You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 122 No. 4, April 1986 TABLE OF CONTENTS
  Archives
  •  Online Features
  STUDIES
 This Article
 •References
 •Full text PDF
 •Correction
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Dermatitis Herpetiformis

Cutaneous Deposition of Polyclonal IgA1

Suzanne M. Olbricht, MD; Thomas J. Flotte, MD; A. Bernard Collins; Clifford M. Chapman, MS; Terence J. Harrist, MD

Arch Dermatol. 1986;122(4):418-421.


Abstract

• Dermatitis herpetiformis (DH) is a pruritic papulovesicular skin disorder of unknown cause, characterized by granular IgA deposits in the dermis along the dermoepidermal junction. It is associated with gluten-sensitive enteropathy and increased IgA production by gut lymphoid tissue. We report four cases of immunologically documented DH studied by immunofluorescence technique. Monoclonal antibodies against the IgA subclasses IgA1 and IgA2 were used. IgA1 without IgA2 was found in the cutaneous deposits in each case. The IgA1 had both {kappa} and X light chains in approximately equal quantities. Because normal gut-associated lymphoid tissue produces 70% IgA1 and 30% IgA2, while circulating IgA is primarily IgA1, it could be concluded that the IgA in the skin of DH patients is not produced in the gut. However, the subclass restriction of the IgA produced by pathologic gut-associated lymphoid tissue is unknown. Alternatively, both IgA1 and IgA2 may be produced by the gut, but only IgA1 is involved in the production of cutaneous lesions.

(Arch Dermatol 1986;122:418-421)



Author Affiliations

From the Department of Dermatology, Beth Israel Hospital (Dr Olbricht), the Department of Pathology, Massachusetts General Hospital (Drs Flotte and Harrist and Mr Collins), and the Harvard Medical School and Pathology Services (Dr Harrist and Mr Chapman), Boston.


Footnotes

Accepted for publication Dec 20, 1985.

Presented in part at the 73rd annual meeting of the United States-Canadian Division of the International Academy of Pathology, San Francisco, March 12, 1984.

Reprint requests to Department of Dermatology, Beth Israel Hospital, 330 Brookline Ave, Boston, MA 02215 (Dr Olbricht).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Dermatitis Herpetiformis Bodies: Ultrastructural Study on the Skin of Patients Using Direct Preembedding Immunogold Labeling
Karpati et al.
Arch Dermatol 1990;126:1469-1474.
ABSTRACT  

Dietary Management of Dermatitis Herpetiformis
Hall
Arch Dermatol 1987;123:1378a-1380a.
ABSTRACT  

The Cause of Dermatitis Herpetiformis
Fry et al.
Arch Dermatol 1987;123:293-293.
ABSTRACT  

The Cause of Dermatitis Herpetiformis-Reply
Olbricht and Harrist
Arch Dermatol 1987;123:293-293.
ABSTRACT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1986 American Medical Association. All Rights Reserved.