Histology of linear IgA disease, dermatitis herpetiformis, and bullous pemphigoid

Blenkinsopp, W. K.; Haffenden, G P; Fry, Lionel; Leonard, J.N.

doi:10.1097/00000372-198312000-00005

Cited by 64 publications

(20 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…15,16 Dermatitis herpetiformis can also induce subepidermal blisters, but it is also accompanied by dermal microabscesses. 17 The limitation of this case report is the inability to prove the etiology of BP. There have been many etiologies in humans, such as HLA genes, an imbalance between autoreactive T helper and T regulatory cells, drug intake, physical agents (e.g., radiation therapy, ultraviolet radiation, thermal or electrical burns, surgical procedures, and transplants), viral infections, and environmental agents.…”

Section: Case Presentationmentioning

confidence: 91%

Bullous pemphigoid‐like skin blistering disease in a rhesus macaque (Macaca mulatta)

Kim

Min

et al. 2016

J of Medical Primatology

View full text Add to dashboard Cite

Autoimmune bullous disease is very uncommon in non-human primates. We observed a bullous skin disease in a male rhesus monkey while conducting porcine islet xenotransplantation. Fifty days after the transplantation, multiple bullous skin lesions were observed. There was no mucosal involvement. Skin biopsy results demonstrated a subepidermal blister with no necrotic keratinocytes. Immunofluorescent staining showed linear IgG deposition at the roof of the blister. These skin lesions spontaneously disappeared. Considering these results, this monkey was diagnosed with bullous pemphigoid (BP). As far as we know, this is the first report of BP in non-human primates.

show abstract

Section: Case Presentationmentioning

confidence: 91%

Bullous pemphigoid‐like skin blistering disease in a rhesus macaque (Macaca mulatta)

Kim

Min

et al. 2016

J of Medical Primatology

View full text Add to dashboard Cite

show abstract

“…Nie jest badaniem rekomendowanym i koniecznym do wykonania w rutynowej diagnostyce. Nie rozstrzyga różnicowania z LABD [37].…”

Section: Badanie Histopatologiczne Skóryunclassified

“…Wskazane jest więc, aby do badania histopatologicznego pobierać materiał z okolicy obejmującej rumieniowo lub pokrzywkowo zmienione najbliż-sze otoczenie świeżego, trwającego krócej niż dobę wykwitu ewoluującego w kierunku pęcherzyka. Uzyskuje się wtedy charakterystyczny obraz mikroropni ze znaczną przewagą liczbową neutrofilów i domieszką eozynofilów na szczytach brodawek skórnych i podnaskórkowymi szczelinami ponad tymi mikroropniami [1,3,9,37].…”

Section: Badanie Histopatologiczne Skóryunclassified

Diagnostic and therapeutic guidelines of dermatitis herpetiformis (Duhring’s disease) – consensus of Polish Dermatological Society

Żebrowska¹,

Waszczykowska²,

Kowaléwski³

et al. 2016

View full text Add to dashboard Cite

StreSzczenieOpryszczkowate zapalenie skóry (dermatitis herpetiformis -DH, choroba Duhringa) jest autoimmunizacyjną chorobą pęcherzową z charakterystyczną, polimorficzną osutką świądową. Procesowi autoimmunologicznemu wobec transglutaminaz (TGs) w skórze towarzyszy zwykle klinicznie bezobjawowa lub skąpoobjawowa jelitowa nadwrażliwość na gluten. Postępowanie diagnostyczne w DH powinno się opierać na badaniu klinicznym, bezpośrednim badaniu immunofluorescencyjnym skóry klinicznie niezmienionej z otoczenia wykwitów i oznaczeniu surowiczych przeciwciał IgA techniką ELISA z jednym substratem z zakresu do wyboru (tTG, eTG, npG, neo-tTG) lub przeciwciał IgAEmA. U chorych z niejednoznacznym obrazem kliniczno-laboratoryjnym takie postępowanie można uzupełnić o badanie histopatologiczne wycinka ze skóry chorobowo zmienionej i badanie haplotypu HLA DQ2/ DQ8. Powiązanie leczenia farmakologicznego dapsonem i stosowania diety bezglutenowej lub ograniczenie glutenu jest postępowaniem terapeutycznym z wyboru w DH. AbStrActDermatitis herpetiformis (Duhring's disease) is an autoimmune blistering dermatosis with a characteristic polymorphic, itchy rash. The autoimmune process against transglutaminases (TGs) is connected with asymptomatic or with mild symptoms of gluten-sensitive enteropathy (GSE). The diagnostic approach in DH should rely on clinical evaluation, direct immunofluorescence of perilesional skin and evaluation of serum IgA antibodies with ELISA with one substrate of four substrates from which to choose (tTG, eTG, npG, neo-tTG) using the ELISA

show abstract

“…1,2 It occurs both in adults (adult LAD) and in children (chronic bullous disease of childhood). 3 There is a body of evidence suggesting that LAD is a heterogeneous disease as regards its clinical features which may be bullous pemphigoid (BP)-like, dermatitis herpetiformis (DH)-like or 'jewel'-like, 4 histopathological findings (BPlike or DH-like) 5 and immunopathological patterns. The histopathology of LAD appears similar to that of DH, with neutrophilic microabscesses and fibrin at the papillary tips associated with oedema of the papillae, or similar to that of BP, with a subepidermal blister and a predominance of eosinophils.…”

mentioning

confidence: 99%

The role of lymphocytes, granulocytes, mast cells and their related cytokines in lesional skin of linear IgA bullous dermatosis

Caproni

Rolfo

Bernacchi

et al. 1999

British Journal of Dermatology

View full text Add to dashboard Cite

Linear IgA bullous dermatosis (LAD) is an acquired, heterogeneous, subepidermal blistering disease characterized by linear IgA deposits at the dermoepidermal basement membrane zone (BMZ), often with circulating IgA antibodies to the BMZ. The pathogenetic mechanism, possibly related to the immunophenotype of infiltrating cells, as well as the potential role of cytokines in determining bullous lesions, have not yet been elucidated. An immunohistochemical study was performed with a large panel of monoclonal antibodies [to CD3, CD4, CD8, CD25, CD1a, CD30, CD54, CD50, endothelial leucocyte adhesion molecule-1, vascular cell adhesion molecule-1, myeloperoxidase (MPO), eosinophil cationic protein EG1 and EG2, tryptase, HLA-DR, human interleukin (IL)-3, human IL-5, human IL-8, human IL-4, tumour necrosis factor (TNF)-alpha, interferon (IFN)-gamma and granulocyte/macrophage colony-stimulating factor] using the alkaline phosphatase-antialkaline phosphatase procedure on lesional and perilesional skin of nine patients (one male, eight female; age range 8 months-80 years) with clinical, histological and immunofluorescent proven LAD. The predominant infiltrating cells, distributed mostly inside and below the bullae, were neutrophils and eosinophils which showed intense activation (MPO +, EG1 +, EG2 +). The lymphocytic infiltrate, consisting principally of CD4 +, HLA-DR + and CD30 + T cells, had a predominantly perivascular distribution. Proinflammatory cytokines, such as TNF-alpha and IFN-gamma, showed a moderate focal expression on the dermal perivascular sites; IL-8 was found to have a particularly intense staining on all the epidermal cell layers and at perivascular and vascular sites. Other cytokines, such as IL-4 and IL-5, showed a prevalent intracytoplasmic staining on some cells of the dermal infiltrate (probably mastocytes and lymphocytes), and at the dermal-epidermal separation sites there was also an intense scattered distribution of IL-5. The specific tissue lesions of LAD may be the consequence of the IgA deposits at the BMZ and also of the release of these cytokines together with tissue damage enzymes derived from neutrophils or eosinophils.

show abstract

Histology of linear IgA disease, dermatitis herpetiformis, and bullous pemphigoid

Cited by 64 publications

References 0 publications

Bullous pemphigoid‐like skin blistering disease in a rhesus macaque (Macaca mulatta)

Bullous pemphigoid‐like skin blistering disease in a rhesus macaque (Macaca mulatta)

Diagnostic and therapeutic guidelines of dermatitis herpetiformis (Duhring’s disease) – consensus of Polish Dermatological Society

The role of lymphocytes, granulocytes, mast cells and their related cytokines in lesional skin of linear IgA bullous dermatosis

Contact Info

Product

Resources

About