skin lesions in melanoma and kaposi s sarcoma394476/uq394476... · 2019. 10. 11. · daniele...

DIAGNOSIS IN ONCOLOGYArthur Skarin, MD, Consultant Editor

Skin Les ions in Melanoma and Kaposi ’ s SarcomaCASE 1. DETECTION OF CIRCULATING MALIGNANT CELLS BY RT-PCR IN A CASE OF CUTANEOUS MELANOMA

IN COMPLETE REGRESSION

A healthy 37-year-old woman with a familial history of cutaneous melanoma and a recent history (6 months) of atypicalnevus was seen in consultation by a dermatologist. Complete skin mapping revealed only an oval, 6 � 4-mm pigmentedlesion on her upper left arm that had a history of rapid growth and a variegated chromatic pattern (Fig 1A). In vivo digitalepiluminescence microscopy showed digitated radial streaming, grayish-blue reticular patterns, opaque gypseous alabasterlacunas, brown-black dots on a blue-gray background, pseudopodia at the periphery, blue-in-pink areas, and a blue-grayvelum (Fig 1B). Surprisingly, histologic examination of the excised lesion (Fig 1C and 1D) displayed all the typicalpathologic features of completely regressed melanocytic lesion and led to a diagnosis of atypical pigmented lesion in

Fig 1.

1411Journal of Clinical Oncology, Vol 20, No 5 (March 1), 2002: pp 1411-1418

Downloaded from ascopubs.org by University of Queensland on February 1, 2017 from 130.102.082.083Copyright © 2017 American Society of Clinical Oncology. All rights reserved.

regression and a suspicion of melanoma (uninvolved flattened epidermis, fibrosis parallel to the epidermis together withmany melanophages, and chronic inflammatory cell infiltration consisting mainly of lymphocytes). Although partialregression in malignant cutaneous melanoma occurred in 10% to 58% in several large series, spontaneous completeregression of primary melanomas are rarely described in the literature.1,2 The present case did not meet all the stringentcriteria for the diagnosis of spontaneous complete regression of primary melanoma because of the absence of clinicallytumor-involved lymph nodes draining the area where the regressed pigmented lesion was localized. Because of the diagnosticdilemma, 3 months after surgical excision we performed a reverse transcriptase–polymerase chain reaction (RT-PCR)–basedassessment of malignant melanoma cells in three sequential peripheral-blood samplings.3-5 Tyrosinase-positive circulatingcells (Fig 1E) were detected in all the samples (lanes 1, 2, and 3: peripheral blood from the patient obtained in three sequentialsamplings at different time points; lane 4: peripheral blood from a healthy donor; lane 5: A375M melanoma cell line).

A skin and systemic search for an occult primary melanoma and systemic staging with axillary ultrasonography, total-bodycomputed tomography, and total-bone scintigraphy were negative. On the basis of these data, a diagnosis of completespontaneous regression of cutaneous malignant melanoma was suggested and a local surgical resection was performed.Results of an RT-PCR assay for tyrosinase from peripheral blood continued to be positive 10 months after the diagnosis inthe absence of any other sign of systemic disease or atypical skin lesions. To the best of our knowledge, this is the first reportof a diagnosis of a completely regressed primary cutaneous melanoma formulated with the help of RT-PCR tyrosinasedetection.

Daniele Santini, Giuseppe Tonini, Bruno Vincenzi, Raffaele Murace, Giulio Ferranti, and Alfonso BaldiUniversita Campus Bio-Medico, Centro Diagnostico, and Istituto Dermopatico dell’Immacolata, Rome, and Seconda

Universita di Napoli, Naples, Italy

Copyright © 2002 American Society of Clinical Oncology

REFERENCES

1. Bottger D, Dowden RV, Kay PP: Complete spontaneous regres-sion of cutaneous primary malignant melanoma. Plast Reconstr Surg89:548-553, 1992

2. Menzies SW, McCarthy WH: Complete regression of primarycutaneous malignant melanoma. Arch Surg 132:553-556, 1997

3. Smith B, Selby P, Southgate J, et al: Detection of melanoma cellsin peripheral blood by means of reverse transcriptase and polymerasechain reaction. Lancet 338:1227-1229, 1991

4. Brossart P, Schmier JW, Kruger S, et al: A polymerase chainreaction-based semiquantitative assessment of malignant melanomacells in peripheral blood. Cancer Res 55:4065-4068, 1995

5. Reinhold U, Berkin C, Bosserhoff A-K, et al: Interlaboratoryevaluation of a new reverse transcriptase polymerase chain reaction–based enzyme-linked immunosorbent assay for the detection of circu-lating melanoma cells: A multicenter study of the DermatologicCooperative Oncology Group. J Clin Oncol 19:1723-1727, 2001

CASE 2. DERMOSCOPIC FEATURES OF METASTASES FROM CUTANEOUS MELANOMA MIMICKING BENIGN NEVIAND PRIMARY MELANOMA

A 39-year-old woman presented in December 1999 with a 4 � 5-cm brown-black plaque with an irregular margin on theleft parietal region of the scalp. The lesion was subsequently excised and histopathologic examination revealed malignantmelanoma, Clark level IV, with Breslow thickness of 1.5 mm. At that time, no metastases were detected. Six months later,11 new pigmented skin lesions, about 4 mm in size, appeared on the right parietal, frontal, and nuchal sites of the scalp andon the upper trunk. Previously, no melanocytic skin lesions were present in these sites. Four of these lesions were examineddermatoscopically, photographed at 10 times magnification, and then excised. The lesions presented clinical anddermatoscopic features simulating either benign melanocytic nevi (Fig 1A and 1B) or primary cutaneous melanoma (Fig 2Aand 2B). In three dermatoscopic images, a globular pattern usually ascribed to a benign dermal nevus was recognizable,characterized by grayish-blue globules extending throughout the entire lesion (Fig 1B).1 In contrast, a multicomponentpattern was detectable in one image.2

This was typified by irregular blue-gray pigmentation at the periphery featuring pseudopods and black to grayish dots inthe center of the lesion on a reddish background (Fig 2B). Pseudopods have been reported to represent a specific criterionfor early invasive melanoma.2 Histopathology of the two lesions revealed metastases from melanoma (Fig 3A and 3B), withdermal involvement only in the former and with dermoepidermal involvement suggestive of a primary cutaneous melanomain the latter. In January 2001, the patient developed meningeal metastases.

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The differentiation of cutaneous melanoma metastasis from primary melanoma is often difficult, not only clinically butalso dermatoscopically. A series of dermatoscopic variables have been identified that allow the dermatoscopic diagnosis ofcutaneous melanoma metastases.3 However, in our patient, these criteria did not permit differentiation of cutaneousmelanoma metastases from benign melanocytic lesions and melanoma in situ. Interestingly enough, other authors describeda globular pattern in cutaneous melanoma metastases as well.4

Fig 1.

Fig 2.

1413DIAGNOSIS IN ONCOLOGY


Fig 3.

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In conclusion, the evaluation of patients with a history of melanoma and clinically unequivocal pigmented skin lesionscannot rely on dermatoscopic features alone. In cases of recent onset or history of growth, excision is warranted.

Maria A. Pizzichetta, Vincenzo Canzonieri, Alessandro Gatti, Clelia de Giacomi, Giusto Trevisan,Andrea Veronesi, and H. Peter Soyer

National Cancer Institute, Aviano, and University of Trieste, Trieste, Italy, and University of Graz, Graz, Austria


REFERENCES

1. Kenet RO, Kang S, Kenet BJ, et al: Clinical diagnosis ofpigmented lesions using digital epiluminescence microscopy. ArchDermatol 129:157-174, 1993

2. Menzies SW, Ingvar C, McCarthy WH: A sensitivity and speci-ficity analysis of the surface microscopy features of invasive mela-noma. Melanoma Res 6:55-62, 1996

3. Schulz H: Epiluminescence microscopy features of cutaneousmalignant melanoma metastases. Melanoma Res 10:273-280, 2000

4. Ferrari A, Peris K, Piccolo D, et al: Dermoscopic features ofcutaneous local recurrent melanoma. J Am Acad Dermatol 43:722-724,2000

CASE 3. FAMILIAL CLASSIC MEDITERRANEAN KAPOSI’S SARCOMA

An 82-year-old white man of Syrian descent presented with purplish raised skin lesions involving both feet. The skin lesionson the left foot preceded the occurrence of lesions on the right foot by 4 months and were associated with severe edema ofthe foot (Fig 1). The lesions progressed gradually and spread to the trunk, involving the right flank and left lateral chest wall.

Fig 1.



His 35-year-old son had similar purple-blue skin lesions localized to the face that were histologically proven to be Kaposi’ssarcoma. The son’s serum human immunodeficiency virus (HIV) antibodies were negative. The facial skin lesions had acomplete response to intralesional interferon therapy, and this patient remains in complete remission after 3 years.

Examination of our elderly patient showed that the skin lesions had irregular borders, were slightly raised, and werenontender to palpation. The rest of the physical examination showed left inguinal lymphadenopathy and edema of the leftleg. The biopsy of one of the skin lesions revealed irregular vascular spaces lined by endothelial cells with slightly enlargedand hyperchromatic nuclei (Fig 2). Between the vascular spaces, there were aggregates of spindle cells, extravasatederythrocytes, and hemosiderin pigment (Fig 2, arrows; hematoxylin and eosin, � 100). These features are characteristic ofKaposi’s sarcoma. Serum antibodies to HIV-1, HIV-2, and human T-cell leukemia virus-1 were not present. Computedtomography scans of the chest, abdomen, and pelvis did not reveal visceral metastases. The disease was extensive and notamenable to local treatment with surgery or radiation or to topical treatment with cryotherapy, liquid nitrogen, or intralesionalvinblastine. This prompted the initiation of paclitaxel as an antiangiogenic agent at 60 mg/m2 administered for 3 consecutiveweeks followed by 1 week of rest. After 12 weeks of therapy, the lesions showed significant improvement, with flatteningof surface, decrease in size, and fading of color. The edema of the left leg also showed significant improvement (Fig 3). Thelesions continue to improve after 5 months of paclitaxel therapy (Fig 4).

The classic form of Kaposi’s sarcoma is rare and is seen primarily in older men of Eastern European and Mediterraneanorigin. The lesions typically appear initially on the hands and feet and gradually progress up the arms and legs. Lymphedemausually follows the development of skin lesions, but it may precede them. If untreated, the disease can spread to involve theviscera or mucosa. Familial classic Kaposi’s sarcoma is exceedingly rare. Our case adds to the few documented casesreported in the English literature (Table 1).1-6

Fig 2.

1416 FATA, MIRZA, AND BERNATH


Single lesions can be treated with excisional biopsy, and patients with a few lesions in a limited area can be treated withradiation therapy. Patients with extensive disease can be treated with chemotherapy including vinblastine, doxorubicin, anddacarbazine alone or in combination, but it has limited efficacy.7

Paclitaxel has antiangiogenic and apoptotic effects.8 Its antitumor activity has been reported in AIDS-associated Kaposi’ssarcoma,9,10 but there are limited data describing efficacy in classic Kaposi’s sarcoma, an unusual form of hemangiosarcoma.We have previously reported paclitaxel to be an active agent in the treatment of angiosarcoma of the scalp and face, ahemangiosarcoma similar to Kaposi’s sarcoma.11 This case reveals that paclitaxel should be considered an appropriatetherapy with good palliative effects in the treatment of classic Kaposi’s sarcoma.

Farid Fata, Ayoub Mirza, and Albert BernathGeisinger Medical Center, Danville, PA


REFERENCES

1. McGinn JT, Ricca JJ, Currin JF: Kaposi’s sarcoma followingallergic angiitis. Ann Intern Med 42:921-927, 1955

2. Zeligman I: Kaposi’s sarcoma in a father and son. Bull JohnsHopkins Hosp 107:208-212, 1960

Fig 3.

Fig 4.

Table 1. Reported Cases of Familial Kaposi’s Sarcoma in Two or MoreMembers of the Same Family

First Author (ref) Year of Publication Cases of Familial Non-HIV–associated KS

McGinn1 1955 An uncle and a niece of Italiandescent

Zeligman2 1960 A Jewish father and his sonEpstein3 1972 Two Latvian brothersBrowstein4 1973 One patient and brother in a series of

100 patients with KSDigiovanna5 1981 A Jewish patient and his brotherPerniciaro6 1996 A German/English patient and his

sister

Abbreviation: KS, Kaposi’s sarcoma.



3. Epstein E: Kaposi’s sarcoma and parapsoriasis en plaque inbrothers. JAMA 219:1477-1478, 1972 (letter)

4. Brownstein MH, Shapiro L, Skolnik P: Kaposi’s sarcoma incommunity practice. Arch Dermatol 107:137-138, 1973 (letter)

5. Digiovanna J, Safai B: Kaposi’s sarcoma: Retrospective study of90 cases with particular emphasis on the familial occurrence, ethnicbackground and prevalence of other diseases. Am J Med 71:779-783,1981

6. Perniciaro C, Gross DJ, White JW, et al: Familial Kaposi’ssarcoma. Cutis 57:220-2222, 1996

7. Antman K, Yuan C: Medical progress: Kaposi’s sarcoma. N EnglJ Med 342:1027-1038, 2000

8. Belotti N, Vergani V, Drudis T: The microtubule-affecting drugpaclitaxel has anti-angiogenic activity. Clin Cancer Res 2:1843-1849,1996

9. Welles L, Saville W, Lietzau J, et al: Phase II trial with dosetitration of paclitaxel for the therapy of human immunodeficiencyvirus-associated Kaposi’s sarcoma. J Clin Oncol 16:1112-1121, 1998

10. Gill P, Tulpule A, Byron E, et al: Paclitaxel is safe and effectivein the treatment of advanced AIDS-related Kaposi’s sarcoma. J ClinOncol 17:1876-1883, 1999

11. Fata F, O’Reilly E, Ilson D, et al: Paclitaxel in the treatment ofpatients with angiosarcoma of the scalp or face. Cancer 86:2034-2037,1999

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skin lesions in melanoma and kaposi s sarcoma394476/uq394476... · 2019. 10. 11. · daniele...

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