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Background/introductionWhile oral acetazolamide is a cornerstone of management of adult and pediatric PTCS, previous studies have suggested that acetazolamide used in children with other conditions may influence growth.Aims and methodsRetrospective chart review involving a single tertiary medical center. Thirty-four children with definite or probable PTCS were identified. Analysis was restricted to individuals from whom anthropometric data were available before and during acetazolamide treatment (n=22).ResultsHalf of individuals (n=11/22) showed a decline in BMI Z-scores. Sixty-three percent (n=14/22) showed a decrease in height Z-scores during treatment with acetazolamide; in 6 of these 14 children who had complete data, 3 showed at least a partial recovery of height Z-scores after discontinuation of acetazolamide.ConclusionAcetazolamide may be associated with growth suppression in some children treated for pediatric PTCS. In some cases, the growth suppression appears to reverse once the acetazolamide is stopped.

In recent years, the substantial burden of medical comorbidities in autism spectrum disorder (ASD) populations has been described. We report a retrospective observational case series of pediatric patients with suspected idiopathic intracranial hypertension (IIH) and concurrent ASD. Pediatric subjects with suspected IIH aged 2–18 years were identified by review of a pediatric neuro-ophthalmologist’s database spanning from July 1993 to April 2013. ASD diagnoses were identified within this cohort by an ICD-9 diagnosis code search and database review. Three subjects had concurrent ASD diagnoses; all were non-obese males. Since the retrospective observational case series was performed in April 2013, we identified three additional IIH cases in boys with ASD. Our experience suggests that IIH may be a comorbidity of ASD, particularly in non-obese boys.

Purpose: Vitamin A deficiency is a very rare condition in the developed world and can lead to a variety of ocular changes from xerosis and xerophthalmia to corneal ulcer and perforation. The treatment of this devastating disease is simple and inexpensive. It is therefore important to recognize and treat accordingly, especially in the event of ulcers unresponsive to treatment or in the presence of severe malnutrition/malabsorption syndromes. The purpose of this case report is to remind physicians of the potentially devastating effects of vitamin A deficiency on the eyes and to demonstrate outcomes after vitamin A treatment. Methods: Single observational case report. Results: A 29-year-old male with known eosinophilic gastroenteropathy was treated with oral steroids for peripheral ulcerative keratitis. Two weeks after resolution, the patient suffered from peripheral ulcerative keratitis in his other eye, with a self-sealing perforation. Vitamin A deficiency was confirmed and successfully treated, leading to subsequent resolution of signs and symptoms. Conclusions: Vitamin A deficiency can be present in patients with malabsorption and malnutrition syndromes and should be considered as cause of corneal ulceration.