Dependence of indicators of the biochemical profile of children with psoriasis on the severity of the pathological process | Ukrainian Medical Journal

Murzina E.O.

Main
Publications
Dependence of indicators of the biochemical profile of children with psoriasis on the severity of the pathological process

Dependence of indicators of the biochemical profile of children with psoriasis on the severity of the pathological process

October 30, 2020

611

Dermatology and Venereology

Pediatrics

Murzina E.O.

Keywords :

children,

gamma-glutamyltransferase,

indices of psoriasis severity,

metabolic panel indicators,

psoriasis,

uric acid

Specialities :

Dermatology and Venereology

Pediatrics

Resume

Objective — to assess indicators of a metabolic panel in children with psoriasis depending on the severity of the disease process.

Materials and methods. A metabolic panel, including total protein level, total bilirubin, cholesterol, liver enzymes (alanine aminotransferase, aspartate aminotransferase, gamma-glutamyltransferase (GGT), triglycerides, low-density lipoproteins, creatinine, urea, uric acid (UA), was done in 108 children, who underwent inpatient treatment. PASI, BSA and PGA indices were calculated. Study records were statistically processed using the «Statistica 13.3» («StatSoft Inc.»).

Results. The analysis of metabolic panel results, obtained in children with psoriasis, revealed that the mean values (total bilirubin, cholesterol, alanine aminotransferase, aspartate aminotransferase, GGT, triglycerides, low-density lipoproteins, creatinine, urea, UA) remain within normal age limits, however make significant difference to identic indicators in children from the control group. In case of an increase in the PASI index in children with psoriasis, the level of UA increases as well, particularly in groups of children with PASI ranging from 10 to 20 and more than 20, the mean level of UA is significantly higher than the value in the control group and mean value in the group of children having PASI up to 10. With an increase in the PASI index, GGT levels rise as well, which, in groups of children with PASI varying from 10 to 20 and more than 20, makes a statistically significant difference to the same indicator in the control group, and in children with PASI higher than 20 — significantly higher than the values in other groups. After the intensification of psoriatic skin lesions (in accordance with the PGA index), mean GGT levels gradually increase, there is a statistically significant difference between the mean levels of serum GGT in children having 3–4-point PGA index and the indicator in controls. The highest mean value of UA was reported in children holding 3-point PGA index, significantly exceeding mean values in groups of children having 1–2- and 4-point PGA index. In the group of children with psoriasis, metabolic panel indicators did not make any statistical difference depending on the BSA index and can be comparable with indicators in the control group, except for GGT values. This indicator, in children with psoriasis of both groups, significantly exceeds the same indicator in controls according to the BSA index.

Conclusions. Regardless of metabolic panel results ranging within age limits, there are signs of impaired UA metabolism and the damage to hepatic cell membranes (as evidenced by increased GGT levels) and they become more intensive with an increase in the severity of the disease process, as well as lead to the durable exacerbation of psoriasis and the resistance to the medication prescribed.

References:

Aizyatulov R.F., Yukhimenko V.V. (2001) The importance of risk factors in the onset and course of psoriatic disease, Vest. Dermatol, 1: 41-43.
Butov Yu.S.,Vasenova V.Yu., Shmakova A.S. etc. (2009) Clinical and biochemistry status at patients with psoriasis and methods of its correction. Russian Journal of Skin and Sexually Transmitted Diseases., 5: 23-27.
Dyudyun A.D.Fedotov V.P., Polyon N.N., et al. (2009) Complex treatment of patients with psoriasis with the use of the medication Karsil®forte. Dermatovenereology. Cosmetology. Sexopathology, 12(1-2): 245-250.
Compendium (2020) Gout: Looking Ahead. Uric acid metabolism and pathogenesis of disorders (https://compendium.com.ua/tutorials/podagra/obmen-mochevoj-kisloty-i-patogenez-narushenij/).
Mamedov M.N. Manual on diagnostics and treatment of a metabolic syndrome. M.: Multiprint. 2005.
Rozumbaeva LP, Kozlova IV, Bykova AP. et al. (2014) Psoriasis and pathology of the hepatobiliary system: the relationship and mutual influence. Sovremennye problemy nauki i obrazovaniya, 4: 1–7.
Smirnova SV, Barilo AA, Smolnikova MV. (2016) Hepatobiliary System Diseases as the Predictors of Psoriasis Progression. Annals of the Russian Academy of Medical Sciences, 71(2): 102-108. doi: 10.15690/vramn636
Falko E.V., Khyshiktuev B.S. Metabolic disorders in psoriatic disease ttp://www.fesmu.ru/SITE/files/editor/file/dmj/2009/200902/200902_39.pdf
Khrustaleva E.A. (2001) The effectiveness of phosphogliv and moslecithin in the complex treatment of patients with psoriasis: author. dis. … D.
Shmakova A.S., Vasyenova V.Yu., Butov Yu.S. et al. (2010) Correction of cholesterol metabolism in patients with psoriasis. RGMU Bulletin, 4: 55–59.
Yakubovich A. I. (2011) Correction of violations of a lipidic exchange at patients with psoriasis. Russian Journal of Skin and Sexually Transmitted Diseases. 6: 29-32.
Akcali C., Buyukcelik B., Kirtak N. et al. (2014) Clinical and laboratory parameters associated with metabolic syndrome in Turkish patients with psoriasis. J. Int. Med. Res., 42(2): 386–394. doi.org/10.1177/0300060513502891.
Akhyani M., Ehsani A.H., Robati R.M., Robati A.M. (2007) The lipid profile in psoriasis: a controlled study. J. Eur. Acad. Dermatol. Venereol., 21(10): 1330–1332. doi.org/10.1111/j.1468-3083.2007.02260.x.
Aksu F., Caliskan M., Yilmaz Y. (2016) Gamma-glutamyltransferase and Markers of Subclinical Atherosclerosis in Patients with Psoriasis Kenan Demircioglu, Originally published. Arteriosclerosis, Thrombosis, and Vascular Biology, 36: A441.
Al-Mutairi N., Al-Farag S., Al-Mutairi A. et al. (2010) Comorbidities associated with psoriasis: an experience from the Middle East. J. Dermatol., 37: 146–155. doi.org/10.1111/j.1346-8138.2009.00777.x.
Augustin M., Glaeske G., Radtke M.A. et al. (2010) Epidemiology and comorbidity of psoriasis in children. Br. J. Dermatol., 162(3): 633–636. doi.org/10.1111/j.1365-2133.2009.09593.x.
Cassano N., Carbonara M., Panaro M. et al. (2011) Role of serum uric acid in conditioning the association of psoriasis with metabolic syndrome. Eur. J. Dermatol., 21: 808–809. doi.org/10.1684/ejd.2011.1478.
Christophers E. (2007) Comorbidities in psoriasis. Clin. Dermatol., 25(6): 529–534. doi.org/10.1016/j.clindermatol.2007.08.006.
Elmets C.A., Korman N.J., Prater E.F. et al. (2020) Joint AAD-NPF Guidelines of care for the management and treatment of psoriasis with topical therapy and alternative medicine modalities for psoriasis severity measures. Jul. 29. DOI:https://doi.org/10.1016/j.jaad.2020.07.087 jaad.2020.07.087.
Gisondi P., Targher G., Cagalli A. et al. (2014) Hyperuricemia in patients with chronic plaque psoriasis. J. Am. Acad. Dermatol., 70: 127–130. doi.org/10.1016/j.jaad.2013.09.005.
Gisondi P., Tessari G., Conti A. et al. (2007) Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case-control study. Clinical and laboratory investigations. Br. J. Dermatol., 157: 68–73. doi.org/10.1111/j.1365-2133.2007.07986.x.
Goldminz A.M., Buzney C.D., Kim N. et al. (2013) Prevalence of the metabolic syndrome in children with psoriatic disease. Pediatr. Dermatol., 30(6): 700–705. doi.org/10.1111/pde.12218.
Jones S.M., Harris C.P., Uoyd J. et al. (2008) Lipoproteins and their subfractions in psoriatic arthritis: identification of an atherogenic profile with active joint disease. Ann. Rheum. Dis., 59: 904–909.
Kural B.V., Orem A., Cimsit G. et al. (2003) Evaluation of the atherogenic tendency of lipids and lipoprotein content and their relationships with oxidant – antioxidant system in patients with psoriasis. Clin. Chimica Acta, 328: 71–82. doi.org/10.1016/s0009-8981(02)00373-x.
Lea W.A. Jr., Curtis A.C., Bernstein I.A. (1958) Serum uric acid levels in psoriasis. J. Invest. Dermatol., 31(5): 269–271.
Li X., Miao X., Wang H. et al. (2016) Association of Serum Uric Acid Levels in Psoriasis. A Systematic Review and Meta-Analysis. Medicine, 95(19): 1–8. doi.org/10.1097/md.0000000000003676.
Lonardo A., Romagnoli D. (2016) Gamma glutamyl transferase: а novel cardiovascular outfit for an old liver test. Indian J. Med. Res., 143(1): 4–7. doi: 10.4103/0971-5916.178574.
Loria P., Ballestri S., Lonardo A. (2008) Gli enzimi epatobiliari nella diagnostica clinica delle epatopatie. Intern. Emerg. Med., 3: 1–6.
Ma C., Harskamp C.T., Armstrong E.J., Armstrong A.W. (2013) The association between psoriasis and dyslipidaemia: a systematic review. Br. J. Dermatol., 168(3): 486–495. doi.org/10.1111/bjd.12101.
Mahe E., Maccari F., Beauchet A. et al. (2013) Childhood-onset psoriasis: association with future cardiovascular and metabolic comorbidities. Br. J. Dermatol., 169(4): 889–895. doi.org/10.1111/bjd.12441.
Mallbris L., Ritchlin C.T., Stahle M. (2006) Psoriasis is associated with lipid abnormalities at the onset of skin disease. J. Am. Acad. Dermatol., 54: 614–616. doi.org/10.1016/j.jaad.2005.11.1079.
Menter A., Cordoro K.M., Davis D.M.R. et al. (2020) Joint American Academy of Dermatology National Psoriasis Foundation guidelines of care for the management and treatment of psoriasis in pediatric patients. J. Am. Acad. Dermatol., 82(1): 161–201. doi.org/10.1016/j.jaad.2019.08.049.
Rocha-Pereira P., Santos-Silva A., Rebelo I. et al. (2001) Dislipidemia and oxidative stress in mild and in severe psoriasis as a risk for cardiovascular disease. Clin. Chim. Acta, 303(1–2): 33–39. doi.org/10.1016/s0009-8981(00)00358-2.
Tom W.L., Playford M.P., Admani S. et al. (2016) Characterization of lipoprotein composition and function in pediatric psoriasis reveals a more atherogenic profile. J. Invest. Dermatol., 136(1): 67–73. doi.org/10.1038/jid.2015.385.