Journal of Pathology and Translational Medicine

Original Article

Inflammation and tissue remodeling contribute to fibrogenesis in stricturing Crohn’s disease: image processing and analysis study: Mustafa Erdem Arslan, Rupinder Brar, Lianna Goetz, Dipti Karamchandani, Michael W. Mikula, Kyle Hodge, Hua Li, Sangtae Ahn, Hwajeong Lee; J Pathol Transl Med. 2022;56(5):239-248. Published online July 4, 2022; DOI: https://doi.org/10.4132/jptm.2022.05.18

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Abstract PDF Supplementary Material: Background
Inflammation and structural remodeling may contribute to fibrogenesis in Crohn’s disease (CD). We quantified the immunoexpression of calretinin, CD34, and calprotectin as a surrogate for mucosal innervation, telocytes (interstitial cells playing a role in networking), and inflammation, respectively, and correlated them with bowel alterations in stricturing CD.
Methods
Primary resection specimens for ileal CD (n = 44, 31 stricturing CD, 13 inflammatory CD) were identified. Left-sided ulcerative colitis and trauma cases were used as controls. Proximal and distal margin and middle (diseased) sections were stained for calretinin, CD34, and calprotectin. Microscopic images were captured from the mucosa (calretinin), submucosa (calprotectin), and myenteric plexus (CD34), and the immunostaining was quantified using image processing and analysis. Bowel thickness at the corresponding sections were measured and correlated with the amount of immunoexpression.
Results
A total of 2,037 images were analyzed. In stricturing CD, submucosal alteration/thickening at the stricture site correlated with calprotectin staining and inversely correlated with calretinin staining at the proximal margin. Muscularis propria alteration/thickening at the stricture site correlated with mucosal calretinin staining at the proximal margin. Submucosal alteration/thickening at the proximal margin correlated with calretinin and CD34 staining at the proximal margin and inversely correlated with CD34 staining at the stricture site. Calretinin immunostaining at the distal margin was significantly higher in stricturing CD than the controls.
Conclusions
Inflammation and tissue remodeling appear to contribute to fibrogenesis in stricturing CD. Increased mucosal calretinin immunostaining distal to the diseased segment could be helpful in diagnosing CD in the right clinical context.

Corrigendum

Correction of Ethics Statement: Metastatic Insulinoma Presenting as a Liver Cyst: Hua Li, Tony El Jabbour, Ankesh Nigam, Hwajeong Lee; J Pathol Transl Med. 2019;53(6):415-415. Published online November 5, 2019; DOI: https://doi.org/10.4132/jptm.2019.08.12; Corrects: J Pathol Transl Med 2019;53(2):148

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Brief Case Report

Metastatic Insulinoma Presenting as a Liver Cyst: Hua Li, Tony El Jabbour, Ankesh Nigam, Hwajeong Lee; J Pathol Transl Med. 2019;53(2):148-151. Published online January 16, 2019; DOI: https://doi.org/10.4132/jptm.2019.01.15; Correction in: J Pathol Transl Med 2019;53(6):415

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Citations

Citations to this article as recorded by

Hyperechogenicity and histopathological features of focal liver lesions
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Review

Idiopathic Noncirrhotic Portal Hypertension: An Appraisal: Hwajeong Lee, Aseeb Ur Rehman, M. Isabel Fiel; J Pathol Transl Med. 2016;50(1):17-25. Published online November 11, 2015; DOI: https://doi.org/10.4132/jptm.2015.09.23

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Abstract PDF

Idiopathic noncirrhotic portal hypertension is a poorly defined clinical condition of unknown etiology. Patients present with signs and symptoms of portal hypertension without evidence of cirrhosis. The disease course appears to be indolent and benign with an overall better outcome than cirrhosis, as long as the complications of portal hypertension are properly managed. This condition has been recognized in different parts of the world in diverse ethnic groups with variable risk factors, resulting in numerous terminologies and lack of standardized diagnostic criteria. Therefore, although the diagnosis of idiopathic noncirrhotic portal hypertension requires clinical exclusion of other conditions that can cause portal hypertension and histopathologic confirmation, this entity is under-recognized clinically as well as pathologically. Recent studies have demonstrated that variable histopathologic entities with different terms likely represent a histologic spectrum of a single entity of which obliterative portal venopathy might be an underlying pathogenesis. This perception calls for standardization of the nomenclature and formulation of widely accepted diagnostic criteria, which will facilitate easier recognition of this disorder and will highlight awareness of this entity.

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