Apoptotic enteropathy caused by antimetabolites and TNF-α antagonists

Abstract

Pathologists should be aware of the expanding spectrum of drugs that can cause apoptotic enteropathy, including antimetabolites and tumour necrosis factor-α inhibitors.

Consensus diagnostic histopathological criteria for acute gastrointestinal graft versus host disease improve interobserver reproducibility

“…The remaining diagnostic divergences were mostly due to unresolved differential diagnoses, especially viral infection (such as CMV and adenovirus) and therapy-related toxicity, which may produce histological features similar to those of GvHD [11,18]. This underscores the need for microbiological and immunohistological studies.…”

“…Discrepancies may be marginal when pathologists from single or cooperating institutions have an opportunity to adjust each other's diagnostic criteria [5,20], but when there is no such exchange of experience, they could more profoundly affect inter-institutional reproducibility [19,24]. Additionally, other diagnostic considerations include infection [2,3] and toxic side effects of applied therapies [11,18], which are both frequent in patients after HCT and could mimic GvHD histologically as well as clinically.…”

Olmesartan-Associated Enteropathy

“…In that situation, the most likely culprit is olmesartan, with complete recovery expected when the drug is withdrawn. Colchicine (5,6,(20)(21)(22) Infliximab (6,20) Etanercept (20) Capecitabine (20) Neomycin (20) Sulindac (23) Alcohol with folic acid deficiency (5) …”

Antibiotic-Associated Apoptotic Enterocolitis in the Absence of a Defined Pathogen: The Role of Intestinal Microbiota Depletion*

“…Several other conditions like infections (e.g., cytomegalovirus), immunodeficiencies, autoimmune enteropathy, cord colitis, or thymoma could be accompanied by gastrointestinal epithelial apoptosis; however, the severe phenotype reported here is mainly seen in intestinal GvHD (24, 25). Interestingly, cytotoxic CD8 + T cells were significantly increased in the colon, CD4 + T cells concomitantly reduced during acute disease, whereas regulatory T cells were not changed in cases.…”