International Journal of Dermatology

2005,

44

, 969–970 © 2005

The International Society of Dermatology

970 Correspondence

capacity under

in vitro

or

in vivo

conditions. Moreover, therewas no significant improvement in facial vitiligo after4 months of treatment.

Acknowledgments

This study was supported by a donation from the DeutscheVitiligo-Verein eV Hamburg, Germany. We kindly acknow-ledge the help of the patients and volunteers.

Karin U. Schallreuter

,

MD

Hartmut Rokos

,

PhD

Bradford, UK

References

1 Maresca V, Roccella M, Roccella F,

et al.

Increased sensitivity to peroxidative agents as a possible pathogenic factor of melanocyte damage in vitiligo.

J Invest Dermatol

1997;

109

: 310–313.2 Dell’Anna ML, Urbanelli S, Mastrofrancesco A,

et al.

Alterations of mitochondria in peripheral blood mononuclear cells of vitiligo patients.

Pigment Cell Res

2003;

16

: 553–559.3 Dell’Anna ML, Maresca V, Briganti S,

et al.

Mitochondrial impairment in peripheral blood mononuclear cells during the active phase of vitiligo.

J Invest Dermatol

2001;

117

: 908–913.

4 Schallreuter KU, Moore J, Wood JM,

et al.

In vivo and in vitro evidence for hydrogen peroxide (H

2

O

2

) accumulation

in the epidermis of patients with vitiligo and its successful removal by a UVB-activated pseudocatalase.

J Invest Dermatol Symp Proc

1999;

4

: 91–96.5 Schallreuter KU, Moore J, Wood JM,

et al.

Epidermal H

2

O

2

accumulation alters tetrahydrobiopterin (6BH

4

) recycling in vitiligo: identification of a general mechanism in regulation of all 6BH

4

-dependent processes?

J Invest Dermatol

2001;

116

: 167–174.6 Hasse S, Gibbons NC, Rokos H,

et al.

Perturbed 6-tetrahydrobiopterin recycling via decreased dihydropteridine reductase in vitiligo: more evidence for H

2

O

2

stress.

J Invest Dermatol

2004;

122

: 307–313.7 Schallreuter KU, Wood JM, Lemke KR,

et al.

Treatment of vitiligo with a topical application of pseudocatalase and calcium in combination with short-term UVB exposure: a case study on 33 patients.

Dermatology

1995;

190

: 223–229.

8 Schallreuter KU, Moore J, Behrens-Williams S,

et al.

Rapid initiation of repigmentation in vitiligo with Dead Sea climatotherapy in combination with pseudocatalase (PC-KUS).

Int J Dermatol

2002;

41

: 482–487.9 Schallreuter KU, Elwary SM, Gibbons NC,

et al.

Activation/deactivation of acetylcholinesterase by H

2

O

2

: more evidence for oxidative stress in vitiligo.

Biochem Biophys Res Commun

2004;

315

: 502–508.10 Schallreuter KU, Moore J, Behrens-Williams S,

et al.

In vitro and in vivo identification of pseudocatalase activity in Dead Sea water using Fourier transform Raman spectroscopy.

J Raman Spectrosc

2002;

33

: 586–592.

Correspondence

CorrespondenceCorrespondenceCORRESPONDENCE

Role of direct immunofluorescence test in cutaneous leukocytoclastic vasculitis

Dear Sir,We would like to comment on the recent article by

Barnadas

et al

.

1

addressing the diagnostic, prognostic andpathogenic value of the direct immunofluorescence test incutaneous leukocytoclastic vasculitis.

Although classification criteria for Schönlein-Henochpurpura by the American College of Rheumatology do notinclude direct immunofluorescence findings,

2

historically,Schönlein-Henoch purpura, the most frequent vasculitis ofchildhood, has been considered an IgA-mediated small-vesselvasculitis with direct immunofluorescence test showingisolated or predominant deposition of IgA along the dermalvessels and in the kidney. However, deposition of IgA in thecutaneous vessels are not restricted to Schönlein-Henochpurpura and its diagnostic value when considering the differ-ent vasculitic syndromes is still a matter of controversy.

3–5

Intheir study Barnadas and coworkers conclude that IgA isthe immunoglobulin most frequently found in vessels ofboth lesional and perilesional skin in leukocytoclastic vas-culitis and that the presence of IgA in the skin is associatedwith renal involvement. The authors do not include dataconcerning how frequent was the detection of isolated IgA

(without associated IgG or IgM) in the cutaneous vasculiticlesions, and the final vasculitic syndromes diagnosed intheir patients are not provided. Moreover, the authorssuggest that the value of DIF findings in the skin in dis-criminating patients with Shönlein-Henoch purpura isprobably low.

In our study,

6

including 160 patients (most adults) withhistologically documented cutaneous leukocytoclasticvasculits a direct immunofluorescence test was undertaken in102 cases. Our results showed deposition of IgA in dermalvessels in 64.7% of cases, of IgM in 49%, of IgG in 42.2%and of C3 in 80.4%. In 15.8% of the patients, DIF wasnegative, and we found that the positivity of DIF wasinversely correlated with the duration of the biopsied lesion(

P <

0.001). So, as Barnadas and coworkers mention in theirstudy, we found that IgA was the immunoglobulin mostfrequently detected in cutaneous lesions of leukocytoclasticvasculitis. In only 5.2% of the patients of our series was afinal diagnosis of Schönlein-Henoch purpura performed.However, as discussed in our report, in only eight cases wasdeposition of IgA in dermal vessels not associated with IgM orIgG deposition, and in most of these eight patients (including,Schönlein-Henoch purpura and severe alcohol abuse) a directpathogenic role of IgA could be proposed.

International Journal of Dermatology

2005,

44

, 970–971 © 2004

The International Society of Dermatology

© 2005

The International Society of Dermatology International Journal of Dermatology

2005,

44

, 969–970

971Correspondence

So, while we agree with Barnadas

et al

. that in the contextof cutaneous leukocytoclastic vasculitis the finding of IgAassociated with other immunoglobulins in the vessels oflesional skin has a low specificity for discriminatingSchönlein-Henoch purpura from other small-vessel vasculitis,an isolated IgA (or with C3) finding may be, in our opinion,characteristic of Schönlein-Henoch disease.

A second question that arises when considering the roleof DIF in cutaneous vasculitis is whether the detection ofcirculating ANCA correlates with the existence of a pauci-immune vasculitis with negative results in the DIF tests, asstated by some authors

7–9

or, as we have previously sug-gested, whether the pathogenesis of vasculitis involving theskin includes a variety of mechanisms acting in concertand the presence of circulating ANCA and deposition ofimmunocomplexes (a time-dependent finding) are notmutually exclusive.

10

We would be very grateful if the authors could provide dataconcerning their ANCA results and its relationship with theimmunoreactants deposited in the skin and kidney.

Sais Gemma

Hospital de Mataró, Barcelona, Spain

Vidaller Antonio

C.S.U. Bellvitge University of Barcelona, Barcelona, Spain

References

1 Barnadas MA, Perez E, Gich I,

et al.

Diagnostic, prognostic and pathogenic value of the direct immunofluorescence test in cutaneous leukocytoclastic vasculitis.

Int J Dermatol

2004;

43

: 19–26.

2 Mills JA, Michel BA, Bloch DA,

et al.

The American College of Rheumatology 1990 criteria for the classification of Henoch-Schönlein purpura.

Arthr Rheum

1990;

33

: 1114–1121.3 Helander SD, De Castro FR, Gibson LE. Henoch-Schönlein

purpura: clinicopathologic correlation of cutaneous vascular IgA deposits and the relationship to leukocytoclastic vasculitis.

Acta Derm Venereol

1995;

75

: 125–129.4 Van Hale HM, Gibson LE, Shroeter AL. Henoch-Schönlein

vasculitis: direct immunofluorescence of uninvolved skin.

J Am Acad Dermatol

1986;

15

: 665–670.5 Tsai CC, Giangiacomo J, Zuckner J. Dermal IgA depositis in

Henoch-Schönlein purpura and Berger’s nephritis.

Lancet

1975;

1

: 342–343.6 Sais G, Vidaller A, Jucglà A,

et al.

Prognostic factors in leukocytoclastic vasculitis. A clinicopathologic study of 160 patients.

Arch Dermatol

1998;

134

: 309–315.7 Sais G, Vidaller A. Prognostic facotrs in leukocytoclastic

vasculitis: What is the role of antineutrophil cytoplasmic antibody ?

In Reply Arch Dermatol

1999;

135

: 714–715.8 Jennette JC, Falk RJ. Antineutrophil cytoplasmic antibodies

and associated diseases: a review.

Am J Kidney Dis

1990;

15

: 517–529.9 Cohen Tervaert JW, Goldschmeding R, Elema JD,

et al.

Association of autoantibodies to myeloperoxidase with different forms of vasculitis.

Arthritis Rheum

1990;

33

: 1264–1272.10 Falk RJ, Jennette JC. Anti-neutrophil cytoplasmic

autoantibodies with specificity for myeloperoxidase in patients with systemic vasculitis and idiopathic necrotizing and crescentic glomerulonephritis.

N Engl J Med

1988;

318

: 1651–1657.

Correspondence

Dear Sir,We are grateful to Sais

et al

. for their interest in andcomments on our article.

Concerning the first question, we did not observe a clearrelationship between the finding of isolated IgA in cutaneousvessels and kidney involvement. In two of the nine patientswith mesangial deposits of IgA in the kidney, we also observedIgM, associated with IgA, in skin vessels. These findings arein concordance with the early reports of cutaneous bloodvessel wall deposits of IgA in Henoch-Schönlein patients:Baart de la Faille detected IgG and IgM,

1

and Tsai et al.detected IgM and/or IgG, both in association with IgA.2 Weagree with the aforementioned authors and others that thereis a predominant, but not exclusive, presence of IgA in skinvessels in this entity.1–4 Furthermore, we detected IgA, neitherwith IgG nor with IgM, in some patients with leucocytoclasticvasculitis (LV) without kidney involvement. We cannottherefore conclude that isolated IgA deposits in skin vesselsare specific to Henoch-Schönlein purpura.

With respect to antineutrophil cytoplasmic antibodies(ANCA), by means of the indirect immunofluorescence test,we detected a specific antineutrophil pattern only in twopatients: one with a perinuclear pattern and the other with acytoplasmic pattern. Owing to the small number of cases wedid not perform a statistical analysis.

Maria A. BarnadasHospital de la Sta. Creu i St. Pau, Barcelona, Spain José BallarínFundació Puigvert, Barcelona, Spain

References1 Baart de la Faille-Kuyper EH, Kater L, Kooiker CJ, et al.

IgA deposits in cutaneous blood-vessel walls and mesangium in Henoch–Schönlein syndrome. Lancet 1973; i: 892–893.

2 Tsai CC, Giangiacomo J, Zuckner J. Dermal IgA deposits in Henoch-Schönlein purpura and Berger’s nephritis. Lancet 1975; i: 342–343.

© 2004 The International Society of Dermatology International Journal of Dermatology 2005, 44, 971–972