Underlying Organic Causes in Lebanese Autistic Pediatric Patients in a Single-Center Cohort



EL SABBAGH Jana1, MANSOUR Hicham1-2*

¹Faculty of Medicine, Saint George University of Beirut, Beirut, Lebanon.

²Department of Pediatrics, Saint George Hospital University Medical Center, Beirut, Lebanon.

*Corresponding Author: MANSOUR Hicham, Department of Pediatrics, Saint George University Medical Center, Lebanon.

https://doi.org/10.58624/SVOAPD.2026.05.017

Received: May 26, 2026

Published: June 18, 2026

Citation: El Sabbagh J, Mansour H. Underlying Organic Causes in Lebanese Autistic Pediatric Patients in a Single-Center Cohort. SVOA Paediatrics 2026, 5:3, 120-125. doi: 10.58624/SVOAPD.2026.05.017

 

Abstract

This is a prospective observational study at a university hospital pediatric clinic between June 2025 and June 2026. During the study period, 242 new unique consults of patients already diagnosed with autism/cognitive delay were seen for neurological evaluation, 44 among which were included in the study. Among 44 analyzed children, the mean age was 6.3 ± 2.7 years and mean age at presentation was 4.7 ± 2.4 years. Presenting features were: Speech delay (93.2%), hyperlaxity (43.2%) and poor attention/hyperactivity (15.9%). Consanguinity was present in 18.2%. Lactic acidosis in (88.6%), white-matter delay on MRI in 12 (27.3%), and a positive WES finding in all 5 children who underwent testing. The most frequent treatment regimen was L-Carnitine, Coenzyme Q 10, Vitamin B2, Biotin combination. Thirty-four patients (77.3%) improved after treatment. In this selected cohort, children referred under an autism/cognitive-delay label frequently showed biochemical or clinical clues suggestive of an underlying organic disorder, and more than 75% improved after targeted mitochondrial-oriented supplementation. These findings support a more etiologic approach to selected ASD presentations rather than reliance on behavioral labeling alone.

Keywords: Autism spectrum disorder; Cognitive delay; Lactic acidosis; Mitochondrial disease; mitochondrial dysfunction; Whole-exome sequencing; Pediatrics; Lebanon