Skin barrier disorders in atopic dermatitis: from the history of the study to the development of «emollients plus»

Мұқаба

Дәйексөз келтіру

Толық мәтін

Ашық рұқсат Ашық рұқсат
Рұқсат жабық Рұқсат берілді
Рұқсат жабық Рұқсат ақылы немесе тек жазылушылар үшін

Аннотация

Background. Modern clinical guidelines for the treatment of patients with atopic dermatitis (AD) include the mandatory use of specialized dermatocosmetics - emollients (recommendation grade A), regardless of the severity of the process and the period of the disease (exacerbation, remission). During an exacerbation of AD, emollients are prescribed as part of complex therapy; during an remission, they can be used as a monotherapy. Objective. Evaluation of the effectiveness of complex therapy in patients with atopic dermatitis using a topical glucocorticosteroid (activity class 2) and Atopi Control products. Methods. The study included 27 patients aged 10 to 48 years (mean age 16.2±4.3 years) with AD in the acute stage with severe symmetrical erythema and itching on the forearms (modified SCORing Atopic Dermatitis (SCORAD) index 10.0±2.0). In accordance with clinical recommendations, all patients were prescribed a topical glucocorticosteroid (GCS) of the activity class 2, Atopi Control1 lotion 2 times a day on the right forearm and basic emollient2 2 times a day on the left forearm. After the exacerbation was removed (after 2 weeks), GCS was canceled, and patients continued to use emollients for 12 weeks. The number of relapses and the severity of symptoms at each exacerbation (local SCORAD) on the right and left hands were recorded, taking into account the presence of erythema, exudation, rash, excoriation, lichenification, and dry skin. The intensity of itching in the study area was assessed by patients using a visual analog scale (VAS) from 0 (no itching) to 10 (severe itching). Results. As a result of therapy, after 2 weeks the local SCORAD index decreased by 68%. In the control area (basic emollient application), the reduction in local SCORAD after 2 weeks was 45%. The number of relapses (persistent erythema for 3 or more days) in the Atopi Control group was 64% lower than in the basic emollient group (8 versus 22 reported exacerbations in 12 weeks), the severity of itching during exacerbations was also significantly lower in the Atopi Control group. All patients noted the comfort of using Atopi Control products, their excellent organoleptic properties. Conclusion. The inclusion of Atopi Control in therapy provides control over the course of AD: it quickly reduce the symptoms of the disease during exacerbations, reduce the number of relapses and their severity.

Толық мәтін

Рұқсат жабық

Авторлар туралы

L. Kruglova

Central State Medical Academy of the Administrative Department of the President of the Russian Federation

Moscow, Russia

D. Zaslavsky

St. Petersburg State Pediatric Medical University

St. Petersburg, Russia

N. Pereverzina

Central State Medical Academy of the Administrative Department of the President of the Russian Federation

Moscow, Russia

Yu. Sokolovskaya

LLC Baiersdorf

Moscow, Russia

Әдебиет тізімі

  1. Yoshida Т., Beck L. A., De Benedetto A. Skin barrier defects in atopic dermatitis: From old idea to new opportunity. Allergol Int. 2022;71(1):3-13. doi: 10.1016/j.alit.2021.11.006.
  2. Kramer O.N., Strom M.A., Ladizinski B., Lio PA. The history of atopic dermatitis. Clin Dermatol. 2017;35:344-48. Doi: 10.1016/j. clindermatol.2017.03.005.
  3. Barber H.W., Oriel G.H. A clinical and biochemical study of allergy. Lancet. 1928;212:1064-70.
  4. Rackemann F.M. Eczema. N Engl J Med. 1945;232:649-54.
  5. Blackfan K.D. Cutaneous reaction from proteins in eczema. Am J Dis Child. 1916;11:441-54.
  6. Ramirez M.A. Protein sensitization in eczema: report of seventy-eight cases. Arch Derm Syphilol. 1920;2:365-67.
  7. Hill L.W., Sulzberger M.B. Evolution of atopic dermatitis. Arch Derm Syphilol. 1935;32:451-63
  8. Alvaro M., Garcia-Paba M.B., Giner M.T., et al. Tolerance to egg proteins in egg-sensitized infants without previous consumption. Allergy. 2014;69:1350-56. doi: 10.1111/all.12483.
  9. Brough H.A., Simpson A., Makinson K., et al. Peanut allergy: effect of environmental peanut exposure in children with filaggrin loss-of-function mutations. J Allergy Clin Immunol. 2014;134:867-75. doi: 10.1016/j.jaci.2014.08.011.
  10. Brough H.A., Liu A.H., Sicherer S., et al. Atopic dermatitis increases the effect of exposure to peanut antigen in dust on peanut sensitization and likely peanut allergy. J Allergy Clin Immunol. 2015;135(1):164-70. Doi: 10.1016/j. jaci.2014.10.007.
  11. Brough H.A., Kull I., Richards K., et al. Environmental peanut exposure increases the risk of peanut sensitization in high- risk children. Clin Exp Allergy. 2018;48:586-93. Doi: 10.1111/ cea.13111.
  12. Abe Т., Ohkido M., Yamamoto K. Studies on skin surface barrier functions:- skin surface lipids and transepidermal water loss in atopic skin during childhood. J Dermatol. 1978;5:223-29. doi: 10.1111/j.1346-8138.1978.tb01857.x.
  13. Finlay A.Y, Nicholls S., King C.S., Marks R. The ‘dry' non-eczematous skin associated with atopic eczema. Br J Dermatol. 1980;103:249-56. doi: 10.1111/j.1365-2133.1980.tb07241.x.
  14. Agner T Susceptibility of atopic dermatitis patients to irritant dermatitis caused by sodium lauryl sulphate. Acta Derm Venereol. 1991;71:296-300.
  15. Winsor Т., Burch G.E. Differential roles of layers of human epigastric skin on diffusion rate of water. Arch Intern Med. 1944;74:428-36.
  16. Blank I.H. Further observations on factors which influence the water content of the stratum corneum. J Invest Dermatol. 1953;21:259-71. doi: 10.1038/jid.1953.100.
  17. Monash S., Blank H. Location and reformation of the epithelial barrier to water vapor. AMA. Arch Derm. 1958;78:710-14. Doi: 10.1001/ archderm.1958.01560120030005.
  18. Bosko C.A. Skin Barrier Insights: From Bricks and Mortar to Molecules and Microbes. J Drugs Dermatol. 2019;18(1s):S63-67.
  19. Wickett R.R., Visscher M.O. Structure and function of the epidermal barrier. Am J Infect Control. 2006;34(10):S98-110. Doi: 10.1016/j. ajic.2006.05.295.
  20. Otani Т., Nguyen T.P., Tokuda S., et al. Claudins and JAM-A coordinately regulate tight junction formation and epithelial polarity. J Cell Biol. 2019;218:3372-96. Doi: 10.1083/ jcb.201812157.
  21. Matsui T., Amagai M. Dissecting the formation, structure and bar- rier function of the stratum corneum.Int Immunol. 2015;27(6):269-80. doi: 10.1093/intimm/dxv013.
  22. Yokouchi M., Atsugi T., Logtestijn M.V., et al. Epidermal cell turnover across tight junctions based on Kelvin's tetra- kaidecahedron cell shape. Elife. 2016;5:е19593. Doi: 10.7554/ eLife.19593.
  23. Toulza E., Mattiuzzo N.R., Galliano M.F., et al. Large- scale identification of human genes implicated in epidermal barrier function. Genome Biol. 2007;8:R107. doi: 10.1186/gb-2007-8-6-r107.
  24. Kypriotou M., Huber M., Hohl D. The human epidermal differentiation com- plex: cornified envelope precursors, S100 proteins and the ‘fused genes' family. Exp Dermatol. 2012;21:643-49. doi: 10.1111/j.1600-0625.2012.01472.x.
  25. Sugiura H., Ebise H., Tazawa T., et al. Large-scale DNA microarray analysis of atopic skin lesions shows overexpression of an epidermal differentiation gene cluster in the alternative pathway and lack of protective gene expression in the cornified envelope. Br J Dermatol. 2005;152:146-49. doi: 10.1111/j.1365-2133.2005.06352.x.
  26. Ehrhardt P., Brandner Johanna M., Jens-Michael J. The skin: an indispensable barrier. Exp. Dermatol. 2008;17(12):1063- 72. doi: 10.1111/j.1600-0625.2008.00786.x.
  27. Круглова Л.С., Переверзина Н.О. Филаггрин: от истории открытия до применения модуляторов филаггрина в клинической практике (обзор литературы). Медицинский алфавит. 2021;27:8-12.
  28. Presland R.B., Boggess D., Lewis S.P., et al. Loss of normal profilaggrin and filaggrin in flaky tail (ft/ft) mice: an animal model for the filaggrin-deficient skin disease ichthyosis vulgaris. J Invest Dermatol. 2000;115:1072-81. doi: 10.1046/j.1523-1747.2000.00178.x.
  29. Brown S.J., Elias M.S., Bradley M. Genetics in atopic dermatitis: historical perspective and future prospects. Acta Derm Venereol. 2020;100:adv00163. doi: 10.2340/000155553513.
  30. Janssens M., van Smeden J., Puppels G.J., et al. Lipid to protein ratio plays an important role in the skin barrier function in patients with atopic eczema. Br J Dermatol. 2014;170:1248-55. doi: 10.1111/bjd.12908.
  31. Berdyshev E., Goleva E., Bronova I., et al. Lipid abnormalities in atopic skin are driven by type 2 cytokines. JCI. Insight. 2018;3:e98006. doi: 10.1172/jci.insight.98006.
  32. Горский В.С., Блюмина В.А. Современные представления о патогенезе атопического дерматита. Иммунопатология, Аллергология, Инфектология. 2022;3:71.
  33. Roggenkamp D., Falkner S., Stab F., et al. Atopic keratinocytes induce increased neurite outgrowth in a coculture model of porcine dorsal root ganglia neurons and human skin cells. J Invest Dermatol. 2012;132:1892-900. Doi: 10.1038/ jid.2012.44.
  34. EADV Congress 2020. Virtual. Poster №PO241
  35. IAngelova-Fischer G., Neufang K., Jung T.W., et al. Department of Dermatology, University of Lubeck, Lubeck, Germany, Beiersdorf AG, Hamburg, Germany. JEADV. 2014;28(Suppl. 3):9-15.
  36. EADV Congress 2020. Virtual. Poster №PO232.
  37. Study results presented as poster presentation at the European Academy of Dermatology and Venereology 2015 (EADV 2015) Standalone Emollient Treatment Reduces Flares After Discontinuation of Topical Steroid Treatment in Atopic Dermatitis: A Double-blind, Randomized, Vehicle-controlled, Left-right Comparison Study.

Қосымша файлдар

Қосымша файлдар
Әрекет
1. JATS XML
Жүктеу

© Bionika Media, 2022

Осы сайт cookie-файлдарды пайдаланады

Біздің сайтты пайдалануды жалғастыра отырып, сіз сайттың дұрыс жұмыс істеуін қамтамасыз ететін cookie файлдарын өңдеуге келісім бересіз.< / br>< / br>cookie файлдары туралы< / a>