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Atypical Mole (Clark Nevus or Dysplastic Nevus)

Updated : January 30, 2024





Background

Atypical moles, also known as dysplastic nevi, are melanocytic neoplasms that have developed and have an abnormal architecture and melanocyte atypia. Atypical moles have a variety of names; they are often referred to as B-K moles, Clark nevi, and dysplastic nevi; though strict sense, the word “dysplastic nevus” only refers to a particular microscopic morphology, and only a small percentage of atypical moles meet the requirements. Since dysplastic nevi frequently exhibit ABCDE morphological melanoma traits, they mirror the disease clinically.

Atypical moles are often diagnosed clinically if three or more of the following characteristics are present: diameter greater than 5 mm, uneven margins, poorly defined borders, & color change of the lesion. Healthcare professionals frequently perform biopsies on lesions with this characteristic to rule out melanoma because making the distinction purely based on microscopic inspection may be challenging. Individual atypical nevi have a low likelihood of malignant development, however, patients with many atypical moles are more likely to develop melanoma.

 

Epidemiology

Atypical moles are slightly more prevalent in men than in women around the globe and have a wide geographic range. The prevalence is 2% – 18% worldwide, with European populations and people with fair complexion showing greater incidences (7% – 24%). There are several notable exemptions, such as in the Japanese population, where despite having a light-skinned phenotype, the occurrence of atypical moles is minimal. Additionally, rare is pediatric occurrence.

In the US, the risk of developing melanoma in one’s lifetime is only 1%, but it is much higher in people who have atypical moles, which are thought to account for more than 10 percent of all moles. In the US population, the probability of developing melanoma from a common mole is approximately 1:30,000 for men & 1:40,000 for women.

Frequently diagnosed moles do not often turn into atypical moles; instead, 75% of aberrant moles appear suddenly, with no previous history of moles at the afflicted site. Patients with family atypical multiple-mole melanoma syndrome (FAMMM), with a nearly 100% lifetime prevalence of an atypical mole developing into melanoma in situ, are among those at increased risk.

 

Anatomy

Pathophysiology

Although the pathophysiology of atypical moles is incompletely understood, it is generally agreed that a complex interplay of genetic and environmental variables is responsible for its development. Allelic deletion of particular chromosomal locations, such as 9p21–22 & 1p36, is one genetic change that has been linked to the etiology of atypical moles.

Furthermore, pathogenesis is directly correlated with mutations in the protooncogenes BRAF & CDK4 as well as the tumor suppressor melastatin. These moles’ melanocytic cellular atypia is caused by the repair of DNA mismatch mechanisms that produce excessive telomerase activity, as determined by the telomerase activity markers Ki-67 & cyclin D1. Atypical moles frequently don’t have the CDKN2A alteration that melanoma frequently possesses.

Etiology

Scientifically speaking, the origin of atypical moles needs to be better understood. Genetic (inside) & environmental (exterior) factors combine to form the possible causes. Their prevalence is linked to particular hereditary traits like pale skin, thinner (blond) hair, lighter eye colors, a propensity for freckles, & sun sensitivities. Epidemiological data have shown that those with a history of elevated UV sunlight exposure had a higher incidence of atypical moles.

Nevi have genetic ties to a number of chromosomal locations. PLA2G6, IRF4, & MTAP have been shown in genome-wide investigations to have a strong correlation with the number of melanocytic nevi. Atypical moles are the transitional stage between banal nevi and the formation of melanoma, according to Clark’s sequential progression hypothesis, which is still favored by some dermatologists.

There is, however, less evidence that atypical moles and melanoma share genetic alterations. For instance, CDKN2A is represented by the greater part of familial melanoma individuals but not frequently in those with atypical moles. There are additional concerns about the veracity of this idea, given that 75% of melanoma develops from scratch.

 

Genetics

Prognostic Factors

Clinical History

Clinical Presentation

History

It is important to collect a thorough family and personal history, paying close attention to any moles & melanoma. Sun exposure patterns and recent nevi changes are additional crucial considerations. A patient’s lifespan may see the development of atypical moles at any time. Atypical moles can grow new lesions and evolve over time.

While persons with nonfamilial (sporadic) atypical moles often have just 1–10 tumors, they may also appear with several hundred lesions, and familial atypical multiple-mole melanoma (FAMMM) syndrome patients may have one to several hundred atypical moles. A person with atypical moles who comes from a family where melanoma is common has a significant lifetime risk of getting the disease. To rule out melanoma, rapid and distinctive alterations should warrant consideration for excision or biopsy.

 

Physical Examination

Physical Examination

Complete skin examinations should be performed on FAMMM syndrome patients at their initial outpatient clinic and thereafter at least once every twelve months for the rest of their lives. Atypical moles frequently have a distinctive look, albeit specific lesions might not exhibit all the symptoms. They often have a diameter of 5 to 15 mm and are big, pigmented lesions in general. Atypical moles typically measure more than 5 millimeters in diameter.

Typically, borders need to be ill-defined, notched, and irregular. One lesion may have both macular and papular patches (sometimes known as a “fried egg” & “target” appearance). There is a wide spectrum of colors, from tan to dark brown to pink. Atypical nevi can develop any part of the body, although the chest, back, breasts, buttocks, & scalp are where they most usually manifest. Both sun-exposed & sun-protected regions might have lesions.

Individuals with FAMMM syndrome may well have over 100 tumors, which is a significant increase over the typical 50 common moles found in most people. Although the clinical diagnosis of a single unusual mole may be straightforward, patients frequently have several nevi, which could complicate monitoring.

For histologic validation of dysplastic nevi vs. melanoma in the initial assessment of an unusual mole, an excisional sample should be taken into consideration. If the pigmented lesions are completely eliminated & care is given to provide appropriate depth for correct staging in melanoma, shallow scoop saucerizations can be performed with at minimum a 2-mm border of apparently healthy skin covering the pigmentation lesion.

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

Differential Diagnoses

Spitz Nevus

Seborrheic Keratosis

Melanocytic Nevi

Lentigo

Dermatofibroma

Cutaneous Melanoma

Blue Nevi

Basal Cell Carcinoma

 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

Although there is no known way to stop the growth of atypical moles, people who have a history of them should take extra precautions to wear high-factor sun protection. However, it is believed that routine skin inspections by a qualified healthcare professional to look for any suspicious lesions and evaluate changes within already-existing moles are the most efficient way to identify malignant alterations early on. Dermatologists disagree on how best to treat unusual moles.

When there is any clinical concern about atypical moles that have arisen on their own or when morphological alterations are noticed in already-existing atypical moles, excision biopsies are typically performed. When margins are incomplete or lesions reappear, more than half of the doctors questioned by the American Academy of Dermatology said it is normal protocol to re-excise atypical moles. Reexcision of clear borders is based on the idea that the “pseudo-melanoma” phenomenon, or the reappearance of excised tumors along a biopsy scarring, may make them difficult to distinguish from melanoma.

There is strong evidence, nonetheless, that most atypical moles don’t require additional excision. There are several exceptions, such as when there is the worry that the clinical assessment does not match the histology, when there is acute atypia, or when a histological investigation is unable to distinguish between the lesion & melanoma. In these situations, the lesion should be re-excised with the proper margins and managed in accordance with the melanoma management guidelines.

 

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Media Gallary

References

https://www.ncbi.nlm.nih.gov/books/NBK560606/

https://emedicine.medscape.com/article/1056283-clinical

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Atypical Mole (Clark Nevus or Dysplastic Nevus)

Updated : January 30, 2024




Atypical moles, also known as dysplastic nevi, are melanocytic neoplasms that have developed and have an abnormal architecture and melanocyte atypia. Atypical moles have a variety of names; they are often referred to as B-K moles, Clark nevi, and dysplastic nevi; though strict sense, the word “dysplastic nevus” only refers to a particular microscopic morphology, and only a small percentage of atypical moles meet the requirements. Since dysplastic nevi frequently exhibit ABCDE morphological melanoma traits, they mirror the disease clinically.

Atypical moles are often diagnosed clinically if three or more of the following characteristics are present: diameter greater than 5 mm, uneven margins, poorly defined borders, & color change of the lesion. Healthcare professionals frequently perform biopsies on lesions with this characteristic to rule out melanoma because making the distinction purely based on microscopic inspection may be challenging. Individual atypical nevi have a low likelihood of malignant development, however, patients with many atypical moles are more likely to develop melanoma.

 

Atypical moles are slightly more prevalent in men than in women around the globe and have a wide geographic range. The prevalence is 2% – 18% worldwide, with European populations and people with fair complexion showing greater incidences (7% – 24%). There are several notable exemptions, such as in the Japanese population, where despite having a light-skinned phenotype, the occurrence of atypical moles is minimal. Additionally, rare is pediatric occurrence.

In the US, the risk of developing melanoma in one’s lifetime is only 1%, but it is much higher in people who have atypical moles, which are thought to account for more than 10 percent of all moles. In the US population, the probability of developing melanoma from a common mole is approximately 1:30,000 for men & 1:40,000 for women.

Frequently diagnosed moles do not often turn into atypical moles; instead, 75% of aberrant moles appear suddenly, with no previous history of moles at the afflicted site. Patients with family atypical multiple-mole melanoma syndrome (FAMMM), with a nearly 100% lifetime prevalence of an atypical mole developing into melanoma in situ, are among those at increased risk.

 

Although the pathophysiology of atypical moles is incompletely understood, it is generally agreed that a complex interplay of genetic and environmental variables is responsible for its development. Allelic deletion of particular chromosomal locations, such as 9p21–22 & 1p36, is one genetic change that has been linked to the etiology of atypical moles.

Furthermore, pathogenesis is directly correlated with mutations in the protooncogenes BRAF & CDK4 as well as the tumor suppressor melastatin. These moles’ melanocytic cellular atypia is caused by the repair of DNA mismatch mechanisms that produce excessive telomerase activity, as determined by the telomerase activity markers Ki-67 & cyclin D1. Atypical moles frequently don’t have the CDKN2A alteration that melanoma frequently possesses.

Scientifically speaking, the origin of atypical moles needs to be better understood. Genetic (inside) & environmental (exterior) factors combine to form the possible causes. Their prevalence is linked to particular hereditary traits like pale skin, thinner (blond) hair, lighter eye colors, a propensity for freckles, & sun sensitivities. Epidemiological data have shown that those with a history of elevated UV sunlight exposure had a higher incidence of atypical moles.

Nevi have genetic ties to a number of chromosomal locations. PLA2G6, IRF4, & MTAP have been shown in genome-wide investigations to have a strong correlation with the number of melanocytic nevi. Atypical moles are the transitional stage between banal nevi and the formation of melanoma, according to Clark’s sequential progression hypothesis, which is still favored by some dermatologists.

There is, however, less evidence that atypical moles and melanoma share genetic alterations. For instance, CDKN2A is represented by the greater part of familial melanoma individuals but not frequently in those with atypical moles. There are additional concerns about the veracity of this idea, given that 75% of melanoma develops from scratch.

 

Clinical Presentation

History

It is important to collect a thorough family and personal history, paying close attention to any moles & melanoma. Sun exposure patterns and recent nevi changes are additional crucial considerations. A patient’s lifespan may see the development of atypical moles at any time. Atypical moles can grow new lesions and evolve over time.

While persons with nonfamilial (sporadic) atypical moles often have just 1–10 tumors, they may also appear with several hundred lesions, and familial atypical multiple-mole melanoma (FAMMM) syndrome patients may have one to several hundred atypical moles. A person with atypical moles who comes from a family where melanoma is common has a significant lifetime risk of getting the disease. To rule out melanoma, rapid and distinctive alterations should warrant consideration for excision or biopsy.

 

Physical Examination

Complete skin examinations should be performed on FAMMM syndrome patients at their initial outpatient clinic and thereafter at least once every twelve months for the rest of their lives. Atypical moles frequently have a distinctive look, albeit specific lesions might not exhibit all the symptoms. They often have a diameter of 5 to 15 mm and are big, pigmented lesions in general. Atypical moles typically measure more than 5 millimeters in diameter.

Typically, borders need to be ill-defined, notched, and irregular. One lesion may have both macular and papular patches (sometimes known as a “fried egg” & “target” appearance). There is a wide spectrum of colors, from tan to dark brown to pink. Atypical nevi can develop any part of the body, although the chest, back, breasts, buttocks, & scalp are where they most usually manifest. Both sun-exposed & sun-protected regions might have lesions.

Individuals with FAMMM syndrome may well have over 100 tumors, which is a significant increase over the typical 50 common moles found in most people. Although the clinical diagnosis of a single unusual mole may be straightforward, patients frequently have several nevi, which could complicate monitoring.

For histologic validation of dysplastic nevi vs. melanoma in the initial assessment of an unusual mole, an excisional sample should be taken into consideration. If the pigmented lesions are completely eliminated & care is given to provide appropriate depth for correct staging in melanoma, shallow scoop saucerizations can be performed with at minimum a 2-mm border of apparently healthy skin covering the pigmentation lesion.

Differential Diagnoses

Spitz Nevus

Seborrheic Keratosis

Melanocytic Nevi

Lentigo

Dermatofibroma

Cutaneous Melanoma

Blue Nevi

Basal Cell Carcinoma

 

Although there is no known way to stop the growth of atypical moles, people who have a history of them should take extra precautions to wear high-factor sun protection. However, it is believed that routine skin inspections by a qualified healthcare professional to look for any suspicious lesions and evaluate changes within already-existing moles are the most efficient way to identify malignant alterations early on. Dermatologists disagree on how best to treat unusual moles.

When there is any clinical concern about atypical moles that have arisen on their own or when morphological alterations are noticed in already-existing atypical moles, excision biopsies are typically performed. When margins are incomplete or lesions reappear, more than half of the doctors questioned by the American Academy of Dermatology said it is normal protocol to re-excise atypical moles. Reexcision of clear borders is based on the idea that the “pseudo-melanoma” phenomenon, or the reappearance of excised tumors along a biopsy scarring, may make them difficult to distinguish from melanoma.

There is strong evidence, nonetheless, that most atypical moles don’t require additional excision. There are several exceptions, such as when there is the worry that the clinical assessment does not match the histology, when there is acute atypia, or when a histological investigation is unable to distinguish between the lesion & melanoma. In these situations, the lesion should be re-excised with the proper margins and managed in accordance with the melanoma management guidelines.

 

https://www.ncbi.nlm.nih.gov/books/NBK560606/

https://emedicine.medscape.com/article/1056283-clinical

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