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2019, Número 4

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Dermatología Cosmética, Médica y Quirúrgica 2019; 17 (4)


Abordaje diagnóstico y terapéutico actual de la dermatitis herpetiforme

Ramos CCJ, Ocampo CJ, Gómez FM

Idioma: Español
Referencias bibliográficas: 60
Paginas: 244-254
Archivo PDF: 395.40 Kb.


RESUMEN

La dermatitis herpetiforme (dh) es una enfermedad ampollosa autoinmune crónica, polimorfa, caracterizada por la presencia de pápulas y vesículas, intensamente pruriginosas, que se distribuyen en superficies de extensión de las extremidades y la región sacra. Se considera que es la manifestación cutánea de una enteropatía sensible al gluten de la dieta, y su asociación con la enfermedad celíaca (ec) se ha demostrado ampliamente. Afecta sobre todo a población con ascendencia escandinava, y en mayor proporción a hombres entre la cuarta y quinta décadas de vida. Su patogénesis consiste en una sumatoria de factores genéticos, perfil inmunológico idiosincrático y la exposición a factores ambientales desencadenantes, donde el más importante es el gluten presente sobre todo en el trigo, la cebada y el centeno. Además de las manifestaciones cutáneas, se acompaña de alteraciones subclínicas de la mucosa intestinal, las cuales se traducen en una amplia sintomatología que incluye distensión abdominal, cólicos, dolor, diarrea y/o estreñimiento. Además de la ec, se asocia a hipotiroidismo, diabetes mellitus tipo 1, anemia perniciosa, enfermedad de Addison, vitiligo y alopecia areata. El diagnóstico se establece uniendo datos clínicos con hallazgos de histopatología, serología y de inmunofluorescencia directa (ifd), esta última considerada el estándar de oro para dh. El abordaje terapéutico actual se orienta a la combinación temprana del uso de dapsona como inductor de la remisión de la enfermedad y la dieta libre de gluten (dlg) como terapia de mantenimiento. Asimismo, la dh es una enfermedad que requiere manejo interdisciplinario y seguimiento por las áreas de dermatología y nutrición clínica.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Mendes FBR, Hissa-Elian A, De Abreu MA y Gonçalves VS, Review: dermatitis herpetiformis, An Bras Dermatol 2013; 88:594-9 .

  2. Fry L, Dermatitis herpetiformis: problems, progress and prospects, European Journal of Dermatology 2002; 12(6):523-31.

  3. Bolotin D, y Petronic-Rosic V, Dermatitis herpetiformis: Part ii. Diagnosis, management, and prognosis, Journal of the American Academy of Dermatology 2011; 64(6)1027-33.

  4. Caproni M, Antiga E, Melani L y Fabbri P, Guidelines for the diagnosis and treatment of dermatitis herpetiformis, Journal of the European Academy of Dermatology and Venereology 2009; 23(6):633-8.

  5. Hervonen K et al., Reduced mortality in dermatitis herpetiformis: a population- based study of 476 patients, Br J Dermatol 2012; 167(6)1331-7.

  6. Bolotin D y Petronic-Rosic V, Dermatitis herpetiformis: Part i. Epidemiology, pathogenesis, and clinical presentation, J Am Acad Dermatol 2011; 64:1017-24.

  7. Bonciani D et al., Dermatitis herpetiformis: from the genetics to the development of skin lesions, Clin Dev Immunol 2012; 1:239691.

  8. Alonso-Llamazares J, Gibson LE y Rogers RS, Clinical, pathologic, and immunopathologic features of dermatitis herpetiformis: review of the Mayo Clinic experience, Int J Dermatol 2007; 46:910-9.

  9. Lever’s histopathology of the skin, 10ª ed., J Cutan Pathol-Wiley Online Library, 2009.

  10. Reunala TL, Dermatitis herpetiformis, Clinics in Dermatology 2001; 144:196-7.

  11. Zone JJ, Meyer LJ y Petersen MJ, Deposition of granular iga relative to clinical lesions in dermatitis herpetiformis, Arch Dermatol 1996; 132(8):912-8.

  12. Dieterich W et al., Antibodies to tissue transglutaminase as serologic markers in patients with dermatitis herpetiformis, J Invest Dermatol 1999; 113(1)133-6.

  13. Sárdy M, Kárpáti S, Merkl B, Paulsson M y Smyth N, Epidermal transglutaminase (tgase 3) is the autoantigen of dermatitis herpetiformis, J Exp Med 2002; 195(6):747-57.

  14. Zone JJ et al., Dermatitis herpetiformis sera or goat anti-transglutaminase- 3 transferred to human skin-grafted mice mimics dermatitis herpetiformis immunopathology, J Immunol 2011; 186(7):4474-80.

  15. Mobacken H, Kastrup W y Nilsson LA, Incidence and prevalence of dermatitis herpetiformis in Western Sweden, Acta Derm Venereol 1984; 64(5):400-4.

  16. Reunala T y Lokki J, Dermatitis herpetiformis in Finland, Acta Derm Venereol 1978.

  17. Smith JB, Tulloch JE, Meyer LJ y Zone JJ, The incidence and prevalence of dermatitis herpetiformis in Utah, Arch Dermatol 1992; 128:1608-10.

  18. Lanzini A et al., Epidemiological, clinical and histopathologic characteristics of celiac disease: results of a case-finding population-based program in an Italian community, Scand J Gastroenterol 2005; 40(8)950-7.

  19. Llorente-Alonso MJ, Fernández-Aceñero MJ y Sebastián M, Gluten intolerance: sex- and age-related features, Can J Gastroenterol 2006; 20(11)719-22.

  20. Reunala T, Incidence of familial dermatitis herpetiformis, Br J Dermatol 1996; 134:394-8.

  21. Chmurova N, Parnicka Z, Svecova D, Manova A y Simaljakova M, Dermatitis herpetiformis in siblings, Bratisl Lek Listy 2007.

  22. Forabosco P et al., Meta-analysis of genome-wide linkage studies in celiac disease, Hum Hered 2009; 68(4):223-30.

  23. Chorzepa C, Dermatitis herpetiforme y enfermedad celíaca, tesis, Universidad Nacional de Rosario, 2011.

  24. Clarindo MV et al., Dermatitis herpetiformis: pathophysiology, clinical presentation, diagnosis and treatment, An Bras Dermatol 2014; 89, 865-77.

  25. Rostom A, Murray JA y Kagnoff MF, American Gastroenterological Association (aga) Institute Technical Review on the Diagnosis and Management of Celiac Disease; Gastroenterology 2006; 131(6): 1981-2002.

  26. Kárpáti S, Dermatitis herpetiformis: close to unravelling a disease, Journal of Dermatological Science 2004; 34:83-90.

  27. Reif S y Lerner A, Tissue transglutaminase-the key player in celiac disease: a review, Autoimmun Rev 2004; 3(1):40-5.

  28. Caputo I, Barone MV, Martucciello S, Lepretti M y Esposito C, Tissue transglutaminase in celiac disease: role of autoantibodies, Amino Acids 2009; 36(4):693-9.

  29. Bolognia JL, Jorizzo JL y Rapini RP, Dermatology 2: volume set, 2003.

  30. Cinats AK, Parsons LM y Haber RM, Facial involvement in dermatitis herpetiformis: a case report and review of the literature, Journal of Cutaneous Medicine and Surgery 2019; 23(1):35-7..

  31. Tu H et al., Acral purpura as leading clinical manifestation of dermatitis herpetiformis: report of two adult cases with a review of the literature, Dermatology 2013; 227(1):1-4.

  32. Kárpáti S, An exception within the group of autoimmune blistering diseases: dermatitis herpetiformis, the gluten-sensitive dermopathy, Immunol Allergy Clin North Am 2012; 32:255-62.

  33. Kaplan RP y Callen JP, Dermatitis herpetiformis: autoimmune disease associations, Clin Dermatol 1991; 9(3):347-60.

  34. Londei M et al., Gliadin as a stimulator of innate responses in celiac disease, Mol Immunol 2005; 42(8):913-18.

  35. Askling J et al., Cancer incidence in a population-based cohort of individuals hospitalized with celiac disease or dermatitis herpetiformis, Gastroenterology 2002; 123(5):1726-9.

  36. Weedon D, Weedon’s skin pathology, Londres, Elsevier, 2009.

  37. Ko CJ, Colegio OR, Moss JE y McNiff JM, Fibrillar i iga deposition in dermatitis herpetiformis: an underreported pattern with potential clinical significance, J Cutan Pathol 2010; 37(4):475-7.

  38. Bonciolini V et al., Newly described clinical and immunopathological feature of dermatitis herpetiformis, Clin Dev Immunol 2012; 2012:967964.

  39. Van L, Browning JC, Krishnan RS, Kenner-Bell BM y Hsu S, Dermatitis herpetiformis: potential for confusion with linear iga bullous dermatosis on direct immunofluorescence, Dermatology Online Journal 2008.

  40. Reunala T et al., iga antiepidermal transglutaminase antibodies in dermatitis herpetiformis: a significant but not complete response to a gluten-free diet treatment, British Journal of Dermatology 2015; 172(4):1139-41.

  41. Borroni G et al., iga anti-epidermal transglutaminase autoantibodies: a sensible and sensitive marker for diagnosis of dermatitis herpetiformis in adult patients J Eur Acad Dermatology Venereol 2013; 27(7):836-41.

  42. Rose C et al., Autoantibodies against epidermal transglutaminase are a sensitive diagnostic marker in patients with dermatitis herpetiformis on a normal or gluten-free diet, J Am Acad Dermatol 2009; 61(1):39-43.

  43. Marietta E et al., A new model for dermatitis herpetiformis that uses hla-dq8 transgenic nod mice, J Clin Invest 2004; 114(8):1090-7.

  44. Jaskowski TD et al., iga anti-epidermal transglutaminase antibodies in dermatitis herpetiformis and pediatric celiac disease, Journal of Investigative Dermatology 2009; 129(11):2728-30.

  45. Ferguson A, Arranz E y O’Mahony S, Clinical and pathological spectrum of coeliac disease: active, silent, latent, potential, Gut 1993; 34(2):150-1.

  46. Fry L et al., Long term follow-up of dermatitis herpetiformis with and without dietary gluten withdrawal, Br J Dermatol 1982; 107(6):631-40.

  47. Cardones ARG y Hall RP, Management of dermatitis herpetiformis, Immunology and Allergy Clinics of North America 2012; 32:271-81.

  48. Ermacora E et al., Long-term follow-up of dermatitis herpetiformis in children, J Am Acad Dermatol 1986; 15:24-30.

  49. Cardones ARG y Hall RP, Management of dermatitis herpetiformis, Immunology and Allergy Clinics of North America 2012; 32:271-81.

  50. Egan CA, O’Loughlin S, Gormally S y Powell FC, Dermatitis herpetiformis: a review of fifty-four patients, Ir J Med Sci 1997; 166(4):241-4.

  51. Reunala T et al., Dermatitis herpetiformis: jejunal findings and skin response to gluten free diet, Archives of Disease in Childhood 1984; 59:517-22.

  52. Wozel G, Blasum C, Winter C y Gerlach B, Dapsone hydroxylamine inhibits the ltb4-induced chemotaxis of polymorphonuclear leukocytes into human skin: results of a pilot study, Inflammation Research 1997; 46(10):420-2.

  53. Sanders SW y Zone JJ, The relationship between dapsone dose, serum concentration and disease severity in dermatitis herpetiformis, Arzneimittelforschung 1986; 36(1):146-9.

  54. Luzzatto L y Seneca E, g6pd deficiency: a classic example of pharmacogenetics with on-going clinical implications, British Journal of Haematology 2014; 164(4):469-80.

  55. Willsteed E, Lee M, Wong LC y Cooper A, Sulfasalazine and dermatitis herpetiformis, Australas J Dermatol 2005; 46: 101-3.

  56. Klotz U, Clinical pharmacokinetics of sulphasalazine, its metabolites and other prodrugs of 5-aminosalicylic acid, Clinical Pharmacokinetics 1985; 10(4):285-302 .

  57. Shah SA y Ormerod AD, Dermatitis herpetiformis effectively treated with heparin, tetracycline and nicotinamide, Clin Exp Dermatol 2000; 25(3):204-5.

  58. Stenveld HJ, Starink TM, Van Joost T y Stoof TJ, Efficacy of cyclosporine in two patients with dermatitis herpetiformis resistant to conventional therapy, J Am Acad Dermatol 1993; 38(5):1014-5.

  59. Silvers DN, Juhlin EA, Berczeller PH y Mcsorley J, Treatment of dermatitis herpetiformis with colchicine, Arch Dermatol 1980; 116:1373-4.

  60. Albers LN, Zone JJ, Stoff BK y Feldman RJ, Rituximab treatment for recalcitrant dermatitis herpetiformis, jama Dermatology 2017; 153:315-8.




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