RESUMEN
INTRODUCTION: Eosinophilic esophagitis is a chronic, antigen-mediated inflammation of the esophagus. The disease is most common at young ages, with a male to female ratio of 3:1. Eosinophilic granulocyte infiltration induced by oral/aeroantigens in the esophagus, mucosal hyperplasia, and fibrosis of the subepithelial layers can lead to constriction, dysphagia, blockage and esophageal perforation. CASE REPORT: A 36-year-old male patient presented in June 2016 with dysphagia as the main complaint. Workup with plain chest radiography with a water soluble contrast swallow did not reveal any pathological lesions. The patient's swallowing difficulties persisted and one year later he was treated by esophageal food bolus impaction (EFBI) in another institution. A new plain chest radiography with a water soluble contrast swallow confirmed a 9 cm long stricture in the middle third with an EFBI. During gastroscopy, a clinical picture of eosinophilic esophagitis was noted, with partially destroyed foreign body at 25cm and iatrogenic perforation at the upper half of the esophagus. After preoperative intensive care unit valuation and preparation, transhiatal esophagectomy without thoracotomy and cervical esophagostomy was performed with pyloromyotomy and feeding jejunostomy. The postoperative period was uneventful. Histological examination confirmed the presence of strictures and perforation on the background of eosinophilic esophagitis. Elective esophageal reconstruction with cervical esophagogastric anastomosis was performed on January 2018. Control blood tests revealed persistent eosinophilia, while the plain chest radiography with a water soluble contrast swallow showed no contrast leakage. Per os nutrition was resumed and the patient was discharged in good general condition. CONCLUSIONS: Eosinophilic esophagitis is a rare and difficult to diagnose entity due to its non-specific clinical presentation. In order to avoid complications and undesired delay in diagnosis, one should take into consideration this entity in every clinical situation of a young male patient with swallowing complaints.
RESUMEN
Both adipose-derived stem cells (ADSCs) and fat grafting promote burn wound healing, but whether adipogen-derived cells using various inducers such as 3-isobutyl-1-methylxanthine (IBMX) and insulin affect wound healing is unknown. Herein, ADSC-differentiated adipogenic lineages were used in rat burn wounds to evaluate wound healing potential. ADSCs were cultivated using six different adipogenic differentiation conditions (IBMX ± insulin, IBMX for 5 days, high and low Dulbecco's modified Eagle's medium) and in vitro morphological changes and cell proliferations during adipogenic differentiation were recorded. Intermediate burn wounds were inflicted in 15 Wistar male rats. Afterwards, the rats were divided into five groups for subcutaneous injections under the wounds: control; ADSCs; differentiated adipocytes (-IBMX+INSULIN and +IBMX[D1-5]+INSULIN) and fat prepared by Coleman technique. Macroscopic changes and histology were documented for 3 weeks. Repeated measures analysis of variance was performed to analyze cell growth and wound healing with a statistical level set of P < .05. Induction cocktails significantly reduced proliferation and induced lipid droplet accumulation. Conditioning without insulin induced the least lipid accumulation, while discontinuing IBMX generated larger adipocytes (P < .001). Adipogenic differentiated ADSCs had similar wound healing abilities with ADSC and fat injections, but differentiated adipocytes (+IBMX[D1-5]+INSULIN) and fat grafting accelerated the early healing process relative to ADSC (P < .001). Reduced fibrosis and mild inflammatory infiltration limited to superficial dermis were observed in +IBMX(D1-5)+INSULIN and fat injection groups, while those reactions were mild to moderate in ADSC group. Differentiated adipocytes achieve similar wound healing results compared with ADSC and fat injections, but differentiated adipocytes (+IBMX[D1-5]+INSULIN) and fat grafting accelerate early healing relative to ADSC.