Antinuclear antibodies in patients with lichen planus

Abstract

Lichen planus (LP) is a mucocutaneous syndrome of yet uncertain pathogenesis, and it has usually been considered to be a dermatosis without antinuclear antibodies (ANA) nor other specific auto-antibodies. Over 10 years ago a series of indirect immunofluorescence researches with patients' lesional skin and serum disclosed the presence of lichen planus specific antigens (LPSA). After this, a number of substrates have been submitted for evaluation. In this study we have carried out indirect immunofluorescent test in relation with different substrates, with the aim of verifying whether the negative results previously obtained were due to poor sensitivity of the substrates employed. Subsequently we have compared the results obtained in the erosive forms of LP with those obtained in the non-erosive forms. We have concluded that rat oesophagus is a better substrate for the detection of ANA in patients with LP, as it has proved to have a positivity rate of 40.42%. Monkey oesophagus has provided a rate of 27.6%, and HEP-2 cells and rat liver have proved to be unsuitable. In addition, we have observed that the frequency of ANA is higher in the erosive forms of LP (P = 0.0389). In this article we demonstrate that the presence of ANA in patients with LP depends on the substrate employed, the most suitable substrate being rat oesophagus. Also, we demonstrate that ANA is more frequently observed in patients with erosive LP.

Lichen planus is associated with human herpesvirus type 7 replication and infiltration of plasmacytoid dendritic cells

“…1,2 The aetiology is unknown but it is speculated that LP is caused by a viral infection. 3 Hepatitis C virus (HCV) has been suggested as a causal agent for LP, 4 but epidemiological correlations are not strong. 5 Nevertheless, viral causality in LP seems plausible because of the acute onset and the overall single episode presentation.…”

“…Lichen planus (LP) is an inflammatory skin disease with a self‐limiting course 1,2 . The aetiology is unknown but it is speculated that LP is caused by a viral infection 3 . Hepatitis C virus (HCV) has been suggested as a causal agent for LP, 4 but epidemiological correlations are not strong 5 .…”

Absence of leukocyte microchimerism in oral lichen planus (OLP): an in situ hybridisation study

“…Anti-epithelial and anti-nuclear antibodies have also been found in some OLP patients (36)(37)(38)(39)(40)(41), as well as basal cell cytoplasmic autoantibodies in oral lichenoid reactions (42). It is interesting to note in such a context that oral and skin lichenoid lesions are also observed in graft-versus-host-disease (GVHD), which is a frequent complication in patients who have undergone allogeneic bone marrow transplantation, thus implicating an immune mechanism for such lesions (43,44).…”

Prevalence of stratified epithelium-specific antinuclear antibodies in 138 patients with lichen planus

“…7 In addition, antiebasal cell antibodies have been detected using rat esophagus as substrate and found to be directed to the cytoplasm or, more frequently, to the membrane of epitheliocytes. 8 In 1997, Carrizosa, Elorza, and Carnacho, 9 using monkey and rat esophagus as substrates, found ANAs (possibly SESANAs) in a high proportion of LP patients (40.4% for rat esophagus and 27.6% for monkey esophagus), mostly exhibiting a speckled pattern and being more frequent in the erosive forms. In the same year, Lodi et al, 10 SES-ANAs are considered the immunological marker of chronic ulcerative stomatitis.…”