PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 7387898

Transient acantholytic dermatosis.

P J Heenan·C J Quirk
View original source ↗Export metadata ↓

Abstract

A series of twenty-four cases of transient acantholytic dermatosis (TAD) is presented. All patients were male and their eruptions tended to be more persistent than those of previously reported cases. The epidermal changes included four patterns of acantholysis, of which the pemphigus-like pattern was associated with the more persistent eruptions. Although twenty-three of the twenty-four patients had other actinic-associated skin lesions, no direct relationship between the onset of TAD and episodes of excessive sun exposure was found. Oral vitamin A treatment has been effective in some cases.

Explore related subjects

AcantholysisAdultAgedHumansMaleMiddle AgedPhotosensitivity DisordersSex FactorsSkin DiseasesTime FactorsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P J Heenan, C J Quirk. 1980. Transient acantholytic dermatosis.. https://doi.org/10.1111/j.1365-2133.1980.tb07648.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Changes in desmoglein 1 expression and subcellular localization in cultured keratinocytes subjected to anti-desmoglein 1 pemphigus autoimmunity.

The complexity of pemphigus acantholysis together with the weak expression of desmoglein 1 (Dsg1) in cultured keratinocytes have made the study on the pathogenic action of anti-Dsg1 antibodies quite difficult. The pathophysiology of the acantholytic phenomenon could depend on the reduction of Dsg1 adhesion function occurring after its massive internalization or decrease of its synthesis. Here, we have investigated this hypothesis by using sera of patients having antibodies against Dsg1 or monoclonal anti-Dsg1 antibodies to simulate pemphigus autoimmunity in Dsg1-rich keratinocytes. Similar to pemphigus foliaceus (PF) and vulgaris (PV) sera, monoclonal anti-Dsg1 antibodies induced transient internalization of Dsg1 and reduced the adhesion strength among keratinocytes. However, binding of IgG to Dsg1 did not determine its early depletion from the adhesion complexes but reduced the amount of Dsg1 found in the Triton X-100 soluble pool of proteins. Taken together, our results represent the first demonstration that anti-Dsg1 antibodies induce similar alterations on the subcellular distribution of Dsg1 irrespective of the disease where they come from. Furthermore, the present study provides insight into the mechanisms underlying epithelial blistering observed in the skin type of pemphigus.

Acantholysis↗
PubMed2006

Pathogenic human monoclonal antibody against desmoglein 3.

Pemphigus vulgaris (PV) is a potentially fatal autoimmune mucocutaneous disease associated with production of IgG autoantibodies to desmoglein 3 (Dsg3), a 130-kDa epidermal cadherin protein. The binding of pathogenic antibody to Dsg3 on epidermal keratinocytes leads to loss of intercellular adhesion and results in intraepithelial blister formation. Here, we describe a human monoclonal antibody, PVMAB786, a Dsg3-specific IgG4 antibody, from an untreated patient with active PV. The antibody reacts with a 130-kDa protein on keratinocyte cell surfaces and recombinant Dsg3 protein, but not desmoglein 1 protein. PVMAB786 induces acantholysis in normal human skin and mucous membranes and induces a clinical and histological profile similar to human PV when injected into neonatal mice. PVMAB786 will be a valuable tool in identifying the role of Dsg3 in epithelial cell adherence and acantholysis, mechanisms of Dsg3 processing/presentation and V gene and isotype usage in PV pathogenesis.

Acantholysis↗