https://www.cidjournal.com/article/S0738-081X(11)00084-8/pdf

Linear immunoglobulin A bullous dermatosis

https://www.cidjournal.com/article/S0738-081X(13)00007-2/pdf

Bullous pemphigoid: etiology, pathogenesis, and inducing factors: facts and controversies

Linijna IgA dermatoza/choroba pêcherzowa (linear IgA bullous dermatosis/disease, linear IgA disease) (LABD) jest przewlek31 podnaskórkow1 dermatoz1 pêcherzow1, wystêpuj1c1 u doros3ych i dzieci z autoimmunizacji wobec ró¿nych antygenów po31czenia skórno-naskórkowego (DEJ). Cech1 tej choroby s1 autoprzeciwcia3a w klasie IgA, które w technikach immunofluorescencji reaguj1 wzd3u¿nie w DEJ. Ostatnio, po stwierdzeniu na poziomie molekularnym zwi1zków z innymi autoimmunizacyjnymi chorobami pêcherzowymi skóry, odrêbnoœæ nozologiczna tej dermatozy jest coraz powszechniej dyskutowana. Upowszechnia siê pogl1d, ¿e wiêkszoœæ przypadków tej choroby powinno siê umieœciæ w krêgu pemfigoidu pêcherzowego (BP), b1dŸ krêgu nabytego pêcherzowego oddzielania siê naskórka (EBA). S1 te¿ przypadki molekularnie odrêbne od innych autoimmunizacyjnych dermatoz podnaskórkowych. Autor zdecydowa3 siê na wydzielenie tej dermatozy ze wzglêdu na to, ¿e dlaczego dochodzi w niej do odpowiedzi autoimmunologicznej g3ównie w klasie IgA, lecz nie IgG, nie zosta3o do tej pory zadowalaj1co naœwietlone.

Linear IgA bullous dermatosis

Atypical presentations of bullous pemphigoid: Clinical and immunopathological aspects.

Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease affecting mainly the elderly. The subtype of the disease induced by physical agents represents a rare and, therefore, insufficiently characterized form. In the present study, we aimed to contribute to a better understanding of the pathogenetic mechanisms involved in the onset of BP induced by different trigger factors. We have retrospectively analyzed nine cases of BP. All patients were characterized based on clinical, epidemiological and immunological parameters. For each case, the trigger factor involved was specified. In addition to our retrospective analysis, a comprehensive review of the 59 published cases was conducted, regarding the involvement of trigger factor in BP, and clinical, epidemiological and immunological data were collected. In the local study, conducted on nine patients diagnosed with BP, various trigger factors were identified: contrast substance injection, surgical procedure, mechanical trauma, insect bite, thermal burn, radiotherapy and ultraviolet exposure associated with pre-existing psoriasis. The autoantibodies from all patients were shown to activate granulocytes and induce dermal-epidermal split. Different hypotheses regarding the pathogenetic mechanism involving the trigger factors have been discussed. In regard of the pathogenetic mechanism, we believe that the most reliable hypothesis is that BP patients already have low titers of anti-basement membrane autoantibodies which activate the granulocytes. However, more studies are needed for a better understanding of the pathogenetic mechanism of the intervention of trigger factors.

Role of physical factors in the pathogenesis of bullous pemphigoid: Case report series and a comprehensive review of the published work.

References 1 Knol AC, Guilloux Y, Quereux G, et al. CD8 T lymphocytes reactive against Epstein–Barr virus antigens in skin lesions of a patient with Sezary syndrome. J Am Acad Dermatol 2005; 53: 897–900. 2 Agnarsson BA, Vonderheid EC, Kadin ME. Cutaneous T cell lymphoma with suppressor/cytotoxic (CD8) phenotype. J Am Acad Dermatol 1990; 22: 569–577. 3 Lu D, Patel KA, Duvic M, et al. Clinical and pathological spectrum of CD8-positive cutaneous T-cell lymphomas. J Cutan Pathol 2002; 29: 465–472. 4 Diamandidou E, Colome-Grimmer M, Fayad L, et al. Transformation of mycosis fungoides/Sezary syndrome: clinical characteristics and prognosis. Blood 1998; 92: 1150–1159. 5 Berti E, Tomasini D, Vermeer MH, et al. Primary cutaneous CD8-positive epidermotropic cytotoxic T-cell lymphoma: a distinct clinicopathological entity with an aggressive clinical behavior. Am J Pathol 1999; 155: 483–492. 6 Willemze R, Jaffe ES, Burg G, et al. WHO–EORTC classification for cutaneous lymphomas. Blood 2005; 105: 3768–3785. 7 Bekkenk MW, Vermeer MH, Jansen PM, et al. Peripheral T-cell lymphomas unspecified presenting in the skin: analysis of prognostic factors in a group of 82 patients. Blood 2003; 102: 2213–2219. 8 Ralfkiaer E, Muller-Hermelink HK, Jaffe ES. Peripheral T-cell lymphoma, unspecified. In: Jaffe ES, Harris NL, Stein H, et al., eds. Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues. World Health Organization Classification of Tumours, Vol. 3. Lyon: IARC Press, 2001: 227–229. 9 Pinkus GS, Said JW. Peripheral T-cell lymphomas. In: Knowles DM, ed. Neoplastic Hematopathology, 2nd edn. Philadelphia, PA: Williams & Wilkins, 2000: 1091–1125. 10 Agnarsson BA, Vonderheid EC, Kadin ME. Cutaneous T-cell lymphoma with suppressor/cytotoxic (CD8) phenotype: identification of rapidly progressive and chronic subtypes. J Am Acad Dermatol 1990; 22: 569–577.

Bullous pemphigoid initially localized around a urostomy.

Subacute prurigo-like linear IgA disease A 72-year-old white woman was referred to our clinic with a 2-year history of generalized pruritus that had never been investigated or treated. She also suffered from arterial hypertension, carotid artery stenosis, noninsulin-dependent diabetes mellitus, generalized anxiety disorder, and osteoporosis. She was taking chlorthalidone 25 mg, acetylsalicylic acid 100 mg, and delorazepam 1 mg daily. Physical examination showed numerous roundish, excoriated papules, studded by erosions or serosanguineous crusts, distributed on the face, neck, upper trunk, forearms, and thighs (Fig. 1). Laboratory blood investigation revealed a slight increase in glucose (130 mg/dL; normal range, 2–30 mg/dL), uric acid (7.3 mg/dL; normal range, 2–7 mg/dL), and fibrinogen (432 mg/dL; normal range, 200–400 mg/dL). Histopathologic examination of an excoriated papular lesion showed an epidermal ulceration and a dense inflammatory infiltrate, localized in the perivascular and junctional dermis, and composed of lymphocytes, histiocytes, neutrophils, and scant numbers of eosinophils (Fig. 2a). Direct immunofluorescence (DIF) assay on perilesional skin demonstrated linear deposits of immunoglobulin (Ig) A, IgM, C3, and fibrinogen along the basement membrane zone (BMZ). Indirect immunofluorescence (IIF) assay, using monkey esophagus and human healthy skin as substrates, was negative for serum IgG, IgA, and IgM. Salt-split skin (SSS)-DIF revealed linear deposits of IgA along the epidermal side of split perilesional skin (Fig. 2b), and SSS-IIF showed a linear discontinuous deposit of IgA along the epidermal side of normal human skin. Immunoblot (IB) analysis of an epidermal extract detected an IgA band at 230 kDa (Fig. 2c), whereas IB analysis of a dermal extract was negative. On the basis of these findings, we made a diagnosis of linear IgA disease (LAD) and, having excluded glucose-6phosphate dehydrogenase deficiency, oral therapy with dapsone 50 mg daily, prednisone 25 mg daily, and hydroxyzine 10 mg daily was started. During the following weeks, the patient reported a decrease in pruritus and there was an improvement in the cutaneous lesions. Unfortunately, after 2 months, the patient developed methemoglobinemia. Therefore, dapsone was stopped and treatment with progressively decreasing doses of prednisone was continued, with near-total maintenance of the previously achieved results.

Subacute prurigo-like linear IgA disease.

Its potential for confusion with skin lesions of systemic candidiasis. Arch Intern Med 1982; 142:2126–9. 8 Rosen T, Schell JB, Orengo I. Anti-inflammatory activity of antifungal preparations. Int J Dermatol 1997; 36:788–92. 9 Faergemann F, Bergbrant IM, Dohse M et al. Seborrhoeic dermatitis and Pityrosporum (Malassezia) folliculitis: characterization of inflammatory cells and mediators in the skin by immunohistochemistry. Br J Dermatol 2001; 144:549–56. 10 Hill MK, Goodfield JD, Rodgers FG et al. Skin surface electron microscopy in Pityrosporum folliculitis: the role of follicular occlusion in disease and the response to oral ketoconazole. Arch Dermatol 1990; 126:181–4.

Linear IgA disease presenting as prurigo nodularis.

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Bullous pemphigoid initially localized around a urostomy.

Subacute prurigo-like linear IgA disease.

Linear IgA disease presenting as prurigo nodularis.