Counterpoint: The Dysplastic Nevus: What I Do and Do Not Believe

dysplastic nevusIn this issue of the Journal, Rosendahl et al (1), sacrifice yet a few more trees in the ongoing, seemingly never-ending controversy surrounding the so-called dysplastic nevus. Is this latest sacrifice going to make significant changes in how these lesions are named and treated or is this yet another quixotic tilting at windmills? There is an almost religious zeal that has burned hotly and brightly about this issue virtually since the description of this new cancer syndrome was published in 1978 by Wallace Clark and his coworkers.(2) Rosendahl et al have done an excellent job at reviewing the literature and pointing out quite convincingly that perhaps we should stop with the nonsense and move on to other more important issues related to diagnosis and treatment of melanoma. Should we? Will we?
As one who has been involved in this issue almost since it came on the scene, who sat at the microscope with Wallace Clark and Bernard Ackerman in the early 1980s and has made the diagnosis of dysplastic nevus literally hundreds of thousands of times, I can offer a personal observation that few others can. As facts, fiction, religion, zeal, and Don Quixote have all been alluded to, I will share my experiences of over 30 years of dealing with this. Furthermore, since we have not agreed on what term to call ‘‘dysplastic’’ nevi, I will use the term in quotes as I do in my practice to reflect that it is a name, much like we use the term‘‘mycosis fungoides’’ to refer to a form of cutaneous T-cell lymphoma, even though it has nothing to do with fungi.

I believe that many ‘‘dysplastic’’ nevi are difficult to clinically distinguish from melanoma, especially evolving melanoma, as many of them display the ABCD clinical features of melanoma.  

This poses a significant problem, especially when a patient presents with many lesions, as they cannot all be biopsied or excised. Fortunately, most do not exhibit the ‘‘E’’ evolving feature so they can be followed up safely, and they do not all need to be excised. Those that undergo change are the ones that should be targeted.

I believe that there are patients with ‘‘dysplastic’’ nevi, especially when numerous and who have a personal history of or a first degree relative with melanoma, who are at increased risk for developing melanoma.  

Although Rosendahl et al point out the heterogeneity of the dysplastic nevus syndrome descriptions, I have personally witnessed and treated a number of patients over the years who developed melanoma in this setting. Most of the patients I have seen who developed this had many lesions, many of which were large with atypical clinical features. I have also seen patients, as Rosendahl et al note, who had many nevi but without atypical features or a personal or family history of melanoma develop melanoma as well, however.


I do not believe that having one or a few lesions with clinical features of ‘‘dysplastic’’ nevi poses an increased risk for developing melanoma.  

Just as having one or a few coincidental neurofibromas is not equivalent to having Von Recklinghausen disease, so, too, is having a few coincidental nevi with clinical features of dysplastic nevi not equivalent to having a melanoma-cancer syndrome.

I do not believe that dysplastic nevi are precursors of melanoma or that they lie on a spectrum of malignancy with melanoma.  

This concept is discussed by Rosendahl et al and I agree with it. It is not analogous to the relationship between a solar keratosis with its potential to develop into squamous cell carcinoma. It does not demonstrate a genetic profile of malignancy as a solar keratosis does. In some cases, ‘‘dysplastic’’ nevi may be markers for the development of melanoma as noted above, however.

I believe that melanoma may occasionally arise within dysplastic nevi.

Melanoma can arise in any nevus so these lesions are certainly not exempt. However, melanoma is no more likely to arise in these nevi than in any others, in my experience.

I believe that the histologic features of dysplastic nevi may be seen in very many settings and are extremely common findings.

Bernie Ackerman (3) published that the ‘‘dysplastic’’ nevus is the commonest nevus in man, an opinion that may be correct, especially when applying the published histologic criteria for diagnosis of ‘‘dysplastic’’ nevi to all melanocytic nevi. These findings are seen in growing nevi in childhood, eruptive nevi, congenital nevi, and nevi on special sites and perhaps others. In 1985, I and a colleague evaluated what diagnoses were given to ‘‘dysplastic’’ nevi in 1978 before the term was coined. (4) We found that they were all diagnosed as compound or junctional nevi.

I do not believe that there is a histologic distinction between a so-called ‘‘mildly’’ and ‘‘moderately’’ ‘‘dysplastic’’ nevus.

As Rosendahl et al point out, there are many studies that have documented the inability of dermatopathologists to agree as to what comprises so-called ‘‘mild’’ and ‘‘moderate’’ ‘‘dysplasia.’’ I agree whole-heartedly with this and in my experience, the less experience the pathologist has in examining these lesions, the greater the degree of ‘‘dysplasia’’ that gets reported and the greater the number of lesions recommended for excision. We recently published an article stating that if these lesions are to be graded, there should be only 2 grades: high grade, which refers to lesions that have features suggestive of melanoma evolving within them, and low grade, which refers to all others. (5)

I do not believe there is a correlation between the histologic features of a ‘‘dysplastic’’ nevus and a patient’s risk for
developing melanoma.

I have seen patients with the most banal-appearing lesion histologically yet with a family or personal risk for melanoma and multiple nevi develop melanoma and die. Conversely, I  have seen patients with lesions that would be considered severely ‘‘dysplastic’’ histologically with a solitary lesion and they never develop melanoma.

I believe that most so-called ‘‘severely dysplastic’’ nevi are either melanoma or melanoma in situ arising in the lesion.

There is no one ‘‘severely dysplastic’’ nevus entity as there are a number of histologic criteria that can be applied to designate a lesion as being ‘‘severely dysplastic.’’ Most of these are histologic criteria for the diagnosis of melanoma. Many lesions that I have evaluated over the years that have been diagnosed as ‘‘severely dysplastic’’ in consultation, I have diagnosed as melanoma, at least in situ and certainly recommended excision. However, as noted above, less experienced pathologists tend to use the term ‘‘severe dysplasia’’ more liberally and over diagnose lesions that, in my opinion, were benign.

I do not believe that all ‘‘dysplastic’’ nevi need to be excised on the basis of medical necessity.

Although it may be reasonable to excise these lesions in certain settings, as these are benign lesions that are not precursors to melanoma, just as with any other nevus, they can be biopsied when appropriate and followed up. If the pathologist comments that the lesion has features in common with melanoma yet the diagnosis of melanoma cannot be rendered with certainty, it is appropriate to excise such a lesion. However, this should be a relatively rare comment and if the pathologist is recommending re-excision of all ‘‘dysplastic’’ nevi, this is not appropriate. Furthermore, in cases in which there is uncertainty about the diagnosis, additional techniques such as genetic testing are now available and can be used on the tissue itself to help clarify the diagnosis.

I believe it would be reasonable to change the name dysplastic nevus.

Just like ‘‘actinic keratosis’’ does not do justice to the potential dangerous nature of a lesion that is an incipient squamous cell carcinoma, the term ‘‘dysplastic’’ nevus implies a more serious nature to a wholly benign lesion. Bernie Ackerman (6) proposed using the term ‘‘Clark nevus’’ for these lesions and as Rosendahl et al point out, the term ‘‘nevus with architectural disorder’’ was proposed in 1992.  Neither have been widely adopted and the term ‘‘dysplastic’’ nevus remains wildly popular. As the histologic features of these lesions do not correlate with clinical risk for the development of melanoma, I would prefer to diagnose these lesions as compound or junctional nevi as was done before 1978 and if I observe microscopic features that suggest evolving melanoma, I would report those and recommend excision. However, many clinicians do not care much about my preferences and believe that using the term dysplastic nevus with grading is a reasonable way to diagnose and treat these patients.

I do not believe the name dysplastic nevus will disappear anytime soon.

Now, at least one generation of dermatologists, other physicians, and extenders have been trained in the era of the dysplastic nevus. Other efforts to expunge inaccurate or misleading terms in medicine and dermatology have been made over the years, largely to no avail. Furthermore, as long as clinicians are reimbursed for treating these lesions as potential malignancies, there will be a strong incentive to retain the term. Thus, although the effort of Rosendahl et al are noble, I fear that in this case, as with many others before them, the windmills will prevail.

                                                                                                                                                  

From the Department of Dermatology, University of Texas Southwestern Medical Center, and Cockerell Dermatopathology.
Funding sources: None.
Conflicts of interest: None declared.
Reprints not available from the author.
Correspondence to: Clay J. Cockerell, MD, Cockerell Dermatopathology, 2110 Research Row #100, Dallas, TX 75235. E-mail: ccockerell@dermpath.com.
J Am Acad Dermatol 2015;73:515-7. 0190-9622/$36.00
 2015 by the American Academy of Dermatology, Inc.
http://dx.doi.org/10.1016/j.jaad.2015.05.037

REFERENCES
1. Rosendahl CO, Grant-Kels JM, Que SKT. Dysplastic nevus: Fact and fiction. J Am Acad Dermatol. doi: http://dx.doi.org/10.1016/j.jaad.2015.04.029. Published online May 30, 2015.
2. Clark WH, Reimer RR, Greene M. Origin of familial malignant melanomas from heritable melanocytic lesions: ‘The B-K mole syndrome’. Arch Dermatol. 1978;114(5):732-738.
3. Ackerman AB. What nevus is dysplastic, a syndrome and the commonest precursor of malignant melanoma? A riddle and an answer. Histopathology. 1988;13(3):241-256.
4. Cockerell CJ, Berson DS. A retrospective look at dysplastic nevi. What were they in 1978 and how have they fared since? Am J Dermatopathol. 1985;(7 Suppl):93-97.
5. Abdoul-Fotouh H, Baker LA, Lucero Jackson M, Cockerell CJ.
Reassessment of the dysplastic nevus concept in the 21st century: A proposal for a two-tiered system of classification. Clinical Investigation. 2013;3(12):1105-1107.
6. Ackerman AB, Milde P. Naming acquired melanocytic nevi: Commonand dysplastic, normal and atypical, or Unna Miescher, Spitz, and Clark? Am J Dermatopathol. 1992;14(5):447-453.