Abstrait

Esophageal Candidiasis in an Immunocompetent Girl with Chronic Anaemia

Barros Garc

Infection is an uncommon cause of esophagitis among the paediatric population. The main risk factor is immunodeficiency. In children immunocompromised due HIV infection, certain endocrine diseases, and corticosteroid or immunosuppressive therapy, Candida albicans is the most common etiologic agent. The prevalence of Candida esophagitis has increased because of an improvement in survival and management of immunological diseases. Even though it is not frequent in immunocompetent children, there have been reported cases related with risk factors (Chocarro, 2000) such as antibiotic intake (which allow bacterial overgrowth and fungal colonization), proton pump inhibitors (which produce hypochlorhydria allowing oral bacteria to colonize gastric mucosa, and to increase the risk of infectious esophagitis), esophageal obstruction (aperistalsis and stasis helps the fungal overgrowth) and systemic or inhalated corticotherapy (that suppresses lymphocyte and granulocyte function) (Simon, 1997). Candida esophagitis has also been reported in healthy patients, with no evidence of causal mechanism (Alemán, 1996). The most common symptomatology consists in odynophagia, dysphagia and retrosternal chest pain, but epigastralgia, vomiting and gastrointestinal bleeding can also occur. Chronic or acute anaemia could be the sole sign of an asymptomatic presentation (Ortuño Cortés, 1997., Weerasuriya, 2006). The absence of oral candidiasis does not exclude the diagnosis of Candida esophagitis (Mathieson, 1983). The pathophysiology of the infection is complicated. It includes a large number of factors, such as fungal virulence, mucosal integrity and host susceptibility. Esophagoscopy is the most specific and sensitive method of diagnosis. Characteristic endoscopic findings are confluent or isolated white plaques adhered to the mucosa with edema, erythema and friability, with or without ulcers covered by exudate. The diagnostic confirmation is performed by demonstrating the presence of pseudohyfae or by obtaining evidence of tissue invasion on mucosal biopsy (Ahuja, 2016). Fungal culture does not allow differentiation of colonization from infection (Mathieson, 1983). The treatment of choice is fluconazole, but there are new therapeutic options (Ahuja, 2016).