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{{Infobox medical condition (new)
'''Linear IgA bullous dermatosis''' (also known as "Linear IgA dermatosis") is frequently associated with medication exposure, especially ], with men and women being equally affected.<ref name="Andrews">James, William; Berger, Timothy; Elston, Dirk (2005). ''Andrews' Diseases of the Skin: Clinical Dermatology''. (10th ed.). Saunders. ISBN 0-7216-2921-0.</ref>{{rp|135}} Linear IgA dermatosis is a rare immune-mediated blistering skin disease that may be divided into two types, ] and ].<ref name="Fitz2">Freedberg, et al. (2003). ''Fitzpatrick's Dermatology in General Medicine''. (6th ed.). McGraw-Hill. ISBN 0-07-138076-0.</ref>{{rp|587}}
| name = {{PAGENAME}}
| synonyms = Linear IgA dermatosis
| image = Linear IgA bullous dermatosis.jpg
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| caption = (a) Widespread vesiculobullous eruption on the lower limbs with elements in a “string of pearls” arrangement; <br>(b) targetoid vesicular lesions on erythematous skin involving the dorsa of the hands; <br>(c) blisters with a “string of pearls” configuration and crusts in the perioral area;<br> (d) erythematous, vesicular lesions partially eroded on the posterior aspects of both thighs;<br> (e) vesicles involving the vulvar area in a child.<ref>{{cite journal|last1=Genovese|first1=Giovanni|last2=Venegoni |first2=Luigia|last3=Fanoni|first3=Daniele |last4=Muratori|first4=Simona|last5=Berti|first5=Emilio |last6=Marzano|first6=Angelo Valerio|title=Linear IgA bullous dermatosis in adults and children: a clinical and immunopathological study of 38 patients|journal=Orphanet Journal of Rare Diseases|volume=14|issue=1|year=2019|page=115|issn=1750-1172|doi=10.1186/s13023-019-1089-2|pmid=31126328|pmc=6534856|doi-access=free}}
*"This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/)"</ref>
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'''Linear IgA bullous dermatosis''' is a rare immune-mediated blistering skin disease frequently associated with medication exposure, especially ], with men and women being equally affected.<ref name="Andrews">James, William; Berger, Timothy; Elston, Dirk (2005). ''Andrews' Diseases of the Skin: Clinical Dermatology''. (10th ed.). Saunders. {{ISBN|0-7216-2921-0}}.</ref>{{rp|135}} It was first described by ] in 1979 and may be divided into two types:<ref name="Fitz2">Freedberg, et al. (2003). ''Fitzpatrick's Dermatology in General Medicine''. (6th ed.). McGraw-Hill. {{ISBN|0-07-138076-0}}.</ref>{{rp|587}}


Adult linear IgA disease is an acquired, ] blistering disease that may present with a clinical pattern of vesicles indistinguishable from ], or with vesicles and bullae in a bullous ]-like appearance.<ref name="Andrews"/> This disease can often be difficult to treat even with usually effective medications such as ].<ref>{{cite journal |vauthors=He Y, Shimoda M, Ono Y, Villalobos IB, Mitra A, Konia T, Grando SA, Zone JJ, Maverakis E | title = Persistence of Autoreactive IgA-Secreting B Cells Despite Multiple Immunosuppressive Medications Including Rituximab | journal = JAMA Dermatol | volume = 151 | issue = 6 | pages = 646–50 | year = 2015 | pmid = 25901938 | doi = 10.1001/jamadermatol.2015.59| doi-access = }}</ref>
==See also==
* ]
* ]


Childhood linear IgA disease (also known as "Chronic bullous disease of childhood") is an acquired, self-limited bullous disease that may begin by the time the patient is age 2 to 3 and usually remits by age 13.<ref name="Andrews"/>
==References==

== Signs and symptoms ==
Lesions on the skin, ], or both may be seen in cases with linear IgA bullous dermatosis (LABD). While LABD can affect both adults and children, there are variations in the disease's clinical features between these two groups of people.<ref name="UpToDate">{{cite web | title=UpToDate | website=UpToDate |url=https://www.uptodate.com/contents/linear-iga-bullous-dermatosis | access-date=2024-02-17}}</ref>

The most common symptom of LABD of childhood, also called chronic bullous disease of childhood, is the sudden growth of vesicles or bullae on areas of skin that are either inflammatory or not. An arciform or annular appearance is frequently the consequence of new ] forming at the margins of lesions that are healing.<ref name="UpToDate"/> These lesions are often described as looking like rosettes, crowns of jewels, or strings of pearls.<ref name="Autoimmune Blistering Diseases in Children">{{cite journal | last1=Lara-Corrales | first1=Irene | last2=Pope | first2=Elena | title=Autoimmune Blistering Diseases in Children | journal=Seminars in Cutaneous Medicine and Surgery | publisher=Frontline Medical Communications, Inc. | volume=29 | issue=2 | year=2010 | issn=1085-5629 | doi=10.1016/j.sder.2010.03.005 | pages=85–91| pmid=20579597 }}</ref> Skin lesions typically occur in a wide range of locations, including the hands, feet, genitalia, trunk, and face, especially the perioral area. The lower abdomen, inner thighs, and perineum are frequently the most severely affected areas.<ref name="A study">{{cite journal | last1=MARSDEN | first1=R.A. | last2=McKEE | first2=P.H. | last3=BHOGAL | first3=B. | last4=BLACK | first4=M.M. | last5=KENNEDY | first5=L.A. | title=A study of benign chronic bullous dermatosis of childhood and comparison with dermatitis herpetiformis and bullous pemphigoid occurring in childhood | journal=Clinical and Experimental Dermatology | publisher=Oxford University Press (OUP) | volume=5 | issue=2 | year=1980 | issn=0307-6938 | doi=10.1111/j.1365-2230.1980.tb01684.x | pages=159–172| pmid=7002380 | s2cid=25865844 }}</ref><ref name="Clinical Features">{{cite journal | last1=Mintz | first1=Emily M. | last2=Morel | first2=Kimberly D. | title=Clinical Features, Diagnosis, and Pathogenesis of Chronic Bullous Disease of Childhood | journal=Dermatologic Clinics | publisher=Elsevier BV | volume=29 | issue=3 | year=2011 | issn=0733-8635 | doi=10.1016/j.det.2011.03.022 | pages=459–462| pmid=21605812 }}</ref><ref name="Chronic bullous disease of childhood">{{cite journal | last1=Wojnarowska | first1=Fenella | last2=Marsden | first2=R.A. | last3=Bhogal | first3=B. | last4=Black | first4=M.M. | title=Chronic bullous disease of childhood, childhood cicatricial pemphigoid, and linear IgA disease of adults | journal=Journal of the American Academy of Dermatology | publisher=Elsevier BV | volume=19 | issue=5 | year=1988 | issn=0190-9622 | doi=10.1016/s0190-9622(88)70236-4 | pages=792–805| pmid=3056993 }}</ref> Children who are affected may show no symptoms, yet ] is frequent and can get quite bad. For certain people, severe itching signals the beginning of the illness again.<ref name="Guide 2001">{{cite journal | last1=Guide | first1=Shireen V. | last2=Marinkovich | first2=M.Peter | title=Linear IgA bullous dermatosis | journal=Clinics in Dermatology | publisher=Elsevier BV | volume=19 | issue=6 | year=2001 | issn=0738-081X | doi=10.1016/s0738-081x(00)00185-1 | pages=719–727| pmid=11705681 }}</ref><ref name="adults">{{cite journal | last1=Chorzelski | first1=Tadeusz P. | last2=Jabłońska | first2=Stephania | last3=Maciejowska | first3=EWA | title=Linear IgA bullous dermatosis of adults | journal=Clinics in Dermatology | publisher=Elsevier BV | volume=9 | issue=3 | year=1991 | issn=0738-081X | doi=10.1016/0738-081x(91)90030-o | pages=383–392| pmid=1806226 }}</ref>

Adult patients with LABD usually have a sudden onset of skin lesions; however, the condition can develop more slowly. Bullae and tight vesicles can form inside inflammatory plaques or on healthy skin. Adults experience a lower incidence of developing annular lesions exhibiting peripheral vesiculation compared to children.<ref name="Venning 2011">{{cite journal | last=Venning | first=Vanessa A. | title=Linear IgA Disease: Clinical Presentation, Diagnosis, and Pathogenesis | journal=Dermatologic Clinics | publisher=Elsevier BV | volume=29 | issue=3 | year=2011 | issn=0733-8635 | doi=10.1016/j.det.2011.03.013 | pages=453–458| pmid=21605811 }}</ref> Lesion formation is prevalent in the trunk, extensor extremities, buttocks, and face (especially the perioral area).<ref name="Fortuna 2012">{{cite journal | last1=Fortuna | first1=Giulio | last2=Marinkovich | first2=M. Peter | title=Linear immunoglobulin A bullous dermatosis | journal=Clinics in Dermatology | publisher=Elsevier BV | volume=30 | issue=1 | year=2012 | issn=0738-081X | doi=10.1016/j.clindermatol.2011.03.008 | pages=38–50| pmid=22137225 }}</ref> There have also been reports of localized variations of LABD that manifest as annular inflammatory plaques or restricted blistering eruptions.<ref name="Gamo Aguilar Gónzalez‐Valle Houmani 2007 pp. 544–545">{{cite journal | last1=Gamo | first1=R | last2=Aguilar | first2=A | last3=Gónzalez-Valle | first3=O | last4=Houmani | first4=M | last5=Martín | first5=L | last6=Gallego | first6=MA | title=Localized linear IgA disease associated with monoclonal gammapathy of undetermined significance | journal=Journal of the European Academy of Dermatology and Venereology | publisher=Wiley | volume=21 | issue=4 | date=2007-03-05 | issn=0926-9959 | doi=10.1111/j.1468-3083.2006.01943.x | pages=544–545| pmid=17373989 | s2cid=39379260 }}</ref><ref name="He Xu Xiao Geng 2007 pp. 500–502">{{cite journal | last1=He | first1=Chundi | last2=Xu | first2=Honghui | last3=Xiao | first3=Ting | last4=Geng | first4=Long | last5=Chen | first5=Hong-Duo | title=Localized linear IgA dermatosis induced by UV light-treatment for herpes zoster | journal=International Journal of Dermatology | publisher=Wiley | volume=46 | issue=5 | date=2007-04-30 | issn=0011-9059 | doi=10.1111/j.1365-4632.2007.02966.x | pages=500–502| pmid=17472682 | s2cid=31441124 }}</ref><ref name="Shimanovich Rose Sitaru Bröcker 2004 pp. 95–98">{{cite journal | last1=Shimanovich | first1=Iakov | last2=Rose | first2=Christian | last3=Sitaru | first3=Cassian | last4=Bröcker | first4=Eva-B | last5=Zillikens | first5=Detlef | title=Localized linear IgA disease induced by ampicillin/sulbactam | journal=Journal of the American Academy of Dermatology | publisher=Elsevier BV | volume=51 | issue=1 | year=2004 | issn=0190-9622 | doi=10.1016/j.jaad.2004.03.027 | pages=95–98| pmid=15243532 }}</ref> Strong ] may cause excoriated ] or lesions resembling ] to appear.<ref name="Torchia Caproni Del Bianco Cozzani 2006 pp. 479–480">{{cite journal | last1=Torchia | first1=D. | last2=Caproni | first2=M. | last3=Del Bianco | first3=E. | last4=Cozzani | first4=E. | last5=Ketabchi | first5=S. | last6=Fabbri | first6=P. | title=Linear IgA disease presenting as prurigo nodularis | journal=British Journal of Dermatology | publisher=Oxford University Press (OUP) | volume=155 | issue=2 | date=2006-05-03 | issn=0007-0963 | doi=10.1111/j.1365-2133.2006.07315.x | pages=479–480| pmid=16882196 | s2cid=28166468 }}</ref>

Both adults and children can experience ] involvement. Up to 80% of adult patients experience mucosal illness.<ref name="Chronic bullous disease of childhood" /> Mucosal lesions usually manifest as erosions or ulcers; complete vesicles or bullae are not frequently found. Any mucosal surface, such as those in the mouth, ], nose, genitalia, ], ], ], and ], could be impacted.<ref name="Fortuna 2012"/><ref name="Chronic bullous disease of childhood" /><ref name="Venning 2011"/><ref name="Upper aerodigestive">{{cite journal | last1=Gluth | first1=Michael B | last2=Witman | first2=Patricia M | last3=Thompson | first3=Dana M | title=Upper aerodigestive tract complications in a neonate with linear IgA bullous dermatosis | journal=International Journal of Pediatric Otorhinolaryngology | publisher=Elsevier BV | volume=68 | issue=7 | year=2004 | issn=0165-5876 | doi=10.1016/j.ijporl.2004.02.014 | pages=965–970| pmid=15183590 }}</ref> The mucosal areas most frequently affected are the oral and ocular mucosa.<ref name="Chronic bullous disease of childhood" /><ref name="Venning 2011"/> Lesions on the palate, palatine arches, or buccal mucosa are commonly seen in patients with oral diseases.<ref name="Venning 2011"/> Additionally, erosive ] and ] might be signs of oral LABD.<ref name="KELLY FRITH MILLARD WOJNAROWSKA 1988 pp. 161–170">{{cite journal | last1=KELLY | first1=SUSAN E. | last2=FRITH | first2=PEGGY A. | last3=MILLARD | first3=P. R. | last4=WOJNAROWSKA | first4=FENELLA | last5=BLACK | first5=M. M. | title=A clinicopathological study of mucosal involvement in linear IgA disease | journal=British Journal of Dermatology | publisher=Oxford University Press (OUP) | volume=119 | issue=2 | year=1988 | issn=0007-0963 | doi=10.1111/j.1365-2133.1988.tb03197.x | pages=161–170| pmid=3048368 }}</ref> Conjunctival redness, ocular discharge, ocular pain, or a feeling of a foreign body can all be symptoms of ocular illness.<ref name="Chronic bullous disease of childhood" />

== Causes ==
Circulating ] anti-basement membrane zone antibodies directed against the 97 kDa component of ] (bullous pemphigoid antigen 2) in the ] are the primary cause of linear IgA bullous dermatosis (LABD).<ref name="Sarikaya Solak Ficicioglu 2019 p. e12927">{{cite journal | last1=Sarikaya Solak | first1=Sezgi | last2=Ficicioglu | first2=Sezin | title=Cephalosporin-induced linear IgA dermatosis in a child: Case report and literature review | journal=Dermatologic Therapy | publisher=Hindawi Limited | date=2019-06-03 | volume=32 | issue=4 | issn=1396-0296 | doi=10.1111/dth.12927 | page=e12927| pmid=30977941 | doi-access=free }}</ref><ref name="Matsumoto Nakamura Ishii Umemoto 2019 pp. 220–221">{{cite journal | last1=Matsumoto | first1=Takanao | last2=Nakamura | first2=Satoshi | last3=Ishii | first3=Norito | last4=Umemoto | first4=Naoka | last5=Kawase | first5=Masaaki | last6=Demitsu | first6=Toshio | last7=Hashimoto | first7=Takashi | title=Erythrodermic linear IgA/IgG bullous dermatosis | journal=European Journal of Dermatology | publisher=John Libbey Eurotext | volume=29 | issue=2 | year=2019 | issn=1952-4013 | doi=10.1684/ejd.2019.3503 | pages=220–221| pmid=30973330 | s2cid=108295628 }}</ref>

=== Risk factors ===
The most frequent benign condition linked to LABD is ].<ref name="213 cases in Japan">{{cite journal | last1=HORIGUCHI | first1=Yuji | last2=IKOMA | first2=Akihiko | last3=SAKAI | first3=Rie | last4=MASATSUGU | first4=Asako | last5=OHTA | first5=Miyuki | last6=HASHIMOTO | first6=Takashi | title=Linear IgA dermatosis: Report of an infantile case and analysis of 213 cases in Japan | journal=The Journal of Dermatology | publisher=Wiley | volume=35 | issue=11 | year=2008 | issn=0385-2407 | doi=10.1111/j.1346-8138.2008.00561.x | pages=737–743| pmid=19120770 | s2cid=32517522 }}</ref><ref name="Taniguchi Maejima Saito Katsuoka 2009 pp. 1284–1285">{{cite journal | last1=Taniguchi | first1=Tomonori | last2=Maejima | first2=Hideki | last3=Saito | first3=Norimitsu | last4=Katsuoka | first4=Kensei | last5=Haruki | first5=Satomi | title=Case of linear IgA bullous dermatosis-involved ulcerative colitis | journal=Inflammatory Bowel Diseases | publisher=Oxford University Press (OUP) | volume=15 | issue=9 | year=2009 | issn=1078-0998 | doi=10.1002/ibd.20795 | pages=1284–1285| pmid=19023862 }}</ref> It is unknown why there is a correlation between ] and LABD. According to some writers, aberrant ] production by the inflamed colon may have a role in the emergence of LABD.<ref name="Paige Leonard Wojnarowska Fry 1997 pp. 779–782">{{cite journal | last1=Paige | first1=D.G. | last2=Leonard | first2=J.N. | last3=Wojnarowska | first3=F. | last4=Fry | first4=L. | title=Linear IgA disease and ulcerative colitis | journal=British Journal of Dermatology | volume=136 | issue=5 | date=1997 | doi=10.1046/j.1365-2133.1997.6751622.x | pages=779–782| pmid=9205518 | s2cid=33294097 }}</ref>

Many case reports have documented the incidence of LABD in conjunction with solid organ cancers and ].<ref name="Holló Preisz Nemes Bíró 2003 pp. 143–146">{{cite journal | last1=Holló | first1=P. | last2=Preisz | first2=K. | last3=Nemes | first3=L. | last4=Bíró | first4=J. | last5=Kárpáti | first5=S. | last6=Horváth | first6=A. | title=Linear IgA dermatosis associated with chronic clonal myeloproliferative disease | journal=International Journal of Dermatology | publisher=Wiley | volume=42 | issue=2 | year=2003 | issn=0011-9059 | doi=10.1046/j.1365-4362.2003.01438_2.x | pages=143–146| pmid=12709006 | s2cid=31443626 }}</ref><ref name="GODFREY WOJNAROWSKA LEONARD 2006 pp. 447–452">{{cite journal | last1=GODFREY | first1=K. | last2=WOJNAROWSKA | first2=FENELLA | last3=LEONARD | first3=J. | title=Linear IgA disease of adults: association with lymphoproliferative malignancy and possible role of other triggering factors | journal=British Journal of Dermatology | publisher=Oxford University Press (OUP) | volume=123 | issue=4 | date=2006-07-29 | issn=0007-0963 | doi=10.1111/j.1365-2133.1990.tb01448.x | pages=447–452| pmid=2095175 | s2cid=29409150 }}</ref><ref name="Adamič Potočnik Pavlović 2008 pp. 503–505">{{cite journal | last1=Adamič | first1=M. | last2=Potočnik | first2=M. | last3=Pavlović | first3=M. D. | title=Linear IgA bullous dermatosis in a patient with advanced pancreatic carcinoma | journal=Clinical and Experimental Dermatology | publisher=Oxford University Press (OUP) | volume=33 | issue=4 | year=2008 | issn=0307-6938 | doi=10.1111/j.1365-2230.2008.02767.x | pages=503–505| pmid=18498404 | s2cid=43629819 }}</ref>

],<ref name="Takagi Sawada Yamauchi Amagai 2000 pp. 513–516">{{cite journal | last1=Takagi | first1=Y. | last2=Sawada | first2=S. | last3=Yamauchi | first3=M. | last4=Amagai | first4=M. | last5=Niimura | first5=M. | title=Coexistence of psoriasis and linear IgA bullous dermatosis | journal=British Journal of Dermatology | publisher=Oxford University Press (OUP) | volume=142 | issue=3 | date=2000-03-01 | issn=1365-2133 | doi=10.1046/j.1365-2133.2000.03367.x | pages=513–516| pmid=10735961 | s2cid=37297071 }}</ref> ],<ref name="Tobón Toro Bravo Cañas 2007 pp. 391–393">{{cite journal | last1=Tobón | first1=Gabriel J. | last2=Toro | first2=Carlos E. | last3=Bravo | first3=Juan-Carlos | last4=Cañas | first4=Carlos A. | title=Linear IgA bullous dermatosis associated with systemic lupus erythematosus: a case report | journal=Clinical Rheumatology | publisher=Springer Science and Business Media LLC | volume=27 | issue=3 | date=2007-10-12 | issn=0770-3198 | doi=10.1007/s10067-007-0752-5 | pages=391–393| pmid=17932615 | s2cid=20800832 }}</ref> and a number of infections have also been linked to LABD in a small number of patients.<ref name="Smitt Leusen Stas Teeuw 1997 pp. 150–152">{{cite journal | last1=Smitt | first1=J H S. | last2=Leusen | first2=J H W | last3=Stas | first3=H G | last4=Teeuw | first4=A H | last5=Weening | first5=R S | title=Chronic bullous disease of childhood and a paecilomyces lung infection in chronic granulomatous disease | journal=Archives of Disease in Childhood | publisher=BMJ | volume=77 | issue=2 | date=1997-08-01 | issn=0003-9888 | doi=10.1136/adc.77.2.150 | pages=150–152| pmid=9301356 | pmc=1717284 }}</ref><ref name="Simon Dietrich Kapp Schopf 1995 pp. 485–489">{{cite journal | last1=Simon | first1=Jan C. | last2=Dietrich | first2=Andrea | last3=Kapp | first3=Alexander | last4=Schopf | first4=Erwin | title=Chronisch bullose Dermatose des Kindesalters Assoziation mit einer Salmonellen-Enteritis | journal=Der Hautarzt | publisher=Springer Science and Business Media LLC | volume=46 | issue=7 | date=1995-07-01 | issn=0017-8470 | doi=10.1007/s001050050287 | pages=485–489| pmid=7672989 | s2cid=23651196 }}</ref> There have also been reports of LABD developing after ] exposure.<ref name="Salmhofer Soyer Wolf Födinger 2004 pp. 109–115">{{cite journal | last1=Salmhofer | first1=Wolfgang | last2=Soyer | first2=H.Peter | last3=Wolf | first3=Peter | last4=Födinger | first4=Dagmar | last5=Hödl | first5=Stefan | last6=Kerl | first6=Helmut | title=UV light–induced linear IgA dermatosis | journal=Journal of the American Academy of Dermatology | publisher=Elsevier BV | volume=50 | issue=1 | year=2004 | issn=0190-9622 | doi=10.1016/s0190-9622(03)02120-0 | pages=109–115| pmid=14699378 }}</ref><ref name="Wozniak Kalinska-Bienias Hashimoto Kowalewski 2014 pp. 1578–1581">{{cite journal | last1=Wozniak | first1=K. | last2=Kalinska-Bienias | first2=A. | last3=Hashimoto | first3=T. | last4=Kowalewski | first4=C. | title=Ultraviolet-induced linear IgA bullous dermatosis: a case report and literature survey | journal=British Journal of Dermatology | publisher=Oxford University Press (OUP) | volume=171 | issue=6 | date=2014-10-30 | issn=0007-0963 | doi=10.1111/bjd.13154 | pages=1578–1581| pmid=24888577 | s2cid=45413559 }}</ref>

=== Triggers ===
Drug exposure has been shown in several case reports to be a contributing factor. The pharmacologic medication most commonly mentioned as a possible initiating cause is ].<ref name="Fortuna Salas-Alanis Guidetti Marinkovich 2012 pp. 988–994">{{cite journal | last1=Fortuna | first1=Giulio | last2=Salas-Alanis | first2=Julio Cesar | last3=Guidetti | first3=Eugenio | last4=Marinkovich | first4=M. Peter | title=A critical reappraisal of the current data on drug-induced linear immunoglobulin A bullous dermatosis: A real and separate nosological entity? | journal=Journal of the American Academy of Dermatology | publisher=Elsevier BV | volume=66 | issue=6 | year=2012 | issn=0190-9622 | doi=10.1016/j.jaad.2011.09.018 | pages=988–994| pmid=22169257 }}</ref> A number of ], ], ], ], ], ], ], ], ], and ] are a few other medications that may be connected to LABD.<ref name="Fortuna 2012"/><ref name="Ho Ng Tan Giam 2007 p. ">{{cite journal | last1=Ho | first1=Jean Chin Ching | last2=Ng | first2=Pei Lin Patricia | last3=Tan | first3=Suat Hoon | last4=Giam | first4=Yoke Chin | title=Childhood Linear IgA Bullous Disease Triggered by Amoxicillin-Clavulanic Acid | journal=Pediatric Dermatology | publisher=Wiley | volume=24 | issue=5 | date=2007-08-06 | pages=E40-3 | issn=0736-8046 | doi=10.1111/j.1525-1470.2007.00438.x | pmid=17958778 | s2cid=7278884 }}</ref><ref name="Polat Lenk Kürekçi Öztaş 2007 pp. 389–391">{{cite journal | last1=Polat | first1=Muhterem | last2=Lenk | first2=Nurdan | last3=Kürekçi | first3=Emin | last4=Öztaş | first4=Pinar | last5=Artüz | first5=Ferda | last6=Alli | first6=Nuran | title=Chronic Bullous Disease of Childhood in a Patient with Acute Lymphoblastic Leukemia | journal=American Journal of Clinical Dermatology | publisher=Springer Science and Business Media LLC | volume=8 | issue=6 | year=2007 | issn=1175-0561 | doi=10.2165/00128071-200708060-00010 | pages=389–391| pmid=18039023 | s2cid=9453819 }}</ref><ref name="Kocyigit Akay Karaosmanoðlu 2009 pp. e123–e124">{{cite journal | last1=Kocyigit | first1=P. | last2=Akay | first2=B. N. | last3=Karaosmanoðlu | first3=N. | title=Linear IgA bullous dermatosis induced by interferon-α 2a | journal=Clinical and Experimental Dermatology | publisher=Oxford University Press (OUP) | volume=34 | issue=5 | year=2009 | issn=0307-6938 | doi=10.1111/j.1365-2230.2008.03160.x | pages=e123–e124| pmid=19508467 | s2cid=23778144 }}</ref>

=== Genetics ===
Development of LABD may also be influenced by genetic factors. There have been reports of associations between LABD and the ]-2 allele, ] (HLA) B8, HLA Cw7, HLA DR3, and HLA DQ2.<ref name="Collier Wojnarowska Welsh Mcguire 1999 pp. 867–875">{{cite journal | last1=Collier | first1=P.M. | last2=Wojnarowska | first2=F. | last3=Welsh | first3=K. | last4=Mcguire | first4=W. | last5=Black | first5=M.M. | title=Adult linear IgA disease and chronic bullous disease of childhood: the association with human lymphocyte antigens Cw7, B8, DR3 and tumour necrosis factor influences disease expression | journal=British Journal of Dermatology | publisher=Oxford University Press (OUP) | volume=141 | issue=5 | year=1999 | issn=0007-0963 | doi=10.1046/j.1365-2133.1999.03110.x | pages=867–875| pmid=10583169 | s2cid=652581 }}</ref>

== Mechanism ==
While it is acknowledged that one of the hallmarks of linear IgA bullous dermatosis (LABD) is the presence of ] antibodies linked to the ], the process by which lesions occur in this condition is not well known. The pathophysiology of this disease may involve both cellular and humoral immune responses.<ref name="UpToDate" /> Specifically, the formation of cutaneous and mucosal lesions may be facilitated by tissue damage brought on by an antibody-induced local inflammatory response as well as the release of proteolytic enzymes by ] along with other inflammatory cells.<ref name="Fortuna 2012" />

The majority of LABD patients exhibit ] antibodies that are specific to the ] zone's 97 kDa and 120 kDa antigens.<ref name="UpToDate" /> Bullous pemphigoid antigen 2 (BP180/]), a transmembrane protein essential for epidermal-dermal adhesion, is broken down into pieces in both of these antigens.<ref name="adults" /><ref name="Guide 2001" /> Less commonly, the NC16a epitope on BP180 has been linked to LABD.<ref name="Ishii Ohyama Yamaguchi Hashimoto 2008 pp. 1151–1153">{{cite journal | last1=Ishii | first1=N. | last2=Ohyama | first2=B. | last3=Yamaguchi | first3=Z. | last4=Hashimoto | first4=T. | title=IgA autoantibodies against the NC16a domain of BP180 but not 120-kDa LAD-1 detected in a patient with linear IgA disease | journal=British Journal of Dermatology | publisher=Oxford University Press (OUP) | volume=158 | issue=5 | year=2008 | issn=0007-0963 | doi=10.1111/j.1365-2133.2008.08492.x | pages=1151–1153| pmid=18363761 | s2cid=31976851 }}</ref><ref name="Zillikens Herzele Georgi Schmidt 1999 pp. 947–953">{{cite journal | last1=Zillikens | first1=Detlef | last2=Herzele | first2=Karin | last3=Georgi | first3=Matthias | last4=Schmidt | first4=Enno | last5=Chimanovitch | first5=Iakov | last6=Bröcker | first6=Eva-B | last7=Schumann | first7=Hauke | last8=Mascaro | first8=Jose M. | last9=Diaz | first9=Luis A. | last10=Bruckner-Tuderman | first10=Leena | last11=Giudice | first11=George J. | title=Autoantibodies in a Subgroup of Patients with Linear IgA Disease React with the NC16A Domain of BP1801 | journal=Journal of Investigative Dermatology | publisher=Elsevier BV | volume=113 | issue=6 | year=1999 | issn=0022-202X | doi=10.1046/j.1523-1747.1999.00808.x | pages=947–953| pmid=10594735 | doi-access=free }}</ref> ] antibodies directed against various basement membrane antigens, such as ] (COL7), ], or ], are present in certain patients with LABD.<ref name="Tsuchisaka Ohara Ishii Nguyen 2015 pp. 626–629">{{cite journal | last1=Tsuchisaka | first1=Atsunari | last2=Ohara | first2=Koji | last3=Ishii | first3=Norito | last4=Nguyen | first4=Ngon T. | last5=Marinkovich | first5=M Peter | last6=Hashimoto | first6=Takashi | title=Type VII Collagen Is the Major Autoantigen for Sublamina Densa–Type Linear IgA Bullous Dermatosis | journal=Journal of Investigative Dermatology | publisher=Elsevier BV | volume=135 | issue=2 | year=2015 | issn=0022-202X | doi=10.1038/jid.2014.381 | pages=626–629| pmid=25207819 | doi-access=free }}</ref> The target antigen in certain people with ]-induced LABD appears to be ].<ref name="Yamagami Nakamura Nagao Funakoshi 2018 pp. 1473–1480">{{cite journal | last1=Yamagami | first1=Jun | last2=Nakamura | first2=Yoshio | last3=Nagao | first3=Keisuke | last4=Funakoshi | first4=Takeru | last5=Takahashi | first5=Hayato | last6=Tanikawa | first6=Akiko | last7=Hachiya | first7=Takahisa | last8=Yamamoto | first8=Toshiyuki | last9=Ishida-Yamamoto | first9=Akemi | last10=Tanaka | first10=Toshihiro | last11=Fujimoto | first11=Noriki | last12=Nishigori | first12=Chikako | last13=Yoshida | first13=Tetsuya | last14=Ishii | first14=Norito | last15=Hashimoto | first15=Takashi | last16=Amagai | first16=Masayuki | title=Vancomycin Mediates IgA Autoreactivity in Drug-Induced Linear IgA Bullous Dermatosis | journal=Journal of Investigative Dermatology | publisher=Elsevier BV | volume=138 | issue=7 | year=2018 | issn=0022-202X | doi=10.1016/j.jid.2017.12.035 | pages=1473–1480| pmid=29410066 | pmc=8054301 }}</ref>

== Diagnosis ==
The clinical manifestations of various mucocutaneous disorders may be confused with those of linear IgA bullous dermatosis (LABD). Therefore, laboratory studies are usually used to confirm the diagnosis when available.<ref name="UpToDate" /> The gold standard for diagnosing LABD is the detection of linear IgA deposits along the ] zone using direct ] (DIF), even though the results of a regular histopathologic examination of the affected tissue may suggest LABD.<ref name="Guide 2001" />

Linear IgA bullous dermatosis histopathologic features are vague and frequently mimic ].<ref name="UpToDate" /> Characteristic is a subepidermal blister with an underlying dermal infiltration that is primarily composed of ].<ref name="Fortuna 2012" /> There may also be papillary microabscesses, ], and ] that resemble those found in ].<ref name="Guide 2001" />

== Treatment ==
First-line treatment for LABD is thought to be ], an immunomodulatory ] that has been successfully used to treat a variety of dermatologic illnesses marked by neutrophilic infiltrates.<ref name="213 cases in Japan" /> Treatment with ] or ], ] drugs with chemical similarities to ], may be beneficial for patients who cannot tolerate ].<ref name="Guide 2001" />

== Gallery ==
<gallery>
File:Micrograph of linear IgA bullous dermatosis.jpg|]: Subepidermal blister formation and neutrophils
File:IgA bullous dermatosis.jpg
</gallery>

== See also ==
* ]
* ]

== References ==
{{reflist}} {{reflist}}


== Further reading ==
]
* {{cite journal | last1=Kasperkiewicz | first1=Michael | last2=Meier | first2=Markus | last3=Zillikens | first3=Detlef | last4=Schmidt | first4=Enno | title=Linear IgA Disease: Successful Application of Immunoadsorption and Review of the Literature | journal=Dermatology | publisher=S. Karger AG | volume=220 | issue=3 | year=2010 | issn=1018-8665 | doi=10.1159/000279318 | pages=259–263 | pmid=20130384 | s2cid=19960443 | ref=none}}
]
* {{cite journal | last1=M | first1=Kharfi | last2=A | first2=Khaled | last3=A | first3=Karaa | last4=I | first4=Zaraa | last5=B | first5=Fazaa | last6=MR | first6=Kamoun | title=Linear IgA bullous dermatosis: the more frequent bullous dermatosis of children | journal=Dermatology Online Journal | date=15 January 2010 | publisher=Dermatol Online J | volume=16 | issue=1 | page=2 | doi=10.5070/D32TS975M4 | issn=1087-2108 | pmid=20137744 |url=https://pubmed.ncbi.nlm.nih.gov/20137744/ | access-date=2024-02-18 | ref=none}}


== External links ==
*
*

{{Medical resources
| ICD11 = {{ICD11|EB42}}
| ICD10 = {{ICD10|L10.8}}
| ICD10CM = <!-- {{ICD10CM|Xxx.xxxx}} -->
| ICD9 = <!-- {{ICD9|xxx}} -->
| ICDO =
| OMIM =
| MeshID = D062027
| DiseasesDB = 7487
| SNOMED CT = 95330001
| Curlie =
| MedlinePlus =
| eMedicineSubj = article
| eMedicineTopic = 1063590
| PatientUK = linear-iga-dermatosis
| NCI =
| GeneReviewsNBK =
| GeneReviewsName =
| NORD =
| GARDNum = 10960
| GARDName = Linear IgA disease
| RP =
| AO =
| WO =
| OrthoInfo =
| Orphanet = 46488
| Scholia = Q5405504
| OB =
}}


{{Cutaneous-condition-stub}}
{{Vesiculobullous disease}} {{Vesiculobullous disease}}


]
]
]
]

Latest revision as of 08:37, 22 August 2024

Medical condition
Linear IgA bullous dermatosis
Other namesLinear IgA dermatosis
(a) Widespread vesiculobullous eruption on the lower limbs with elements in a “string of pearls” arrangement;
(b) targetoid vesicular lesions on erythematous skin involving the dorsa of the hands;
(c) blisters with a “string of pearls” configuration and crusts in the perioral area;
(d) erythematous, vesicular lesions partially eroded on the posterior aspects of both thighs;
(e) vesicles involving the vulvar area in a child.
SpecialtyImmunology, dermatology Edit this on Wikidata

Linear IgA bullous dermatosis is a rare immune-mediated blistering skin disease frequently associated with medication exposure, especially vancomycin, with men and women being equally affected. It was first described by Tadeusz Chorzelski in 1979 and may be divided into two types:

Adult linear IgA disease is an acquired, autoimmune blistering disease that may present with a clinical pattern of vesicles indistinguishable from dermatitis herpetiformis, or with vesicles and bullae in a bullous pemphigoid-like appearance. This disease can often be difficult to treat even with usually effective medications such as rituximab.

Childhood linear IgA disease (also known as "Chronic bullous disease of childhood") is an acquired, self-limited bullous disease that may begin by the time the patient is age 2 to 3 and usually remits by age 13.

Signs and symptoms

Lesions on the skin, mucous membranes, or both may be seen in cases with linear IgA bullous dermatosis (LABD). While LABD can affect both adults and children, there are variations in the disease's clinical features between these two groups of people.

The most common symptom of LABD of childhood, also called chronic bullous disease of childhood, is the sudden growth of vesicles or bullae on areas of skin that are either inflammatory or not. An arciform or annular appearance is frequently the consequence of new blisters forming at the margins of lesions that are healing. These lesions are often described as looking like rosettes, crowns of jewels, or strings of pearls. Skin lesions typically occur in a wide range of locations, including the hands, feet, genitalia, trunk, and face, especially the perioral area. The lower abdomen, inner thighs, and perineum are frequently the most severely affected areas. Children who are affected may show no symptoms, yet pruritus is frequent and can get quite bad. For certain people, severe itching signals the beginning of the illness again.

Adult patients with LABD usually have a sudden onset of skin lesions; however, the condition can develop more slowly. Bullae and tight vesicles can form inside inflammatory plaques or on healthy skin. Adults experience a lower incidence of developing annular lesions exhibiting peripheral vesiculation compared to children. Lesion formation is prevalent in the trunk, extensor extremities, buttocks, and face (especially the perioral area). There have also been reports of localized variations of LABD that manifest as annular inflammatory plaques or restricted blistering eruptions. Strong pruritus may cause excoriated papules or lesions resembling prurigo nodularis to appear.

Both adults and children can experience mucous membrane involvement. Up to 80% of adult patients experience mucosal illness. Mucosal lesions usually manifest as erosions or ulcers; complete vesicles or bullae are not frequently found. Any mucosal surface, such as those in the mouth, conjunctiva, nose, genitalia, pharynx, larynx, anus, and esophagus, could be impacted. The mucosal areas most frequently affected are the oral and ocular mucosa. Lesions on the palate, palatine arches, or buccal mucosa are commonly seen in patients with oral diseases. Additionally, erosive cheilitis and gingivitis might be signs of oral LABD. Conjunctival redness, ocular discharge, ocular pain, or a feeling of a foreign body can all be symptoms of ocular illness.

Causes

Circulating IgA anti-basement membrane zone antibodies directed against the 97 kDa component of BPAG2 (bullous pemphigoid antigen 2) in the lamina lucida are the primary cause of linear IgA bullous dermatosis (LABD).

Risk factors

The most frequent benign condition linked to LABD is ulcerative colitis. It is unknown why there is a correlation between ulcerative colitis and LABD. According to some writers, aberrant IgA1 production by the inflamed colon may have a role in the emergence of LABD.

Many case reports have documented the incidence of LABD in conjunction with solid organ cancers and lymphoproliferative diseases.

Psoriasis, systemic lupus erythematosus, and a number of infections have also been linked to LABD in a small number of patients. There have also been reports of LABD developing after UV radiation exposure.

Triggers

Drug exposure has been shown in several case reports to be a contributing factor. The pharmacologic medication most commonly mentioned as a possible initiating cause is vancomycin. A number of antibiotics, nonsteroidal anti-inflammatory medications, lithium, amiodarone, captopril, cyclosporine, phenytoin, interferon alfa, furosemide, and somatostatin are a few other medications that may be connected to LABD.

Genetics

Development of LABD may also be influenced by genetic factors. There have been reports of associations between LABD and the tumor necrosis factor-2 allele, human leukocyte antigen (HLA) B8, HLA Cw7, HLA DR3, and HLA DQ2.

Mechanism

While it is acknowledged that one of the hallmarks of linear IgA bullous dermatosis (LABD) is the presence of IgA antibodies linked to the basement membrane zone, the process by which lesions occur in this condition is not well known. The pathophysiology of this disease may involve both cellular and humoral immune responses. Specifically, the formation of cutaneous and mucosal lesions may be facilitated by tissue damage brought on by an antibody-induced local inflammatory response as well as the release of proteolytic enzymes by neutrophils along with other inflammatory cells.

The majority of LABD patients exhibit IgA1 antibodies that are specific to the basement membrane zone's 97 kDa and 120 kDa antigens. Bullous pemphigoid antigen 2 (BP180/type XVII collagen), a transmembrane protein essential for epidermal-dermal adhesion, is broken down into pieces in both of these antigens. Less commonly, the NC16a epitope on BP180 has been linked to LABD. IgA antibodies directed against various basement membrane antigens, such as type VII collagen (COL7), laminin-332, or laminin gamma 1, are present in certain patients with LABD. The target antigen in certain people with vancomycin-induced LABD appears to be type VII collagen.

Diagnosis

The clinical manifestations of various mucocutaneous disorders may be confused with those of linear IgA bullous dermatosis (LABD). Therefore, laboratory studies are usually used to confirm the diagnosis when available. The gold standard for diagnosing LABD is the detection of linear IgA deposits along the basement membrane zone using direct immunofluorescence (DIF), even though the results of a regular histopathologic examination of the affected tissue may suggest LABD.

Linear IgA bullous dermatosis histopathologic features are vague and frequently mimic dermatitis herpetiformis. Characteristic is a subepidermal blister with an underlying dermal infiltration that is primarily composed of neutrophils. There may also be papillary microabscesses, eosinophils, and lymphocytes that resemble those found in dermatitis herpetiformis.

Treatment

First-line treatment for LABD is thought to be dapsone, an immunomodulatory sulfone that has been successfully used to treat a variety of dermatologic illnesses marked by neutrophilic infiltrates. Treatment with sulfapyridine or sulfamethoxypyridazine, sulfonamide drugs with chemical similarities to dapsone, may be beneficial for patients who cannot tolerate dapsone.

Gallery

  • Micrograph: Subepidermal blister formation and neutrophils Micrograph: Subepidermal blister formation and neutrophils

See also

References

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  32. Salmhofer, Wolfgang; Soyer, H.Peter; Wolf, Peter; Födinger, Dagmar; Hödl, Stefan; Kerl, Helmut (2004). "UV light–induced linear IgA dermatosis". Journal of the American Academy of Dermatology. 50 (1). Elsevier BV: 109–115. doi:10.1016/s0190-9622(03)02120-0. ISSN 0190-9622. PMID 14699378.
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Further reading

External links

ClassificationD
External resources
Vesiculobullous disease
Acantholysis
(epidermis)
Pemphigus
Other
Pemphigoid
(dermis)
IgG:
IgA:
Other bullous
In diseases
classified elsewhere
Categories: