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Agminated Atypical (Dysplastic) Nevi:  Case Report and Review of the Literature FREE

Ashfaq A. Marghoob, MD; Robin Blum, BS; Robert Nossa, MD; Klaus J. Busam, MD; Dana Sachs, MD; Allan Halpern, MD
[+] Author Affiliations

From the Dermatology Service, Department of Medicine, Memorial Sloan-KetteringCancer Center, New York, NY (Drs Marghoob, Busam, Sachs, and Halpern); andthe Departments of Dermatology, State University of New York at Stony Brook(Dr Marghoob) and Mount Sinai Medical Center, New York (Ms Blum and Dr Nossa).


Arch Dermatol. 2001;137(7):917-920. doi:10-1001/pubs.Arch Dermatol.-ISSN-0003-987x-137-7-dob00064.
Text Size: A A A
Published online

ABSTRACT

Background  Patients with the atypical mole syndrome have multiple dysplastic nevithat appear to be randomly distributed on certain preferred anatomical sitessuch as the upper back. These dysplastic nevi are thought to be acquired melanocyticnevi that begin appearing at puberty. To our knowledge, the presence of agminatedatypical (dysplastic) nevi has not been reported.

Observation  We describe a patient with the atypical mole syndrome who has more than100 melanocytic nevi, many of which are clinically atypical and one of whichproved to be a melanoma. Among his many melanocytic nevi is a cluster of approximately50 nevi that are distributed in an area measuring 5 × 3 cm. The histopathologicfeatures of these nevi are consistent with the diagnosis of "dysplastic nevus."

Conclusions  To our knowledge, agminated atypical (dysplastic) nevi have not beendescribed previously. The presence of agminated atypical (dysplastic) neviin a patient with the atypical mole syndrome can be theorized to arise becauseof loss of heterozygosity.

Figures in this Article

ATYPICAL MOLES and the atypical mole (dysplastic nevus) syndrome arerecognized as distinct clinical entities.1,2Most dermatopathologists also agree on the existence of the histologic entityknown as a dysplastic nevus.3,4Clinically, most atypical nevi are solitary lesions that begin to appear aroundpuberty. We describe a patient with the atypical mole syndrome who had multipleagminated atypical nevi that were histologically characterized as dysplasticnevi. Agminated as it pertains to melanocytic neviis defined as a circumscribed grouping of pigmented lesions confined to abody segment. Our patient had approximately 50 nevi clustered in a 5 ×3-cm area of skin on his right arm. Although the existence of agminated melanocyticnevi has been documented,5 to our knowledgeagminated atypical (dysplastic) nevi have never been reported in the literature.

REPORT OF A CASE

A 44-year-old man was referred to the dermatology clinic for evaluationof multiple irregular moles. The patient reported that his nevi developedduring his teenage years. He denied a family history of multiple moles ormelanoma.

On physical examination, the patient had more than 100 melanocytic nevi,and a few of these nevi appeared clinically atypical. The largest nevus, onthe right side of his chest, measured 1 cm in greatest diameter (Figure 1). The patient also had an irregularmelanocytic neoplasm on the right side of his mandible that on subsequentbiopsy proved to be melanoma in situ.

Place holder to copy figure label and caption
Figure 1.

Anterior chest and abdomen showingmultiple melanocytic nevi. The patient's largest nevus is on the right sideof his chest near the midline.

Graphic Jump Location

The patient had a cluster of approximately 50 melanocytic nevi on hisright arm, all distributed in an area 5 × 3 cm in diameter (Figure 2 and Figure 3). The patient stated that this cluster of nevi first becameapparent at the age of 15 years. No background café-au-lait pigmentationwas noted clinically or with the aid of a Wood light examination. Dermoscopyrevealed that all the nevi had a "diffuse and patchy" network pattern6 (Figure 4A).However, one area was darker (Figure 3)and on dermoscopy had black dots, globules, and structureless areas (Figure 4B). Because this area had nevi thatdiffered from the other surrounding nevi, it was excised.7The histopathologic findings revealed a lentiginous compound melanocytic nevuswith architectural disorder of its intraepidermal component and irregularplacement of nests of variable size and shape, fusion of nests, and asymmetricextension of the junctional component beyond the confines of the intradermalnevus component (Figure 5A). Severalmelanocytes contained abnormally large nuclei, some that were twice the normalsize, and the nuclei had irregular contours. Furthermore, papillary dermalfibroplasia with a sparse lymphohistiocytic infiltrate was present (Figure 5B). In light of the presence of architecturaldisorder and cytologic atypia, a diagnosis of dysplastic nevus was made.

Place holder to copy figure label and caption
Figure 2.

The agminated atypical nevi areseen on the right arm.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 3.

The agminated atypical nevi. Abiopsy of the area within the oval was performed. A indicates the area fromwhich the dermoscopic image seen in Figure 4A was taken; and B, the area fromwhich the dermoscopic image seen in Figure 4B was taken.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 4.

A, Dermoscopy of the agminatednevi showing a "diffuse and patchy" network pattern, a feature commonly seenin dysplastic nevi. B, Dermoscopy showing an area with globules, black dots,a network, and structureless areas. A biopsy of this area was performed.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 5.

A, Histopathologic features underscanning magnification show the lesion to have a slightly asymmetric silhouette(original magnification ×4). B, A higher magnification reveals a lentiginousmelanocytic proliferation with papillary dermal fibrosis and scattered clustersof lymphocytes (original magnification ×10).

Graphic Jump Location

COMMENT

Atypical moles (dysplastic nevi) are acquired pigmented lesions thatdevelop during puberty and continue to develop and change throughout life.Although they may appear anywhere on the body, they primarily develop on thetrunk.

Clinically, atypical nevi share many features of malignant melanoma,including asymmetry, border irregularity, color variability, and a diametergreater than 6 mm.8 They can be multiple orsolitary, and can develop in patients with or without a family history ofsimilar lesions.

We describe a patient with the atypical mole syndrome who had an unusualpresentation of multiple, clustered, clinically atypical (dysplastic) nevi.To our knowledge, this is the first reported case of agminated atypical (dysplastic)nevi. In this patient, the diagnosis of atypical (dysplastic) nevi was basedon clinical and histologic features. Clinically, some of the patient's neviwere irregular, demonstrated variegation of color, and were greater than 6mm in diameter. The dermoscopic feature of a patchy network was also consistentwith a diagnosis of dysplastic nevi.6 The histologicdiagnosis of the biopsied section was that of a dysplastic nevus or a nevuswith "architectural disorder and cytologic atypia."9

A review of the literature revealed that the term agminated has been used to describe several different cutaneous lesions.Pigmented lesions that have been described as agminated include melanocyticnevi,5 congenital melanocytic nevi,10 Spitz nevi,11,12nevi spilus,13,14 blue nevi,15,16 and multiple lentigines.17 Other nonpigmented agminated lesions reported inthe literature include xanthogranulomas,18angiofibromas,19 and neurilemomas.20 Historically, atypical (dysplastic) nevi have notbeen reported to occur in an agminated distribution.

Based on this patient's clinical and histologic features, the diagnosisof agminated atypical (dysplastic) nevi, and not any of the other previouslyreported agminated lesions, is most accurate. By definition, congenital melanocytic nevi are melanocytic nevi that are present atbirth or develop shortly after birth. Because our patient's nevi developedduring his teenage years, it is unlikely that they were congenital melanocyticnevi.21 In addition, the histopathologic featureswere not consistent with congenital melanocytic nevi.

It is unlikely that the cluster of lesions were Spitz nevi. Althoughmultiple agminated Spitz nevi have been reported,22the histologic features of Spitz nevi are quite different and demonstrateadmixed spindle and epitheliod cells arranged in irregular nests with occasionalmitotic figures. These features were not seen in this patient's biopsy specimen.In addition, the clinical features of agminated Spitz nevi are also different.Spitz nevi tend to develop in early childhood, predominately occur on theface, and are pink.11 In our patient, the nevidid not develop until puberty, occurred on his arm, and were brown.

The diagnoses of nevus spilus,23 bluenevi, and lentiginosis can be ruled out based on clinical and histologic features.Unlike our patient, who developed his "agminated atypical moles" at the ageof 15 years, nevus spilus is usually apparent by early infancy or childhood.21,23 The diagnosis of nevus spilus isalso not consistent with the clinical examination because of the obvious lackof background pigmentation, a feature commonly seen in a nevus spilus. Furthermore,the pathological features of our patient's agminated lesions also failed todemonstrate the background of lentigo, as would be seen in a nevus spilus.The diagnosis of blue nevi was not made because clinically they did not appearas blue or black dome-shaped papules, and histologically they did not demonstratedermal melanocytes grouped in irregular bundles admixed with melanophages.16 The diagnosis of agminated lentiginosis was not madebecause the histologic features did not demonstrate elongation of the reteridges and hyperplasia of melanocytes.17

It has been proposed that the atypical mole syndrome has either an autosomaldominant mode of inheritance with incomplete penetrance or a polygenic modeof inheritance.2 The specific gene or genesthat predispose to the development of dysplastic nevi and the precipitantsfor the formation of individual melanocytic nevi have not been identified.However, sun exposure has been implicated in the development of melanocyticnevi.24 Furthermore, it has been postulatedthat some atypical melanocytic nevi may develop through loss of heterozygosity(LOH).25,26 Loss of heterozygosityis the loss of a normal wild-type allele, leading to the expression of a mutantor recessive allele.27 One mechanism for acquiredloss of an allele may be through mutations induced by UV exposure.28 The specific etiology of agminated nevi is not known.Local environmental factors, such as UV radiation, may play a role in thedevelopment of clustered lesions. However, it is also possible that this agminatedpattern may represent LOH, occurring during embryogenesis, as has been postulatedto account for the segmental distribution of lesions such as neurofibromas,porokeratosis, and Becker nevi.27 In our patient,the agminated dysplastic nevi occurred in the presence of the atypical molesyndrome. Other examples of segmental clustering of skin lesions superimposedon a generalized less severe form of the condition may shed light on the pathogenesisin our case. Autosomal dominant skin disorders, such as neurofibromatosis,sometimes occur in a segmental pattern superimposed on a less severe but diffuseform of the same disorder.27 This phenomenonmay be explained by an early postzygotic mutational event giving rise to LOHat the locus responsible for the trait. A person can also have a segmentalmanifestation of a polygenic skin disorder, such as segmental severe psoriasis,superimposed on symmetric involvement of ordinary psoriasis.27This too can be explained by LOH occurring in a somatic cell during earlyembryogenesis, resulting in either homozygosity or hemizygosity for one ofthe genes predisposing to psoriasis. Future studies of the distribution oflesions in cases of agminated nevi such as ours coupled with genetic analysisof microdissected tissues may shed light on the timing and nature of theseevents.

In conclusion, based on a review of clinical entities occurring in anagminated distribution, we believe that our case is the first report of agminatedatypical (dysplastic) nevi. This is a new, previously undescribed, clinicalvariant of atypical (dysplastic) nevi occurring in a patient with the atypicalmole syndrome and adds to the phenotypic spectrum of this entity. In addition,this case raises the possibility that LOH may play a role in the developmentof some cases of dysplastic nevi or atypical mole syndrome.

ARTICLE INFORMATION

Accepted for publication February 26, 2001.

We thank Nathan Ellis, PhD, for reviewing the manuscript and helpingus to better understand the concept of loss of heterozygosity.

Corresponding author and reprints: Ashfaq A. Marghoob, MD, DermatologyService, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, New York,NY 10021.

REFERENCES

Tucker  MAHalpern  AHolly  EA  et al.  Clinically recognized dysplastic nevi: a central risk factor for cutaneousmelanoma. JAMA. 1997;2771439- 1444
Link to Article
Slade  JMarghoob  AASalopek  TGRigel  DSKopf  AWBart  RS Atypical mole syndrome: risk factors for cutaneous malignant melanomaand implications for management. J Am Acad Dermatol. 1995;32479- 494
Link to Article
Clemente  CCochran  AJElder  DE  et al.  Histopathologic diagnosis of dysplastic nevi: concordance among pathologistsconvened by the World Health Organization Melanoma Programme. Hum Pathol. 1991;22313- 319
Link to Article
Weinstock  MABarnhill  RLRhodes  ARBrodsky  GL Reliability of the histopathologic diagnosis of melanocytic dysplasia. Arch Dermatol. 1997;133953- 958
Link to Article
Stolz  WBraun-Falco  OBilek  PLandthaler  MCognetta  AB Color Atlas of Dermatoscopy.  Oxford, England Blackwell Science Ltd1993;64
Kopf  AW Dermoscopic diagnosis of dysplastic nevi. Melanoma Res. 2001;11521
Grob  JJBonerandi  JJ The "ugly duckling" sign: identification of the common characteristicsof nevi in an individual as a basis for melanoma screening. Arch Dermatol. 1998;134103- 104
Link to Article
Marghoob  AA The dangers of atypical mole (dysplastic nevus) syndrome. Postgrad Med. 1999;105147- 164
Link to Article
NIH Consensus Development Panel on Early Melanoma, Diagnosis and treatment of early melanoma. JAMA. 1992;2681314- 1319
Link to Article
Brunner  MVardarman  EMegahed  MRuzicka  T Congenital agminated segmental naevi. Br J Dermatol. 1995;133315- 316
Link to Article
Hamm  HHapple  RBrocker  EB Multiple agminate Spitz naevi: review of the literature and reportof a case with distinctive immunohistochemical features. Br J Dermatol. 1987;117511- 522
Link to Article
Lancer  HAMuhlbauer  JESober  AJ Multiple agminated spindle cell nevi: unique clinical presentationand review. J Am Acad Dermatol. 1983;8707- 711
Link to Article
Betti  RInselvini  EPalvarini  MCrosti  C Agminated intradermal Spitz nevi arising on an unusual speckled lentiginousnevus with localized lentiginosis: a continuum? Am J Dermatopathol. 1997;19524- 527
Link to Article
Aloi  FTomasini  CPippione  M Agminated Spitz nevi occurring within a congenital speckled lentiginousnevus. Am J Dermatopathol. 1995;17594- 598
Link to Article
Shenfield  HTMaize  JC Multiple and agminated blue nevi. J Dermatol Surg Oncol. 1980;6725- 728
Link to Article
Velez  Adel-Rio  EMartin-de-Hijas  CFurio  VSanchez Yus  E Agminated blue nevi: case report and review of the literature. Dermatology. 1993;186144- 148
Link to Article
Micali  GNasca  MRInnucenzi  DLembo  D Agminated lentiginosis: case report and review of the literature. Pediatr Dermatol. 1994;11241- 245
Link to Article
Tangoren  IAWeinberg  JMHumphreys  TMurphy  GFMargolis  DJSpiers  EM Agminated xanthogranuloma: an unusual presentation of juvenile xanthogranuloma. Acta Derm Venereol. 1998;7868- 69
Link to Article
Anliker  MDDummer  RBurg  G Unilateral agminated angiofibromas: a segmental expression of tuberoussclerosis? Dermatology. 1997;195176- 178
Link to Article
Berger  TGLapins  NAEngel  ML Agminated neurilemomas. J Am Acad Dermatol. 1987;17891- 894
Link to Article
Schaffer  JVOrlow  SJLazova  RBolognia  JL Speckled lentiginous nevus: within the spectrum of congenital melanocyticnevi. Arch Dermatol. 2001;137172- 178
Link to Article
Paniago-Pereira  CMaize  JCAckerman  AB Nevus of large spindle and/or epitheliod cells: Spitz's nevus. Arch Dermatol. 1978;1141811- 1823
Link to Article
Rhodes  ARMihm  MC Origin of cutaneous melanoma in a congenital dysplastic nevus spilus. Arch Dermatol. 1990;126500- 505
Link to Article
Kelly  JWRivers  JKMacLennan  RHarrison  SLewis  AETate  BJ Sunlight: a major factor associated with the development of melanocyticnevi in Australian schoolchildren. J Am Acad Dermatol. 1994;3040- 48
Link to Article
Boni  RZhuang  ZAlbuquerque  AVortmeyer  ADuray  P Loss of heterozygosity detected on 1p and 9q in microdissected atypicalnevi. Arch Dermatol. 1998;134882- 883
Link to Article
Birindelli  STragni  GBartoli  C  et al.  Detection of microsatellite alterations in the spectrum of melanocyticnevi in patients with or without individual or family history of melanoma. Int J Cancer. 2000;86255- 261
Link to Article
Happle  R Loss of heterozygosity in human skin. J Am Acad Dermatol. 1999;41143- 161
Link to Article
Boni  RMatt  DBurg  GTronnier  MVortmeyer  AZhuang  Z Ultraviolet-induced acute histological changes in irradiated nevi arenot associated with allelic loss. Arch Dermatol. 1998;134853- 856

Figures

Place holder to copy figure label and caption
Figure 1.

Anterior chest and abdomen showingmultiple melanocytic nevi. The patient's largest nevus is on the right sideof his chest near the midline.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

The agminated atypical nevi areseen on the right arm.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 3.

The agminated atypical nevi. Abiopsy of the area within the oval was performed. A indicates the area fromwhich the dermoscopic image seen in Figure 4A was taken; and B, the area fromwhich the dermoscopic image seen in Figure 4B was taken.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 4.

A, Dermoscopy of the agminatednevi showing a "diffuse and patchy" network pattern, a feature commonly seenin dysplastic nevi. B, Dermoscopy showing an area with globules, black dots,a network, and structureless areas. A biopsy of this area was performed.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 5.

A, Histopathologic features underscanning magnification show the lesion to have a slightly asymmetric silhouette(original magnification ×4). B, A higher magnification reveals a lentiginousmelanocytic proliferation with papillary dermal fibrosis and scattered clustersof lymphocytes (original magnification ×10).

Graphic Jump Location

Tables

References

Tucker  MAHalpern  AHolly  EA  et al.  Clinically recognized dysplastic nevi: a central risk factor for cutaneousmelanoma. JAMA. 1997;2771439- 1444
Link to Article
Slade  JMarghoob  AASalopek  TGRigel  DSKopf  AWBart  RS Atypical mole syndrome: risk factors for cutaneous malignant melanomaand implications for management. J Am Acad Dermatol. 1995;32479- 494
Link to Article
Clemente  CCochran  AJElder  DE  et al.  Histopathologic diagnosis of dysplastic nevi: concordance among pathologistsconvened by the World Health Organization Melanoma Programme. Hum Pathol. 1991;22313- 319
Link to Article
Weinstock  MABarnhill  RLRhodes  ARBrodsky  GL Reliability of the histopathologic diagnosis of melanocytic dysplasia. Arch Dermatol. 1997;133953- 958
Link to Article
Stolz  WBraun-Falco  OBilek  PLandthaler  MCognetta  AB Color Atlas of Dermatoscopy.  Oxford, England Blackwell Science Ltd1993;64
Kopf  AW Dermoscopic diagnosis of dysplastic nevi. Melanoma Res. 2001;11521
Grob  JJBonerandi  JJ The "ugly duckling" sign: identification of the common characteristicsof nevi in an individual as a basis for melanoma screening. Arch Dermatol. 1998;134103- 104
Link to Article
Marghoob  AA The dangers of atypical mole (dysplastic nevus) syndrome. Postgrad Med. 1999;105147- 164
Link to Article
NIH Consensus Development Panel on Early Melanoma, Diagnosis and treatment of early melanoma. JAMA. 1992;2681314- 1319
Link to Article
Brunner  MVardarman  EMegahed  MRuzicka  T Congenital agminated segmental naevi. Br J Dermatol. 1995;133315- 316
Link to Article
Hamm  HHapple  RBrocker  EB Multiple agminate Spitz naevi: review of the literature and reportof a case with distinctive immunohistochemical features. Br J Dermatol. 1987;117511- 522
Link to Article
Lancer  HAMuhlbauer  JESober  AJ Multiple agminated spindle cell nevi: unique clinical presentationand review. J Am Acad Dermatol. 1983;8707- 711
Link to Article
Betti  RInselvini  EPalvarini  MCrosti  C Agminated intradermal Spitz nevi arising on an unusual speckled lentiginousnevus with localized lentiginosis: a continuum? Am J Dermatopathol. 1997;19524- 527
Link to Article
Aloi  FTomasini  CPippione  M Agminated Spitz nevi occurring within a congenital speckled lentiginousnevus. Am J Dermatopathol. 1995;17594- 598
Link to Article
Shenfield  HTMaize  JC Multiple and agminated blue nevi. J Dermatol Surg Oncol. 1980;6725- 728
Link to Article
Velez  Adel-Rio  EMartin-de-Hijas  CFurio  VSanchez Yus  E Agminated blue nevi: case report and review of the literature. Dermatology. 1993;186144- 148
Link to Article
Micali  GNasca  MRInnucenzi  DLembo  D Agminated lentiginosis: case report and review of the literature. Pediatr Dermatol. 1994;11241- 245
Link to Article
Tangoren  IAWeinberg  JMHumphreys  TMurphy  GFMargolis  DJSpiers  EM Agminated xanthogranuloma: an unusual presentation of juvenile xanthogranuloma. Acta Derm Venereol. 1998;7868- 69
Link to Article
Anliker  MDDummer  RBurg  G Unilateral agminated angiofibromas: a segmental expression of tuberoussclerosis? Dermatology. 1997;195176- 178
Link to Article
Berger  TGLapins  NAEngel  ML Agminated neurilemomas. J Am Acad Dermatol. 1987;17891- 894
Link to Article
Schaffer  JVOrlow  SJLazova  RBolognia  JL Speckled lentiginous nevus: within the spectrum of congenital melanocyticnevi. Arch Dermatol. 2001;137172- 178
Link to Article
Paniago-Pereira  CMaize  JCAckerman  AB Nevus of large spindle and/or epitheliod cells: Spitz's nevus. Arch Dermatol. 1978;1141811- 1823
Link to Article
Rhodes  ARMihm  MC Origin of cutaneous melanoma in a congenital dysplastic nevus spilus. Arch Dermatol. 1990;126500- 505
Link to Article
Kelly  JWRivers  JKMacLennan  RHarrison  SLewis  AETate  BJ Sunlight: a major factor associated with the development of melanocyticnevi in Australian schoolchildren. J Am Acad Dermatol. 1994;3040- 48
Link to Article
Boni  RZhuang  ZAlbuquerque  AVortmeyer  ADuray  P Loss of heterozygosity detected on 1p and 9q in microdissected atypicalnevi. Arch Dermatol. 1998;134882- 883
Link to Article
Birindelli  STragni  GBartoli  C  et al.  Detection of microsatellite alterations in the spectrum of melanocyticnevi in patients with or without individual or family history of melanoma. Int J Cancer. 2000;86255- 261
Link to Article
Happle  R Loss of heterozygosity in human skin. J Am Acad Dermatol. 1999;41143- 161
Link to Article
Boni  RMatt  DBurg  GTronnier  MVortmeyer  AZhuang  Z Ultraviolet-induced acute histological changes in irradiated nevi arenot associated with allelic loss. Arch Dermatol. 1998;134853- 856

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