Pathophysiological Mechanisms of Drug-Induced Appendicitis and Current Therapeutic Options

Review Article

Abstract

Acute appendicitis remains a primary cause of emergency abdominal surgery worldwide. While classical etiology focuses on mechanical luminal obstruction by fecaliths or lymphoid hyperplasia, growing clinical evidence associates specific pharmacological classes with an elevated risk of appendiceal inflammation. Glucagon-like peptide-1 receptor agonists delay gastric emptying and alter gastrointestinal motility, potentially accelerating fecal stasis and fecalith development. Angiotensin-converting enzyme inhibitors trigger localized bradykinin-mediated angioedema within the appendiceal wall, provoking mechanical luminal occlusion. Immunosuppressive therapies attenuate systemic inflammatory responses, obscuring early clinical presentations while promoting subclinical bacterial translocation and rapid tissue necrosis. Nonsteroidal anti-inflammatory drugs similarly mask diagnostic pain pathways through cyclooxygenase inhibition, leading to delayed surgical interventions and high perforation rates. Atypical antipsychotics, mainly clozapine, exert potent anticholinergic effects that induce severe gastrointestinal hypomotility and fecal impaction. Managing these drug-induced appendiceal complications requires a careful selection of therapeutic modalities. Conservative management utilizing targeted broad-spectrum antibiotics provide a viable alternative to surgical intervention in uncomplicated cases, supplemented by probiotics to restore microflora homeostasis. For advanced or complicated presentations, laparoscopic appendectomy remains the definitive intervention, offering superior postoperative outcomes compared to open procedures. Recommending lifestyle modifications, including high dietary fiber intake and adequate hydration, serves to mitigate the underlying gastrointestinal stasis associated with these offending agents