M J Brito-Luna1, D G Villanueva-Quintero2, A K Sandoval-Talamantes3, M Fafutis-Morris4, O Graciano-Machuca5, P E Sanchez-Hernandez6, A Alvarado-Navarro7. 1. Jalisco Dermatology Institute "Dr. José Barba Rubio", Secretary of Health, Jalisco, Mexico, Av. Federalismo Norte 3102, Atemajac del Valle, CP 45190 Zapopan, Jalisco, Mexico. Electronic address: jbrito.lunapiel@gmail.com. 2. Jalisco Dermatology Institute "Dr. José Barba Rubio", Secretary of Health, Jalisco, Mexico, Av. Federalismo Norte 3102, Atemajac del Valle, CP 45190 Zapopan, Jalisco, Mexico. Electronic address: luviq_16@yahoo.com.mx. 3. Centre for Research in Immunology and Dermatology, Health Sciences University Centre, University of Guadalajara, Mexico, Av. Federalismo Norte 3102, Atemajac del Valle, CP 45190 Zapopan, Jalisco, Mexico. Electronic address: dra_talamantes@hotmail.com. 4. Centre for Research in Immunology and Dermatology, Health Sciences University Centre, University of Guadalajara, Mexico, Av. Federalismo Norte 3102, Atemajac del Valle, CP 45190 Zapopan, Jalisco, Mexico. Electronic address: mfafutis@gmail.com. 5. Centre for Research in Immunology and Dermatology, Health Sciences University Centre, University of Guadalajara, Mexico, Av. Federalismo Norte 3102, Atemajac del Valle, CP 45190 Zapopan, Jalisco, Mexico. Electronic address: omargmachuca@gmail.com. 6. Immunology Laboratory, Department of Physiology, Health Sciences University Centre, University of Guadalajara, México, Sierra Mojada 950, Col. Independencia, CP 44340 Guadalajara, Jalisco, Mexico. Electronic address: pedro.e.sanchez@gmail.com. 7. Centre for Research in Immunology and Dermatology, Health Sciences University Centre, University of Guadalajara, Mexico, Av. Federalismo Norte 3102, Atemajac del Valle, CP 45190 Zapopan, Jalisco, Mexico. Electronic address: bell2000_mx@yahoo.com.
Abstract
BACKGROUND: Psoriasis is an autoimmune skin disease characterised by proliferation of keratinocytes, primarily due to cytokines Th1 and Th17. This profile is involved in pathogenesis of metabolic syndrome, a frequently found comorbidity in patients with psoriasis. OBJECTIVE: In this study we determine the correlation of levels of pro-inflammatory cytokines TNF-α, IL-23, IL-12, and IL-22 in patients with psoriasis with and without metabolic syndrome and clinically healthy controls. METHODS: We included 55 patients with plaque psoriasis: 30 with metabolic syndrome (PPMS), 25 without metabolic syndrome (PP), 15 healthy subjects (HS) and 15 with metabolic syndrome (MS). Quantification of serum levels of IL-12, TNF-α, IL-22, and IL-23 was done by ELISA. RESULTS: We observed that serum levels of IL-12 were more elevated in PP group, while the lowest levels of TNF-α were seen in HS group. IL-22 was found to be higher in PP than in PPMS (p<0.05). PP patients with PASI scores rating as severe showed higher levels of IL-12. TNF-α level analysis showed significant differences in HS group compared with the others; levels of this cytokine were lower in patients with PP and moderate PASI scores than in MS group (p<0.05). We found no correlation between cytokine levels and psoriasis or between cytokines and PASI scores. In PP group, a positive correlation was observed between IL-23 and fasting glucose (r=0.432, p<0.05), as well as a negative correlation between IL-23, IL-22, and IL-12 versus waist circumference (r=-0.504, r=-0.556 and r=-0.511, respectively; p<0.05). CONCLUSIONS: Psoriasis is not just a skin disorder, but rather a condition with systemic implications, with intervention of pro-inflammatory cytokines that contribute to metabolic syndrome and other comorbidities, which in turn increases the risk of developing cardiovascular disease.
BACKGROUND:Psoriasis is an autoimmune skin disease characterised by proliferation of keratinocytes, primarily due to cytokines Th1 and Th17. This profile is involved in pathogenesis of metabolic syndrome, a frequently found comorbidity in patients with psoriasis. OBJECTIVE: In this study we determine the correlation of levels of pro-inflammatory cytokines TNF-α, IL-23, IL-12, and IL-22 in patients with psoriasis with and without metabolic syndrome and clinically healthy controls. METHODS: We included 55 patients with plaque psoriasis: 30 with metabolic syndrome (PPMS), 25 without metabolic syndrome (PP), 15 healthy subjects (HS) and 15 with metabolic syndrome (MS). Quantification of serum levels of IL-12, TNF-α, IL-22, and IL-23 was done by ELISA. RESULTS: We observed that serum levels of IL-12 were more elevated in PP group, while the lowest levels of TNF-α were seen in HS group. IL-22 was found to be higher in PP than in PPMS (p<0.05). PP patients with PASI scores rating as severe showed higher levels of IL-12. TNF-α level analysis showed significant differences in HS group compared with the others; levels of this cytokine were lower in patients with PP and moderate PASI scores than in MS group (p<0.05). We found no correlation between cytokine levels and psoriasis or between cytokines and PASI scores. In PP group, a positive correlation was observed between IL-23 and fasting glucose (r=0.432, p<0.05), as well as a negative correlation between IL-23, IL-22, and IL-12 versus waist circumference (r=-0.504, r=-0.556 and r=-0.511, respectively; p<0.05). CONCLUSIONS:Psoriasis is not just a skin disorder, but rather a condition with systemic implications, with intervention of pro-inflammatory cytokines that contribute to metabolic syndrome and other comorbidities, which in turn increases the risk of developing cardiovascular disease.