Abstract
Functional gastrointestinal disorders represent the most common cause of gastrointestinal complaints and do not require extensive diagnostic evaluation. However, the presence of so-called red flag symptoms, such as dysphagia or nocturnal abdominal pain, necessitates further investigation, including esophagogastroduodenoscopy (EGD). Eosinophilic esophagitis (EoE) is an increasingly recognized chronic, immune-mediated esophageal disorder. Its hallmark clinical manifestation is dysphagia, frequently presenting as food bolus impaction. In the pediatric population, symptoms may be nonspecific, and up to one-third of patients demonstrate no macroscopic abnormalities on endoscopic examination of the esophagus. Therefore, histopathological assessment of esophageal biopsy specimens remains the diagnostic gold standard (with an eosinophil count of ≥15 eosinophils per high-power field). First-line therapeutic options include proton pump inhibitors (PPIs), swallowed topical glucocorticosteroids, or dietary elimination therapy. These modalities demonstrate comparable efficacy, and treatment selection is typically based on shared decision-making between the clinician and the patient (and caregivers). Therapeutic response should be confirmed not only by clinical remission but also by normalization of both endoscopic and histological findings on follow-up evaluation. The disease is chronic, relapsing, and progressive if left untreated. Importantly, the presence of one gastrointestinal pathology does not preclude the coexistence of another. Chronic gastritis is a considerably more prevalent condition, and in children, it is often characterized by a paucity of symptoms despite its chronic course. Most cases are associated with infection by Helicobacter pylori (H. pylori). Although H. pylori infection may remain asymptomatic, nausea and epigastric pain have been associated with its presence and may constitute early manifestations of chronic gastritis. In pediatric patients, detection of H. pylori infection in the absence of destructive gastric mucosal lesions does not necessitate eradication therapy. For more than two decades, accumulating evidence has suggested a potential inverse association between H. pylori infection and EoE; however, the underlying pathophysiological mechanisms of this relationship, if causal, remain incompletely elucidated. We present the case of a patient hospitalized in a pediatric department with a diagnosis of EoE and chronic gastritis. A unique feature of this clinical case is the coexistence of these two disease entities and the selection of an appropriate therapy that allows both conditions to be treated simultaneously.