Correspondence

Malignant melanoma following scalp irradiation?

SIR, A 75-year-old man presented with a rapidly growingpigmented lesion on the occipital region of the scalp. A clinicaldiagnosis of malignant melanoma was made and the lesion wastreated by excision and skin grafting. Histology demonstratedthis lesion to be a primary nodular malignant melanomaarising in an area of lentigo maligna (Breslow 5.6 mm, Clarke’slevel IV). Six years previously he had developed a squamous cellcarcinoma in an adjacent area of the scalp which had also beensurgically excised. As a child he had been treated with radiationepilation for scalp ringworm, from which he had long-standingscarring alopecia. He was otherwise well and there was nohistory of previous arsenic exposure, nor any family history ofskin malignancies.

Roentgen’s discovery of X-rays in 1895 led to a widespreadand indiscriminate use of this modality. By 1897 a variety ofadverse cutaneous effects had been noted, including hair loss.By 1904 X-ray epilation was used therapeutically in the treat-ment of ringworm. Some years later the potential of ionizingradiation to promote nonmelanoma skin cancer, after a vari-able latent interval from exposure, was recognized. Indeed,many of the pioneers of radiation physics, and of therapeuticuse of radiation themselves developed squamous cell carcinomaof the hand. Historical aspects of the subject are graphicallydescribed by Hunter.1

A large number of benign dermatoses were treated withX-rays, in addition to ringworm. These included eczema,psoriasis and warts. Analyses of large series of such patientsindicate an incidence of 10–28% of nonmelanoma skin cancerfollowing such therapy.2 These radiation-induced tumoursappear to have a latency of 10 years onwards. Indeed, Derma-tologists have long been familiar with nonmelanoma skincancers arising on the scalp as a late effect of radiotherapyused for the treatment of childhood ringworm infection, andsuch cases continue to present up to 60 years after the originalexposure.

By contrast, the relationship between malignant melanomaand radiation is less well established. A literature review foundonly a single case report detailing the development of amalignant melanoma in an irradiation field 10 years afterexternal beam radiotherapy for endometrial carcinoma.3

Unfortunately, no histological subtype was reported in thistext. In addition, large studies on the morbidity and mortalityassociated with radiation exposure to the scalp during child-hood for the treatment of ringworm show an increased risk of

malignancies, including leukaemias, bone and soft tissue sar-comas and skin cancer, mainly basal cell but also squamous cellcarcinomas,4,5 but not malignant melanoma. The developmentof nonmelanoma skin malignancies in the above cohort ofpatients has been shown to be significantly higher than inmatched controls.

It is thought that a variety of factors are involved, includingthe additive effect of sun-exposure. The present case appearsinteresting as the patient would seem to have received sufficientradiation exposure to develop a squamous cell carcinoma aftera long latency. Subsequent to this he developed a malignantmelanoma of the scalp. Both of these tumours could have beenthe result of sun exposure alone and the role of radiotherapymerely coincidental. However, both developed on the irradiatedscalp and this gentleman has not suffered from skin malignan-cies in any other site.

C. L. A. Currie, B. E. Monk and R. J. Haywood

Laser Treatment Centre, Bedford Hospital, South Wing, Kempston Road,Bedford MK429DJ, UK

REFERENCES

1 Hunter D. The Diseases of Occupations. 5th edn. London: TheEnglish Universities Press Ltd, 1975.

2 Landthaler M, Hagspiel H-J, Braun-Falco O. Late irradiationdamage to the skin caused by soft X-ray therapy to cutaneoustumours. Arch Dermatol 1995; 131: 182–6.

3 Inbar M, Matzkin H, Rozin RR et al. Malignant melanoma devel-oping in an irradiation field. Br J Radiol 1988; 61: 519–20.

4 Ron AE, Modan B, Boice JD. Mortality after radiotherapy for ring-worm of the scalp. Am J Epidemiol 1988; 127: 713–25.

5 Teloh HA, Mason ML, Wheelock MC. A histopathologic study ofradiation injuries of the skin. Surg Gynae Obstet 1950; 90: 335–48.

Treatment of unilateral Darier’s disease with topicalisotretinoin

SIR, A 46-year-old woman presented with a 5-year history of anitchy linear rash affecting the left side of her trunk. In theprevious year this had increased significantly in size and hadbecome increasingly itchy. She had noticed no abnormality ofher nails. The eruption had not been provoked or aggravatedby sunlight. There was no previous or family history of skin diseaseand she was otherwise healthy and was taking no medication.

On examination there were multiple brown pigmented,

q 1999 Blackwell Science Ltd • Clinical and Experimental Dermatology, 24, 425–430 425

Viewpoints in dermatology • Correspondence

follicular papules in a zosteriform distribution (Fig. 1a) affectingher left flank. There were no other cutaneous lesions, inparticular there was no evidence of palmar pits or mucosal

lesions. Longitudinal lines with sandwiching of red and whitelines were present on the right thumb and left ring and littlefinger nails. No V-shaped nicks at the free margins of the nailswere present. A skin biopsy revealed acanthosis, papillomatosis,hyper-keratosis, focal parakeratosis and suprabasal acantholy-sis (Fig. 2). Corp ronds were present. Histology was consistentwith Darier’s disease.

The patient was commenced on topical Isotretinoin gel0.05% (Isotrex) twice daily. This resulted in clearing of therash after 3 months of treatment (Fig. 1b). This remained clearat follow-up 6 months later. Several months following treat-ment she developed an identical rash affecting her left shoulder,upper arm and left lower leg in a linear distribution. Thisoccurred during a sunny holiday abroad. Topical isotretinoinwas commenced with excellent clearing of this rash after2 months treatment.

The late onset of our case and the lack of family historywould favour an acantholytic dyskeratotic epidermal naevus.However the presence of bilateral nail changes and the devel-opment of the rash on the left side of her body are moresupportive of Darier’s disease. Photoaggravation of Darier’sdisease is common1 and occurred in the case reported here.Many of the clinical features of localized Darier’s disease suggestthat it is a genetic mosaic of generalized Darier’s disease.3 Thiscase and other reports of unilateral naevoid keratosis follicu-laris in which other features of Darier’s disease are present aresupportive of the latter.4,5

Darier’s disease improves in more than 90% of patientstaking oral retinoids but this treatment is limited by side-effectsand their teratogenic potential.2 To avoid these problemsboth topical tretinoin (all-trans-retinoic acid)6 and isotretinoin(13-cis-retinoic acid)7–9 have been used to treat Darier’sdisease. Using 0.1% isotretinoin Steijlen et al. found markedimprovement in one man with Darier’s disease after treatmentfor 12 weeks7 and a moderate reduction in hyperkeratosis intwo patients.8 Burge and Buxton9 reported on the use of topical

q 1999 Blackwell Science Ltd • Clinical and Experimental Dermatology, 24, 425–430426

Figure 1 (a) Multiple brown papules in zosteriform distributionaffecting the left flank. (b) Response to topical isotretinoin follow-ing 3 months of therapy.

Figure 2 Skin biopsy showinghyperkeratosis, suprabasal acantholysisand corp ronds (haematoxylin &eosin × 100).

Correspondence • Correspondence

0.05% isotretinoin on test patches of the skin of 11 patientswith Darier’s disease. Hyperkeratosis and papules improved insix patients after treatment for 3 months. Local irritationoccurred in over 50% of these patients.

Topical isotretinoin was effective in clearing unilateralDarier’s disease in this reported case with no adverse events.Because of the risk of local irritation, topical isotretinoin is moreappropriate for localized rather than widespread Darier’sdisease.

K. E. McKenna, M. Y. Walsh† and D. Burrows*

Department of Dermatology, Craigavon Area Hospital Group Trust,Craigavon, Departments of *Dermatology and †Pathology, Royal VictoriaHospitals Trust, Belfast, Northern Ireland, UK

References

1 Starink ThM, Woerdeman MJ. Unilateral systematized keratosisfollicularis. A variant of Darier’s disease or an epidermal naevus(acantholytic dyskeratotic epidermal naevus) ? Br J Dermatol1981; 105: 207–14.

2 Burge SM, Wilkinson JD. Darier–White disease: a review of the clini-cal features in 163 patients. J Am Acad Dermatol 1992; 27: 40–50.

3 O’Malley MP, Haake A, Goldsmith L, Berg D. Localized Darierdisease. Implications for genetic studies. Arch Dermatol 1997;133: 1134–8.

4 Munro CS, Cox NH. An acantholytic dyskeratotic epidermalnaevus with other features of Darier’s disease on the same side ofthe body. Br J Dermatol 1992; 127: 168–71.

5 Cambiaghi S, Brusasco A, Grimalt R, Caputo R. Acantholytic dys-keratotic epidermal naevus as a mosaic form of Darier’s disease. JAm Acad Dermatol 1995; 32: 284–6.

6 Gunther S. Vitamin A acid in Darier’s disease. Acta Derm Venereol(Stockh) 1975; 74: 146–51.

7 Steijlen PM, Happle R, van Muijen GNP, van de Kerkhof PCM.Topical treatment with 13-cis-retinoic acid improves Darier’s dis-ease and induces the expression of a unique keratin pattern. Der-matologica 1991; 182: 178–83.

8 Steijlen PM, Reifenschweiler DOH, Ramaekers FCS et al. Topicaltreatment of ichthyoses and Darier’s disease with 13-cis-retinoicacid. A clinical and immunohistological study. Arch Dermatol Res1993; 285: 221–6.

9 Burge SM, Buxton PK. Topical isotretinoin in Darier’s disease. Br JDermatol 1995; 133: 924–8.

Minimum requirements for digital images indermatological publications

SIR, In recent years, opportunities have increased for the use ofdigital images in dermatological practice. For dermatologicalmeetings and publications, clinical photographs can be takenusing a digital camera and used to make slides directly from acomputer. In addition, pathological pictures can be imported toa computer via a digital CCD camera connected to a lightmicroscope. The concept of desktop publishing has been intro-duced into the dermatological field, simplifying the productionof impressive slides and complex figures for manuscripts sub-mitted for publication. However, many people unfamiliar withdigital imaging overload their computer with unnecessary data.

In this communication I propose some minimum requirementsfor dermatological publishing.

Digital images are composed of pixels (dots). An imagecomposed of 1280 × 1000 pixels, for example, has a total of1 280 000 pixels. Obtaining the final print size of an image is amatter of simple arithmatic: a digital image of approximately1.3 million pixels (1280 × 1000) printed on a 400 dpi (dots perinch) printer produces a print of 3.2 (1280/400) × 2.5 (1000/400) inches. At a print density of 267 dpi, however, the imagewill be 4.8 × 3.7 inches (Fig. 1).

To produce a print for submission of 5 × 3.5 inches, the printdensity must first be decided. Although a high quality colourprinter such as the Pictrography 3000 (Xerox), for example,produces colour photographs at 400 dpi, such high density isusually not required. We conducted an informal blinded com-parison of two clinical photographs, one printed at 400 dpi andthe other at 200 dpi. All other settings were the same. Three outof five dermatologists selected the 200 dpi print as better,although they could not identify any reason for their preference.From this, the necessary pixel size can easily be calculated: printsize (5 × 3.5 inches) times print density (200 dpi) produces adigital density of only 1000 × 700 pixels. Thus, 1.3-millionpixel digital cameras provide sufficient image quality for derma-tological publishing.

A second important factor is image brightness. An imagewhich appears satisfactory on a PC monitor needs to bebrightened for printing. With Photoshop (Adobe Systems),this is easily done using by choosing the image-variation tagand making the image 2 steps brighter.

For authors with existing 35 mm colour positive slides, a filmscanner can be used. To make a colour print of 5 × 3.5 incheswith a density of 200 dpi, a slide would need to be scanned at700 dpi, as the image will be enlarged approximately 3.5 times.

On the basis of the above, I suggest that figures of approxi-mately 1 300 000 pixels printed at 200 dpi should providesatisfactory resolution for dermatological publications.

M. Tanaka

Department of Dermatology, Keio University School of Medicine,Tokyo 160–8582, Japan

Figure 1 The size of a digital image is determined by pixels.When you choose a print density, the final print size will be fixed.Digital size ¼ density × print size.

Correspondence • Correspondence

q 1999 Blackwell Science Ltd • Clinical and Experimental Dermatology, 24, 425–430 427

Livedo reticularis as a presenting symptom ofpolycythaemia vera

SIR, Polycythaemia vera (PV; Vaquez disease, primary poly-cythaemia) is a progressive clonal myeloproliferative diseasecharacterized by the pathological proliferation of erythro-poiesis, myelopoiesis and megakaryopoiesis in the bonemarrow. PV usually presents with various mild initial clinicalsymptoms supporting the diagnosis, including cutaneousmanifestation. However, < 30–35% of the patients showsevere thrombotic or haemorrhagic complications as the firstobjective symptoms of the disease. Cutaneous lesions in PVdisplay diverse morphology. Sometimes an extensive pruritusafter thermic stimuli occurs. We report a case in which skinlesions of the livedo reticularis (LR) type presented as an initialmanifestation of PV and healed after phlebotomy.

A 68-year-old man, retired, with history of pericarditis(1978), coronary thrombosis (1979), apoplexy (1985) andhyperuricaemia presented in 1996 with painful reddish-violetpatches on his thighs and gluteal regions. Similar less extensivelesions developed on his chest later. In 1997 the patient wasreferred to our clinic. At time of admission livid, bizarre, light-ning-like macules on the gluteal regions and right thigh werelocated asymmetrically. Clinical presentation was consistentwith the diagnosis of LR. Histological evaluation of the gluteallesion showed inflammatory changes of various intensity,affecting vessels located in the lower dermis. The inflammatoryinfiltrate consisted of lymphocytes, histiocytes and polymor-phonuclear cells. Venules showed intimal and/or endothelialproliferation, formation of fibrin thrombi and fibrin deposits inthe walls. Extravasation of erythrocytes and vasodilatationwere encountered focally. Laboratory studies showed an ery-throcyte sedimentation rate of 1/3, white blood cell count9.5 × 109/L, erythrocyte count 6.14 × 1012/L, haemoglobin178 g/L, haematocrit 35%, basophilia, uric acid 532 mmol/L,platelet count 709 × l09/L. Haematological evaluations of bonemarrow revealed hyperplasia of erythropoiesis and mega-karyopoiesis. Trephine biopsy of the bone marrow showedintermediate hypercellularity with proliferation of megakaryo-poiesis and erythroid cell line, mild diffuse fibrosis anddecreased iron stores. Investigation of haemostasis did notprove activation of haemostatic system, nor DIC. Taking intoconsideration clinical and histological features, diagnosis of PVwith cutaneous changes of the LR type was established. Thera-peutic phlebotomy 400 mL twice a week was initiated.Cutaneous lesions healed and haematocrit returned to thenormal range after four phlebotomies.

PV is a myeloproliferative disease with various clinical fea-tures. Often cutaneous symptoms such as cyanosis and purplecoloration of the face are the first manifestion of the disease andthis provides a clue to the diagnosis. As a rule, the definitivediagnosis of PV, based on pathological findings in the blood andthe bone marrow, is confirmed in the later stage of the disease.Early clinical features such as cephalea, paraesthesia andreduced efficiency are nondiagnostic. Hepatomegaly and sple-nomegaly, representing organ involvement, develops later.

Cutaneous symptoms could be divided into three groups/related to:• vasodilation and higher blood viscosity resulting in purplecoloration of the skin and mucous membranes, haemangiomasand spider naevi, acne urticata, pruritus, eczema, haemor-rhagia, rosacea, skin dryness, erythrodermia, lingua scrotalis;• organic changes of vessels presenting as purple-violet colora-tion of extremities, thrombosis, ulcerative nodules on lowerextremities, erythromelalgia, vasospastic Raynaud’s phenom-enon, sclerodermiform changes or necrosis of distal parts offingers;• effect of heat or cold, for which the damaged circulation isnot able to compensate, leads to the intensification of symptomsspecified in the above mentioned groups.

Perhaps the most frequent feature is cyanosis and purplecoloration of the face. About 15% of the patients present withpruritus,1 3% with erythromelalgia.2 Aquagenic pruritus,3

urticaria vasculitis,4 repeated attacks of erythromelalgia5

were described as initial features of PV. LR is a cutaneoussymptom caused by inflammatory changes of vessels locatedparticularly in the deeper parts of dermis, with stasis of blood incapillaries and venules, occasionally connected with occlusionof lumina. Several subtypes of LR are recognized such ascongenital (cutis marmorata), idiopathic/acquired or in asso-ciation with systemic involvement – Sneddon’s syndrome, andsecondary to intravascular obstruction or vessel wall disease.LR is also described in anti-phospholipid syndrome, polyarter-itis nodosa and other principal diseases. We consider LR as aninitial clinical feature of PV a rarity, and we failed to find similarreports in literature. Resorption of livedo lesions after phlebot-omy proved a relationship between LR and PV.

V. Filo, D. Brezova, P. Hlavcak* and A. Filova†

Department of Dermatology, University Hospital, Bratislava, Slovakia,*National Cancer Institute, Bratislava, Slovakia, †Department ofHaematology and Transfusiology, University Hospital, Bratislava Slovakia

References

1 Winkelmann RK, Muller SA. Pruritus. Ann Rev Med 1964; 15:53–64.

2 Redding KG. Trombocythemia as a cause of erythermalgia. ArchDermatol 1977; 113: 468–71.

3 Abdel-Naser MB, Gollnick H, Orfanos CE. Aquagenic pruritus as apresenting symptom of polycythemia vera. Dermatology 1993;187: 13O–133.

4 Farrel AM, Sabroe RA, Bunker CB. Urticarial vasculitis associatedwith polycythaemia rubra vera. Clin Exp Dermatol 1996; 21:302–4.

5 Ongenae K, Janssens A, Noens L, Wieme N et al. Erythromelalgia:a clue to the diagnosis of polycytemia vera. Dermatology 1996;192: 408–10.

Unilateral linear syringomata. A case report

SIR, Syringoma is a benign adnexal tumour arising from theducts of eccrine sweat glands. The development of multiple

Correspondence • Correspondence

q 1999 Blackwell Science Ltd • Clinical and Experimental Dermatology, 24, 425–430428

syringomata following Blaschko’s lines suggests a somaticmutation may underlie the pathogenesis of this dermatosis. A17-year-old girl presented with a 3-year history of an erythe-matous papular eruption over the right shoulder with anteriorextension down the upper arm. There were no associatedsymptoms, the patient was otherwise healthy and gave nopast history of skin disease. The dermatosis had been treatedunsuccessfully with topical corticosteroids.

Examination of the skin revealed multiple erythematouspapules distributed over the right deltoid region with linearextensions onto the proximal arm and anterior chest (Fig. 1).Distribution of the lesions followed Blaschko’s lines. Individualpapules were firm and measured 2–5 mm in diameter. Generalexamination was unremarkable. Histological examination of abiopsy specimen taken from the main portion of the lesiondemonstrated strands and islands of epithelium showing pro-nounced ductal differentiation within the mid-dermis (Fig. 2).The duct-like strucures, some displaying a ‘comma’-shapedappearance, were lined by two layers of cells. Other ducts

contained amorphous material. Histological findings were con-sistent with syringomata.

Treatment with electrocautery was discussed, but the area ofinvolvement was considered too extensive to attempt ablativetherapy.

Syringomata are fairly common benign adnexal tumourswhich usually occur scattered symmetrically on the lowereyelids and cheeks. Individual lesions are skin-coloured oryellowish papules of diameter 1–3 mm. The surface may berounded or flat-topped and the outline is sometimes angular.1

Syringomata appear predominantly in young women, are morecommonly observed in Oriental people, and are occasionallyfamilial. Eighteen per cent of individuals with Down’s syndromedevelop syringomata, a predilection that is not observed inother chromosomal abnormality syndromes.2

A number of clinical variants of syringomata have beenreported, including eruptive and plaque forms.3,4 There havebeen two previous reports of linear syringoma, both involvingthe upper trunk.5,6 Atypical sites of involvement include thepenis and scalp.7,8

The discrimination of syringomata from other lesions follow-ing a linear pattern may be difficult. Individual lesions ofnaevoid basal cell epithelioma, epidermal naevus and verrucaplana can all resemble syringoma, making histological exam-ination important. In contrast to the epidermal naevus andnaevoid basal cell epithelioma syndromes, there were no ske-letal or central nervous system anomalies in our case, or otherpublished cases, of naevoid syringoma.

Linear lesions may result from exogenous or endogenouscauses. Of the latter, recognition of a lesion following Blaschko’slines invokes mosaicism, in which genetically distinct cellpopulations are produced by postzygotic mutations. Lesionaltissue in cutaneous mosaicism is distributed in the character-istic linear and whorled patterns of Blaschko’s lines whichreflect the dorso-ventral migration paths of embryonic cellpopulations.9

Figure 1 Multiple syringomata distributed over the right shoulderwith linear extensions occurring across the chest and down theright arm.

Figure 2 Histology of a representativelesion demonstrating islands of epitheliumwithin mid-dermis showing ductaldifferentiation, some displaying a‘comma’-shaped appearance.

Correspondence • Correspondence

q 1999 Blackwell Science Ltd • Clinical and Experimental Dermatology, 24, 425–430 429

An early postzygotic mutation can enter the germ-cell lineresulting in transmission to the offspring. In other pathologiesfollowing Blashko’s lines, gene mutations have been identifiedin cells of lesional but not nonlesional skin, confirming thepresence of somatic chromosomal anomalies.10

The pathogenesis of syringoma is unclear, however, racial,familial and Down’s syndrome associations suggest the involve-ment of hereditary factors. The description of syringomataoccurring in the context of genetic mosaicism strengthens thehypothesis of an underlying genetic abnormality.

D. Creamer, A. Macdonald* and W. A. D. Griffiths

St John’s Institute of Dermatology, St Thomas’ Hospital, UMDS, London,*Department of Dermatology, Sevenoaks Hospital, Kent.

References

1 MacKie RM. Tumours of the skin appendages. In: Champion RH,Burton JL, Ebling FJG, eds. Textbook of Dermatology 5th edn. Vol 2Oxford: Blackwell Scientific Publications, 1992: 1519–20.

2 Butterworth T. Dermatologic disorders in institutionalised mentaldefectives. Birth Defects 1971; 7: 178–85.

3 Hashimoto K, DiBella RJ, Borsuk GM, Lever WF. Eruptive hidrade-noma and syringoma. Arch Dermatol 1967; 96: 500–19.

4 Rongioletti F, Semino MT, Rebora A. Unilateral multiple plaque-like syringoma. Br J Dermatol 1996; 135: 623–5.

5 Yung CW, Soltani K, Bernstein JE, Lorincz AL. Unilateral linearnaevoidal syringoma. J Am Acad Dermatol 1981; 4: 412–6.

6 Sala GP, Marinaro P, Rossi E et al. Einseitige navoide Syringome.Hautarzt 1990; 41: 272–3.

7 Lo JS, Dijkstra JW, Bergfeld WF. Syringoma of the penis. Int J Der-matol 1990; 29: 309–10.

8 Shelley WB, Wood MG. Occult syringomas of scalp associatedwith progressive hair loss. Arch Dermatol 1980; 116: 843–4.

9 Savin JA. Cutaneous mosaicism. Q J Med 1996; 89: 489–91.10 Paller AS, Syder AJ, Chan Y-M et al. Genetic and clinical mosai-

cism in a type of epidermal nevus. New Eng J Med 1994; 331:1408–15.

A case of leukocytoclastic vasculitis associated withhaloperidol

SIR, Haloperidol is an antipsychotic drug, and may induceadverse drug reactions such as hypotension and psychologicalproblems. Skin eruptions secondary to haloperidol have beenseldom reported with no mention of leucocytoclastic vasculitis.I report a patient who developed palpable purpura after taking

haloperidol; the relationship was supported by intradermal andoral provocation tests.

A 59-year-old Korean man had been in hospital for manage-ment of neurologic problems with a diagnosis of metabolicencephalopathy. He had taken several kinds of drugs such asnimodipine, indeloxazine HCl, flurazepam HCl for a few monthsand haloperidol additionally for 11 days before the skin erup-tion. The dose of haloperidol was 1 mg per day for the first7 days and increased to 1.5 mg per day for a further 4 days. Ondermatological examination, palpable purpura with oedemaappeared on both legs and feet. Laboratory tests includingbleeding time, prothrombin time, activated partial thrombo-plastin time, antinuclear antibody, hepatitis C antibody, coldagglutinin, cryoglobulin, immunoglobulins (IgA, IgG, IgM, IgD,IgE), and complement (C3, C4, CH50) were within normalranges. Histopathological findings revealed leukocytoclasticvasculitis with eosinophilic infiltration. Skin tests with ingesteddrugs were performed after clearing of the skin lesion. Intra-dermal testing with haloperidol produced erythematous,infiltrated papules, the histology of which, on the second day,was similar to the original findings. Oral provocation tests wereperformed with all of the drugs that he had been taking.Haloperidol, the last drug tested for oral provocation, inducedpurpura after 3 days. The purpura disappeared 1 day after thediscontinuation of haloperidol.

Drugs are often the cause of leucocytoclastic vasculitis.1,2 Incausative drug identification topical provocation tests are saferthan systemic tests, but they are less reliable. This patientdeveloped a definite reaction after an intradermal test withhaloperidol which was confirmed by histopatholgical analysis.Re-administration and withdrawal of haloperidol made thediagnosis reliable. Interestingly, the time required for systemicprovocation in this patient was as long as 3 days and with-drawal cleared the provoked lesions quickly. This differsfrom some types of drug eruption, and might be related topathogenesis.

A-Y. Lee

Department of Dermatology, Eulji Hospital College of Medicine, 280-1,Hagye-1-dong, Nowon-gu, Seoul 139-711, Korea

REFERENCES

1 Lotti T, Ghersetich I, Comacchi C, Jorizzo JL. Cutaneous small-vessel vasculitis. J Am Acad Dermatol 1998; 39: 667–87.

2 Gibson LE. Cutaneous vasculitis: approach to diagnosis and sys-temic associations. Mayo Clin Proc 1990; 65: 221–229.

Correspondence • Correspondence

q 1999 Blackwell Science Ltd • Clinical and Experimental Dermatology, 24, 425–430430