cirrhosis having complete follow-up data (n = 702) were analysed. Median follow-up duration was 21 months (range: 1-84 months). Mortality among them was 51% (n = 358 out of 702). Development of HCC (OR 2.8: 95%CI 1.8-4.2, P < 0.0001), male gender (OR 1.4: 95% CI 1.0-1.8, P = 0.009) and higher Child score at the time of diagnosis (OR 1.2: 95%CI 1.1-1.3, P < 0.0001) were predictors of mortality. Survival after the diagnosis of cirrhosis was significantly shorter in alcohol (16.5 month; range 1-51)- and HCV (16 month; range 1-48)-related cirrhosis in comparison to HBV (23 month; range 1-48)-related and cryptogenic cirrhosis (22 month; range 1-84) (P = 0.014).
Conclusion
Majority of the patients with cirrhosis had decompensation at the time of diagnosis. Shorter survival was noticed in alcohol- and HCV-related cirrhosis.
{"title":"Mortality pattern in cirrhosis: A reflection of liver disease burden in India","authors":"Debashis Misra, Kausik Das, Saswata Chatterjee, Parthasarathi Mukherjee, Abhijit Chowdhury","doi":"10.1002/ygh2.497","DOIUrl":"https://doi.org/10.1002/ygh2.497","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction and objective</h3>\u0000 \u0000 <p>Mortality data from high-income group countries are frequently used in developing countries for healthcare planning. This study was planned to explore the mortality pattern of cirrhosis in India in terms of survival after diagnosis of cirrhosis, predictors of death and aetiology specific effect on mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This observational study enrolled newly diagnosed patients with liver disease (n = 3193) attending a tertiary care hospital in Kolkata, India between April 2010 and October 2012 and were followed up to September 2015.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Patients with cirrhosis having complete follow-up data (n = 702) were analysed. Median follow-up duration was 21 months (range: 1-84 months). Mortality among them was 51% (n = 358 out of 702). Development of HCC (OR 2.8: 95%CI 1.8-4.2, <i>P</i> < 0.0001), male gender (OR 1.4: 95% CI 1.0-1.8, <i>P</i> = 0.009) and higher Child score at the time of diagnosis (OR 1.2: 95%CI 1.1-1.3, <i>P</i> < 0.0001) were predictors of mortality. Survival after the diagnosis of cirrhosis was significantly shorter in alcohol (16.5 month; range 1-51)- and HCV (16 month; range 1-48)-related cirrhosis in comparison to HBV (23 month; range 1-48)-related and cryptogenic cirrhosis (22 month; range 1-84) (<i>P</i> = 0.014).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Majority of the patients with cirrhosis had decompensation at the time of diagnosis. Shorter survival was noticed in alcohol- and HCV-related cirrhosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":12480,"journal":{"name":"GastroHep","volume":"3 6","pages":"409-416"},"PeriodicalIF":0.0,"publicationDate":"2021-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71939529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Liver stiffness (LS) as measured by magnetic resonance elastography (MRE) and the presence of intrahepatic nonhypervascular hypointense nodules (NHHNs) during the hepatobiliary phase of gadolinium-ethoxybenzyl diethylenetriamine-pentaacetic acid–enhanced magnetic resonance imaging are non-invasive MR-based biomarkers of hepatocarcinogenesis.
Methods
We retrospectively evaluated the ability of these two MR-based biomarkers to stratify the risk of hepatocellular carcinoma (HCC) development in patients with chronic liver disease. Between September 2013 and April 2020, 868 consecutive patients underwent MRE and gadolinium-ethoxybenzyl diethylenetriamine-pentaacetic acid–enhanced magnetic resonance imaging, among whom 487 were enrolled in this study. Factors associated with hepatocarcinogenesis were analysed by a Cox proportional hazard model.
Results
Thirty-two patients developed hypervascular HCC. According to the time-dependent receiver operating characteristic analysis, an LS value of 3.94 kPa was selected as the optimal cut-off value for predicting HCC development. Multivariate analyses identified high LS (≥3.94 kPa) and the presence of NHHN as independent predictive factors for HCC development. Patients were classified as follows: high LS/NHHN+ (Group 1), high LS/NHHN− (Group 2), low LS/NHHN+ (Group 3) and low LS/NHHN− (Group 4). The 5-year incidence rates of HCC in Groups 1, 2, 3 and 4 were 49.0%, 16.3%, 10.0% and 2.5% respectively. The HCC development rate was highest in Group 1 and lowest in Group 4 (P < 0.01).
Conclusion
MRE-based LS measurements and the presence of NHHN are useful biomarkers to stratify the risk of HCC development among chronic liver disease patients. Combining these biomarkers can provide a detailed classification of the risk of HCC development.
{"title":"Risk stratification of hepatocellular carcinoma in patients with chronic liver disease by combining gadolinium-ethoxybenzyl diethylenetriamine-pentaacetic acid–enhanced magnetic resonance imaging and magnetic resonance elastography","authors":"Emi Meren, Yoshiyuki Sawai, Kazuto Fukuda, Takumi Igura, Sachiyo Kogita, Yoshihiro Yukimura, Yasushi Seki, Norihiko Fujita, Masahide Oshita, Yasuharu Imai","doi":"10.1002/ygh2.495","DOIUrl":"https://doi.org/10.1002/ygh2.495","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Liver stiffness (LS) as measured by magnetic resonance elastography (MRE) and the presence of intrahepatic nonhypervascular hypointense nodules (NHHNs) during the hepatobiliary phase of gadolinium-ethoxybenzyl diethylenetriamine-pentaacetic acid–enhanced magnetic resonance imaging are non-invasive MR-based biomarkers of hepatocarcinogenesis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We retrospectively evaluated the ability of these two MR-based biomarkers to stratify the risk of hepatocellular carcinoma (HCC) development in patients with chronic liver disease. Between September 2013 and April 2020, 868 consecutive patients underwent MRE and gadolinium-ethoxybenzyl diethylenetriamine-pentaacetic acid–enhanced magnetic resonance imaging, among whom 487 were enrolled in this study. Factors associated with hepatocarcinogenesis were analysed by a Cox proportional hazard model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Thirty-two patients developed hypervascular HCC. According to the time-dependent receiver operating characteristic analysis, an LS value of 3.94 kPa was selected as the optimal cut-off value for predicting HCC development. Multivariate analyses identified high LS (≥3.94 kPa) and the presence of NHHN as independent predictive factors for HCC development. Patients were classified as follows: high LS/NHHN+ (Group 1), high LS/NHHN− (Group 2), low LS/NHHN+ (Group 3) and low LS/NHHN− (Group 4). The 5-year incidence rates of HCC in Groups 1, 2, 3 and 4 were 49.0%, 16.3%, 10.0% and 2.5% respectively. The HCC development rate was highest in Group 1 and lowest in Group 4 (<i>P</i> < 0.01).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>MRE-based LS measurements and the presence of NHHN are useful biomarkers to stratify the risk of HCC development among chronic liver disease patients. Combining these biomarkers can provide a detailed classification of the risk of HCC development.</p>\u0000 </section>\u0000 </div>","PeriodicalId":12480,"journal":{"name":"GastroHep","volume":"3 7","pages":"435-442"},"PeriodicalIF":0.0,"publicationDate":"2021-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71991047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Kao, J. Almenoff, Dana D. Portenier, Kely L. Sheldon
Helicobacter pylori infection affects ~35% of Americans and may lead to serious sequelae if left untreated, including gastric cancer. Obesity is a significant risk factor for antibiotic treatment failure; however, little work has been done to understand the influence of high body mass index (BMI) on the success rates of H pylori eradication regimens in treatment‐naïve and refractory adult patients.
{"title":"Helicobacter pylori eradication by low‐dose rifabutin triple therapy (RHB‐105) is unaffected by high body mass index","authors":"J. Kao, J. Almenoff, Dana D. Portenier, Kely L. Sheldon","doi":"10.1002/ygh2.494","DOIUrl":"https://doi.org/10.1002/ygh2.494","url":null,"abstract":"Helicobacter pylori infection affects ~35% of Americans and may lead to serious sequelae if left untreated, including gastric cancer. Obesity is a significant risk factor for antibiotic treatment failure; however, little work has been done to understand the influence of high body mass index (BMI) on the success rates of H pylori eradication regimens in treatment‐naïve and refractory adult patients.","PeriodicalId":12480,"journal":{"name":"GastroHep","volume":"64 1","pages":"426 - 434"},"PeriodicalIF":0.0,"publicationDate":"2021-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91539860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E. Meren, Yoshiyuki Sawai, K. Fukuda, T. Igura, S. Kogita, Yoshihiro Yukimura, Y. Seki, Norihiko Fujita, M. Oshita, Y. Imai
Liver stiffness (LS) as measured by magnetic resonance elastography (MRE) and the presence of intrahepatic nonhypervascular hypointense nodules (NHHNs) during the hepatobiliary phase of gadolinium‐ethoxybenzyl diethylenetriamine‐pentaacetic acid–enhanced magnetic resonance imaging are non‐invasive MR‐based biomarkers of hepatocarcinogenesis.
{"title":"Risk stratification of hepatocellular carcinoma in patients with chronic liver disease by combining gadolinium‐ethoxybenzyl diethylenetriamine‐pentaacetic acid–enhanced magnetic resonance imaging and magnetic resonance elastography","authors":"E. Meren, Yoshiyuki Sawai, K. Fukuda, T. Igura, S. Kogita, Yoshihiro Yukimura, Y. Seki, Norihiko Fujita, M. Oshita, Y. Imai","doi":"10.1002/ygh2.495","DOIUrl":"https://doi.org/10.1002/ygh2.495","url":null,"abstract":"Liver stiffness (LS) as measured by magnetic resonance elastography (MRE) and the presence of intrahepatic nonhypervascular hypointense nodules (NHHNs) during the hepatobiliary phase of gadolinium‐ethoxybenzyl diethylenetriamine‐pentaacetic acid–enhanced magnetic resonance imaging are non‐invasive MR‐based biomarkers of hepatocarcinogenesis.","PeriodicalId":12480,"journal":{"name":"GastroHep","volume":"1 1","pages":"435 - 442"},"PeriodicalIF":0.0,"publicationDate":"2021-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83187874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
John Y. Kao, June S. Almenoff, Dana D. Portenier, Kely L. Sheldon
Background
Helicobacter pylori infection affects ~35% of Americans and may lead to serious sequelae if left untreated, including gastric cancer. Obesity is a significant risk factor for antibiotic treatment failure; however, little work has been done to understand the influence of high body mass index (BMI) on the success rates of H pylori eradication regimens in treatment-naïve and refractory adult patients.
Aim
This analysis evaluated the association of subject obesity on overall H pylori eradication rates for RHB-105 (rifabutin, amoxicillin, and omeprazole magnesium; Talicia®) and its comparators using data from two Phase 3 clinical trials.
Methods
A post hoc analysis of the eradication rates of RHB-105 vs comparators in a total of 269 subjects who tested positive for H pylori was conducted. Comparators in the two studies included placebo (placebo comparator) and amoxicillin and omeprazole (active comparator). Subjects were treated for 14 days and returned for follow-up test-of-cure at 28-59 days post-therapy using urea breath testing.
Results
Subjects receiving RHB-105 with 30 ≤ BMI < 40 or BMI ≥ 40 had pooled modified intent to treat (mITT) eradication rates of 88.1% (95% CI: 81.1-92.8) and 90.9% (95% CI: 72.2-97.5) [P = .707], respectively, compared to active comparator rates of 62.9% (95% CI: 52.5-72.2) and 31.8% (95% CI: 16.4-52.7) [P = .008].
Conclusions
Obese patients treated with RHB-105 were associated with efficacy rates comparable to the overall study population. This supports further evaluation of the efficacy of RHB-105 in obese populations, where H pylori is prevalent. ClinTrials.gov # NCT01980095 & NCT031985070.
{"title":"Helicobacter pylori eradication by low-dose rifabutin triple therapy (RHB-105) is unaffected by high body mass index","authors":"John Y. Kao, June S. Almenoff, Dana D. Portenier, Kely L. Sheldon","doi":"10.1002/ygh2.494","DOIUrl":"https://doi.org/10.1002/ygh2.494","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p><i>Helicobacter pylori</i> infection affects ~35% of Americans and may lead to serious sequelae if left untreated, including gastric cancer. Obesity is a significant risk factor for antibiotic treatment failure; however, little work has been done to understand the influence of high body mass index (BMI) on the success rates of <i>H pylori</i> eradication regimens in treatment-naïve and refractory adult patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>This analysis evaluated the association of subject obesity on overall <i>H pylori</i> eradication rates for RHB-105 (rifabutin, amoxicillin, and omeprazole magnesium; Talicia<sup>®</sup>) and its comparators using data from two Phase 3 clinical trials.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A post hoc analysis of the eradication rates of RHB-105 vs comparators in a total of 269 subjects who tested positive for <i>H pylori</i> was conducted. Comparators in the two studies included placebo (placebo comparator) and amoxicillin and omeprazole (active comparator). Subjects were treated for 14 days and returned for follow-up test-of-cure at 28-59 days post-therapy using urea breath testing.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Subjects receiving RHB-105 with 30 ≤ BMI < 40 or BMI ≥ 40 had pooled modified intent to treat (mITT) eradication rates of 88.1% (95% CI: 81.1-92.8) and 90.9% (95% CI: 72.2-97.5) [<i>P</i> = .707], respectively, compared to active comparator rates of 62.9% (95% CI: 52.5-72.2) and 31.8% (95% CI: 16.4-52.7) [<i>P</i> = .008].</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Obese patients treated with RHB-105 were associated with efficacy rates comparable to the overall study population. This supports further evaluation of the efficacy of RHB-105 in obese populations, where <i>H pylori</i> is prevalent. ClinTrials.gov # NCT01980095 & NCT031985070.</p>\u0000 </section>\u0000 </div>","PeriodicalId":12480,"journal":{"name":"GastroHep","volume":"3 7","pages":"426-434"},"PeriodicalIF":0.0,"publicationDate":"2021-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ygh2.494","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71993025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Achalasia is a rare condition characterised by an absent oesophageal peristalsis and a non-relaxing lower oesophageal sphincter. The incidence of paediatric achalasia is poorly studied and inconsistently reported. We aimed to provide an up to date incidence of paediatric achalasia in the UK.
Methods
All United Kingdom hospitals with paediatric gastroenterology and/or paediatric surgery were contacted to provide data on achalasia diagnosis and myotomies performed (2008-2020). Hospital Episode Statistics includes diagnostic and procedural data for all hospitals in England that were searched for achalasia and myotomy in children (1998-2020). Proxy data (epilepsy diagnosis) were used to compare diagnosis.
Results
The incidence of paediatric achalasia in the UK was 0.38 (England 0.43, Wales 0.09, Scotland 0.15 and Northern Ireland 0.17) per 100 000 population per year. The number of myotomies performed remained stable with an average of (±SD) 11.6 (±5) from 2000 to 2020, however, there was a gradual increase in achalasia admissions 58.4 (±19) in the same time period. Using epilepsy as proxy condition, hospitals appear to diagnose achalasia predominantly from their geographic catchment population raising concerns about underdiagnosing achalasia in children.
Conclusion
The incidence of paediatric achalasia in the UK is significantly higher than previously reported. Although this is still lower than the incidence in adults, the gap is narrowing. There is evidence to suggest an ongoing underdiagnosis of achalasia in childhood contributing to the wide variation in care across the UK.
{"title":"An updated incidence of paediatric achalasia and number of myotomies performed in the United Kingdom","authors":"Kitt Dokal, Mohamed Mutalib","doi":"10.1002/ygh2.493","DOIUrl":"https://doi.org/10.1002/ygh2.493","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Achalasia is a rare condition characterised by an absent oesophageal peristalsis and a non-relaxing lower oesophageal sphincter. The incidence of paediatric achalasia is poorly studied and inconsistently reported. We aimed to provide an up to date incidence of paediatric achalasia in the UK.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>All United Kingdom hospitals with paediatric gastroenterology and/or paediatric surgery were contacted to provide data on achalasia diagnosis and myotomies performed (2008-2020). Hospital Episode Statistics includes diagnostic and procedural data for all hospitals in England that were searched for achalasia and myotomy in children (1998-2020). Proxy data (epilepsy diagnosis) were used to compare diagnosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The incidence of paediatric achalasia in the UK was 0.38 (England 0.43, Wales 0.09, Scotland 0.15 and Northern Ireland 0.17) per 100 000 population per year. The number of myotomies performed remained stable with an average of (±SD) 11.6 (±5) from 2000 to 2020, however, there was a gradual increase in achalasia admissions 58.4 (±19) in the same time period. Using epilepsy as proxy condition, hospitals appear to diagnose achalasia predominantly from their geographic catchment population raising concerns about underdiagnosing achalasia in children.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The incidence of paediatric achalasia in the UK is significantly higher than previously reported. Although this is still lower than the incidence in adults, the gap is narrowing. There is evidence to suggest an ongoing underdiagnosis of achalasia in childhood contributing to the wide variation in care across the UK.</p>\u0000 </section>\u0000 </div>","PeriodicalId":12480,"journal":{"name":"GastroHep","volume":"3 7","pages":"420-425"},"PeriodicalIF":0.0,"publicationDate":"2021-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71974037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Up to 10% of patients who have had cholecystectomies suffer from symptomatic diarrhoea. The mechanism of this diarrhoea is not fully understood. It is often assumed that the diarrhoea is caused by increased bile acid. The evidence for this is based on studies which show that twothirds of patients who experience diarrhoea after the operation have excess bile acid and respond to cholestyramine, a bile acid sequestrant.1 Other poorly understood neuroendocrine effects of cholecystectomy may also be contributory factor and may account for the remaining third of patients. The mechanism by which there is increased bile acid in the lower gut after cholecystectomy is unclear. There are several proposals: a faster enterohepatic recycling of bile acids with increased bile acid synthesis or a change in the composition of the bile acid pool could play a role. The bile synthesis rate may be assessed with plasma 7αhydroxy4cholesten3one (C4), whereas ileal reabsorption of bile acids may be assessed with plasma fibroblast growth factor 19 (FGF19).2 In patients with bile acid diarrhoea, lower fasting FGF19 and higher fasting C4 have been previously demonstrated. In this paper, Borup et al tries to shed more light into this intriguing condition.3 They measured FGF19 and C4 levels in 18 individuals before and after cholecystectomy. FGF19 is stimulated in the ileum in response to bile acid and is thus a useful biomarker for ileal bile acid load. They assessed their symptoms and looked at fasting and postprandial levels of FGF19 in these individuals before and after cholecystectomy. They demonstrated that fasting levels of FGF19 are unchanged but postprandial levels are significantly increased after cholecystectomy. They also found that fasting C4 levels to be unchanged after cholecystectomy in their cohort. These results are puzzling and could lead to a rethink as to the mechanism of postcholecystectomy diarrhoea. Unfortunately, none of the patients they studied had symptomatic diarrhoea. This is likely to be a statistical fluke and rather unfortunate as these results suggest that both bile acid production and recycling is increased after cholecystectomy. Perhaps if they could continue their studies and recruit a larger cohort they may start to further elucidate the pathophysiology of postcholecystectomy diarrhoea.
{"title":"Post-cholecystectomy diarrhoea: New light on old problem","authors":"Her Hsin Tsai","doi":"10.1002/ygh2.492","DOIUrl":"https://doi.org/10.1002/ygh2.492","url":null,"abstract":"Up to 10% of patients who have had cholecystectomies suffer from symptomatic diarrhoea. The mechanism of this diarrhoea is not fully understood. It is often assumed that the diarrhoea is caused by increased bile acid. The evidence for this is based on studies which show that twothirds of patients who experience diarrhoea after the operation have excess bile acid and respond to cholestyramine, a bile acid sequestrant.1 Other poorly understood neuroendocrine effects of cholecystectomy may also be contributory factor and may account for the remaining third of patients. The mechanism by which there is increased bile acid in the lower gut after cholecystectomy is unclear. There are several proposals: a faster enterohepatic recycling of bile acids with increased bile acid synthesis or a change in the composition of the bile acid pool could play a role. The bile synthesis rate may be assessed with plasma 7αhydroxy4cholesten3one (C4), whereas ileal reabsorption of bile acids may be assessed with plasma fibroblast growth factor 19 (FGF19).2 In patients with bile acid diarrhoea, lower fasting FGF19 and higher fasting C4 have been previously demonstrated. In this paper, Borup et al tries to shed more light into this intriguing condition.3 They measured FGF19 and C4 levels in 18 individuals before and after cholecystectomy. FGF19 is stimulated in the ileum in response to bile acid and is thus a useful biomarker for ileal bile acid load. They assessed their symptoms and looked at fasting and postprandial levels of FGF19 in these individuals before and after cholecystectomy. They demonstrated that fasting levels of FGF19 are unchanged but postprandial levels are significantly increased after cholecystectomy. They also found that fasting C4 levels to be unchanged after cholecystectomy in their cohort. These results are puzzling and could lead to a rethink as to the mechanism of postcholecystectomy diarrhoea. Unfortunately, none of the patients they studied had symptomatic diarrhoea. This is likely to be a statistical fluke and rather unfortunate as these results suggest that both bile acid production and recycling is increased after cholecystectomy. Perhaps if they could continue their studies and recruit a larger cohort they may start to further elucidate the pathophysiology of postcholecystectomy diarrhoea.","PeriodicalId":12480,"journal":{"name":"GastroHep","volume":"3 5","pages":"276"},"PeriodicalIF":0.0,"publicationDate":"2021-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/ygh2.492","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71963878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D. Misra, K. Das, Saswata Chatterjee, Parthasarathi Mukherjee, A. Chowdhury
Mortality data from high‐income group countries are frequently used in developing countries for healthcare planning. This study was planned to explore the mortality pattern of cirrhosis in India in terms of survival after diagnosis of cirrhosis, predictors of death and aetiology specific effect on mortality.
{"title":"Mortality pattern in cirrhosis: A reflection of liver disease burden in India","authors":"D. Misra, K. Das, Saswata Chatterjee, Parthasarathi Mukherjee, A. Chowdhury","doi":"10.1002/ygh2.497","DOIUrl":"https://doi.org/10.1002/ygh2.497","url":null,"abstract":"Mortality data from high‐income group countries are frequently used in developing countries for healthcare planning. This study was planned to explore the mortality pattern of cirrhosis in India in terms of survival after diagnosis of cirrhosis, predictors of death and aetiology specific effect on mortality.","PeriodicalId":12480,"journal":{"name":"GastroHep","volume":"55 1","pages":"409 - 416"},"PeriodicalIF":0.0,"publicationDate":"2021-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79432726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Up to 10% of patients who have had cholecystectomies suffer from symptomatic diarrhoea. The mechanism of this diarrhoea is not fully understood. It is often assumed that the diarrhoea is caused by increased bile acid. The evidence for this is based on studies which show that twothirds of patients who experience diarrhoea after the operation have excess bile acid and respond to cholestyramine, a bile acid sequestrant.1 Other poorly understood neuroendocrine effects of cholecystectomy may also be contributory factor and may account for the remaining third of patients. The mechanism by which there is increased bile acid in the lower gut after cholecystectomy is unclear. There are several proposals: a faster enterohepatic recycling of bile acids with increased bile acid synthesis or a change in the composition of the bile acid pool could play a role. The bile synthesis rate may be assessed with plasma 7αhydroxy4cholesten3one (C4), whereas ileal reabsorption of bile acids may be assessed with plasma fibroblast growth factor 19 (FGF19).2 In patients with bile acid diarrhoea, lower fasting FGF19 and higher fasting C4 have been previously demonstrated. In this paper, Borup et al tries to shed more light into this intriguing condition.3 They measured FGF19 and C4 levels in 18 individuals before and after cholecystectomy. FGF19 is stimulated in the ileum in response to bile acid and is thus a useful biomarker for ileal bile acid load. They assessed their symptoms and looked at fasting and postprandial levels of FGF19 in these individuals before and after cholecystectomy. They demonstrated that fasting levels of FGF19 are unchanged but postprandial levels are significantly increased after cholecystectomy. They also found that fasting C4 levels to be unchanged after cholecystectomy in their cohort. These results are puzzling and could lead to a rethink as to the mechanism of postcholecystectomy diarrhoea. Unfortunately, none of the patients they studied had symptomatic diarrhoea. This is likely to be a statistical fluke and rather unfortunate as these results suggest that both bile acid production and recycling is increased after cholecystectomy. Perhaps if they could continue their studies and recruit a larger cohort they may start to further elucidate the pathophysiology of postcholecystectomy diarrhoea.
{"title":"Post‐cholecystectomy diarrhoea: New light on old problem","authors":"H. Tsai","doi":"10.1002/ygh2.492","DOIUrl":"https://doi.org/10.1002/ygh2.492","url":null,"abstract":"Up to 10% of patients who have had cholecystectomies suffer from symptomatic diarrhoea. The mechanism of this diarrhoea is not fully understood. It is often assumed that the diarrhoea is caused by increased bile acid. The evidence for this is based on studies which show that twothirds of patients who experience diarrhoea after the operation have excess bile acid and respond to cholestyramine, a bile acid sequestrant.1 Other poorly understood neuroendocrine effects of cholecystectomy may also be contributory factor and may account for the remaining third of patients. The mechanism by which there is increased bile acid in the lower gut after cholecystectomy is unclear. There are several proposals: a faster enterohepatic recycling of bile acids with increased bile acid synthesis or a change in the composition of the bile acid pool could play a role. The bile synthesis rate may be assessed with plasma 7αhydroxy4cholesten3one (C4), whereas ileal reabsorption of bile acids may be assessed with plasma fibroblast growth factor 19 (FGF19).2 In patients with bile acid diarrhoea, lower fasting FGF19 and higher fasting C4 have been previously demonstrated. In this paper, Borup et al tries to shed more light into this intriguing condition.3 They measured FGF19 and C4 levels in 18 individuals before and after cholecystectomy. FGF19 is stimulated in the ileum in response to bile acid and is thus a useful biomarker for ileal bile acid load. They assessed their symptoms and looked at fasting and postprandial levels of FGF19 in these individuals before and after cholecystectomy. They demonstrated that fasting levels of FGF19 are unchanged but postprandial levels are significantly increased after cholecystectomy. They also found that fasting C4 levels to be unchanged after cholecystectomy in their cohort. These results are puzzling and could lead to a rethink as to the mechanism of postcholecystectomy diarrhoea. Unfortunately, none of the patients they studied had symptomatic diarrhoea. This is likely to be a statistical fluke and rather unfortunate as these results suggest that both bile acid production and recycling is increased after cholecystectomy. Perhaps if they could continue their studies and recruit a larger cohort they may start to further elucidate the pathophysiology of postcholecystectomy diarrhoea.","PeriodicalId":12480,"journal":{"name":"GastroHep","volume":"47 2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82772810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Khanna, N. Cianci, Husnain Abbas Shah, A. Goel, A. Jebril, J. Chauhan, M. Pipe, S. Shetty, C. Weston, H. Venkataraman, Stacey Smith, S. Vickrage, J. Kemp-Blake, T. Shah
Diarrhoea is a common and debilitating symptom of Carcinoid syndrome. Effective control of symptoms is achieved with somatostatin analogues (SSAs) and additional loperamide and/or codeine phosphate. Symptom control is lost with time and disease progression. There is, therefore, a strong need for additional and more effective therapies. Telotristat‐ethyl is a peripheral tryptophan‐hydroxylase inhibitor approved for treatment of diarrhoea. Here, we present our experience of Telotristat for treating carcinoid diarrhoea in a large cohort of patients outside of clinical trials. The primary outcome was reduction in stool frequency of >30%, as defined in most studies.
{"title":"Telotristat in the management of Carcinoid diarrhoea – A real world experience of patients from ENETs centre of excellence in Neuroendocrine tumours","authors":"A. Khanna, N. Cianci, Husnain Abbas Shah, A. Goel, A. Jebril, J. Chauhan, M. Pipe, S. Shetty, C. Weston, H. Venkataraman, Stacey Smith, S. Vickrage, J. Kemp-Blake, T. Shah","doi":"10.1002/ygh2.491","DOIUrl":"https://doi.org/10.1002/ygh2.491","url":null,"abstract":"Diarrhoea is a common and debilitating symptom of Carcinoid syndrome. Effective control of symptoms is achieved with somatostatin analogues (SSAs) and additional loperamide and/or codeine phosphate. Symptom control is lost with time and disease progression. There is, therefore, a strong need for additional and more effective therapies. Telotristat‐ethyl is a peripheral tryptophan‐hydroxylase inhibitor approved for treatment of diarrhoea. Here, we present our experience of Telotristat for treating carcinoid diarrhoea in a large cohort of patients outside of clinical trials. The primary outcome was reduction in stool frequency of >30%, as defined in most studies.","PeriodicalId":12480,"journal":{"name":"GastroHep","volume":"70 1","pages":"291 - 297"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84099708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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