Benign Neoplasms



Benign Neoplasms


Juliana L. Basko-Plluska



Neoplasms of the skin are derived from proliferation of the different types of cells residing in the epidermis, dermis, or subcutaneous tissue. Epidermal growths are due to the proliferation of basal cells and keratinocytes and are characterized clinically by excessive accumulation of keratin or scale. Pigmented growths are due to the proliferation of pigment-forming cells and melanocytes, and they have a characteristic light to dark brown color. Finally, dermal growths are derived from the proliferation of the various types of cells residing in the dermis (e.g., fibroblasts, neurons, endothelial cells) and present clinically as firm, indurated papules or nodules. This chapter will provide a general overview of the most commonly encountered benign neoplasms of the skin.


Skin Tags



Background/Epidemiology

A skin tag, also known as an acrochordon, is a very common, benign epidermal growth in middle-aged individuals and the elderly. The overall prevalence in the adult population is approximately 25%; the prevalence reaches 60% at the age of 70. Skin tags are more common in females than males and typically affect the intertriginous areas (axilla, groin, and inframammary regions) as well as the neck and the eyelids. Patients usually complain of slow-growing fleshy bumps, which are cosmetically unappealing.


Pathogenesis

The pathogenesis of acrochordons remains unknown. They are an obligatory lesion in acanthosis nigricans (Fig. 11-2), and are commonly associated with acromegaly and pregnancy, suggesting that high levels of circulating growth hormone may play a role. Recent studies have shown that patients with multiple skin tags have a higher frequency of diabetes (23% versus 8.51%). It is likely that multiple skin tags may serve as a cutaneous marker for impaired insulin sensitivity in patients with no previously known impaired glucose metabolism.








Figure 11-1 Small, 1- to 2-mm furrowed papules, commonly found in the neck and the axilla.






Figure 11-2 Large, pedunculated papillomas on the lower parts of the body.

Occasionally, multiple acrochordons and multiple flesh-colored facial papules (fibrofolliculoma/trichodiscoma) are seen. These patients should be evaluated for Birt-Hogg-Dube (BHD) syndrome, although it remains to be determined whether skin tags can be used as markers for these two conditions. In patients with other skin findings of BHD syndrome, consider gene analysis for definite diagnosis. Patients with BHD have an increased risk for pulmonary cysts/spontaneous pneumothoraces and renal cell carcinoma; therefore, screening abdominal ultrasounds are suggested for the patient and first-degree family members.

Unlike adult skin tags, childhood skin tags deserve special attention, as they may be the first manifestation of nevoid basal cell carcinoma syndrome, a rare autosomal dominant syndrome characterized by multiple basal cell carcinomas and multiple systemic anomalies.


Clinical Presentation

Three types of acrochordon have been classically described:



  • Small, 1- to 2-mm furrowed papules, commonly found in the neck and the axilla (often called “skin tags”) (Fig. 11-1)


  • Single or thread-like, 2- to 5-mm papules on areas other than the neck and the axilla


  • Large, pedunculated papillomas on the lower parts of the body, often called “fibroepithelial polyps” (Fig. 11-2)

Wiggling of the pedunculated lesions back and forth does not ordinarily elicit any tenderness, unless there is irritation or torsion of the skin tag.


Diagnosis


Differential Diagnosis

Skin tags can be confused with pedunculated seborrheic keratosis (SK), compound melanocytic nevus, solitary neurofibroma, viral warts, or molluscum contagiosum (Table 11-1).


Diagnostic Methods

Diagnosis is made by visual inspection.









Table 11-1 Differential Diagnosis of Skin Tags




















DIAGNOSIS KEY FEATURES
Pedunculated seborrheic keratosis Tan to dark-brown papules or plaques with stuck-on appearance and greasy surface. Mainly on the sun-exposed areas, sparing the palms and soles. Often asymptomatic, but may itch or bleed.
Compound melanocytic nevus Tan to brown, up to 6 mm dome-shaped nevus with symmetric borders and uniform pigmentation. May be congenital or acquired.
Solitary neurofibroma Asymptomatic hyperpigmented nodules measuring few mm to 4–5 cm. Occasional positive Tinel sign.
Viral warts Firm papules with verrucous surface, mainly on the fingers and soles. Often asymptomatic, except plantar warts. Transmission by autoinoculation, direct skin contact, or sexual contact.
Molluscum contagiosum Dome-shaped papule with central umbilication and pearly appearance. Tends to spare the palms and soles. Children and immunosuppressed patients are mostly affected.



Treatment

Asymptomatic skin tags are removed if indicated for cosmetic purposes.



  • Cryotherapy: liquid nitrogen is used to freeze the lesion at the base. Side effect: temporary posttreatment hypopigmentation.


  • Snipping with scissors at the base: no local anesthesia is required


  • Excision with sharp blade: no local anesthesia is required


  • Ligation with suture tied around the base: no local anesthesia is required, but it hurts


  • Electrodessication: an electric current is used to destroy the skin tag; cauterization can be used to stop the bleeding. Side effects: temporary posttreatment hypopigmentation


“At a Glance” Therapy



  • First-line therapy:



    • Liquid nitrogen: quick and easy. Downside is that LN2 hurts more and it takes about a week for the lesion to fall off.


    • Scissors (sharp Gradle scissors work best): snip at base of lesion


  • Second-line therapy:



    • Sharp blade excision (#15 blade)


    • Ligation at base with a tied suture


    • Electrodessication



Course and Complications

Skin tags are permanent growths with no potential for malignant transformation. They tend to recur after surgical removal.

ICD9 Code





701.9 Unspecified hypertrophic and atrophic conditions of skin



Seborrheic Keratosis



Background/Epidemiology

Seborrheic keratosis (SK) is a common benign epidermal tumor, which results from the clonal proliferation of immature keratinocytes. It is found with increasing numbers and increasing age. In one study, individuals older than age 64 years were examined and 88% had at least one SK lesion. These lesions are less common on darker-skinned individuals and there is no gender predominance.



Pathogenesis

The precise etiology of SK is not well understood. Higher incidence on the sun-exposed areas suggests that chronic sun exposure may play a role. Some studies suggest SK may be inherited in an autosomal dominant fashion; a clear genetic locus has not yet been determined. Mutations in fibroblast growth factor receptor 3, which regulates cell growth, have been noted in 40% to 85% of examined SK lesions. The deeply pigmented variant of SK often has a mutation in endothelin-1. The exact cause of the growth due to these mutations is not yet known.


Clinical Presentation

Seborrheic keratosis starts as a sharply defined, light-brown macule, which later develops into a verrucous, warty-like papule with a “stuck-on” appearance. It affects mainly middle-aged to elderly individuals; almost everyone over the age of 50 has at least one SK. The lesions are usually asymptomatic, but can occasionally itch or bleed upon irritation. The trunk is most often affected; the palms, soles, and the mucosal surfaces are often spared. Dark-skinned individuals tend to develop a variant of SK, called dermatosis papulosa nigra, which presents as smaller, heavily pigmented lesions in younger individuals, often presenting on the face (Fig. 11-4).

Seborrheic keratoses are totally benign. Collision tumors of SK and other skin malignancies have been reported, mainly squamous cell carcinoma and rarely melanoma. In cases of a typical-appearing SK, a biopsy is not necessary for confirmation. When a typical SK changes or the appearance is atypical, a biopsy is indicated.

An association between the sudden, explosive appearance of multiple seborrheic keratoses and internal malignancies, most often adenocarcinoma of the gastrointestinal tract, has also been reported, known as “the sign of Leser-Trélat.” This type of sudden explosive growth of SK may also accompany severe sunburn, eczema flare, or other severe inflammatory dermatosis. Finally, eruptive seborrheic keratoses may also occur in association with leukemia, lymphoma, or human immunodeficiency virus (HIV).


Diagnosis

Upon examination, well-circumscribed, light- to dark-brown papules or plaques with an adherent greasy scale and tiny keratotic dots studding the surface are noted. They may vary in size from 1 mm to 5 cm or greater and are often uniformly pigmented. Close inspection with a hand lens demonstrates the presence of pseudohorn cysts and dark keratin plugs. Typical examples of
benign SK are shown in Figures 11-3 to 11-7. An irritated and subsequently necrotic SK is shown in Figure 11-7.






Figure 11-3 Seborrheic keratosis: this is an atypical-appearing lesion with clearly visible pseudohorn cysts.






Figure 11-4 Dermatosis papulosis nigra on the cheek of an African-American woman.


Differential Diagnosis

SK can oftentimes be confused with malignant melanoma, squamous cell carcinoma, actinic keratosis, viral warts, and solar lentigo (Table 11-2).


Diagnostic Methods

Diagnosis is made by visual inspection. A biopsy is indicated for questionable or changing lesions.






Figure 11-5 Multiple seborrheic keratoses on the back.






Figure 11-6 Waxy-appearing seborrheic keratosis.






Figure 11-7 Necrotic and irritated seborrheic keratosis.


Therapy

Benign-appearing seborrheic keratoses are treated, if indicated, for cosmetic purposes. The following treatment modalities exist:



  • Cryotherapy: the standard treatment for thin seborrheic keratoses, which produces cosmetically acceptable results to patients. The downside is the risk for posttreatment hypopigmentation and recurrence.









    Table 11-2 Differential Diagnosis of Seborrheic Keratosis




















    DIAGNOSIS KEY FEATURES
    Malignant melanoma Dark brown to black, nonhomogenous melanocytic lesions measuring >6 mm in diameter, which may itch or bleed. Lesions have a tendency for rapid growth. Risk factors: light skin, prolonged sun exposure, dysplastic nevi, family history of melanoma
    Squamous cell carcinoma Sharply defined, scaly, erythematous patch, papule, or nodule, which may ulcerate. Risk factors: light skin, chronic sun exposure/phototherapy, exposure to industrial carcinogens, organ transplantation/immunosuppression
    Actinic keratosis Discrete, yellow-brown to slightly erythematous papules with adherent scale and a rough/sandpaper-like consistency on the habitually sun-exposed areas
    Viral wart Firm papules with verrucous surface affecting mainly the fingers and soles
    Solar lentigo Asymptomatic, evenly pigmented light brown patch on the sun-exposed areas. It may not be possible to differentiate lentigo from flat SK.


  • Electrocautery: less effective than cryotherapy for thin lesions. The downside risk is for posttreatment skin hypopigmentation.


  • Shave excision: horizontal slicing of the affected skin extending to the level of mid-dermis. Well-suited for epidermal growths. There is postoperative scarring and occasionally pigmentary change.


  • Curettage: lesions are very superficial and “stuck-on.” They can be removed with a curette or edge of a #15 scalpel blade.


“At a Glance” Therapy



  • First-line therapy:



    • Cryotherapy: the standard treatment for thin seborrheic keratoses


  • Second-line therapy:



    • Electrocautery: carefully done, this method is very effective for thin SK; not appropriate for thick lesions.


    • Shave excision: horizontal slicing of the affected skin extending to the level of mid-dermis. Well-suited for thicker epidermal growths. There is postoperative scarring and occasionally pigmentary change. Best option for thick SK.




Course and Complications

Seborrheic keratoses are permanent growths that may enlarge and become thicker over time, but have no potential for malignant transformation.

ICD9 Codes








702.11 Inflamed seborrheic keratosis
702.19 Other seborrheic keratosis



Nevi


Jul 21, 2016 | Posted by in Dermatology | Comments Off on Benign Neoplasms

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