He was treated with acyclovir and a proton pump inhibitor, but his follow-up endoscopy showed typical patterns of eosinophilic esophagitis, as well as the biopsy specimens were appropriate for the diagnostic requirements for eosinophilic esophagitis. Korean kid with regular immunity. strong course=”kwd-title” Keywords: Kid, Eosinophilic esophagitis, Herpes virus Intro Eosinophilic esophagitis (EoE) can be thought as an immuneand antigen-mediated persistent esophageal inflammatory disease with eosinophilic build up and esophageal dysfunction symptoms, such as for example throwing up, dysphagia, and meals impactions [1]. Even though the occurrence of EoE can be raising in European countries and america quickly, EoE is an extremely uncommon disease in Korea and there have been limited studies on EoE in Korea and other Asian countries [2,3]. The occurrence of EoE is associated with abnormal esophageal epithelial barrier function, and collapse of the esophageal epithelium is one of the most important factors in the development of EoE [1,4]. This abnormality can easily SR9243 lead to sensitization to food and SR9243 environmental antigens, followed by cytokine mediated recruitment of eosinophils to the esophagus [1]. Herpes simplex virus (HSV) is a common cause of infectious esophagitis in SR9243 immunocompromised patients, but HSV esophagitis is also found in immunocompetent healthy Rabbit Polyclonal to FA7 (L chain, Cleaved-Arg212) children and adults [5-8]. HSV infection in the esophagus can induce the breakdown of the esophageal mucosa and activate an immune reaction that sensitizes the esophagus to foods and aeroallergens [5]. In practice, there have been reports of subsequent occurrences of EoE due to HSV infection [5-7,9-12]. However, active EoE can also cause HSV esophagitis as a result of active untreated EoE disrupting the esophageal mucosa integrity and allowing infectious agents, such as HSV, to invade the esophageal mucosa more easily [10]. The patient described in this report was diagnosed with EoE after esophageal epithelial damage due to HSV esophagitis. Until now, EoE has not been diagnosed after HSV esophagitis in Korea; we report a case where EoE was diagnosed after HSV esophagitis in an immunocompetent SR9243 pediatric patient, and we present a review of relevant literature on the subject. CASE REPORT An 11-year-old boy who had allergic rhinitis without other medical problems was admitted with fever, odynophagia, dysphagia, and chest pain. On examination, his body temperature was 38.2 and he had multiple ulcers on his lip and hard palate. The initial esophagogastroduodenoscopy (EGD) (Olympus GIF-Q260 Video Gastroscope; Olympus, Tokyo, Japan) revealed numerous depressed linear ulcerative lesions at the mid-esophagus. The longitudinal ulcers had erythematous mucosa with raised margins and yellow bases with a volcano-like appearance at the distal esophagus (Fig. 1A). Polymerase chain reaction (PCR) and immunohistochemistry were performed with the EGD biopsy specimens in order to identify the causative infection of the ulcers. Open in a separate window Fig. 1. (A) Longitudinal ulcers with raised margins, yellow bases with a volcano-like appearance on the distal esophagus (black ellipses), and ulcers on the lip are shown. (B) The initial esophageal biopsy specimen shows nonspecific inflammatory and ulcerative findings without cytopathic changes or intranuclear inclusions (hematoxylin and eosin stain, 200). The polymerase chain reaction test is positive for herpes simplex virus (HSV) 1; patient (P), positive control (PC), and negative control (NC). We extracted genomic DNA from the fresh esophageal biopsy tissues using the QIAsymphony kit (Qiagen, Hombrechtikon, Switzerland), following preparation with tissue lysis buffer and proteinase K solution (Qiagen). We mixed the primer mixture of HSV type 1 and type 2 (BioCore, Seoul, Korea) and the genomic DNA. PCR was performed with a cycling condition consisting of a denaturation step for 12 minutes (95C), followed by 35 cycles of 45 seconds at 94C, 67C, and 72C respectively, and a final extension at 72C for 5 minutes. Electrophoresis was performed with the PCR products and the internal control. The marker of the 279 base pair was HSV type 1 and the 180 base pair was HSV type 2. Although HSV type I was positive in the PCR test, HSV was negative in the immunohistochemistry exam, which also showed nonspecific inflammatory and ulcerative findings without SR9243 cytopathic changes and intranuclear inclusions (Fig. 1B). We performed PCR with skin, blood, and gastrointestinal tissues of six patients in parallel. HSV type 1 was only positive in the esophageal tissue of this patient, and so we could.