Apolipoprotein E gene polymorphism, serum lipids, and risk of superficial fungal infections in Egyptian patients - A preliminary case-controlled study

• Main Authors: Amany I Mustafa (Author), Ghada M Shams (Author), Eman M Fawzy (Author), Naglaa F Alhusseini (Author), Rana A Khashaba (Author), Ola S EL-Shimi (Author)
• Format: Book
• Published: Wolters Kluwer Medknow Publications, 2023-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 0019-5154; 1998-3611; 10.4103/ijd.ijd_1001_22
• Keywords: apolipoprotein e; gene polymorphism; superficial fungal infections; Dermatology; RL1-803
• Source: Indian Journal of Dermatology, Vol 68, Iss 2, Pp 233-233 (2023)

Background: Apolipoprotein E (APOE) gene isoforms have been found to affect the risk of superficial fungal infections (SFIs). However, the data only cover a few ethnicities. Aims: The present work intended to investigate the association of APOE gene polymorphism and serum lipids with the susceptibility of SFIs among a group of Egyptian patients. Materials and Methods: Standard laboratory methods were used to estimate the serum lipid profile, and polymerase chain reaction-restriction fragment length polymorphism was used to detect APOE gene polymorphism in deoxyribonucleic acid extracted from 150 SFI patients and an equal number of apparently healthy matched controls. Results: Serum total cholesterol, triglycerides, and low-density lipoprotein cholesterol were significantly higher in the studied patients than in controls. The APOE gene ε2, ε4 alleles, and ε3/4 and ε3/2 genotypes were significantly distributed in the patients than in the controls. APOE ε3/3 genotype was predominant in dermatophytosis and tinea versicolour patients, and ε3/4 genotype was predominant in candidiasis. Conclusions: ApoE alleles ε2 and ε4, and genotypes ε2/3 and ε3/4 are linked to SFI and may be risk factors, whereas allele ε3 and genotype ε3/3 may be protective for SFI in the Egyptian population studied. The lipid profile results suggest that hyperlipidemia may provide evidence for SFI pathogenesis. However; further large-scale studies are still needed to validate our results.