Ponad 7000 publikacji medycznych!
Statystyki za 2021 rok:
odsłony: 8 805 378
Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19

Poniżej zamieściliśmy fragment artykułu. Informacja nt. dostępu do pełnej treści artykułu tutaj
© Borgis - Postępy Nauk Medycznych 10/2012, s. 806-810
Marek Kot, Anna Sysa-Jędrzejowska, *Anna Woźniacka
Alergia kontaktowa na preparaty glikokortykosteroidowe
Contact allergy to corticosteroids**
Department of Dermatology and Venereology, Medical University of Łódź
Head od Department: prof. Anna Sysa-Jędrzejowska, MD, PhD
Streszczenie
Glikokortykosteroidy zaliczają się do najpopularniejszych środków leczniczych stosowanych we współczesnej medycynie. Alergia kontaktowa na glikokortykosteroidy stanowi duże wyzwanie diagnostyczne i terapeutyczne, bowiem właściwości farmakologiczne (przeciwzapalne, immunosupresyjne) tych substancji często maskują ich zdolność do wywoływania reakcji nadwrażliwości kontaktowej. Reakcja nadwrażliwości kontaktowej na hapteny jest klasycznym przykładem immunologicznej reakcji komórkowej występującej wskutek nadwrażliwości typu IV wg klasyfikacji Gella i Coombsa. Za efektywną metodę diagnozy alergii kontaktowej uznawane są naskórkowe testy płatkowe. Nadwrażliwość na glikokortykosteroidy występuje coraz częściej. Steroidy znajdują zastosowanie w dermatologii w wielu różnych dermatozach, głównie przewlekłych i powiązanych z nawracającymi stanami zapalnymi, takimi jak atopowe zapalenie skóry czy egzema. Zdiagnozowanie alergii kontaktowej na glikokortykosteroidy zwiększa szansę na zupełną remisję i poprawia jakość życia pacjenta. Niniejsza praca skupia się na aktualnym stanie wiedzy o alergii kontaktowej na glikokortykosteroidy, które uznano za alergeny roku 2005.
Summary
Glucocorticosteroids are among the most important and popular therapeutic agents in contemporary medicine. Contact allergy to corticosteroids is considered to be a significant diagnostic and therapeutic problem, because pharmacological (anti-inflammatory, immunosuppressive) properties of these agents often mask their ability to induce contact sensitivity reaction. The contact sensitivity reaction to haptens is a classical example of cell-mediated immune response, resulting from type IV hypersensitivity according to Gell and Coombs classification. Patch tests are considered to be the golden standard in the diagnosis of contact allergy. Sensitivity to corticosteroids is characterized with an increasing incidence. In dermatology steroids are applied in many different dermatoses, mainly in those with chronic and recurrent inflammatory origin, like atopic dermatitis or eczema. Diagnosis of contact allergy to corticosteroids increases chances for achieving complete remission and improves patients „quality of life”. The review focuses on the current knowledge about contact allergy to corticosteroids which has been classified as allergens of the year 2005.
Allergic contact eczema named also allergic contact dermatitis (Latin: contact dermatitis, contact eczema) develops after a direct contact with an allergen. Clinically, two types of disease can be distinguished: an acute type (Latin: contact dermatitis acuta, eczema acutum) and a chronic type (contact dermatitis chronic, eczema chronicum) (1).
Most of the allergens evoking the disease are characterized by a low molecular weight (lower than 1000 daltons). Contact allergens are haptens, which acquire a full antigenic capacity only after binding themselves with protein in the skin. From the clinical point of view, an important factor of developing a contact allergy is a fully preserved correct function of the epidermal barrier. Mechanical damages of the epidermis, maceration, dryness, inflammation are the causes of increased hapten penetration into the skin. Occlusive bandages are factors facilitating the penetration.
Allergic contact dermatitis is a result from type IV hypersensitivity according to Gell and Coombs classification. Its development consists of two phases: induction and release. During the induction phase haptens bind in the extravascular space with serum proteins creating an immunological complex, which is then presented by the Langerhans cells to Th1 lymphocytes in the surrounding lymph glands. This presentation occurs with the participation of the MHC histocompatibility antigens of the II class. This leads to the formation of the specific memory Th1 lymphocytes for the presented haptens. During the next contact with a given allergen, after at least 24-48 hours, the release phase starts, which activates the specific memory Th1 lymphocytes producing the proinflammatory cytokines, such as IL-2, IFN-γ and TNF-α (2). The released cytokines are responsible for the activation and migration of the allergic reaction cells including cytotoxic lymphocytes, macrophages and neutrophiles. Keratinocytes also take part in this reaction. Keratinocytes have ICAM-1 adhesive molecules on their surface, which are ligands for the LFA-1 cell receptors of leucocytes. Keratinocytes not only present MHC class II antigens on their surface and produce Il-1 and TNF-α, but also stimulate the inflammatory reaction (3, 4). The release of inflammation mediators and the activation of allergic reaction cells induce epidermal spongiosis and the development of local inflammation. After some time the effector phase is placated by the Treg 1 lymphocytes, which produce Il-10 (5). The antibodies do not play any role in the reaction initiation, which distinguishes contact allergy from other types of allergic reactions.
Oversensitivity to allergens depend on many overlapping factors. On one hand, skin inflammation may cause the development of contact oversensitivity to different antigens. On the other hand, the intolerance of some factors correlates with polyvalent contact allergy shown in patch tests. According to some authors, contact allergy to three or more antigens defines the contact allergy polyvalence. Genetic factors affect this phenomenon (6).
Glucocorticosteroids are drugs commonly used in treating patients suffering from eczema. Synthetic derivatives of adrenal cortex glucocorticosteroids comprise a group of drugs having antiphlogistic, antiproliferative, antiallergic and immunosuppressive properties. Thanks to these properties they constituted a turning point in treating many diseases. They are now being the most often used drugs both in external application, as well as systemically.
Adrenal cortex produces hormones, whose mother substance is cyklopentanoperhydrofenantren, named steroid system. Their traditional name is glucocorticosteroids (gcs), because at first only their effect on glucose transformation was noticed. Thomas Addison described the clinical symptoms of adrenal cortex failure for the first time in 1855. Only in the years 1940-1948 chemical structure was determined. The method of cortisone synthesis was elaborated by an American biochemist Edward Kendall in 1948. In 1949 an American rheumatologist Hench used the synthetically produced cortisone to treat a patient with a rheumatoid joint inflammation (7). It was a 29-year old women immobilized due to intense pains. Two injections of the new drug managed to restore her physical fitness. This spectacular health improvement experienced by her went down to history as a “cortisone miracle”.
In 1950 Edward Kendall, Tadeusz Reichstein and Philip Showalter Hench received a Nobel prize in medicine for their discovery of chemical structure and the function of adrenal cortex hormones and their application in treating rheumatic diseases. For the first time hydrocortisone was used locally for skin diseases treatment in 1952 by Sulzberger and Witten (8). Professor Howard Maibach jokes that the history of dermatopharmacology can be divided into two periods: BC (before corticoids) and AC (after corticoids) (9).
Corticosteroid receptors are located intracellular. They are cytoplasmatic receptors, from which results the concept of their two stages function (two steps model). The first step is creating an active hormone/ /receptor complex, then transferring it to the nucleus and binding with the nuclear chromatin (10). The binding of an active steroid/receptor complex with DNA induces lipocortin-1 synthesis. It is an inflammatory protein from the group of annexines. Lipocortins bind with phospholipids of the cell membranes, disabling A phospholypase to release arachidonic acid from them. As a result, the lipid inflammatory mediators production track breaks (prostaglandin, leukotriene). Glucokorticosteroids restrain the induction of nitric oxide (iNOS) decreasing the inflammatory mediator synthesis this way (11). They also decrease the amount and the activity of mast cells in the skin (12). The most recent studies prove that the active steroid/receptor complex can directly restrain transcriptive factors. The consequence of this process is a reduced expression of adhesive molecules, which blocks the leucocytes migration to the inflammation focus. Also, the proinflammatory cytokines (Il-1, Il-2, Il-6, TFNa) activity and the amount of their receptors decreases.
Gcs currently used in treatment are synthetic derivatives of the adrenal cortex hormones. In comparison to natural compounds they have a stronger anti-inflammatory and immunosuppressive function and produce less unwanted symptoms. For many years the allergy to corticosteroids has been negated, which was caused by their anti-inflammatory properties, which mask the symptoms of contact allergy. The first case of contact allergy to hydrocortisone was recorded in Copenhagen in 1958. Then, 20.000 patients were tested and 0,3% of them had positive results. In Poland, first tests with hydrocortisone were carried out in the years 1980-1981. All of them gave negative results. The first positive results were obtained in 1988 in the Warsaw Dermatological Clinic. The allergy to hydrocortisone was diagnosed in 1% of patients (13).

Powyżej zamieściliśmy fragment artykułu, do którego możesz uzyskać pełny dostęp.
Mam kod dostępu
  • Aby uzyskać płatny dostęp do pełnej treści powyższego artykułu albo wszystkich artykułów (w zależności od wybranej opcji), należy wprowadzić kod.
  • Wprowadzając kod, akceptują Państwo treść Regulaminu oraz potwierdzają zapoznanie się z nim.
  • Aby kupić kod proszę skorzystać z jednej z poniższych opcji.

Opcja #1

19

Wybieram
  • dostęp do tego artykułu
  • dostęp na 7 dni

uzyskany kod musi być wprowadzony na stronie artykułu, do którego został wykupiony

Opcja #2

49

Wybieram
  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 30 dni
  • najpopularniejsza opcja

Opcja #3

119

Wybieram
  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 90 dni
  • oszczędzasz 28 zł
Piśmiennictwo
1. Jabłońska S, Chorzelski T: Choroby skóry – Dla studentów medycyny i lekarzy. Warszawa: Wydawnictwo Lekarskie PZWL 2002; 169-176.
2. Szepietowski JC, McKenzie RC, Keohane SG et al.: Atopic and non-atopic react to nickel challenge in a similar way. A study of the cytokine profile in nickel-induced contact dermatitis. Br J Dermatol 1997; 137: 195-200.
3. Gliński W, Rudzki E: Alergologia dla lekarzy dermatologów. Lublin: Wydawnictwo Czelej 2002; 115-130.
4. Kimber I, Dearman RJ: Allergic contact dermatitis: the cellular effectors. Contact Dermatitis 2002; 46: 1-5.
5. Gołąb J, Jakóbisiak M, Lasek W: Immunologia. Warszawa: Wydawnictwo Naukowe PWN 2002; 405-406.
6. Carlsen BC, Andersen KE, Menne T, Johansen JD: Patients with multiple contact allergies a review Contact Dermatitis 2008; 58: 1-8.
7. Langner A, Stąpór W: Hormony glikokortykosteroidowe w lecznictwie dermatologicznym. [In:] Langner A, Stąpór W, editors. Współczesne leczenie wybranych chorób skóry. Warszawa: Ośrodek Informacji Naukowej „Polfa” 1998; 22-34.
8. Sulzberger MB, Witten VH: The effect of topically applied compoud F in selected dermatoses. J Invest Dermatol 1952; 19: 101-102.
9. Maibach HI: In vivo percutaneous penetration of corticoids in man and unresolved problems in their efficacy. Dermatologica 1976; 152 (Suppl. 1): 11-25.
10. Górski J, Malayer JR, Gregg DW, Lundeen SG: Just where are the steroid receptors anyway? Endocrine J 1994; 2 (2): 99-100.
11. Appleton I, Tomlinson A, Willoughby DA, Lundeen SG: Induction of cyclo-oxygenase and nitric oxide synthase in inflammation. Adv Pharmacol 1996; 35: 27-79.
12. Lavker RM, Schechter NM: Cutaneous mast cell depletion results from topical corticosteroid usage. J Immunol 1985; 135: 2368-2373.
13. Rudzki E, Parapura K: Sensitivity to corticosteroid. Alergia Astma Immunol 2000; 5(1): 31-35.
14. Dooms-Goossens A, Andersen K, Brandao M et al.: Corticosteroid contact allergy. Contact Dermatitis 1996; 35: 40-44.
15. Ljubojevic S, Lipozencic J, Basta-Juzbasic A: Contact allergy to corticosteroids and Malassezia furfur in seborrhoeic dermatitis patients. JEADV 2011; 25: 647-651.
16. Dooms-Goossens A, Andersen K, Brandao M et al.: Corticosteroid contact allergy. Contact Dermatitis 1996; 35: 40-44.
17. Żmudzińska M, Czarnecka-Operacz M, Silny W: Contact allergy to glucocorticosteroids in patients with chronic venous leg ulcers, atopic dermatitis and contact allergy. Acta Dermatovenerol Croat 2008; 16: 72-78.
18. Ljubojevic S, Lipozencic J, Basta-Juzbasic A: Contact allergy to corticosteroids and Malassezia furfur in seborrhoeic dermatitis patients. JEADV 2011; 25: 647-651.
19. Nettis E, Colanardi MC, Calogiuri GF et al.: Allergic reactions to inhalant glucocorticosteroids: a hot topic for pneumologists and allergologists. Immunopharmacol Immunotoxicol 2006; 28: 511-534.
20. Amin N, Brancaccio R, Cohen D: Cutaneous reactions to injectable corticosteroids. Dermatitis 2006; 17: 143-146.
21. Belsito DV: Allergic contact dermatitis to topical glucocorticosteroids. Cutis 1993; 52: 291-294.
22. Whitmore SE: Delayed systemic allergic reactions to corticosteroids. Contact Dermatitis 1995; 32: 193-198.
23. Rasanen L, Hasan T: Allergy to systemic and intralesional corticosteroids. Br J Dermatol 1993; 128: 407-411.
24. Dooms-Goossens A, Degreef H: Clinical aspects of contact allergy to corticosteroids. Dermatology 1994; 189: 54-55.
25. Coskey RJ: Adverse effects of corticosteroids. Topical and intralesional. Clin Dermatol 1986; 4: 155-160.
26. Amin N, Brancaccio R, Cohen D: Cutaneous reactions to injectable corticosteroids. Dermatitis 2006; 17: 143-146.
27. Senff H, Kunz R, Kollner A et al.: Allergic contact dermatitis due to prednicarbate. Hautarzt 1991; 42: 53-55.
28. Laurema AI, Visa K, Pekonen M et al.: Cellular kinetics of delayed hypesensitivity test reactions to topical glucocorticosteroids. Arch Dermatol Res 1987; 279: 379-384.
29. Davis MD, el-Azhary RA, Farmer SA: Results of patch testing to a corticosteroids series a retrospective review of 1188 patients during 6 years at Mayo Clinic. J Am Acad Dermatol 2007; 56: 921-927.
30. Amin N, Brancaccio R, Cohen D: Cutaneous reactions to injectable corticosteroids. Dermatitis 2006; 17: 143-146.
31. Boffa MJ, Wilkinson SM, Beck MH: Screening for corticosteroid contact hypersensitivity. Contact Dermatitis 1995; 33: 149-151.
32. Seukeran DC, Wilkinson SM, Beck MH: Patch testing to detect corticosteroid allergy: Is it adequate? Contact Dermatitis 1997; 36: 127-130.
33. Trautmann A. Allergiediagnose, Allergietherapie. Stuttgart: Georg Thieme Verlag; 2006: 130-155.
34. Hengge UR, Ruzicka T, Schwartz RA et al.: Adverse effects of topical glucocorticosteroids. J Acad Dermatol 2006; 54: 1-15.
35. Davis MD, el-Azhary RA, Farmer SA: Results of patch testing to a corticosteroids series a retrospective review of 1188 patients during 6 years at Mayo Clinic. J Am Acad Dermatol 2007; 56: 921-927.
36. Davis MD, Scalf LA, Yiannias JA et al.: Changing trends and allergens in the patch test standard series: a Mayo Clinic 5-year retrospective review, January 1, 2001, through December 31, 2005. Arch Dermatol 2008; 144: 67-72.
37. Ljubojevic S, Lipozencic J, Basta-Juzbasic A: Contact allergy to corticosteroids and Malassezia furfur in seborrhoeic dermatitis patients. JEADV 2011; 25: 647-651.
38. Isaksson M, Möller H, Bruze M: The reliability of visual scoring of patch test reactions revisited. Contact Dermatitis 2012; 66(3): 163.
39. Dooms-Goossens A, Verschaeve H, Degreef H et al.: Contact allergy to hydrocortisone and tixocortol pivalate problems in the detection of corticosteroid sensitivity. Contact Dermatitis 1986; 14: 94-102.
40. Davis MD, Scalf LA, Yiannias JA, et al.: Changing trends and allergens in the patch test standard series: a Mayo Clinic 5-year retrospective review, January 1, 2001, through December 31. 2005 Arch Dermatol 2008; 144: 67-72.
otrzymano: 2012-08-22
zaakceptowano do druku: 2012-09-28

Adres do korespondencji:
*Anna Woźniacka
Department of Dermatology and Venerology
Medical University of Łódź
ul. Krzemieniecka 5, 94-115 Łódź
tel.: +48 (42) 686-79-81
e-mail: wozniacka@bmp.net.pl

Postępy Nauk Medycznych 10/2012
Strona internetowa czasopisma Postępy Nauk Medycznych