Альманах клинической медицины. 2018; 46: 522-530
Парадоксальная псориазиформная воспалительная реакция на фоне применения блокаторов фактора некроза опухоли-альфа у пациентов с болезнью Крона (обзор литературы, описание двух клинических наблюдений)
https://doi.org/10.18786/2072-0505-2018-46-5-522-530Аннотация
У пациентов с воспалительными заболеваниями кишечника псориазиформные высыпания (парадоксальное воспаление), индуцированные блокаторами фактора некроза опухоли-альфа (ФНО-α), встречаются примерно в 5–10% случаев на фоне применения этих генно-инженерных препаратов. К предикторам относят гендерный признак (преимущественно женщины), курение, повышенный индекс массы тела, образование антинейтрофильных антител. При этом отсутствует корреляция парадоксального воспаления с конкретным препаратом (возникновение высыпаний возможно при применении любого блокатора ФНО-α: инфликсимаба, адалимумаба или цертолизумаба пэгола). При развитии медикаментозно индуцированного псориаза первой линией терапии считаются топические кортикостероиды (преимущественно сильной активности: клобетазол, бетаметазон) и комбинированные с ними препараты (бетаметазон в сочетании с кальципотриолом). При неэффективности терапии или повторном появлении высыпаний на фоне применения блокаторов ФНО-α высыпания расцениваются как класс-специфический эффект, и рассматривается вопрос о переходе на препарат генно-инженерной биологической терапии с иным механизмом действия. В этом случае наиболее показано применение устекинумаба. Несмотря на относительно высокую встречаемость парадоксального воспаления на фоне применения блокаторов ФНО-α и большой массив опубликованных данных, ряд вопросов остаются открытыми. В частности, изучению подлежат сроки развития высыпаний в случае уже достигнутого клинически значимого эффекта блокаторов ФНО-α в отношении симптомов воспалительных заболеваний кишечника, а значит, и возможность отмены препарата и смены тактики ведения, а также долгосрочный прогноз кожного процесса. В этой связи описание случаев из клинической практики и накопленный опыт помогут в дальнейшем актуализировать клинические рекомендации по тактике ведения данной категории пациентов.
Список литературы
1. Bernstein CN, Blanchard JF, Rawsthorne P, Yu N. The prevalence of extraintestinal diseases in inflammatory bowel disease: a population-based study. Am J Gastroenterol. 2001 ;96(4):1116-22. doi: 10.1111/j.1572-0241.2001.03756.x.
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9. de Gannes GC, Ghoreishi M, Pope J, Russell A, Bell D, Adams S, Shojania K, Martinka M, Dutz JP. Psoriasis and pustular dermatitis triggered by TNF-{alpha} inhibitors in patients with rheumatologic conditions. Arch Dermatol. 2007;143(2):223-31. doi: 10.1001/archderm.143.2.223.
10. Brown G, Wang E, Leon A, Huynh M, Wehner M, Matro R, Linos E, Liao W, Haemel A. Tumor necrosis factor-а inhibitor-induced psoriasis: Systematic review of clinical features, histopathological findings, and management experience. J Am Acad Dermatol. 2017;76(2): 334-41. doi: 10.1016/j.jaad.2016.08.012.
11. Guerra I, Perez-Jeldres T, Iborra M, Algaba A, Monfort D, Calvet X, Chaparro M, Manosa M, Hinojosa E, Minguez M, Ortiz de Zarate J, Marquez L, Prieto V, Garcia-Sanchez V, Guardiola J, Rodriguez GE, Martin-Arranz MD, Garcia-Tercero I, Sicilia B, Masedo A, Lorente R, Rivero M, Fernandez-Salazar L, Gutierrez A, Van Domselaar M, Lopez-SanRoman A, Ber Y, Garcia-Sepulcre M, Ramos L, Bermejo F, Gisbert JP; Spanish GETECCU group (ENEIDA pro-ject). Incidence, Clinical Characteristics, and Management of Psoriasis Induced by Anti-TNF Therapy in Patients with Inflammatory Bowel Disease: A Nationwide Cohort Study. Inflamm Bowel Dis. 2016;22(4):894-901. doi: 10.1097/MIB.0000000000000757.
12. Freling E, Baumann C, Cuny JF, Bigard MA, Schmutz JL, Barbaud A, Peyrin-Biroulet L. Cumulative incidence of, risk factors for, and outcome of dermatological complications of anti-TNF therapy in inflammatory bowel disease: a 14-year experience. Am J Gastro-enterol. 2015;110(8):1186-96. doi: 10.1038/ajg.2015.205.
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14. Conrad C, Di Domizio J, Mylonas A, Belkhodja C, Demaria O, Navarini AA, Lapointe AK, French LE, Vernez M, Gilliet M. TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis. Nat Commun. 2018;9(1):25. doi: 10.1038/s41467-017-02466-4.
15. Basavaraj KH, Ashok NM, Rashmi R, Praveen TK. The role of drugs in the induction and/or exacerbation of psoriasis. Int J Dermatol. 2010;49(12):1351-61. doi: 10.1111/j.1365-4632.2010.04570.x.
16. Mrowietz U, Domm S. Systemic steroids in the treatment of psoriasis: what is fact, what is fiction? J Eur Acad Dermatol Venereol. 2013;27(8):1022-5. doi: 10.1111/j.1468-3083.2012.04656.x.
17. Tsankov N, Angelova I, Kazandjieva J. Drug-in-duced psoriasis. Recognition and management. Am J Clin Dermatol. 2000;1(3):159-65.
18. Dika E, Varotti C, Bardazzi F, Maibach HI. Drug-induced psoriasis: an evidence-based overview and the introduction of psoriatic drug eruption probability score. Cutan Ocul Toxicol. 2006;25(1):1-11. doi: 10.1080/15569520500536568.
19. Rongioletti F, Fiorucci C, Parodi A. Psoriasis induced or aggravated by drugs. J Rheumatol Suppl. 2009;83:59-61. doi: 10.3899/jrheum.090227.
20. Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol. 2007;25(6):606-15. doi: 10.1016/j.clindermatol.2007.08.015.
21. Naranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA, Janecek E, Domecq C, Greenblatt DJ. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30(2):239-45. doi: 10.1038/clpt.1981.154.
22. Kim GK, Del Rosso JQ. Drug-provoked psoriasis: is it drug induced or drug aggravated?: understanding pathophysiology and clinical relevance. J Clin Aesthet Dermatol. 2010;3(1):32-8.
23. Armstrong AW. Psoriasis provoked or exacerbated by medications: identifying culprit drugs. JAMA Dermatol. 2014;150(9):963. doi: 10.1001/jamadermatol.2014.1019.
24. Di Meglio P, Villanova F, Navarini AA, Mylonas A, Tosi I, Nestle FO, Conrad C. Targeting CD8(+) T cells prevents psoriasis development. J Allergy Clin Immunol. 2016;138(1): 274-6.e6. doi: 10.1016/j.jaci.2015.10.046.
25. Malkonen T, Wikstrom A, Heiskanen K, Merras-Salmio L, Mustonen H, Sipponen T, Kolho KL. Skin reactions during anti-TNFa therapy for pediatric inflammatory bowel disease: a 2-year prospective study. Inflamm Bowel Dis. 2014;20(8):1309-15. doi: 10.1097/MIB.0000000000000088.
26. Harbord M, Annese V, Vavricka SR, Allez M, Barreiro-de Acosta M, Boberg KM, Burisch J, De Vos M, De Vries AM, Dick AD, Juillerat P, Karlsen TH, Koutroubakis I, Lakatos PL, Orchard T, Papay P, Raine T, Reinshagen M, Thaci D, Tilg H, Carbonnel F; European Crohn's and Colitis Organisation. The First European Evidence-based Consensus on Extraintestinal Manifestations in Inflammatory Bowel Disease. J Crohns Colitis. 2016;10(3):239-54. doi: 10.1093/ecco-jcc/jjv213.
Almanac of Clinical Medicine. 2018; 46: 522-530
Paradoxical psoriasiform inflammatory reaction during the use of tumor necrosis factor-alpha inhibitors in patients with Crohn’s disease (a review of the literature and presentation of two clinical cases)
https://doi.org/10.18786/2072-0505-2018-46-5-522-530Abstract
Psoriasiform rash (paradoxical inflammation) induced by tumor necrosis factor-alpha (TNFα) inhibitors is observed in about 5–10% of patients with inflammatory bowel diseases treated by these genetically engineered agents. Its predictors include gender (mostly female), smoking, higher body mass index, and formation of anti-neutrophil antibodies. There is no correlation between the paradoxical inflammation and specific agent; the rash can develop with the use of any TNFα inhibitor, such as infliximab, adalimumab, or certolizumab pegol. The first line of treatment for pharmacologically induced psoriasis includes topical corticosteroids (mostly, high potency agents clobetasol and betamethasone) and combination steroid-containing agents (betamethasone + calcipotriol). If this treatment is ineffective or the rash recurs during the use of TNFα inhibitors, the rash is qualified as a class-specific effect, with consideration of switching the patient to a genetically engineered product with another mechanism of action. In such a case, there is a strong indication for ustekinumab. Despite a relatively high incidence of the paradoxical inflammation with TNFα inhibitors and a bulk of published data, some questions remain unanswered. In particular, further studiesare required into the time intervals between the achievement of a clinically significant effect of TNFα inhibitors on the symptoms of inflammatory bowel diseases and the skin rash formation, which means the possibility of treatment withdrawal and change of the treatment strategy, as well as studies on the long-term prognosis of the skin lesions. In this context, clinical case presentation and the accumulated experience would subsequently help to formulate actual clinical recommendations on the management of this patient category.
References
1. Bernstein CN, Blanchard JF, Rawsthorne P, Yu N. The prevalence of extraintestinal diseases in inflammatory bowel disease: a population-based study. Am J Gastroenterol. 2001 ;96(4):1116-22. doi: 10.1111/j.1572-0241.2001.03756.x.
2. Rankin GB, Watts HD, Melnyk CS, Kelley ML Jr. National Cooperative Crohn's Disease Study: extraintestinal manifestations and perianal complications. Gastroenterology. 1979;77(4 Pt 2):914-20.
3. Su CG, Judge TA, Lichtenstein GR. Extraintestinal manifestations of inflammatory bowel disease. Gastroenterol Clin North Am. 2002;31(1): 307-27. doi: 10.1016/S0889-8553(01)00019-X.
4. Lowes MA, Suarez-Farinas M, Krueger JG. Immunology of psoriasis. Annu Rev Immunol. 2014;32:227-55. doi: 10.1146/annurevimmunol-032713-120225.
5. Potekaev NN, Kruglova LS. Psoriaticheskaya bolezn'. M.: MDV; 2014. 264 s.
6. Kneilling M, Mailhammer R, Hultner L, Schonberger T, Fuchs K, Schaller M, Bukala D, Massberg S, Sander CA, Braumuller H, Eichner M, Maier KL, Hallmann R, Pichler BJ, Haubner R, Gawaz M, Pfeffer K, Biedermann T, Rocken M. Direct crosstalk between mast cell-TNF and TNFR1-expressing endothelia mediates local tissue inflammation. Blood. 2009;114(8):1696- 706. doi: 10.1182/blood-2008-11-187682.
7. Taylor PC, Feldmann M. Anti-TNF biologic agents: still the therapy of choice for rheumatoid arthritis. Nat Rev Rheumatol. 2009;5(10): 578-82. doi: 10.1038/nrrheum.2009.181.
8. Burmester GR, Panaccione R, Gordon KB, Mcllraith MJ, Lacerda AP. Adalimumab: long-term safety in 23 458 patients from global clinical trials in rheumatoid arthritis, juvenile idiopathic arthritis, ankylosing spondylitis, psoriatic arthritis, psoriasis and Crohn's disease. Ann Rheum Dis. 2013;72(4):517-24. doi: 10.1136/annrheumdis-2011-201244.
9. de Gannes GC, Ghoreishi M, Pope J, Russell A, Bell D, Adams S, Shojania K, Martinka M, Dutz JP. Psoriasis and pustular dermatitis triggered by TNF-{alpha} inhibitors in patients with rheumatologic conditions. Arch Dermatol. 2007;143(2):223-31. doi: 10.1001/archderm.143.2.223.
10. Brown G, Wang E, Leon A, Huynh M, Wehner M, Matro R, Linos E, Liao W, Haemel A. Tumor necrosis factor-a inhibitor-induced psoriasis: Systematic review of clinical features, histopathological findings, and management experience. J Am Acad Dermatol. 2017;76(2): 334-41. doi: 10.1016/j.jaad.2016.08.012.
11. Guerra I, Perez-Jeldres T, Iborra M, Algaba A, Monfort D, Calvet X, Chaparro M, Manosa M, Hinojosa E, Minguez M, Ortiz de Zarate J, Marquez L, Prieto V, Garcia-Sanchez V, Guardiola J, Rodriguez GE, Martin-Arranz MD, Garcia-Tercero I, Sicilia B, Masedo A, Lorente R, Rivero M, Fernandez-Salazar L, Gutierrez A, Van Domselaar M, Lopez-SanRoman A, Ber Y, Garcia-Sepulcre M, Ramos L, Bermejo F, Gisbert JP; Spanish GETECCU group (ENEIDA pro-ject). Incidence, Clinical Characteristics, and Management of Psoriasis Induced by Anti-TNF Therapy in Patients with Inflammatory Bowel Disease: A Nationwide Cohort Study. Inflamm Bowel Dis. 2016;22(4):894-901. doi: 10.1097/MIB.0000000000000757.
12. Freling E, Baumann C, Cuny JF, Bigard MA, Schmutz JL, Barbaud A, Peyrin-Biroulet L. Cumulative incidence of, risk factors for, and outcome of dermatological complications of anti-TNF therapy in inflammatory bowel disease: a 14-year experience. Am J Gastro-enterol. 2015;110(8):1186-96. doi: 10.1038/ajg.2015.205.
13. Tillack C, Ehmann LM, Friedrich M, Laubender RP, Papay P, Vogelsang H, Stallhofer J, Beigel F, Bedynek A, Wetzke M, Maier H, Koburger M, Wagner J, Glas J, Diegelmann J, Koglin S, Dombrowski Y, Schauber J, Wollenberg A, Brand S. Anti-TNF antibody-induced psoriasiform skin lesions in patients with inflammatory bowel disease are characterised by interferon-y-expressing Th1 cells and IL-17A/IL-22-expressing Th17 cells and respond to anti-IL-12/IL-23 antibody treatment. Gut. 2014;63(4):567-77. doi: 10.1136/gutjnl-2012-302853.
14. Conrad C, Di Domizio J, Mylonas A, Belkhodja C, Demaria O, Navarini AA, Lapointe AK, French LE, Vernez M, Gilliet M. TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis. Nat Commun. 2018;9(1):25. doi: 10.1038/s41467-017-02466-4.
15. Basavaraj KH, Ashok NM, Rashmi R, Praveen TK. The role of drugs in the induction and/or exacerbation of psoriasis. Int J Dermatol. 2010;49(12):1351-61. doi: 10.1111/j.1365-4632.2010.04570.x.
16. Mrowietz U, Domm S. Systemic steroids in the treatment of psoriasis: what is fact, what is fiction? J Eur Acad Dermatol Venereol. 2013;27(8):1022-5. doi: 10.1111/j.1468-3083.2012.04656.x.
17. Tsankov N, Angelova I, Kazandjieva J. Drug-in-duced psoriasis. Recognition and management. Am J Clin Dermatol. 2000;1(3):159-65.
18. Dika E, Varotti C, Bardazzi F, Maibach HI. Drug-induced psoriasis: an evidence-based overview and the introduction of psoriatic drug eruption probability score. Cutan Ocul Toxicol. 2006;25(1):1-11. doi: 10.1080/15569520500536568.
19. Rongioletti F, Fiorucci C, Parodi A. Psoriasis induced or aggravated by drugs. J Rheumatol Suppl. 2009;83:59-61. doi: 10.3899/jrheum.090227.
20. Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol. 2007;25(6):606-15. doi: 10.1016/j.clindermatol.2007.08.015.
21. Naranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA, Janecek E, Domecq C, Greenblatt DJ. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30(2):239-45. doi: 10.1038/clpt.1981.154.
22. Kim GK, Del Rosso JQ. Drug-provoked psoriasis: is it drug induced or drug aggravated?: understanding pathophysiology and clinical relevance. J Clin Aesthet Dermatol. 2010;3(1):32-8.
23. Armstrong AW. Psoriasis provoked or exacerbated by medications: identifying culprit drugs. JAMA Dermatol. 2014;150(9):963. doi: 10.1001/jamadermatol.2014.1019.
24. Di Meglio P, Villanova F, Navarini AA, Mylonas A, Tosi I, Nestle FO, Conrad C. Targeting CD8(+) T cells prevents psoriasis development. J Allergy Clin Immunol. 2016;138(1): 274-6.e6. doi: 10.1016/j.jaci.2015.10.046.
25. Malkonen T, Wikstrom A, Heiskanen K, Merras-Salmio L, Mustonen H, Sipponen T, Kolho KL. Skin reactions during anti-TNFa therapy for pediatric inflammatory bowel disease: a 2-year prospective study. Inflamm Bowel Dis. 2014;20(8):1309-15. doi: 10.1097/MIB.0000000000000088.
26. Harbord M, Annese V, Vavricka SR, Allez M, Barreiro-de Acosta M, Boberg KM, Burisch J, De Vos M, De Vries AM, Dick AD, Juillerat P, Karlsen TH, Koutroubakis I, Lakatos PL, Orchard T, Papay P, Raine T, Reinshagen M, Thaci D, Tilg H, Carbonnel F; European Crohn's and Colitis Organisation. The First European Evidence-based Consensus on Extraintestinal Manifestations in Inflammatory Bowel Disease. J Crohns Colitis. 2016;10(3):239-54. doi: 10.1093/ecco-jcc/jjv213.
