ARTICLE
Discussion
Granuloma faciale is an uncommon skin disorder presenting as reddish
brown papules, nodules and plaques on the face. Lesions are usually asymptomatic
although occasionally pruritus and tenderness have been reported. The
disorder typically affects healthy middle-aged white men, but it may also
occur in women and even in children [1]. The color of the lesions ranges
from normal skin color to purple and surface changes are usually limited
to follicular dilatation. Extrafacial lesions, with or without co-existing
facial lesions, have been reported [2, 3].
The etiology and exact pathogenesis of the disorder remain unknown.
Diagnosis is usually established through the histopathological findings
that are quite distinctive. In spite of its name skin biopsies do not
show any granuloma formation or an infiltrate rich in histiocytes. Distinctive
histopathological features include a dense polymorphous dermal infiltrate
consisting of eosinophils, neutrophils, plasma cells, lymphocytes and
histiocytes. The infiltrate is separated from both the epidermis and the
adnexal structures by the characteristic Grenz zone. There may be some
degree of vasculitis involving the papillary and middermal capillaries.
Perivascular deposition of immunglobulins (usually IgG) and complement
has been reported on direct immunofluorescence examination. Based on these
observations some authors consider granuloma faciale as a variant of chronic
leukocytoclastic vasculitis confined to the skin [4, 5]. Immunophenotypic
analysis in an attempt to define the nature of the lymphocytic infiltrate
in granuloma faciale has shown the cells to be almost exclusively T-helper
lymphocytes. Since they express interleukin-2 receptors, ICAM-1, lymphocyte
functional antigen (LFA)-1 and HLA-DR, these lymphocytes have been suggested
as producing gamma-interferon. Under the influence of gamma-interferon,
ICAM-1 expression on keratinocytes, which causes migration of lymphocytes
to the epidermis, is expected to occur. In granuloma faciale, however,
it has been observed that there is a lack of expression of ICAM-1 by basal
keratinocytes and this has been suggested as resulting in the formation
of the Grenz zone [6].
The clinical differential diagnosis includes sarcoidosis, chronic cutaneous
lupus erythematosus, polymorphous light eruption, pseudolymphoma, lymphoma/leukemia
cutis, mycosis fungoides, insect bite reaction and fixed drug eruption.
The clinical course of granuloma faciale is usually chronic with exacerbations
and remissions. Occasionally permanent spontaneous clearing may occur.
Multiple treatment modalities have been employed for the disease, but
none has been consistently successful. Drugs that have been proposed include
dapsone [7], antimalarials, colchicine, topical, intralesional or systemic
corticosteroids and clofazimine. Physical modalities such as surgical
excision, dermabrasion [8], carbon dioxide [8] and argon laser, electrodesiccation
[8], topical PUVA, cryotherapy and combination of cryotherapy and intralesional
corticosteroid injection [9] have also been used with variable results.
Further studies are necessary to define the pathophysiology of granuloma
faciale and to establish the effective mode of treatment.
Article accepted on 16/1/00
REFERENCES
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3. Castano E, et al. Granuloma faciale entirely in an
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