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Journal of the

682 Correspondence American Academy of


Dermatology

years prior to our seeing him, spontaneous and trauma- REFERENCES


induced blisters appeared on the dorsal surfaces of the 1. lablonska S, Orth G: Human papoviruses, in Rook A,
hands, the elbows, the knees, and the legs, with milia Maibach HI, editors: Recent advances in dermatology 6.
formation, mild scarring, nail dystrophy, and skin fra- New York, 1983, Churchill Livingstone, pp. 1-36.
2. Lutzner MA: The human papillomaviruses. Arch Derma-
gility. Other bullous diseases were excluded. Electran tol119:631-635, 1983.
microscopy showed dermoepidermal separation in the 3. Lutzner MA, Blanchet BC, Puissant A: Oral aromatic
papillary dermis, below the lamina densa. This was retinoid (Ro 10-9359) treatment of two patients suffering
confirmed by indirect immunofluorescence of a blister with a severe form of epidermoclysplasia verruciformis, in
biopsy: the bullous pemphigoid antigen, laminin, and Orfanos CE, Braun-Falco 0, Farber E, et aI, editors: Ret-
inoids: Advances in basic research and therapy. Berlin
collagen IV were found in the roof of the blister. How- 1981, Springer-Verlag, pp. 407-410.
ever, direct immunofluorescence test results of perile- 4. Jablonska S, Obalek S, Wolska H, et al: Ro 10-9359 in
sionalskin for IgG, IgA, IgM, and C3 showed negative epidermodysplasia verruciformis. Preliminary report, ill
reactions (7 different biopsies over a 4-year period). Orfanos CE, Braun-Falco 0, Farber E, et al editors: Ret-
No circulating autoantibodies against basement memo inoids: Advances in basic research and therapy. Berlin,
1981 , Springer-Verlag, pp. 401-405.
brane zone were detected. We concluded that absence
5. Marks R: Synthetic retinoids, in Rook A, Maibach HI,
of basement membrane zone immunoreactants is pos- editors: Recent advances in dermatology 6. New York,
sible in epidermolysis bullosa. This could suggest that 1983, Churchill Livingstone, pp. 237-263.
they do not necessarily take part in the pathogenesis of
this disease and that their presence is only secondary. Porokeratosis and immunosuppression
Another explanation could be that our patient had a new To the Editor:
unknown disease, as suggested by Unis et a1. We have read with interest the paper by Lederman,
J. P. Lacour, M.D., and J. P. Ortonne, M.D. Sober, and Lederman entitled, ~ 'Immunosuppression:
University of Nice, H6pital Pasteur A Cause of Porokeratosis?'; (J AM ACAD DERMATOL
Department of Dermatology-IBP No. 69 13:75-79, 1985). We agree with the authors about the
06002 Nice Cedex-France possibility that immunosuppression may be either the
cause or an exacerbating factor in porakeratosis.
REFERENCE Indeed, in a paper published in 1983' we reported
the occurrence of disseminated actinic superficial po-
1. Lacour JP, Juhlin L, EI Baze P, Ortonne JP: Epidermolysis
bullosa acquisita with negative direct' immunofluores- rakeratosis in one woman in a population of 105 kid-
cence. Arch Dermatol 121: II 83-1 ] 85, 1985. ney transplant recipients who were being given con-
ventional immunosuppressive treatment consisting of
daily oral methylprednisolone at a maintenance dose
Epidermodysplasia verruciformis of 0.2 to 0.3 mg/kg and azathiopri ne at a dose of 1 to
To the Editor: 1.3 mg/kg.
I am a regular reader of the Self-Assessment ex- The same population has been evaluated for der-
aminations in the JOURNAL. I find them very useful for matologic lesions at 3- to 6-month intervals, and so far
refreshment of knowledge. However, I think that the two more cases of disseminated actinic superficial po-
discussion of questions 1-4 about epidermodysplasia rakeratosis have emerged in two patients 3 years after
verruciformis (J AM ACAD DERMATOL 10(No. 3):51A, transplantation. In all three patients, actinic keratoses
1984) is not quite up-to-date. and warts also developed. We therefore agree with the
The human papillomaviruses currently thought to assumption that immunosuppression might be a trig-
cause epidermodysplasia verruciformis are types 3, 5, gering or an aggravating factor for the development of
8, 9, 10, 12, 14, and 15. 1 Of these viruses, types 3, disseminated actinic superficial parakeratosis, perh'lps
5, and 8 are believed to be oncogenic in epidermodys~ through the same mechanisms already proposed for
plasia verruciformis patients. 2 Regarding therapy, etret- actinic keratoses. I
inate seems to be a promising drug. It was reported to
P. L. Bencini, M.D., * C. Crosti, M.D.,*
give mild to great improvement in epidermodysplasia
G. MontagnillO, M.D., ** and F. Sala, M.D., *
verruciformis patients, particularly those infected with
Istituto di Clinica Dermatologica I,
oncogenic strains types 3 and 5. 3-5 The effective dose
Universita di Milano, * and
is around 1 mg/kg/day.'
Divisione di Nej'rologia e Dialisi, **
K. El-Hoshy, M.D., 10 Emam-Ali Str. Ospedale Maggiore Policlinico.
Heliopolis, Cairo, Egypt Milan, Italy

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