Utility of gastric biopsy in diagnosing IgG4‐related gastrointestinal disease

The utility of gastric biopsy for diagnosing immunoglobulin (Ig)G4‐related gastrointestinal disease (IgG4‐GID) remains unclear. Bottom‐heavy plasmacytosis (BHP) is a distinct feature of IgG4‐GID. To clarify the feasibility of using gastric biopsies to diagnose BHP in IgG4‐GID, we analyzed the histological features and immunostaining of gastric biopsy specimens from 31 known IgG4‐related disease (IgG4‐RD) patients and we assessed the presence of BHP in 1696 consecutive routine gastric biopsies. Cases with both >10 IgG4‐positive plasma cells per high‐power field and an IgG4/IgG‐positive ratio >40% were defined as IgG4‐high. Ten of the 31 IgG4‐RD patients were concluded to have IgG4‐GID, in which IgG4‐positive plasma cells were notably detected at the deeper part of the mucosa. Six cases displayed BHP whereas the remaining four cases showed transmural infiltration with concomitant Helicobacter pylori‐associated gastritis. In addition to BHP, we identified two unique histologic features for IgG4‐GID: plasmacytic aggregation in the muscularis mucosae and permeative plasmacytic infiltration between fundic glands in the non‐atrophic mucosa. Six of the routine cases (0.35%) displayed BHP, including a case with IgG4‐RD. IgG4‐GID can be suspected by the presence of gastric biopsy specimens with characteristic histological features. Such cases are recommended to undergo further examinations to determine whether IgG4‐RD is present

Periductal Induction of High Endothelial Venule-Like Vessels in Type 1 Autoimmune Pancreatitis

信州大学博士（医学）・学位論文・平成24年3月31日授与（甲第946号）・丸山 雅史This is a non-final version of an article published in final form in PANCREAS. 42(1):53-59 (2013).Objectives: Type 1 autoimmune pancreatitis (AIP) is histologically characterized by dense lymphoplasmacytic infiltration and marked storiform fibrosis, manifestations associated with pancreatic ducts. Such periductal lymphocyte recruitment is thought to be elicited by dysregulation of mechanisms governing physiological lymphocyte homing. The present study was undertaken to determine whether vascular addressins including peripheral lymph node addressin and mucosal addressin cell adhesion molecule 1 (MAdCAM-1) play a role in type 1 AIP histogenesis. Methods: Tissue sections of type 1 AIP and tumor-associated non-AIP chronic pancreatitis, as well as normal pancreas, were subjected to immunohistochemical analysis using vascular addressin-related antibodies. Results: The number of periductal mouse endothelial cell antigen 79-positive high endothelial venule (HEV)-like vessels was increased in type 1 AIP relative to that seen in non-AIP chronic pancreatitis, whereas the number of MAdCAM-1-positive HEV-like vessels did not differ between the 2 conditions. Mouse endothelial cell antigen 79 antigens are expressed on duct-forming epithelial cells not only in pancreas but also in salivary glands, which often harbor extrapancreatic lesions in type 1 AIP. Conclusions: Type 1 AIP can be characterized by periductal induction of MECA-79-positive HEV-like vessels. MECA-79-positive 6-sulfo sialyl Lewis X-related carbohydrate antigens expressed on duct-forming epithelial cells could be associated with type 1 AIP pathogenesis.ArticlePANCREAS. 42(1):53-59 (2013)journal articl

Periodontal Disease Is an Independent Predictor of Intracardiac Calcification

Background. Periodontitis is the most common chronic inflammatory condition worldwide and is associated with incident coronary disease. Hypothesis. We hypothesized that periodontal disease would also be associated with cardiac calcification, a condition which shares many risk factors with atherosclerosis and is considered a marker of subclinical atherosclerosis. Methods. Cross-sectional study at two sites (USA and Japan) involving subjects with both clinical echocardiograms and detailed dental examinations. Semiquantitative scoring systems were used to assess severity of periodontal disease and echocardiographic calcification. Results. Fifty-six of 73 subjects (77%) had cardiac calcifications, and 51% had moderate to severe periodontal disease (score > 2). In unadjusted analysis, a significant relationship between periodontal score and cardiac calcification (Spearman rho = 0.4, P=0.001) was noted, with increases in mean calcification score seen across increasing levels of periodontal disease. On multivariate logistic regression, adjusted for age, gender, race, glomerular filtration rate, and traditional risk factors, this association remained significant (P=0.024). There was no significant interaction by study site, race, or gender. Conclusions. In a multiracial population, we found a significant association between the degree of periodontal disease, a chronic inflammatory condition, and cardiac calcification. Further, higher periodontal scores were associated with greater degrees of calcification