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Journal articles on the topic 'Herpetiformi'

Author: Grafiati

Published: 1 April 2023

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1

Fernandes, Iolanda Conde, Madalena Sanches, Rosário Alves, and Manuela Selores. "Case for diagnosis." Anais Brasileiros de Dermatologia 87, no. 6 (December 2012): 933–35. http://dx.doi.org/10.1590/s0365-05962012000600023.

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We report a clinical case of a rare variant of pemphigus - pemphigus herpetiformis - which combines the clinical features of dermatitis herpetiformis with the immunological findings of pemphigus. Due to its atypical presentation, it is frequently misdiagnosed as dermatitis herpetiformis. It is basically characterized by the herpetiform pattern of skin lesions, severe pruritus and by the presence of eosinophilic spongiosis confirmed on histopathology. We call attention to the excellent response to dapsone.

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2

Poór, Adrienn Katalin, Judit Hársing, Bernadett Hidvégi, Péter Holló, and Sarolta Kárpáti. "Impetigo herpetiformis." Bőrgyógyászati és Venerológiai Szemle 88, no. 4 (October 31, 2012): 117–20. http://dx.doi.org/10.7188/bvsz.2012.88.4.3.

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3

Miziara, Ivan Dieb, Bernardo Cunha Araujo Filho, and Raimar Weber. "Aids e estomatite aftóide recidivante." Revista Brasileira de Otorrinolaringologia 71, no. 4 (August 2005): 517–20. http://dx.doi.org/10.1590/s0034-72992005000400020.

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O estado de imunodeficiência em pacientes HIV positivos tem sido causa de episódios severos de Estomatite Aftóide Recidivante (EAR). OBJETIVO: Este estudo objetiva estabelecer evidências da relação entre o surgimento (ou agravamento) de EAR com o estado de imunossupressão causado pelo vírus HIV, por meio da contagem de células CD4+, CD8+ e da carga viral infectante. FORMA DE ESTUDO: estudo de série. MATERIAL E MÉTODO: Noventa e quatro pacientes HIV (1)-positivos (25 mulheres e 69 homens) com EAR foram acompanhados no ambulatório de Aids da Divisão de Clínica ORL do Hospital das Clínicas da FMUSP no período de janeiro de 1998 a dezembro de 2003. A idade dos pacientes variou de 19 a 63 anos (média = 35,3 anos). RESULTADO: Os pacientes com Aids e soropositivos apresentaram, respectivamente, oito aftas e duas aftas por surto. Da mesma maneira, os pacientes portadores de úlceras do tipo major apresentaram menor contagem de células CD8+, CD4+ e relação CD4+/CD8+ e maior valor médio da carga viral do que os pacientes portadores de aftas herpetiformes e minor. Entre os portadores de aftas minor e herpetiforme não houve diferença estatística. CONCLUSÕES O aparecimento das lesões, principalmente as do tipo major, está diretamente relacionado ao estado imunitário do paciente soropositivo, acarretando déficits nutricionais e piora na qualidade de vida. Desta forma, o diagnóstico e tratamento da EAR é um desafio que não deve ser desprezado.

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4

Nakajima, Kimiko. "Recent Advances in Dermatitis Herpetiformis." Clinical and Developmental Immunology 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/914162.

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Dermatitis herpetiformis is an autoimmune bullous disease that is associated with gluten sensitivity which typically presents as celiac disease. As both conditions are multifactorial disorders, it is not clear how specific pathogenetic mechanisms may lead to the dysregulation of immune responses in the skin and small bowel, respectively. Recent studies have demonstrated that IgA and antibodies against epidermal transglutaminase 3 play an important role in the pathogenesis of dermatitis herpetiformis. Here, we review recent immunopathological progress in understanding the pathogenesis of dermatitis herpetiformis.

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5

Ruvinskaya, Guzel R., E. N. Silantieva, and A. V. Anokhina. "The need for a multidisciplinary approach to the diagnosis and treatment procedures of isolated lesions of the oral mucosa in herpetiform Dühring dermatitis." Russian Journal of Dentistry 24, no. 2 (October 3, 2020): 99–103. http://dx.doi.org/10.17816/1728-2802-2020-24-2-99-103.

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The defeat of the oral mucosa in herpetiform Dhring dermatitis is a rare pathology. According to the literature, it is detected in 9.6% 10% of cases. Granular deposits of immunoglobulin A in the papillae of the dermis in herpetiform Dhring dermatitis are associated with gluten enteropathy, lead to the development of inflammatory processes on the skin and oral mucosa and the appearance of polymorphic itchy rashes and chronic recurrent course of the disease. The article describes a clinical case of a patient diagnosed with herpetiform dermatitis, manifestations in the oral cavity (ICD-10 L13.0X code). The need for a multidisciplinary approach to the diagnosis, differential diagnosis, treatment and dynamic observation of isolated lesions of the oral mucosa in herpetiform Dhring dermatitis is indicated. A scheme of measures required by a dentist is developed.

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Novikov, Yuri A., Denis V. Zaslavsky, Olga V. Pravdina, Elena A. Zykova, Anastasia S. Lipatnikova, Elena S. Bolshakova, Elena S. Manylova, and Lyudmila N. Drozdova. "During’s herpetiform dermatitis in pediatric dermatology: issues of diagnostics and treatment." Pediatrician (St. Petersburg) 11, no. 6 (December 31, 2020): 79–86. http://dx.doi.org/10.17816/ped11679-86.

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This article presents a case of clinical observation of a 5-year-old child with herpetiformis dermatitis (Duhrings). This rare dermatosis is characterized by a chronic relapsing course, the presence of itching polymorphic rashes, typical histological and immunomorphological signs. The diagnosis was made on the basis of the clinical picture, histological and immunohistochemical studies of skin biopsy, as well as the results of HLA typing by PCR. Clinical observation of this case is of interest to practicing physicians-dermatologists due to the rare occurrence of Duhrings herpetiformis in children, the complexity of differential diagnostic search, which requires further generalization of experience using histological, immunohistochemical and molecular genetic research methods. The disease is clearly differentiated from other rashes with the formation of subepidermal blisters according to histological, immunological and gastrointestinal criteria. The prevalence of dermatosis in various populations of the Europian race ranges from 10 to 39 cases per 100,000 population. Duhrings dermatitis herpetiformis can develop at any age (cases of the childhood form of Dhrings dermatitis herpetiformis have been reported), but most often the disease occurs at the age of 4050 years. Dermatitis herpetiformis persists indefinitely with variable severity. In patients with Duhrings dermatitis, associated gluten-sensitive enteropathy is often noted, which in most cases is asymptomatic.

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7

Villegas de la Lama, Juan Carlos, and Marina Lacalle-Calderón. "Mujer de 45 años con lesiones digitales pruriginosas." Revista Española de Casos Clínicos en Medicina Interna 7, no. 2 (August 9, 2022): 9–11. http://dx.doi.org/10.32818/reccmi.a7n2a4.

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La dermatitis herpetiforme es una erupción cutánea autoinmune infrecuente que pone de manifiesto una sensibilidad al gluten. Los pacientes desarrollan típicamente unas pápulas y vesículas inflamatorias intensamente pruriginosas en los antebrazos, las rodillas, el cuero cabelludo o los glúteos. La inmensa mayoría de los pacientes con dermatitis herpetiforme también asocia una enteropatía sensible al gluten (enfermedad celíaca), que normalmente es oligosintomática o asintomática. Este caso clínico es una presentación atípica de dermatitis herpetiforme, dado que la primera manifestación cutánea de nuestra paciente fue una combinación de máculas purpúricas, pápulas y petequias dolorosas localizadas en regiones inusuales: los pulpejos de los dedos.

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8

Klimov, L. Ya, V. A. Kuryaninova, Yu A. Dmitrieva, Ya D. Mironova, A. V. Yagupova, S. V. Dolbnya, M. V. Stoyan, S. N. Kashnikova, T. A. Ivenskaya, and E. A. Cherkasova. "Dermatitis herpetiformis Duhring as one of the forms of gluten-associated pathology: a review of the literature and a description of a clinical case." Meditsinskiy sovet = Medical Council, no. 1 (March 5, 2022): 301–11. http://dx.doi.org/10.21518/2079-701x-2022-16-1-301-311.

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This review presents information on the prevalence, pathogenesis, clinical manifestations, diagnosis and treatment of Duhring’s dermatitis herpetiformis. Although the disease was first clinically described in 1884 by the American dermatologist L.A. Duhring, the study of its pathogenesis and the search for prognostic markers of its occurrence continue. Against the background of a significant expansion of ideas about gluten-dependent diseases and conditions, views on the mechanisms of autoimmune skin damage in dermatitis herpetiformis are detailed. A strong association with hereditary predisposition through the major human leukocyte histocompatibility complex (HLA) DQ2 and DQ8, and a role of epidermal transglutaminase as a major autoantigen in dermatitis herpetiformis are shown. The hypotheses explaining the decline in the incidence of dermatitis herpetiformis in recent decades against the background of increased and more effective serological screening and the resulting earlier diagnosis of celiac disease are commented on. A typical clinical picture of dermatitis herpetiformis, in which erythematous papules, plaques, vesicles are seen, usually clustered on the flexural surfaces of the extremities. Secondary elements are erosions, excoriations and crusts due to rupture of blisters and due to scratching caused by intense itching. A generally favourable prognosis for life and disease is shown with a gluten-free diet and the use of dapsone, glucocorticoids and, if these are ineffective, immunosuppressants. The authors describe a clinical case of the disease in an adolescent girl with a typical clinical history and characteristic rashes on the extensor surfaces of the limbs. The authors show that drug therapy without a gluten-free diet cannot be considered effective, and that the diet for dermatitis herpetiformis, like that for celiac disease, is lifelong. The growing understanding of gluten-associated pathology, which includes dermatitis herpetiformis, in recent decades has led to an intensive search for diagnostic and prognostic markers, as well as the development of ways to correct this group of diseases, including those not related to the lifelong elimination of cereal prolamines.

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9

Sárdy, Miklós, Sarolta Kárpáti, Barbara Merkl, Mats Paulsson, and Neil Smyth. "Epidermal Transglutaminase (TGase 3) Is the Autoantigen of Dermatitis Herpetiformis." Journal of Experimental Medicine 195, no. 6 (March 18, 2002): 747–57. http://dx.doi.org/10.1084/jem.20011299.

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Gluten sensitivity typically presents as celiac disease, a common chronic small intestinal disorder. However, in certain individuals it is associated with dermatitis herpetiformis, a blistering skin disease characterized by granular IgA deposits in the papillary dermis. While tissue transglutaminase has been implicated as the major autoantigen of gluten sensitive disease, there has been no explanation as to why this condition appears in two distinct forms. Here we show that while sera from patients with either form of gluten sensitive disease react both with tissue transglutaminase and the related enzyme epidermal (type 3) transglutaminase, antibodies in patients having dermatitis herpetiformis show a markedly higher avidity for epidermal transglutaminase. Further, these patients have an antibody population specific for this enzyme. We also show that the IgA precipitates in the papillary dermis of patients with dermatitis herpetiformis, the defining signs of the disease, contain epidermal transglutaminase, but not tissue transglutaminase or keratinocyte transglutaminase. These findings demonstrate that epidermal transglutaminase, rather than tissue transglutaminase, is the dominant autoantigen in dermatitis herpetiformis and explain why skin symptoms appear in a proportion of patients having gluten sensitive disease.

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10

Cinats, Allison K., Laurie M. Parsons, and Richard M. Haber. "Facial Involvement in Dermatitis Herpetiformis: A Case Report and Review of the Literature." Journal of Cutaneous Medicine and Surgery 23, no. 1 (August 13, 2018): 35–37. http://dx.doi.org/10.1177/1203475418795818.

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Dermatitis herpetiformis is a cutaneous manifestation of celiac disease that classically presents as a symmetric pruritic vesicular eruption on extensor surfaces. Typical locations include elbows, knees, and buttocks. Facial involvement has been reported rarely. Here, we report a case of a 44-year-old woman with dermatitis herpetiformis presenting as pruritic vesicles on the face that had previously been misdiagnosed as allergic contact dermatitis. Diagnosis was confirmed with direct immunofluorescence demonstrating granular IgA in the papillary dermis. This eruption cleared with topical dapsone 5% gel and a gluten-free diet. We report this case to raise awareness of facial involvement in dermatitis herpetiformis as well as the possibility of topical dapsone as a therapeutic option.

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11

Görög, Anna, Tamás Malkovics, and Miklós Sárdy. "The novel aspects of the diagnostics and therapy of dermatitis herpetiformis." Bőrgyógyászati és Venerológiai Szemle 97, no. 4 (September 1, 2021): 204–16. http://dx.doi.org/10.7188/bvsz.2021.97.4.5.

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In the present review, the authors briefy describe the clinical features and pathomechanism of dermatitis herpetiformis and detail the diagnostic algorithm of the disease. The up-to-date protocol for the management of the disease is presented in light of the evidence- and consensus-based (S2) guideline published by the European Academy of Dermatology (EADV) in 2021.

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12

Shrestha, P., R. B. Tajhya, and A. Pokharel. "Pemphigus herpetiformis : A rare clinical variant of pemphigus." Nepal Journal of Dermatology, Venereology & Leprology 13, no. 1 (January 12, 2016): 61–65. http://dx.doi.org/10.3126/njdvl.v13i1.14308.

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Pemphigus herpetiformis is an autoimmune blistering disease. We report a case of pemphigus herpetiformis, a generalized form, manifested as pruritic grouped vesicles at extremities and trunk, in a seventy years old man. Neutrophil dominant inflammatory substrate was seen in histopathology. Direct immunofluorescene revealed IgG reactivity in net like pattern at upper epidermis, confirming pemphigus. The patient responded well to prednisolone and colchicine combination initially and maintained remission later on colchicine alone. Colchicine has anti-mitotic, anti-inflammatory and immunosuppressive mechanism of actions and proven benefits in neutrophilic dermatoses. Therefore we recommend colchicine as mono therapy or in combination with immunosuppressive, for the treatment of pemphigus herpetiformis where neutrophil is predominant inflammatory infiltrate histologically.NJDVL Vol. 13, No. 1, 2015 Page: 61-65

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13

Kondo, Rogerio Nabor, Fernanda Mendes Araújo, Allamanda Moura Pereira, Vivian Cristina Holanda Lopes, and Ligia Márcia Mario Martins. "Pustular psoriasis of pregnancy (Impetigo herpetiformis) - case report." Anais Brasileiros de Dermatologia 88, no. 6 suppl 1 (December 2013): 186–89. http://dx.doi.org/10.1590/abd1806-4841.20132134.

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Impetigo herpetiformis is a rare dermatosis of pregnancy with typical onset during the last trimester of pregnancy and rapid resolution in the postpartum period. Clinically and histologically, it is consistent with pustular psoriasis. This similarity has led some authors to name the disease "the pustular psoriasis of pregnancy". We report the case of a patient who developed impetigo herpetiformis in two sucessive pregnancies.

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14

MUCENICA, Irina Manuela, Ancuţa IGNAT, Gabriela PĂDURARU, Andrada DRUICĂ, Valeriu Vasile LUPU, and Marin BURLEA. "Celiac disease: diagnosis and dilemmas." Romanian Journal of Medical Practice 11, no. 2 (June 30, 2016): 204–7. http://dx.doi.org/10.37897/rjmp.2016.2.17.

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Celiac disease is an autoimmune disorder of the gastrointestinal tract. The condition may develop at any age, triggered by exposure to dietary gluten in genetically susceptible individuals. The most frequent intestinal manifestations include diarrhea and weight loss. Common extradigestive manifestations include iron deficiency anemia, dermatitis herpetiformis. The authors presents a clinical case diagnosed with celiac disease expressed with gastrointestinal and extradigestive symptoms, such as abdominal pain, flatulence, anemia, impaired hepatic function and dermatitis herpetiformis.

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15

KODERA, Hanako, Mitsuharu KAYABA, Noriyuki MISAGO, and Yutaka NARISAWA. "Impetigo Herpetiformis." Nishi Nihon Hifuka 60, no. 1 (1998): 15–18. http://dx.doi.org/10.2336/nishinihonhifu.60.15.

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16

El Khalifa, J., L. Deschamps, and C. Picard Dahan. "Dermatitis herpetiforme." EMC - Dermatología 56, no. 3 (August 2022): 1–8. http://dx.doi.org/10.1016/s1761-2896(22)46753-7.

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17

Thomas, EmyAbi. "Dermatitis herpetiformis." CHRISMED Journal of Health and Research 1, no. 1 (2014): 51. http://dx.doi.org/10.4103/2348-3334.126793.

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18

Jakes, A. D., S. Bradley, and L. Donlevy. "Dermatitis herpetiformis." BMJ 348, apr16 1 (April 16, 2014): g2557. http://dx.doi.org/10.1136/bmj.g2557.

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19

Barnadas, Maria A. "Dermatitis Herpetiformis." American Journal of Dermatopathology 38, no. 4 (April 2016): 283–88. http://dx.doi.org/10.1097/dad.0000000000000420.

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Nicolas, Marie Eleanore O., Patricia K. Krause, Lawrence E. Gibson, and Joseph A. Murray. "Dermatitis herpetiformis." International Journal of Dermatology 42, no. 8 (August 2003): 588–600. http://dx.doi.org/10.1046/j.1365-4362.2003.01804.x.

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21

Berg, G., C. A. M. Rietmeyer, and Th van Joost. "Dermatitis herpetiformis." British Journal of Dermatology 123, no. 2 (August 1990): 262–63. http://dx.doi.org/10.1111/j.1365-2133.1990.tb01862.x.

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22

Hall, Russell P. "Dermatitis Herpetiformis." Journal of Investigative Dermatology 99, no. 6 (December 1992): 873–81. http://dx.doi.org/10.1111/1523-1747.ep12614868.

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23

Otley, Clark, and Russell P. Hall. "Dermatitis Herpetiformis." Dermatologic Clinics 8, no. 4 (October 1990): 759–69. http://dx.doi.org/10.1016/s0733-8635(18)30463-7.

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24

Doffoel-Hantz, V., A. Sparsa, and J. M. Bonnetblanc. "Dermatitis herpetiforme." EMC - Dermatología 45, no. 3 (January 2011): 1–8. http://dx.doi.org/10.1016/s1761-2896(11)71079-2.

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25

Vergara Hernández, J., and R. Díaz Peral. "Dermatitis herpetiforme." SEMERGEN - Medicina de Familia 30, no. 6 (January 2004): 279–85. http://dx.doi.org/10.1016/s1138-3593(04)74314-2.

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26

Sherif, Abdalla I., Subhash C. Bharija, Mohammed S. Belhaj, and Gurmohan Singh. "Pemphigus Herpetiformis." International Journal of Dermatology 29, no. 10 (December 1990): 737–38. http://dx.doi.org/10.1111/j.1365-4362.1990.tb03785.x.

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27

Jablonska, Stephania, and Tadeusz Chorzelski. "Pemphigus Herpetiformis." International Journal of Dermatology 31, no. 2 (February 1992): 144. http://dx.doi.org/10.1111/j.1365-4362.1992.tb03259.x.

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28

Gómez Sánchez, María Encarnación, Cristina Faura Berruga, Luis Iñiguez de Onzoño Martín, and Syonghyun Nam Cha. "Dermatitis herpetiforme." Medicina Clínica 143, no. 11 (December 2014): e21. http://dx.doi.org/10.1016/j.medcli.2014.04.004.

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29

Reunala, Timo L. "Dermatitis herpetiformis." Clinics in Dermatology 19, no. 6 (November 2001): 728–36. http://dx.doi.org/10.1016/s0738-081x(00)00184-x.

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30

de Las Heras, E., and J. Borbujo-Martínez. "Dermatitis herpetiforme." FMC - Formación Médica Continuada en Atención Primaria 13, no. 3 (March 2006): 140. http://dx.doi.org/10.1016/s1134-2072(06)71292-0.

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31

Bolotin, Diana, and Vesna Petronic-Rosic. "Dermatitis herpetiformis." Journal of the American Academy of Dermatology 64, no. 6 (June 2011): 1027–33. http://dx.doi.org/10.1016/j.jaad.2010.09.776.

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Bolotin, Diana, and Vesna Petronic-Rosic. "Dermatitis herpetiformis." Journal of the American Academy of Dermatology 64, no. 6 (June 2011): 1017–24. http://dx.doi.org/10.1016/j.jaad.2010.09.777.

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33

Oumeish, Oumeish Youssef, and Jennifer L. Parish. "Impetigo herpetiformis." Clinics in Dermatology 24, no. 2 (March 2006): 101–4. http://dx.doi.org/10.1016/j.clindermatol.2005.10.009.

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Kárpáti, Sarolta. "Dermatitis herpetiformis." Clinics in Dermatology 30, no. 1 (January 2012): 56–59. http://dx.doi.org/10.1016/j.clindermatol.2011.03.010.

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35

Wosnitza, M., C. Blazek, and M. Megahed. "Pemphigus herpetiformis." Der Hautarzt 59, no. 6 (May 11, 2008): 459–60. http://dx.doi.org/10.1007/s00105-008-1574-3.

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Sárdy, M., and J. Tietze. "Dermatitis herpetiformis." Der Hautarzt 60, no. 8 (July 1, 2009): 627–32. http://dx.doi.org/10.1007/s00105-008-1679-8.

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Juratli, H. A., A. Görög, and M. Sárdy. "Dermatitis herpetiformis." Der Hautarzt 70, no. 4 (March 12, 2019): 260–64. http://dx.doi.org/10.1007/s00105-019-4378-8.

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38

Harrington, Christine I., and A. G. Messenger. "Dermatitis herpetiformis." British Journal of Dermatology 114, no. 2 (February 1986): 265–66. http://dx.doi.org/10.1111/j.1365-2133.1986.tb02809.x.

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Salmi, T. T. "Dermatitis herpetiformis." Clinical and Experimental Dermatology 44, no. 7 (May 15, 2019): 728–31. http://dx.doi.org/10.1111/ced.13992.

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40

Bernhardt, Mark. "Dermatitis Herpetiformis." JAMA Dermatology 150, no. 8 (August 1, 2014): 806. http://dx.doi.org/10.1001/jamadermatol.2014.239.

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41

Olbricht, Suzanne M. "Dermatitis Herpetiformis." Archives of Dermatology 122, no. 4 (April 1, 1986): 418. http://dx.doi.org/10.1001/archderm.1986.01660160074022.

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42

Zone, John J. "Dermatitis herpetiformis." Current Problems in Dermatology 3, no. 1 (January 1991): 6–41. http://dx.doi.org/10.1016/1040-0486(91)90003-m.

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Reunala, T., P. Collin, K. Holm, P. Pikkarainen, A. Miettinen, N. Vuolteenaho, and M. Mäki. "Tolerance to oats in dermatitis herpetiformis." Gut 43, no. 4 (October 1, 1998): 490–93. http://dx.doi.org/10.1136/gut.43.4.490.

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Objectives—Recent studies on coeliac disease have shown that oats can be included in a gluten-free diet without adverse effects on the small bowel. The presence of a rash is also a sensitive indicator of gluten ingestion in dermatitis herpetiformis, and this was used to study whether patients with this disease could also tolerate oats.Patients/Methods—Eleven patients with dermatitis herpetiformis in remission on a gluten-free diet were challenged daily with 50 g oats for six months. Clinical symptoms were recorded, serum samples taken, and skin and small bowel biopsies performed before and after the oat challenge. A control group comprised of 11 patients with dermatitis herpetiformis on a conventional gluten-free diet was also studied.Results—Eight patients challenged with oats remained asymptomatic, two developed a transient rash, and one withdrew because of the appearance of a more persistent but mild rash. Three of the 11 controls also developed a transient rash. IgA endomysial antibodies remained negative in all patients. The small bowel villous architecture, the densities of intraepithelial CD3 and α/β and γ/δ T cell receptor positive lymphocytes and crypt epithelial cell DR expression remained unaltered during the oat challenge.Conclusions—The results confirm the absence of oat toxicity on the gluten sensitive small bowel mucosa and suggest that the rash in patients with dermatitis herpetiformis is not activated by eating oats.

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44

Khouna, Afaf, Siham Dikhaye, and Nada Zizi. "Impetigo herpetiformis: an unknown dermatosis of pregnancy." International Journal of Scientific Reports 6, no. 9 (August 20, 2020): 364. http://dx.doi.org/10.18203/issn.2454-2156.intjscirep20203551.

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<p>Impetigo herpetiformis or pustular psoriasis of pregnancy is a rare dermatosis of pregnancy that typically starts in the second half of pregnancy and resolves postpartum. It can be life threatening for both mother and fetus and often causes therapeutic problem. We report a case of 37-year-old pregnant woman with history of generalized pustular lesions in the two previous pregnancies, presenting an impetigo herpetiformis during her third pregnancy, resolved one day after the delivery.</p>

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45

TSUTSUMI, Reiko, Tesshin WATANABE, and Osamu YAMAMOTO. "Herpetiform Pemphigus." Nishi Nihon Hifuka 74, no. 4 (2012): 383–84. http://dx.doi.org/10.2336/nishinihonhifu.74.383.

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46

Dias, Margarida, António Pereira Santos, João Sousa, and Manuela Maya. "Herpetiform pemphigus." Journal of the European Academy of Dermatology and Venereology 12, no. 1 (January 1999): 82–85. http://dx.doi.org/10.1111/j.1468-3083.1999.tb00826.x.

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Goidstein, Glenn D., Paramjit Bhatia, and James Kalivas. "Herpetiform Protothecosis." International Journal of Dermatology 25, no. 1 (January 1986): 54–55. http://dx.doi.org/10.1111/j.1365-4362.1986.tb03405.x.

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Wattiez, Víctor, Nidia Aquino, Jesús García, Clara Mendoza, Gloria Mendoza, Luis Celias, Victoria Rivelli, Graciela Gorostiaga, and Arnaldo Aldama. "Dermatitis herpetiforme en joven con enfermedad celiaca silente." Revista Virtual de la Sociedad Paraguaya de Medicina Interna 2, no. 2 (October 12, 2015): 75–81. http://dx.doi.org/10.18004/rvspmi/2312-3893/2015.02(02)75-081.

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Barbosa, Wanessa Simão, Camila Martins Rodarte, Jackeline Gomes Guerra, Vanessa Gomes Maciel, Luiz Fernando Fróes Fleury Júnior, and Maurício Barcelos Costa. "Lúpus eritematoso sistêmico bolhoso: diagnóstico diferencial com dermatite herpetiforme." Anais Brasileiros de Dermatologia 86, no. 4 suppl 1 (August 2011): 92–95. http://dx.doi.org/10.1590/s0365-05962011000700024.

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Abstract:

O lúpus eritematoso sistêmico bolhoso é um subtipo raro do lúpus eritematoso sistêmico, que ocorre ainda de forma mais incomum nos pacientes pediátricos. Relatamos o caso de uma adolescente de 12 anos, apresentando lesões vésico-bolhosas em face, pescoço, tronco, mucosas oral e genital, anemia, leucocitúria estéril, FAN: 1/1280 padrão nuclear pontilhado grosso, Anti-Sm e Anti-RNP positivos. O estudo anatomopatológico sugere dermatite herpetiforme e a imunofluorescência direta revela IgG, IgA e fibrina ao longo da zona de membrana basal. Apresentamos um caso típico de lúpus eritematoso sistêmico bolhoso e enfatizamos a importância do diagnóstico diferencial com a dermatite herpetiforme

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Mendes, Fernanda Berti Rocha, Adaucto Hissa-Elian, Marilda Aparecida Milanez Morgado de Abreu, and Virgínica Scaff Gonçalves. "Review: dermatitis herpetiformis." Anais Brasileiros de Dermatologia 88, no. 4 (August 2013): 594–99. http://dx.doi.org/10.1590/abd1806-4841.20131775.

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Abstract:

Dermatitis herpetiformis (DH) or Duhring-Brocq disease is a chronic bullous disease characterized by intense itching and burning sensation in the erythematous papules and urticarial plaques, grouped vesicles with centrifuge growth, and tense blisters. There is an association with the genotypes HLA DR3, HLA DQw2, found in 80-90% of cases. It is an IgA-mediated cutaneous disease, with immunoglobulin A deposits appearing in a granular pattern at the top of the dermal papilla in the sublamina densa area of the basement membrane, which is present both in affected skin and healthy skin. The same protein IgA1 with J chain is found in the small intestinal mucosa in patients with adult celiac disease, suggesting a strong association with DH. Specific antibodies such as antiendomysium, antireticulina, antigliadin and, recently identified, the epidermal and tissue transglutaminase subtypes, as well as increased zonulin production, are common to both conditions, along with gluten-sensitive enteropathy and DH. Autoimmune diseases present higher levels of prevalence, such as thyroid (5-11%), pernicious anemia (1-3%), type 1 diabetes (1-2%) and collagen tissue disease. The chosen treatment is dapsone and a gluten-free diet.

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