Duodenal Morphometry and Small Bowel Permeability in Children With Portal Hypertension

Borkar, Vibhor; Poddar, Ujjal; Kumari, Niraj; Singh, Suruchi; Roy, Raja; Yachha, Surender Kumar

doi:10.1097/mpg.0000000000000578

Cited by 8 publications

(3 citation statements)

References 35 publications

(96 reference statements)

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“…66 A study in children with portal hypertension reported villous atrophy, capillary dilation, muscularis mucosae thickening, and increased intestinal permeability. 67 In a study in Austria, patients with severe portal hypertension had increased gastroduodenal and intestinal permeability, which was correlated with the degree of the hepatic venous pressure gradient. As markers of the enteric bacteria translocation, lipopolysaccharide (LPS)-binding proteins and interleukin-6 had increased serum levels in patients with portal hypertension patients compared with controls.…”

Section: Role Of the Intestinal Chemical Barrier In The Nafld Develop...mentioning

confidence: 99%

Intestinal Barrier Function in the Pathogenesis of Nonalcoholic Fatty Liver Disease

Liu¹,

Yin²,

Gao³

et al. 2022

J Clin Transl Hepatol

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Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. The mechanisms involved in NAFLD onset are complicated and multifactorial. Recent literature has indicated that altered intestinal barrier function is related to the occurrence and progression of liver disease. The intestinal barrier is important for absorbing nutrients and electrolytes and for defending against toxins and antigens in the enteric environment. Major mechanisms by which the intestinal barrier influences the development of NAFLD involve the altered epithelial layer, decreased intracellular junction integrity, and increased intestinal barrier permeability. Increased intestinal permeability leads to luminal dysbiosis and allows the translocation of pathogenic bacteria and metabolites into the liver, inducing inflammation, immune response, and hepatocyte injury in NAFLD. Although research has been directed to NAFLD in recent decades, the pathophysiological changes in NAFLD initiation and progression are still not completely understood, and the therapeutic targets remain limited. A deeper understanding on the correlation between NAFLD pathogenesis and intestinal barrier regulation must be attained. Therefore, in this review, the components of the intestinal barrier and their respective functions and disruptions during the progression of NAFLD are discussed.

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Section: Role Of the Intestinal Chemical Barrier In The Nafld Develop...mentioning

confidence: 99%

Intestinal Barrier Function in the Pathogenesis of Nonalcoholic Fatty Liver Disease

Liu¹,

Yin²,

Gao³

et al. 2022

J Clin Transl Hepatol

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show abstract

“…Despite some progress in understanding bacterial translocation mechanisms in BA, there remain many unanswered questions, and in particular, data is limited in paediatrics. Urinary excretion of melibiose/rhamnose did suggest increased intestinal permeability in children with cirrhotic portal hypertension but details on disease aetiology were limited (66). One paediatric study revealed an increase in serum markers for intestinal wall integrity in cholestatic versus healthy infants, but could not differentiate BA versus non-BA cholestatic subgroups, suggesting infant cholestasis, indiscriminate of cause, may be associated with intestinal epithelial damage (67).…”

Section: Biliary Atresiamentioning

confidence: 99%

Gut Microbiome

Jain

Alexander

Burford

et al. 2021

J. pediatr. gastroenterol. nutr.

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Biliary atresia (BA) is a fibro-obliterative condition of the biliary tree, presenting in infancy. The bilioenteric conduit formed at Kasai portoenterostomy (KPE), achieves restoration of bile flow in approximately 60% of infants. Even if the operation is successful, cirrhosis and its associated complications are, however, common. BA remains the leading cause for liver transplantation (LT) in children. Antibiotic, choleretic, and steroid therapy post-KPE have not convincingly reduced LT rates. Advances in molecular technology have enabled characterisation of the encoded genes of the gut microbiota (gut microbiome). The gut microbiome plays an important role in host metabolism, nutrition, and immune function, with alterations in its diversity and/or composition, known as dysbiosis, being described in disease states, including liver disease. Liver-gut microbiome exploration in adulthood largely focuses on nonalcoholic liver disease, cirrhosis (mainly alcohol- or viral-based aetiology) and cholestatic liver diseases (eg, primary sclerosing cholangitis), with microbial signatures correlating to disease severity. Investigation of the gut microbiota in BA had been limited to culture-based methodology, but molecular studies are emerging, and although in their infancy, highlight a potential pathogenic role for Enterobacteriaceae and Streptococcus, and a potential beneficial role for Bifidobacteria. Bacterial translocation, and the production of gut microbiome-derived metabolites, are key host-microbiome-mechanistic pathways in liver disease pathogenesis. Microbiome-targeted therapeutics for liver disease are in development, with faecal microbiota transplantation showing promise in cirrhosis. Could the gut microbiome be a novel modifiable risk factor in BA, reducing the need for LT?

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“…In the study from the authors’ center, children with EHPVO showed features of enteropathy as evident by duodenal morphometric features (60%). The features were lower villous to crypt ratio, dilated capillaries, increased thickness of muscularis mucosae) and increased small intestinal permeability (lactulose excretion test) as compared to healthy controls[ 61 ]. Portal hypertensive enteropathy is one of the most important causes of growth failure in children.…”

Section: Ehpvomentioning

confidence: 99%

Pediatric non-cirrhotic portal hypertension: Endoscopic outcome and perspectives from developing nations

Sarma¹,

Seetharaman²

2021

WJH

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Non-cirrhotic portal hypertension (NCPH) forms an important subset of portal hypertension in children. Variceal bleed and splenomegaly are their predominant presentation. Laboratory features show cytopenias (hypersplenism) and preserved hepatic synthetic functions. Repeated sessions of endoscopic variceal ligation or endoscopic sclerotherapy eradicate esophageal varices in almost all cases. After variceal eradication, there is an increased risk of other complications like secondary gastric varices, cholangiopathy, colopathy, growth failure, especially in extra-hepatic portal vein obstruction (EHPVO). Massive splenomegaly-related pain and early satiety cause poor quality of life (QoL). Meso-Rex bypass is the definitive therapy when the procedure is anatomically feasible in EHPVO. Other portosystemic shunt surgeries with splenectomy are indicated when patients present late and spleen-related issues predominate. Shunt surgeries prevent rebleed, improve growth and QoL. Non-cirrhotic portal fibrosis (NCPF) is a less common cause of portal hypertension in children in developing nations. Presentation in the second decade, massive splenomegaly and patent portal vein are discriminating features of NCPF. Shunt surgery is required in severe cases when endotherapy is insufficient for the varices. Congenital hepatic fibrosis (CHF) presents with firm palpable liver and splenomegaly. Ductal plate malformation forms the histological hallmark of CHF. CHF is commonly associated with Caroli’s disease, renal cysts, and syndromes associated with neurological defects. Isolated CHF has a favourable prognosis requiring endotherapy. Liver transplantation is required when there is decompensation or recurrent cholangitis, especially in Caroli’s syndrome. Combined liver-kidney transplantation is indicated when both liver and renal issues are present.

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Duodenal Morphometry and Small Bowel Permeability in Children With Portal Hypertension

Abstract: PHT is often associated with duodenopathy. SIP does occur as a result of increased paracellular permeability. Factors of increased SIP, undernutrition, and PHTD do not have correlation in childhood PHT.

Cited by 8 publications

References 35 publications

Intestinal Barrier Function in the Pathogenesis of Nonalcoholic Fatty Liver Disease

Intestinal Barrier Function in the Pathogenesis of Nonalcoholic Fatty Liver Disease

Gut Microbiome

Pediatric non-cirrhotic portal hypertension: Endoscopic outcome and perspectives from developing nations

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