Frequency of Hepatobiliary Manifestations and Concomitant Liver Disease in Inflammatory Bowel Disease Patients

Silva, Juliana; Brito, Beatriz; Silva, Isaac Neri de N.; Nóbrega, Viviane; Silva, Maria Carolina S. M. da; Gomes, Hemerson Dyego de N.; Fortes, Flora Maria Lorenzo; Pimentel, Andréa; Mota, Jaciane; Almeida, Neogélia; Surlo, Valdiana; Lyra, André Castro; Rocha, Raquel; Santana, Genoile Oliveira

doi:10.1155/2019/7604939

Cited by 31 publications

(34 citation statements)

References 21 publications

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“…Recent research findings have evaluated the presence of liver extrahepatic manifestations associated with IBD. Consistent with the mild inflammation seen in this study, there were no granulomas, hepatic abscesses, amyloidosis, and gallstones which are traditionally observed in CD, while PSC and autoimmune hepatitis are usually described in UC patients (30). One of the important observations made in this investigation is that Ccr6-deficiency serves to reduce the disease severity in the liver and spleen of colitis-afflicted mice.…”

Section: Thesupporting

confidence: 90%

“…In contrast to displaying normal kidney histology, liver pathology indicated significant lobular inflammation in Winnie with milder inflammation in the Ccr6deficient Winnie (29). There are reports which describe the occurrence of concomitant hepatobiliary manifestations in IBD patients, of which the most common complication being primary sclerosing cholangitis (PSC) (30). Recent research findings have evaluated the presence of liver extrahepatic manifestations associated with IBD.…”

Section: Thementioning

confidence: 99%

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Ccr6 Deficiency Attenuates Spontaneous Chronic Colitis in Winnie

Ranasinghe¹,

Fernando²,

Perera³

et al. 2019

Preprint

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The immunomodulatory behaviour of the CCR6/CCL20 axis on multi -system pathophysiology and molecular signalling was investigated at two clinically significant time points, using a Ccr6 - deficient mouse model of spontaneous colitis. Four groups of mice, (C57BL/6J, Ccr6-/- of C57BL/6J, Winnie x Ccr6 -/- and Winnie) were utilized and (I) colonic clinical parameters (2) histology of colon, spleen, kidney and liver (3) T and B lymphocyte distribution in the spleen and MLN by flowcytometry (5) colonic CCL20, PI3K and phosphorylated Akt expression by immunohistochemistry and (6) colonic cytokine expression by RT-PCR were evaluated. CCR6 influenced upregulation of inflammation in the spleen, liver and gut while renal histology remained unaffected. Marked focal lobular inflammation with reactive nuclear features were observed in hepatocytes and a significant neutrophil infiltration in red pulp with extra medullary hemopoiesis in the spleen existed in Winnie. These changes were considerably reduced in Winnie x Ccr6-/- with elevated goblet cell numbers and mucus production in the colonic epithelium. Results indicate that Ccr6- deficiency in the colitis model contributes towards resolution of disease. Our findings demonstrate an intricate networking role for CCR6 in immune activation, which is downregulated by Ccr6 deficiency, and could provide newer clinical therapies in colitis.

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Section: Thesupporting

confidence: 90%

Section: Thementioning

confidence: 99%

Ccr6 Deficiency Attenuates Spontaneous Chronic Colitis in Winnie

Ranasinghe¹,

Fernando²,

Perera³

et al. 2019

Preprint

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“…In contrast to displaying normal kidney histology, liver pathology indicated significant lobular inflammation in Winnie with milder inflammation in the Ccr6-deficient Winnie [28]. There are reports which describe the occurrence of concomitant hepatobiliary manifestations in IBD patients, of which the most common complication being primary sclerosing cholangitis (PSC) [29]. Research findings have evaluated the presence of liver extrahepatic manifestations associated with IBD [30].…”

Section: Discussionmentioning

confidence: 99%

Ccr6 Deficiency Attenuates Spontaneous Chronic Colitis in Winnie

Ranasinghe

Fernando

Perera

et al. 2020

Gastrointestinal Disorders

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Background: The immune-modulator behaviour of the CCR6/CCL20 axis in multi -system pathophysiology and molecular signalling was investigated at two clinically significant time points, using a Ccr6—deficient mouse model of spontaneous colitis. Methods:Four groups of mice, (C57BL/6J, Ccr6−/− of C57BL/6J, Winnie × Ccr6−/− and Winnie) were utilized and (I) colonic clinical parameters (2) histology of colon, spleen, kidney and liver (3) T and B lymphocyte distribution in the spleen and MLN by flowcytometry (5) colonic CCL20, phosphorylated PI3K and phosphorylated Akt expression by immunohistochemistry and (6) colonic cytokine expression by RT-PCR were evaluated. Results: CCR6 deficiency was shown to attenuate inflammation in the spleen, liver and gut while renal histology remained unaffected. Marked focal lobular inflammation with reactive nuclear features were observed in hepatocytes and a significant neutrophil infiltration in red pulp with extra medullary hemopoiesis in the spleen existed in Winnie. These changes were considerably reduced in Winnie × Ccr6−/− with elevated goblet cell numbers and mucus production in the colonic epithelium. Conclusions: Results indicate that Ccr6-deficiency in the colitis model contributes towards resolution of disease. Our findings demonstrate an intricate networking role for CCR6 in immune activation, which is downregulated by Ccr6 deficiency, and could provide newer clinical therapies in colitis.

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“…A disturbed metabolism in IBD patients is causing these diseases to occur in concordance with rapid and large weight changes and steroid use. The prevalence of all liver disease in IBD is probably around 20% [91], among them drug-induced liver disease, vein thrombosis of the hepatic or portal, liver amyloidosis, and granulomatous hepatitis. Autoimmune hepatitis occurs also more frequently in IBD patients, associated with IBD diseases or with PSC.…”

Section: Steatosis and Other Frequent Liver Diseasesmentioning

confidence: 99%

Therapies in Inflammatory Bowel Disease Patients with Extraintestinal Manifestations

Juillerat

Manz²,

Sauter

et al. 2020

Digestion

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Extraintestinal manifestations (EIM) have become an important source of morbidity and disability as well as an identified risk factor for an unfavorably course of disease in inflammatory bowel diseases (IBD). Therefore, efforts have been put into a more global and interdisciplinary management of IBD patients in collaboration with rheumatologists, dermatologists, and ophthalmologists. A real therapeutic success has also been obtained with a more "systemic" IBD treatment associated with the development of monoclonal antibodies against TNF alpha and biological agents derived from the treatment of rheumatological disease (also called biological Disease-Modifying Antirheumatic Drugs). The prevalence of these EIM remains too low to undergo randomized controlled trials with this specific focus and therefore the evidence relies on case series and experts' opinions, which lowers the level of evidence. After a careful review of the most recent literature, this paper aims to update the reader on the latest therapeutic management of IBD patients with EIM.

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Frequency of Hepatobiliary Manifestations and Concomitant Liver Disease in Inflammatory Bowel Disease Patients

Cited by 31 publications

References 21 publications

Ccr6 Deficiency Attenuates Spontaneous Chronic Colitis in Winnie

Ccr6 Deficiency Attenuates Spontaneous Chronic Colitis in Winnie

Ccr6 Deficiency Attenuates Spontaneous Chronic Colitis in Winnie

Therapies in Inflammatory Bowel Disease Patients with Extraintestinal Manifestations

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