Correspondence 283

cians evaluating patients with nail dystrophy shouldattempt to elicit a history of lichen striatus skin le-sions, as this may assist with appropriate diagnosisand prognosis. Interestingly, in this patient the dis-order appeared to respond to the application of top-ical corticosteroids, although we cannot rule outspontaneous involution.

REFERENCE

1. Niren NM, Waldman GD, Barsky S. Lichen striatuswith onychodystrophy. Cutis 1981;27:610-613.

MAKI O. GOSKOWICZ. M.D.LAWRENCE F. EICHENFIELD, M.D.San Diego. California

ONYCHODYSTROPHY IN LICHEN STRIATUS

To the Elditors:Onychodystrophy in lichen striatus is certainly

uncommon, as Karp and Cohen (1993;10:359-361)have written. We therefore call the authors' atten-tion to an article we published in which four caseswere reported (1) and which was quoted in our bookon nails (2).

REFERENCES

1. Baran R, Dupr6 A, Lauret P, Puissant A. Le lichenstriatus onychodystrophique. A propos de 4 cas avecrevue de la littfirature. Ann Dermatoi Venereol 1979;106:885-«90.

2. Baran R, Dawber RPR. Diseases of the nails and theirmanagement. Oxford: Blackwetl, 1984.

ROBERT BARAN, M.D.Cannes, France

AN UNUSUAL CASE OF RECURRENTGIANOTTI-CROSTI SYNDROME

To the Editors:Papular acrodermatitis of childhood, first de-

scribed by Gianotti in 1955, is clinically character-ized by an erythematous, papular, nonrelapsingeruption symmetrically distributed on the face, but-tocks, and limbs (I). In 1970 an anicteric hepatitisinfection, Australia antigen positive (HBSAg), sub-type ayw, was correlated to this disorder (2,3).Other similar papular or papulovesicular acrolo-cated eruptions, not correlated with hepatitis B vi-ms (HBV), were reported in subsequent years; insome of these cases a viral infection or a vetccine-related vims was demonstrated {A-€). RecentlyCaputo et at affirmed that a clinical distinction be-

tween the different etiologic forms of papular acro-located eruption on the basis of cutaneous featureswas not possible, and suggested for all of them theterm Gianotti-Crosti (G-C) syndrome (7).

We report a child who had two episodes of G-Csyndrome over a few months. This 4-year-old girlwas referred to us because of an erythematous, pap-ular eruption on the extensor surfaces of her lowerlimbs and buttocks, spreading within a few days toher face and upper limbs. Several lymphadenopa-thies and a mild hepatomegaly were present. Indi-vidual skin lesions consisted of flat-topped, red, orpurpuric papules, 1 to 3 mm in diameter. Somepetechiae were present on the face, ears, and arms.Laboratory investigations showed alanine ami-notransferase 278IU/L, aspartate aminotransferaselOCX) IU/L, HBSAg positive, HBEAg positive, anti-HBSAg negative, anti-HBC positive, anti-HBEAgnegative; the remainder of laboratory studies werenormal. Serologic investigations (antibodies anti-Epstein-Barr, parainfluenza, adeno, polio, cox-sackie, cytomegalo, rota, mbella vimses) were neg-ative or not significant. Throat swabs and stoolcultures were negative.

Histologic examination showed mild perivascu-lar infiltrates of lymphocytes and histiocytes in theupper dermis.

A diagnosis of G-C syndrome related to HBVwas made. The serum aminotransferase levels in-creased in the following weeks. After about 25 daysthe skin eruption disappeared. Hepatomegaly andlymphadenopathies regressed; serum aminotrans-ferase levels gradually decreased.

Four months later, the chUd was again seen be-cause of a papular emption symmetrically distrib-uted on the face, buttocks, and limbs. Fever wasabsent. Clinical examination showed discrete, flat-topped, flesh-colored papules, 1 to 5 mm in diame-ter; no hepatomegaly or splenomegaly was noted.Laboratory tests showed a fresh increase of alanineaminotransferase (445 IU/L) and aspartate ami-notransferase (1030 IU/L). Serologic viral investiga-tions and viral cultures (throat, stools) were nega-tive apart from a high amount of Ig antimbellavims. Family history revealed a concurrent classicmbella in her brother. The level of Ig antimbella in-creased to I/I024 and then fell gradually to 1/128within six months. The papulovesicular emption re-gressed within three weeks. About 16 months afterthe papular acrodermatitis, the anti-HBS and anti-HBE were detected. The activity of semm ami-notransferases remained elevated for 18 months,and HBSAg persisted for 4 years.

284 Pediatdc Dennatology Vol. 11 No. 3 September 1994

Our patient experienced classic G-C syndromeassociated with an anicteric HBV infection, andfive months later a recurrence associated with m-bella infection.

A relapse of G-C syndrome has never been de-scribed in the literature. In this patient serologic ev-idence of a high amount of antimbella virus antibod-ies that gradually fell in the following weeks and aconcurrent classical mbeUa in the patient's brothersuggested that the second papular emption wascaused by the mbeUa vims. A mild semm Euni-notransferase elevation may occur during viral in-fections; the great increase in the levels observedduring the patient's second papular acrolocatederuption could be related to mbella occurring whenthe B hepatitis was still active.

Nowadays G-C syndrome associated with hepa-titis B infection can be considered very rare; fur-thermore, the introduction in Italy and other coun-tries of antihepatitis B vaccination will contribute tothe reduction of its frequency and consequently ofthe frequency of the skin emption as well. A vims-induced type IV hypersensitivity response recentlywas hypothesized as a pathogenetic mechanism ofthe papular exanthem (7).

Although mbella vims is known to be a commoncause of exanthem in children, the association of ambella vims infection with G-C syndrome has notpreviously been reported in the literature. Earlier,virologic investigations permitted us to find a possi-ble etiologic factor in 12 of 26 children affected by apapular or papulovesicular acrolocated emption.Epstein-Barr vims, adenovims, cytomegalovims,rotavims infections, and vaccine-related vimseswere associated with the skin emption in our pa-tients (8). Other vimses, including coxsackie vims,have been correlated to these particular emptions inthe literature (9-14).

This observation of an unusual recurrence of G-Csyndrome is intriguing and supports the opinion thatG-C emption represents a self-limiting, cutaneous,nonspecific exanthem from different vimses, onlysome of which have been identified so far. Theseexanthems appear to be related more to the host'sreaction, in particular age groups, than to the viralinfection.

REFERENCES

1. Gianotti F. Rilievi di una panicolare casistica tos-sinfettiva caratterizzata da un'eruzione eritemato-infiltrativa desquamativa a focolai lenticolaii, a sedeelettiva acroesposta. G Ital Dermato! 1955;96:678-697.

2. Gianotti F. Papular acrodermatitis of childhood. AnAustralia antigen disease. Arch Dis Child 1973 ;48:794-799.

3. Ishimaru Y, Ishimaru H, Toda G, Baba K, MayumiM. An epidemic of infantile papular acrodermati-tis (Gianotti's disease) in Japan associated withhepatitis-B surface antigen subtype ayw. Lancet1976;2:707-709.

4. Gianotti F. Die infantilen papulosen Akrodermatiti-den. Die Akrodermatitis papulosa un das infantilepapulovesikulose akrolokalisierte Syndrom. Hau-tarzt 1976;27:467^72.

5. Gianotti F. Papular acrodermatitis of childhood andother papulovesicular acrolocated syndrome. Br JDennatol 1979; 100:49-59.

6. Eiloart M. The Gianotti-Crosti syndrome. Br J Der-matol 1966,78:488-492.

7. Caputo R, Gelmetti C, Ermacora E, Gianni E, Silves-tri A. Gianotti-Crosti syndrome: a retrospective anal-ysis of 308 cases. J Am Acad Dermatol 1992;26:207-210.

8. Magyariaki M, Drobnitsch I, Schneider I. Papular ac-rodermatitis of childhood (Gianotti-Crosti disease).Pediatr Dermatol 1991 ;8:224-227.

9. Patrizi A, Di Lemia V, Ricci G, Masi M, Varotti C.Papular and papulovesicular acrolocated eruptionsand viral infections. Pediatr Dennatol 1990;7:22-26.

10. Tayeb A, Plantitie P, Du Pasquier P, Guillet G,MaleviUe J. Gianotti-Crosti syndrome: a study of26 cases. Br J Dennato! 1986;n5:49-59.

11. Rogers S, Connolly JH. Gianotti-Crosti syndromeand viral infections. Br Med J 1974;4:529.

12. Spear KL, Winkelmann RK. Gianotti-Crosti syn-drome. A review of ten cases not associated withhepatitis B. Arch Dermatol 1984; 120:891-896.

13. James WD, Odom RB, Hatch MH. Gianotti-Crostilike eruption associated with coxsackie vims A 16 in-fection. J Am Acad Dermatol 1982;6:862-866,

14. Berant M, Naven Y, Weissmann I. Papular acroder-matitis with cytomegalovims hepatitis. Arch DisChild 1984;58:1024-1025.

15. Sagi EF, Linder N, Shouval D. Papular acrodermati-tis of childhood associated with hepatitis A virus in-fection. Pediatr Dennatol 1985;3:31-33.

ANNALISA PATRIZI, M.D.Vrro DI LERNIA, M.D.IRU NERI, M.D.GL\MPAOLO RICCI, M.D.Bolcigna, Italy