Lymphocytic duodenitis or microscopic enteritis and gluten-related conditions: what needs to be explored?

Abstract

Microscopic enteritis (ME) is characterized by abnormal infiltration of intraepithelial lymphocytes in intestinal mucosa. It was described as duodenal lymphocytosis or lymphocytic duodenitis until the dedicated Consensus Conference of 2015. ME represents a common feature of several gluten-mediated and non-gluten related diseases; therefore, it is an umbrella term embracing several conditions. The most frequent causes of ME are gluten-related disorders (celiac disease, non-celiac gluten sensitivity, wheat allergy), Helicobacter pylori infection and drug-related damages. Less frequently, ME may be secondary to inflammatory bowel disease, some autoimmune conditions, immunoglobulin deficiencies, blood malignancies, infections and irritable bowel syndrome. Therefore, the differential diagnosis of ME may be challenging. The diagnosis of ME needs to be driven by predominant symptoms and patient history. However, it is often difficult to achieve an immediate identification of the underlying condition, and a broad variety of diagnostic tests may be required. Ultimately, long-term surveillance is needed for a final diagnosis in many cases, since a hidden or quiescent condition may be disclosed after a period of latency. In any case, strict collaboration between the clinician and the pathologist is pivotal. The treatment of ME should be personalized, depending on the underlying disease. For gluten-related conditions (celiac disease, gluten sensitivity, wheat allergy, dermatitis herpetiformis), a gluten-free diet may be proposed. For other conditions, a targeted etiologic treatment is necessary. In conclusion, ME represents a novel entity that is attracting increasing interest. The growing epidemiologic trend confirms that it will become a common condition in clinical practice.

Combination of Gluten-Digesting Enzymes Improved Symptoms of Non-Celiac Gluten Sensitivity: A Randomized Single-blind, Placebo-controlled Crossover Study

“…The symptoms of both CD and NCGS are thought to be caused by the indigestible 33-mer peptide, which is generated during the digestion of gliadin in the digestive system and induces mucosal inflammation 3 – 6 . Recently, however, it was considered that the mechanism of NCGS cannot be explained by the 33-mer peptide only 12 , 13 , 24 . We tested whether the symptoms of NCGS were improved by digesting the 33-mer peptide in the digestive system using the digestive enzymes derived from microorganisms and papaya.…”

“…Recently, gliadin was considered not to trigger symptoms of NCGS because only half of the patients with NCGS with the HLA-DQ2 or DQ8 haplotype, or both, showed induction of mucosal inflammation by gliadin 12 , 13 . Several components in wheat are considered as candidates for the triggering factors, e.g., gluten-related proteins, amylase-trypsin inhibitors, fermentable oligosaccharides, disaccharides, and polyols 24 , 28 , 29 . However, the factors and mechanisms of NCGS are still unclear.…”

Transmission electron microscopy helpfulness in Whipple's disease masked by immunosuppressant therapy for arthritis

“…Whipple's disease is a cause of microscopic enteritis, inducing inflammatory changes in duodenal mucosa . Duodenal and ileal samples showed the persistence of PAS‐positive macrophages after 1‐year therapy; this aspect is not surprising since these cells may be found for years in treated patients in clinical remission without indicating a persistent disease .…”

Histopathological evaluation of duodenal biopsy in the PreventCD project. An observational interobserver agreement study

“…In these cases clinical and laboratory data become essential in the diagnosis of CD, together with additional histological studies. Staining with the anti‐CD3 antibody can assist the pathologist in detection and counting of intraepithelial T‐lymphocytes . In our study, the local pathology assessment was based on hematoxylin and eosin stains without routine employment of CD3 immunohistochemistry, and this may explain the discrepancy of four cases assessed as Marsh type 1 by the local pathologist, but found to be type 0 by the referral pathologist when using CD3 immunochemistry.…”