CORRESPONDENCE 605

siCAM-1 levels were observed along with a progression ofthedisease iti four patients who developed multiple metastases,whereas, in six in whom lymph node metastasis occurred, nosignilicant change was seen (Tahle 1).

In Iht' 21) pytienls who presented with metastasis from(naligiianl melanoma, the initial levels of sICAM-1 werehigher than in the group of patients who presented withprimary malignant melanoma (median 3A2 ± 174 ng/ml.riMigo 180-1 520). but this difference did not reach statist if a Isignilicance. In 17 patients, no noliceable change in theNKV\M-1 level was noted with time. Among these, fourpatients had had a constantly high level of sICAM-1(> SOOng/mU without the disease progre.ssiGn. Throepatients had a progression of their malignant melanoma,bul only one showed an increase in slCAM-1 levels.

immunohiHlochemicai study of the six metastatic lesionsof malignant melanoma showed discrete ICAM-1 expressionIn the lymph node metastases. and intense expression in theskin metastase.s. This inlensily correlated wilh the plasmaslCAM-1 levels (Table 2). LFA positive eells were seen toinliltrate the metastases in faint to moderate numbers,but were not found to be in elose contact with ICAM-1positive tumour eells. as is frequently observed in epidermallesions.

Taken together, these data show that slCAM-I levels do notlluctuatc. in time, in most patients {79%) without clinicalchange. They also indicate a differential expression andrelease of ICAM-1 by malignant melanoma cells, which mayexplain Ihc large varialion in the levels of sICAM-l in palicntswith mi'lastatic malignant melanoma."* It is possible that localmicroenvironmenlal factors released by tumour cells mayaccount for the paucity of LFA positive cells in the metastases.Our rcsulls also suggest that sICAM levels might distinguishmulti-organ from lympli node metastases. The levels ofsICAM-I may be a reflection of tumour heterogeneity, hutdo not represent a reliable or early marker for the progressionnf disease.

Aeknowledgment

This work was supported hy the association Vaincre leMelanome and the Association de la Recherche sur leCancer (Contract no. 415).

INSERM U346. J.ViACClinhiiie Dernuilohgique. L .MISHRY

llopiiiil li. HeiTiot, D.ScHMrrr

694 U Lyon U3. A.CLAUDY

France

References

1 Jobn.son |I', Slade BG, tlolzmatm B ei ul. De novo expression oftntercdiular-iidhesion molecule 1 in melanoma correlates wilbincreased risk of metiisttisis. Proe Null AetuI Sci VSA, 1989: 86:641-4.

2 NaLiili I', Niailrii MR. Ciivallerc R fl ni DilTercnOiil expression ol'intcrcelluliiir adhesion molecule 1 in primary and metastatic lesions.Cancer Rts 1990: 50: 1271-8.

3 Altomonte M, Colizsd F. Esposito G. Maio M. Clrculaling inicrcelluiaradbesion molecule 1 as a marker of disease progression incutaneous melanoma. N Engl} Med 1992: 327: 959.

4 Viac |, Guenichc A. Faure M. Claudy A. Soluble intercellularadhesinn molecule I and niiilignanl melanoma. Civwcr Lett 1993:72: 191-4.

5 Viac J. Cbardonnet Y, Fu\Tard S, Scbmill 1). Fpidermolropism ofTcells correlates with intercellular adbe.sinn riiolftule (ICAM-1)expression in bumiui papillomavirus (HPV)-induced lesions. / Patho}1992: 168: 301-6.

Leg ulcers and Klinefelter's syndrome: role of PAI-1

SIR. Klinefelter's syndrome is an abnormality of sexualdifferentiation in men. This syndrome is often associatedwith leg ulcers (prevalence 6-12%). usually related to venousinsufEiciency. Two reports ' ' suggested thai platelet hyperag-grebability was a possible factor in ihe patliogenesis of legulceration. More recently. Veraart et al.^ reported a highplasminogen activator inhibitor -1 (PAI-1) plasma activity intwo patients with Klinefelter s syndrome complicated by legulcers, underlying a possible role for Ihis inhibitor ofQbrinolysis. However, tbe two cases had normal testosleronelevels and there was no indication on the influence ofandrogen therapy on the PAl-1 level.'

We report here a case of Klinefelter's syndrome withleg ulcers associated with bypofibrinolysis and high value ofPAI-1. which decreased only partially with venous occlusion(VO).

Androgen replacement therapy (Androtardyl'. testosteroneenanthate, lOOmg intramuscularly every 3 weeks over 7months) had a benelicial effect on the healing of leg ulceration.It was of particular interest ibal this androgen therapycorrected both the low testosterone level and its highassociated PAI-1 level (Table 1). Thus, androgen therapyseemed to restore a normal librinolyiic response to VO. This isin agreement with the inverse relationship described betweentestosterone and PAM levels"̂ and ihe beneficial role ofandrogen on Hbrinolysis.^

This observation emphasizes the hypothesis ofthe putativerole of PAI-1 in the pathogenesis of leg ulcers in Klinefelter'ssyndrome.

Table I.

Case reported

Variables

Before Afterandnigen androgen Normaltherapy tberapy values

Serum testosterone 6 2 17 ll '6-38-2nmoi/IPAI-1 before VO 17 8-1 < 10!U/mlPAI-1 alter VO 15 0-5 < 10!U/mlDilute blood dot lysis > 100 60

time iifter V,, (mini

1S96 Britisb Assix-ialioii of Dermatologists, British jounial of Dermatology. 1 34, 593-606

606 CORRESPONDENCE

Acknowledgments

The authors thank Prof. j.C.Beani and Prof. S.Halimi for theirassistance.

Uiboratoire d'Hematohgie

Hdpila! Miiluilhm. CHU. Grenoble. France

'Center of Vascular Rehabilitation

Si HUaire dii Tinivet. I'ranee

•[Department of Ancfiokmn

Hopiliil Michallon. CHU. Grenoble, France

B.VILLEMIIR*

J.L.BOSSON

H.TRIJCHE*

A.FRANCotB.POLACK

References

1 Norris PG. Rivers JK. Macbin S el ai Platelet hyperaggregability intwo patients witb Klinefelter's syndrome and leg ulcers. Br //>rm«(oM987; 117: 107-9.

2 Higgins EJ. Tidman MJ. Savidge GF et al. Platelet hyperaggregabilityin two patients wilb Klinefelter's syndrome complicated by legulcers, lir I DermiUoi I9«9: 120: 322.

1 Veraart ]C]M, liamulyak K. Neumann. HAM. hjigelen |. Increasedplasnia activity of plasminogen aclivator inbibitor 1 (PAI-1) in Iwopatients wilb Klinelelter's syndrome complicated by leg ulcers. Br /Derinulol 1994: 130:641-4.

4 Caron P, Bennet A, Camare R fl «(. Plasminogen aclivator inbibilorin plasma is related to testosterone in men. Metabolism 1989: 38:1010-15.

5 Kluft C, Preston FK, Malia RG et ai Stanozolol-induced changes infibrinolysis and coagulalion in bcalthy adults. Tbromh Haernost1984: 51: 157-64.

Nodular solar degeneration following herpes zoster

SIR. A 71-year-old man was seen because of several papuleswhich had developed within a scar. Tbe scar was at the sites ofherpes zoster of the trigeminal area, which bad occurred 4years previously. He had a past history of adenocarcinoma ofthe prostrate, but none of occupational sun exposure.On examination, several yellowisti papules, i - 4 mm indiameter, were present on the left cheek. There were noother lesions. The titre of IgG antibody to varicella zoster virus,in the serum, was 1 : 64. A skin biopsy revealed solardegeneration with amorphous nodular change, which stainedpositively with Victoria blue van Gieson (I ig. 1).

It was a striking feature that this lesion occurred at sites ofpost-herpes zoster scarring. Granuloma annulare has beenreported to occur at tbe site of herpes zosier .scars. ' To ourknowledge, no cases similar to our palieiit have been reported.We speculate that damage to collagen and elastic libres. due toscarring following herpes zoster and to sun exposure, mayplay a part in the induclion of nodular solar degeneration. Il isunclear whether reduced immunocompetcncc plays a part inthis damage.

Department of Dermatoiofiy. T.YAMAMtnti

Tsuclmira Kijodo General Hospitai A.YOKOYAMA

11-7. Manahe-shitimachi.

Tsuchhira-citu.

Ibaraki. japitn

References

1 Zanoli MD. Powell BL. McCalmonl T ft ni (iriinuloma annulare anddisseminated borpes zoster. Int } Onmilo/ 1992; J l : 55-7.

2 Wright AL. Granuloma annuiare following herpes zoster. Int /Dermatol 1992: 31:672.

Figure I. Nodular amorphous change in ibcdermis (Victoria blue van Gieson x40).

1996 British Association of Dennatologists. British journal of Dermatology. 1 J4. 593-606