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The purpose of this study was to determine the risk factors and prevalence of vitiligo in the Saudi population. A comprehensive computerized search of pertinent databases was carried out to find research that satis- fied the requirements of inclusion. To locate relevant studies, PubMed, SCOPUS, Science Direct, Cochrane Library, and Web of Science were all searched. The prevalence of vitiligo among the Saudi population ranged from 0% among school children to 7%. The results indicated that genetic factors, such as family history and parental consanguinity, contribute significantly to the vitiligo prevalence in Saudi Arabia. Localized vitiligo was the most common form, with stress identified as a key trigger for disease progression. Consanguinity in marriages further increased disease prevalence, highlighting the need for genetic counseling and public awareness programs to reduce the impact of vitiligo. This study emphasized the contribution of stress and genetic predisposition to the development of vitiligo in the Saudi population. By focusing on these factors, healthcare providers can improve prevention and management strategies through genetic counseling, stress management, and community education. However, future research with more extensive population data and deeper exploration of various risk factors is essential to refine these strategies and enhance patient care. [ABSTRACT FROM AUTHOR]

One of the most common inborn errors in fatty acid β oxidation (FAO) is a very long-chain acyl-coenzyme A dehydrogenase (VLCAD) deficiency. It is autosomal recessive. The enzyme used in the first phase of FAO is VLCAD. The enzyme is responsible for β oxidation spiral pathway's initial step, the dehydrogenation process of long-chain fatty acyl-CoA. The phenotypes include hypoglycemia, hepatomegaly, cardiomyopathy, and occasionally abrupt mortality. Most VLCAD deficiencies in newborns are now detected during the neonatal period due to the development of newborn screening programs. Mitochondrial DNA depletion syndromes (MTDPS) are one of the rarest metabolic disorders. It is an autosomal recessive disease caused by defects in genes necessary for the maintenance of mitochondrial DNA (mtDNA). One of these FBXL4 (F-box and leucine-rich repeat protein 4) variants causes encephalomyopathic mtDNA depletion syndrome 13 (MTDPS13), which presents as a failure to thrive, severe global developmental delay, hypotonia, early infantile onset of encephalopathy, and lactic acidosis. We report here the case of a Saudi infant born to consanguineous parents who presented to us with severe failure to thrive, profound neurodevelopmental delays, and facial dysmorphic features. Whole-exome sequencing (WES) showed the infants had MTDPS13. The FBXL4 variant c.1698A > G p. (Ile566Met) has previously been described as a disease that causes developmental delay and lactic acidosis, and another variant has also been detected in the patient. The ACADVL variant c.134C > A p. (Ser45*) has previously been described to cause VLCAD deficiency. A comprehensive literature review showed our patient to be the first case of MTDPS13 and VLCAD reported to date worldwide. [ABSTRACT FROM AUTHOR]