Background: Epidermal growth factor (EGF) plays a crucial role in cellular growth, differentiation, and pancreatic β-cell maintenance. Despite reports on EGF deficiency in diabetic animal models, its relevance in type 2 diabetes (T2D), particularly in relation to obesity, remains underexplored. The present study aimed to evaluate plasma EGF levels in individuals with and without T2D, assess its associations with glycaemic status and clinical parameters, and evaluate the influence of obesity on these relationships. Methods: A total of 838 eligible participants were selected from the Kuwait Diabetes Epidemiology Program. Of those, 428 were included in a 1:1 case–control analysis (214 T2D and 214 non-diabetics). EGF was measured in plasma using ELISA. Associations between EGF with glycaemic and clinical variables were evaluated using Pearson’s correlation, multiple linear regression, and logistic regression analyses. Results: Plasma EGF levels were significantly lower in individuals with T2D compared to non-diabetics (P < 0.001). Among non-diabetics, obese participants had a significantly lower EGF level than their non-obese counterparts (P = 0.03), while no such difference was observed in T2D. EGF negatively correlated with fasting blood glucose in both non-diabetics (P = 0.004) and T2D individuals (P < 0.001). In T2D, EGF negatively correlated with haemoglobin A1C (HbA1C) (P = 0.001), triglyceride (TG) (P = 0.021), and waist-to-hip ratio (WHR) (P = 0.014). Logistic regression confirmed that lower EGF levels were independently associated with T2D but not with general obesity (OR = 0.996, P = 0.001). Conclusion: Reduced EGF levels are associated with poor glycaemic control in T2D. These findings highlight EGF’s potential as a biomarker for glycaemic dysregulation and support further investigation into its role in diabetes pathophysiology and complications.
This study was conducted as part of a larger cross-sectional investigation of the microbiological profile of adults with atopic dermatitis (AD) in Kuwait.
30 October 2026 in Journal of International Medical Research
Objectives: To investigate the prevalence of nasal methicillin-resistant Staphylococcus aureus (MRSA) colonization among adults with atopic dermatitis and explore its association with disease severity. Methods: This cross-sectional study included 100 adults (≥18 years) with dermatologist-confirmed atopic dermatitis who attended dermatology outpatient clinics in Kuwait. Patients with nonatopic eczema, major systemic illnesses, or skin malignancy were excluded. Disease severity was assessed using the validated Investigator’s Global Assessment for Atopic Dermatitis. Nasal swabs were collected, and S. aureus isolates were identified using culture, Gram staining, and catalase and coagulase tests, followed by confirmation using the VITEK® 2 system. Methicillin resistance (mecA) and selected staphylococcal virulence genes, including the classical ( sea , seb , sec , sed, and see ) and nonclassical staphylococcal enterotoxins ( seg , seh, and sei ), Panton–Valentine leukocidin ( pvl ), and toxic shock syndrome toxin-1 ( tsst-1 ) were determined using polymerase chain reaction. Antimicrobial susceptibility profiles were assessed using the Clinical and Laboratory Standards Institute disk diffusion method. Results: S. aureus colonization is a key feature of atopic dermatitis and is closely associated with disease activity. This study investigated the prevalence of nasal MRSA colonization among adults with atopic dermatitis and examined its association with disease severity and virulence gene carriage. Overall, 53% of patients were colonized with S. aureus , of whom 71.7% carried MRSA. MRSA colonization was significantly associated with older age and greater disease severity. Virulence gene analysis in MRSA isolates revealed higher frequency of seg and sei , whereas the presence of sea and tsst-1 were significantly associated with more severe atopic dermatitis. Conclusions: Adults with atopic dermatitis showed a high prevalence of nasal MRSA colonization. The predominance of enterotoxin gene cluster genes and the association of sea and tsst-1 with greater disease severity highlight the potential clinical importance of nasal MRSA as a reservoir of virulent strains in atopic dermatitis.