Eye Disorders in Children with Celiac Disease

Dear Editor,

It is not clear if eye examination should be done for all children with celiac disease (CD) at the time of diagnosis and during follow-up whether or not they are at risk of developing eye disorders at older ages. In “Eye disorders in children with celiac disease,” Urganci and Kalyoncu discuss the need for eye examination in these patients (1).

Since its first description in 1500, we have accepted the idea that CD was a condition closely related to the gastrointestinal tract and the ingestion of gluten. However, in recent decades, after the first report of the correlation between neurologic disorders and CD, there has been an increase in the number of reports of patients with neurologic symptoms associated with the presence of the disease (2, 3).

The prevalence of CD in the world population is approximately 1%-2%. The association between CD and ophthalmologic symptoms is rarely reported. Pengiran et al (3), in a retrospective evaluation of neurologic patients, identified depression, epilepsy, and migraine as the most common neurologic manifestations related to CD. In 2004, Zelnik et al (2) identified the coexistence of neurologic symptoms in 51.4% of patients in a pediatric population with CD compared to 19.9% in the control group. In a case report of a 4-year-old patient presenting with epileptic seizures, Lea et al (4) documented the progressive appearance of bilateral parietal intracranial calcifications and a subsequent diagnosis of CD, which resulted in adequate seizure control without the need for medication after instituting dietary changes. The description of the triad of bilateral parietal calcifications, epilepsy, and CD is already widely reported in the literature (2-4). The coexistence of visual symptoms with the disease and its etiology is unknown. The mechanisms involved at the onset of intracranial calcifications, specifically located in the bilateral parietal region, have not yet been elucidated. Some theories have been proposed, such as a deficiency of folic acid, alterations of serum calcium metabolism, and toxicity caused by deposition of silica salts (3, 4). Postmortem analysis of brain tissue from some patients may seem to suggest that immune-mediated phenomena may alter cerebral vascular permeability, favoring the localized deposition of calcium (4).

There are possible differential diagnoses of bilateral intracerebral calcifications with CD. The most important one is the Sturge-Weber syndrome without the presence of nevus flammeus. In the case of Sturge-Weber syndrome, calcifications are present bilaterally in only 15% to 19% of cases and occur predominantly in the cortical area (4). In CD, bilaterality of deposition is mandatory and occurs mainly in the cortical and sub​​cortical areas. Thus, we should investigate occipital calcifications in children with CD and visual impairment.