Section 9. Benign Neoplasms

A 55-year-old man requests removal of multiple skin tags around his neck. He is overweight and has diabetes and acanthosis nigricans. Although some of his skin tags occasionally get caught on his clothing, he just doesn't like the way they look. The patient chose to have many of them removed by the snip excision method.

Skin tags (acrochordons) are flesh-colored, pedunculated lesions that tend to occur in areas of skin folds especially around the neck and in the axillae.

• Also referred to as fibroepithelial polyps.

• In an unselected population study, skin tags were found in 46% of patients, particularly in patients who were obese.1
• Skin tags increase in frequency through the fifth decade of life so that as many as 59% of individuals have them by the time they are 70 years old; however, the increase slows after age 50 years.1

• Three types of skin tags are described:1
  • Small, furrowed papules of approximately 1 to 2 mm in width and height, located mostly on the neck and the axillae (Figure 157-1).
  • Single or multiple filiform lesions of approximately 2 mm in width and 5 mm in length occurring elsewhere on the body (Figure 157-2).
  • Large, pedunculated tumor or nevoid, bag-like, soft fibromas that occur on the lower part of the trunk (Figure 157-3).
• Etiology is unknown, but it is theorized that skin tags occur in localized areas with a paucity of elastic tissue resulting in sessile or atrophic lesions. In addition, hormone imbalances appear to facilitate their development (e.g., high levels of estrogen and progesterone seen during pregnancy) and other factors including epidermal growth factor, tissue growth factor-α, and infection (e.g., human papillomavirus) have been implicated as cofactors.
• Acrochordons also appear to be associated with impaired carbohydrate metabolism and diabetes mellitus (Figure 157-1).2
• Pedunculated lesions may become twisted, infarcted, and fall off spontaneously.
• Very rarely neoplasms are found at the base of skin tags. In a study of consecutive cutaneous pathology reports, 5 of 1335 clinically diagnosed fibroepithelial polyp specimens were malignant (i.e., 4 were basal cell carcinomas and 1 was squamous cell carcinoma in situ).3 There is selection bias in this study because most skin tags are not sent to the pathologist.

Clinical Features

• Small, soft, usually pedunculated lesions.
• Skin colored or hyperpigmented.
• Most vary in size from 2 to 5 mm, but larger ones may be seen.
• Usually asymptomatic, but can be pruritic or become painful and inflamed by catching on clothing or jewelry.

Typical Distribution

• Most typically seen on the neck and in the axillae (Figure 157-1), but any skin fold may be affected. They are also seen on the trunk (Figure 157-3), the abdomen, and the back.

Ancillary Testing

• Dermatoscopy may be a useful diagnostic tool to analyze acrochordon-like lesions in people with basal cell syndromes to facilitate early diagnosis and treatment.4

Biopsy

• Not usually indicated unless the diagnosis is not clear. Typical skin tags do not need to be sent to pathology upon removal. Skin tags, on histology, are characterized by acanthotic, flattened, or frond-like epithelium. A papillary-like dermis is composed of loosely arranged collagen fibers and dilated capillaries and lymphatic vessels.

Lesions that can be confused with skin tags include:

• Warts—Cutaneous neoplasm caused by papilloma virus. Sessile, dome-shaped lesions approximately 1 cm in diameter with hyperkeratotic surface. Paring usually demonstrates a central core of keratinized debris and punctate bleeding points.
• Neurofibromas—Benign Schwann cell tumors; cutaneous tumors tend to form multiple, soft pedunculated masses (Figure 157-4).
• Epidermal hyperplasia in melanocytic nevi (also called keratotic melanocytic nevus [KMN])—Although most common moles are round, tan to brown, less than 6 mm, and flat to slightly elevated, some nevi have overlying hyperplastic epidermis resembling skin tags. In a study of melanocytic nevi submitted for pathology over an 8-month period, 6% were KMN, most often located on the trunk (76%).5 Dermal nevi, can be pedunculated but they are usually larger than skin tags and may appear warty above the stalk.
• Basal cell carcinomas in certain syndromes.4,6

Skin tags may be removed for cosmetic reasons or because of irritation in a number of ways:

• Small lesions may be snipped with a sharp iris scissor with or without anesthesia (Figure 157-5).
• Larger skin tags and fibromas may be removed with shave excision after injecting with lidocaine and epinephrine.
• If there is any bleeding, aluminum chloride on a cotton-tipped applicator is applied for hemostasis.
• Electrodesiccation with or without anesthesia works for very tiny skin tags too small to grab with the forceps.
• Skin tags on the eyelids may be removed with a radiofrequency loop after local anesthesia with lidocaine and epinephrine to minimize bleeding.
• Cryotherapy can be applied directly to the skin tag with a Cryogun or a cotton-tipped applicator. One preferred method involves dipping forceps into liquid nitrogen and then grasping the skin tag until it turns white. This allows you to grasp the skin tag without freezing the skin around it. This is especially helpful on the eyelids. A special cryo forceps is made by Brymill, Inc. that has more metal at the end to hold the cold longer (Figure 157-6). This is a very efficient way to treat multiple skin tags quickly.
• An adhesive patch that applies pressure to the base of a skin tag was found effective in 65% of skin tags in one case series.7
• Most insurance companies will not pay for the cosmetic removal of skin tags.
• To avoid large healthcare costs, only send suspicious looking skin tags to the pathologist.

• Follow-up is not usually necessary.

• Advise patients that these are benign growths that can be removed if irritation occurs or for cosmetic purposes. Patients who are overweight should be encouraged to lose weight for their general health and to avoid new skin tags.

Patient Resources

• http://www.nlm.nih.gov/medlineplus/ency/article/000848.htm.

Provider Resources

• For quick cryosurgery of skin tags, the Cryo Tweezer can be ordered from: http://www.brymill.com/.

An elderly woman noted a growth of a lesion on her chest (Figure 158-1). She was afraid that it might be melanoma. Her family physician recognized the typical features of a seborrheic keratosis (SK) (stuck-on with visible horn cysts) and attempted to reassure her. Dermoscopy was performed and the features were so typical of an SK; the physician was able to convince the patient to not have a biopsy (Figure 158-2). The black comedonal-like openings and white milia-like cysts are typical of an SK and can be seen with the naked eye and magnified with a dermatoscope.

• A SK is a benign skin tumor and a form of localized hyperpigmentation as a result of epidermal alteration; it develops from the proliferation of epidermal cells, although the cause is unknown.

• Most common benign tumor in older individuals; frequency increases with age.
• In an older study of individuals older than age 64 years in North Carolina, 88% had at least one SK. Ten or more SKs were found in 61% of the black men and women, 38% of the white women, and 54% of the white men in the study.1
• In an Australian study preformed in 2 general practices, 23.5% (40 out of 170) of individuals between ages 15 and 30 years had at least 1 SK; prevalence and size increased with age.2
• Approximately half of cases of multiple SKs occur within families, with an autosomal dominant mode of inheritance.3

• In pigmented SKs, the proliferating keratinocytes secrete melanocyte-stimulating cytokines triggering activation of neighboring melanocytes.3
• A high frequency of mutations have been found in certain types of SKs in the gene encoding the tyrosine kinase receptor fibroblast growth factor receptor 3 (FGFR3).3 One study found that FGFR3 and transcription factor forkhead box N1 (FOXN1) were highly expressed in SKs but close to undetectable in squamous cell skin cancer.4 This may represent a positive regulatory loop between FGFR3 and FOXN1 that underlies a benign versus malignant skin tumor phenotype.
• Reticulated SKs, usually found on sun-exposed skin, may develop from solar lentigines.3
• Multiple eruptive seborrheic keratoses (the sign of Leser-Trélat) can be associated with internal malignancy (most often adenocarcinoma of the GI tract) (Figure 158-3),5 although this association has been questioned.6
• An eruption of seborrheic keratoses may develop after an inflammatory dermatosis such as severe sunburn or eczema.3 There is also a report of exacerbation of a SK by topical fluorouracil.7

SKs have a variety of appearances.

Clinical Features

• Typically oval or round brown plaques with adherent greasy scale (Figure 158-4).
• Color ranges from black to tan (Figures 158-4 to 158-6).
• Most often have a velvety to finely verrucous surface and appear to be “stuck on.”
• Some are so verrucous they can appear to be warty (Figure 158-6).
• Lesions may be large (up to 35 × 15 cm), pigmented, and have irregular borders (Figure 158-5).
• Lesions can also be flat (Figure 158-7).
• Many lesions show keratotic plugging of the surface (Figures 158-1 and 158-2).
• May have surface cracks and associated horn cysts (keratin-filled cystic structures). The dermoscopy terms for the horn cysts are comedo-like openings and milia-like cysts (Figures 158-1 and 158-2; see Appendix C, Dermoscopy).
• Occasionally, lesions become irritated and can itch, grow, and bleed; secondary infection may occur.
• Variants of SKs include:
  • Dermatosis papulosa nigra—Consists of multiple brown-black dome-shaped, smooth papules found on the face in young and middle-age persons of color, predominantly African Americans (Figures 158-8 and 158-9).
  • Stucco keratosis—Consists of large numbers of superficial gray-to-light brown flat keratotic lesions usually on the tops of the feet, the ankles, and the back of the hands and forearms (Figure 158-10).

Typical Distribution

• Trunk, face, back, abdomen, extremities; not present on the palms and soles or on mucous membranes. May be present on the areola and breasts (Figures 158-11 and 158-12).
• Dermatosis papulosa nigra is found on the face, especially the upper cheeks and lateral orbital areas (Figures 158-8 and 158-9).

Imaging

• No imaging studies are needed unless there is a sudden appearance of multiple seborrheic keratoses as in the sign of Lesser-Trélat (Figure 158-3). These are associated with adenocarcinoma of the GI tract, lymphoma, Sézary syndrome, and acute leukemia.3,8

Biopsy

• Should be performed if there is a suspicion of melanoma (Figures 158-7 and 158-13). Some melanomas resemble SKs and a biopsy is needed to avoid missing the diagnosis of melanoma. Do not freeze or curette a suspicious SK; these need surgical intervention to send tissue to the pathologist.

• Melanoma—When keratin plugs are visible in the surface of the SK, this helps to distinguish it from a melanoma. Figure 158-7 is a SK that has the ABCDE features (Asymmetry, Border irregular, Color variation, Diameter >6 mm, Evolving) of melanoma (Chapter 172, Melanoma). A biopsy was performed and the lesion was proven to be benign. In Figure 158-13, a possible SK turned out to be a melanoma in situ.
• Solar lentigo—Flat, uniformly medium or dark brown lesion with sharp borders (Chapter 168, Lentigo Maligna). These are flat and seen in sun-exposed areas, typically on the face or back of the hands. Also called liver spots, these hyperpigmented areas are not palpable, whereas a SK is a palpable plaque even when the SK is thin (Figure 158-7).
• Wart—Cutaneous neoplasm caused by papilloma virus (Chapter 131, Common Warts). Sessile, dome-shaped lesions approximately 1 cm in diameter with hyperkeratotic surface. Paring usually demonstrates central core of keratinized debris and punctate bleeding points.
• Pigmented actinic keratosis (AK)—Although most AKs are nonpigmented and don't look like an SK, occasionally a biopsy of an unknown pigmented plaque will be a pigmented AK secondary to sun damage (Chapter 166, Actinic Keratosis and Bowen Disease).
• An inflamed SK may be confused with a malignant melanoma or a squamous cell carcinoma and should be biopsied to determine the diagnosis.
• Even a basal cell carcinoma (BCC) can have features that suggest a SK (Figure 158-14) (Chapter 170, Basal Cell Carcinoma).

• Cryosurgery with liquid nitrogen, with a 1-mm halo, is a quick and easy treatment. The risks include pigmentary changes, incomplete resolution, and scarring. Hypopigmentation is the most common complication of this treatment, especially in dark-skinned individuals.
• Removal of benign lesions by curettage assures complete removal without taking the normal tissue below.
• Light electrofulguration can make the curettage so easy that it can be accomplished with a wet gauze pad.
• If the diagnosis is uncertain but there are no features suggesting a melanoma, a SK may be removed by shave biopsy and the tissue sent to pathology.
• If melanoma or other skin cancers are suspected, perform a full-thickness biopsy by punch or elliptical excision and send to pathology.

• Some experts suggest follow-up for patients with multiple SKs because malignant tumors can develop elsewhere on the body and rarely within a SK.3,8 SOR C

• Reassure patients that SKs are benign lesions that do not become cancer. Although these SKs may grow larger and thicker with time, this is not dangerous.
• Unless the SK is suspicious for cancer or inflamed, removal is for cosmetic purposes only and is often not covered by insurance.
• Although SKs may resolve on occasion, spontaneous resolution does not ordinarily occur.

Patient Resources

• http://www.nlm.nih.gov/medlineplus/ency/article/000884.htm.
• http://www.aad.org/public/Publications/pamphlets/SeborrheicKeratoses.htm.

Provider Resources

• http://emedicine.medscape.com/article/1059477-overview.

A 65-year-old man noted a new growth on his face for 1 year (Figure 159-1). On close examination, the growth was pearly with a few telangiectasias. The doughnut shape and presence of sebaceous hyperplasia scattered on other areas of the face were reassuring that this may be nothing but benign sebaceous hyperplasia. To reassure the patient and to remove the lesion a shave biopsy was performed to rule out basal cell carcinoma (BCC). The patient was relieved when the pathology result was in fact sebaceous hyperplasia. Additionally, he was pleased with the cosmetic result.

Sebaceous hyperplasia (SH) is a common, benign condition of sebaceous glands consisting of multiple asymptomatic small yellow papules with a central depression. The sebaceous lobules of SH are greater in number and higher in the dermis than normal sebaceous glands and only 1 gland appears enlarged.1 Consequently, the term hyperplasia appears to be a misnomer, and SH is more accurately classified as a hamartoma (disorganized overgrowth of tissue normally found at that site).1

• SH occurs in approximately 1% to 26% of the adult population; the latter number is from a population study of hospitalized patients with a mean age of 82 years.1
• The prevalence of SH is increased in those with immunosuppression by 10-fold to 30-fold1; for example, 10% to 16% of patients receiving long-term immunosuppression with cyclosporine in one study had SH.2
• SH has also been reported in infants where they are considered physiologic,3 and in young adults who may have a family history of SH.1
• SH has been reported overlying other skin lesions including neurofibromas, melanocytic nevi, verruca vulgaris, and skin tags.1
• Rare forms of SH include giant linear (up to 5 cm in diameter) and functional familial (also called premature or diffuse SH); the latter occurring typically around puberty as thick plaque-like lesions with pores resembling an orange peel.1

• Sebaceous glands, a component of the pilosebaceous unit, are found throughout the skin, everywhere that hair is found. The greatest number is found on the face, chest, back, and the upper outer arms.
• The glands are composed of acini attached to a common excretory duct. In some areas, these ducts open directly to the epithelial surface, including the lips and buccal mucosa (i.e., Fordyce spots), glans penis or clitoris (i.e., Tyson glands), female areolae (i.e., Montgomery glands), and eyelids (i.e., meibomian glands).1
• Sebaceous glands are highly androgen sensitive and become increasingly active at puberty and reach their maximum by the third decade of life.
• The cells that form the sebaceous gland, sebocytes, accumulate lipid material as they migrate from the basal layer of the gland to the central duct where they release the lipid content as sebum. In younger individuals, turnover of sebocytes occurs approximately every month.
• With aging, the turnover of sebocytes slows; this results in crowding of primitive sebocytes within the sebaceous gland, causing a benign hamartomatous enlargement called SH.1
• Genetic factors include overexpression of the aging-associated gene Smad7 and parathormone-related protein.4
• There is no known potential for malignant transformation, but SH may be associated with nonmelanoma skin cancer in patients following organ transplantation.

• Associated with Muir-Torre syndrome (concurrent or sequential development of a sebaceous neoplasm and an internal malignancy or multiple keratoacanthomas, an internal malignancy, and a family history of Muir-Torre syndrome).
• Immunosuppression
• Ultraviolet radiation4

Clinical Features

• Lesions appear as yellowish, soft, small papules ranging in size from 2 to 9 mm (Figures 159-1, 159-2, and 159-3).1
• Surface varies from smooth to slightly verrucous.
• Lesions can be single or multiple.
• Increasing number of lesions with aging; higher frequencies after 40 to 50 years of age.1
• In functional familial SH, lesions may appear thick and plaque-like, with pores that resemble an orange peel; the skin in these patients is quite oily.1
• Lesions may become red and irritated and bleed after scratching, shaving, or other trauma and may be associated with telangiectasias.
• Central umbilication (doughnut shape) from which a small amount of sebum can sometimes be expressed (Figures 159-1, 159-2, and 159-3).

Typical Distribution

• Most commonly located on the face, particularly the nose, cheeks, and forehead. May also be found on the chest, areola, mouth, and, rarely, the vulva.1,5

Imaging

• Dermoscopy may aid in distinguishing between nodular BCC and SH; a vascular pattern with orderly winding, scarcely branching vessels extending toward the center of the lesion is specific for hyperplastic sebaceous glands.6

Biopsy

• Not usually necessary unless concerned about BCC.

• Nodular BCC—These lesions can appear as waxy papules with a central depression that may ulcerate, most commonly located on the head, neck, and upper back. They may have a pearly appearance, surface telangiectases, and bleed easily (Figures 159-4 and 159-5).
• Fibrous papule of the face is a benign, firm, papule of 1 to 5 mm that is usually dome-shaped and indurated with a shiny, skin-colored appearance. Most lesions are located on the nose and, less commonly, on the cheeks, chin, neck, and, rarely, the lip or forehead.
• Milia are common, benign, keratin-filled cysts (histologically identical to epidermoid cysts) that occur in persons of all ages. They are 1 to 2 mm, superficial, uniform, pearly white to yellowish, domed lesions usually occurring on the face (Figure 159-6).
• Molluscum contagiosum are firm, smooth, usually 2- to 6-mm umbilicated papules that may be present in groups or widely disseminated on the skin and mucosal surfaces. The lesions can be flesh colored, white, translucent, or even yellow in color. Lesions generally are self-limited but can persist for several years (Chapter 130, Molluscum Contagiosum).
• Syringoma is a benign adnexal neoplasm formed by well-differentiated ductal elements. They are 1- to 3-mm skin-colored or yellowish dermal papules with a rounded or flat top arranged in clusters, and symmetrically distributed primarily on the upper parts of the cheeks and lower eyelids (Figure 159-6).
• Xanthomas are deposits of lipid in the skin or subcutaneous tissue that manifest clinically as yellowish papules, nodules, or tumors. They are usually a consequence of primary or secondary hyperlipidemia and occur in patients older than age 50 years. The lesions are soft, velvety, yellow, flat, polygonal papules that are asymptomatic and usually bilateral and symmetric (Chapter 223, Hyperlipidemia).

SH does not require treatment but can be removed for cosmetic purposes or if it becomes irritated. Evidence supporting treatment comes primarily from case series.

• Options for removal include cryotherapy, electrodesiccation, topical chemical treatments (e.g., with bichloracetic acid or trichloroacetic acid), oral isotretinoin (10 to 40 mg a day for 2 to 6 weeks), laser treatment (e.g., with argon, carbon dioxide, or pulsed-dye laser), photodynamic therapy (i.e., combined use of 5-aminolevulinic acid and visible light),7 shave excision, and punch excision.1 Complications of these therapies include atrophic scarring and changes in pigmentation.

No follow-up is needed.

Patient Resources

• http://www.skinsight.com/adult/sebaceousHyperplasia.htm.

Provider Resources

• http://emedicine.medscape.com/article/1059368-overview.

A 25-year-old woman reports a firm nodule on her leg that gets in the way of shaving her leg (Figure 160-1). Upon questioning, the nodule may have started there after she cut her leg shaving 1 year ago. She is worried it could be a cancer and wants it removed. Close observation showed a brown halo and a firm nodule that dimpled down when pinched. A diagnosis of a dermatofibroma (DF) was made and the choices for treatment were discussed.

DF is a benign fibrohistiocytic tumor, usually found in the mid dermis, composed of a mixture of fibroblastic and histiocytic cells. These scar-like nodules are most commonly found on the legs and arms of adults.

Also called benign fibrous histiocytoma.

• Occurs more often in women (male-to-female ratio is 1:4).1
• Found in patients of all races.
• Approximately 20% occur in patients younger than age 17 years.1 In one case series, 80% occurred in people between the ages of 20 and 49 years.2

• Uncertain etiology—Nodule may represent a fibrous reaction triggered by trauma, a viral infection, or insect bite; however, DFs show clonal proliferative growth seen in both neoplastic and inflammatory conditions.3
• Multiple DFs (i.e., >15 lesions) have been reported associated with systemic lupus erythematosus, HIV infection, Down syndrome, Graves disease, or leukemia, and may represent a worsening of immune function.1 A case of familial eruptive DFs has also been reported associated with atopic dermatitis.4

Clinical Features

• Firm to hard nodule; skin is freely movable over the nodule, except for the area of dimpling.
• Color of the overlying skin ranges from flesh to gray, pink, red, blue, brown, or black (Figures 160-2 and 160-3), or a combination of hues (Figure 160-4).
• Dimples downward when compressed laterally because of tethering of the overlying epidermis to the underlying nodule (Figure 160-3).
• Usually asymptomatic but may be tender or pruritic.
• Size ranges from 0.3 to 10 mm; usually less than 6 mm. Rarely, DFs grow to larger than 5 cm.5
• May have a hyperpigmented halo and a scaling surface (Figure 160-4).
• DFs can rarely be located entirely within subcutaneous tissue.6

Imaging

• Dermoscopy is a useful adjunctive diagnostic technique for DF (Figure 160-5). Although the most common finding is a ­peripheral pigment network with a central white area (34.7% of cases), 10 dermoscopic patterns have been identified; in a large case series, pigment network was observed in 71.8% (3% atypical pigment network).7 (See Appendix C: Dermoscopy.)

Typical Distribution

• May be found anywhere, but usually on the legs and arms, especially the lower legs. In one case series, 70% were on the lower extremities.2

Biopsy

• A punch biopsy can be both diagnostic and therapeutic. DFs have been reported with overlying basal cell carcinoma and associated melanoma.8,9
• Histologically, DFs can be fibrocollagenous (40.1%), histiocytic (13.1%), cellular (11.5%), aneurysmal (7.4%), angiomatous (6.5%), sclerotic (6.5%), monster (4.9%), palisading (1.6%), keloidal (0.8%), or mixed type (7.3%).2 Also reported are ossifying DFs10 and a signet-ring cell DF.11
• Electron microscopy and immunohistochemistry may be needed to differentiate atypical or pigmented DFs from other lesions.7

DFs may be confused with the following malignant tumors; diagnosis based on histology and excision should be undertaken for enlarging or ulcerating tumors:

• Dermatofibrosarcoma protuberans—A low-grade malignant fibrotic tumor of the skin and subcutaneous tissues (Figure 160-6). A punch biopsy will provide adequate tissue to make the diagnosis.
• Pseudosarcomatous DF—A rare connective tissue tumor arising on the trunk and limbs in young adults.
• Malignant fibrous histiocytoma—A common soft-tissue sarcomas occurring in the extremities. Presentation as a primary cutaneous lesion is rare and more often presents as a metastasis from another location such as the breast.

Many benign lesions have a similar appearance, including:

• Pigmented seborrheic keratosis—May be macular and often larger than DF. Distinguished by surface cracks, verrucous features, stuck-on appearance, and adherent greasy scale (Chapter 158, Seborrheic Keratosis).
• Epidermal inclusion cyst—Sharply circumscribed, skin-colored nodule often with a central punctum. Most common on face, neck, or trunk. Composed of stratified epithelium surrounding a mass of keratinized material that has a foul odor when it drains.
• Hypertrophic scar—Occurs within previous wounds or lacerations.
• Neurofibroma—Benign Schwann cell tumors; single lesions are seen in normal individuals. Cutaneous tumors tend to form multiple, soft, pedunculated masses, whereas subcutaneous nodules are skin-colored soft nodules attached to peripheral nerves. The latter show similar invagination as DF (Chapter 235, Neurofibromatosis).

• No treatment is necessary unless the diagnosis is questioned or symptoms warrant.
• Punch excision or shave excision may be used for small lesions; with the latter technique, the healed area may remain hard as a result of remaining fibrous tissue.
• Larger lesions may require an elliptical (fusiform) excision, down to the subcutaneous fat.
• One author noted that DFs occurring on the face often have involvement of deeper structures and an increased rate of local recurrences and therefore recommend excision with wider margins in comparison with DFs occurring on the extremities.12
• Cryotherapy has also been used, but the cure rate is low and lesions may recur.
• Several case reports found success in treating multiple DFs with carbon dioxide laser13 or isotretinoin.14

• Although DFs are usually unchanging and persist indefinitely, there are reports of spontaneous regression.15
• Following excision, DFs have a low recurrence rate of less than 2%, with higher recurrence believed to occur in cellular, aneurysmal, and atypical types.7,10
• A higher rate of recurrence has been noted in the subcutaneous and deep types, and in lesions located on the face, in which a recurrence rate of 15% to 19% has been reported.16,17

• DFs are best left alone if they are relatively asymptomatic and stable.

Patient Resources

• www.aocd.org/skin/dermatologic_diseases/DF.html.
• http://www.skinsight.com/adult/DF.htm.

Provider Resources

• http://emedicine.medscape.com/article/1056742

A 20-year-old woman, who was being seen by her family physician for her prenatal care, presents to the office with a new growth on her lip. She stated that the growth on her lip bled very easily but was not painful. She was diagnosed with a pyogenic granuloma (PG) and preferred to wait until her pregnancy was over to have it removed. The lesion did not regress spontaneously after pregnancy and was surgically excised.

PG is the name for a common, benign, acquired, vascular neoplasm of the skin and mucous membranes.

The term lobular capillary hemangioma has been suggested because PG is neither pyogenic (purulent bacterial infection) nor a granuloma.1

• Most often seen in children and young adults (0.5% of children's skin lesions); 42% of cases occur by 5 years of age and approximately 1% are present at birth.1
• Oral lesions occur most often in the second and third decade, more commonly in women (female-to-male ratio is 2:1).1
• Also common during pregnancy.
• PG has also been reported in the GI tract, the larynx, and on the nasal mucosa, conjunctiva, and cornea.

• Etiology is unknown but may be the result of trauma, infection, or preceding dermatoses.
• Consists of dense proliferation of capillaries and fibroblastic stroma that is infiltrated with polymorphonuclear leukocytes.
• Multiple PGs have been reported at burn sites and following use of oral contraceptives, protease inhibitors, and topical application of tretinoin for acne.2
• PGs are known to regress following pregnancy. Vascular endothelial growth factor (VEGF) was found in one study to be high in the granulomas during pregnancy, was almost undetectable after parturition, and was associated with apoptosis of endothelial cells and regression of granuloma.3

• Trauma (up to 50%) or chronic irritation.1
• Multiple lesions can follow manipulation of a primary lesion.4
• Pregnancy or use of oral contraceptives for oral PGs; postulated caused by imbalance between angiogenesis enhancers and inhibitors.1
• Infection with Bartonella.1

Clinical Features

• Usually solitary, erythematous, dome-shaped papule or nodule that bleeds easily (Figures 161-1, 161-2, 161-3, 161-4, 161-5, 161-6, 161-7, and 161-8); rarely causes anemia. Satellite lesions may rarely occur.
• Prone to ulceration, erosion, and crusting.
• Size ranges from a few millimeters to several centimeters (average size is 6.5 mm).1
• Rapid growth over a period of weeks to maximum size.
• Variants include cutaneous, oral mucosal (granuloma gravidarum), satellite, subcutaneous, intravenous, and congenital types.1

Typical Distribution

• Cutaneous PG most often found on the head and neck (62.5%) specifically the gingiva, lips as in Figure 161-1, nose (Figure 161-2), and face, trunk (20%) and extremities (18%) (Figures 161-3, 161-4, 161-5, and 161-6).1
• Pregnancy PG occurs most commonly along the maxillary intraoral mucosal surface (Figure 161-1).

Imaging

• Reddish homogeneous area surrounded by a white collarette is the most frequent dermoscopic pattern in PGs (85%).5 In more advanced lesions, white lines that intersect the central areas may be seen that are likely fibrous septa.

Biopsy

• Early lesions resemble granulation tissue (numerous capillaries and venules with endothelial cells arrayed radially toward the skin surface; stroma is edematous).1
• The mature PG exhibits a fibromyxoid stroma separating the lesion into lobules. Proliferation of capillaries is present, with prominent endothelial cells. The epidermis exhibits inward growth at the lesion base.1
• A regressing PG has extensive fibrosis.

PG may be confused with a number of cutaneous malignancies, including atypical fibroxanthoma, basal cell carcinoma, Kaposi carcoma, metastatic cutaneous lesions, squamous cell carcinoma, and amelanotic melanoma (Figure 161-7). It is especially important to send the excised lesion that appears to be a PG for pathology to make sure that a malignancy is not missed.

Benign tumors that may be confused with PG include:

• Cherry hemangioma—Small, bright-red, dome-shaped papules that represent benign proliferation of capillaries (Figure 161-8).
• Fibrous papule of the nose is a benign tumor of the nose. Most are skin colored and not confused with PG. A benign clear cell variant of a fibrous papule can closely resemble a PG as seen in Figure 161-9.
• Bacillary angiomatosis—A systemic infectious disease caused by two Bartonella species. Globular angiomatous papules appear like PG (Figure 217-6). Nodules affect all age groups and may reach 10 cm in size. This infection is more likely to occur in persons with AIDS. Weight loss and lymphadenopathy may occur.

Removal of the lesion is indicated to alleviate any bleeding or discomfort, for cosmetic reasons, or when the diagnosis is uncertain.

Nonpharmacologic

• Untreated PGs eventually atrophy, become fibromatous, and slowly regress, especially if the causative agent is removed.

Medications

• A case of successful treatment of a recurrent PG was reported using a 14-week course of twice-weekly imiquimod 5% topical application.6 SOR C

Procedures

A number of procedures have been used for elimination of PGs; data are limited to case series reports.7

• Simple surgical excision has a low recurrence rate (<4%) but is associated with scarring (55%).7 SOR C
• Removal can be accomplished with shave excision and electrodesiccation; the latter reduces recurrence (approximately 10%) and scarring appears less than with either simple excision (31%) or cauterization alone (43.5%).1,7 PGs bleed extensively when manipulated or cut. It is important to use lidocaine with epinephrine, wait 10 minutes for the epinephrine to work, and have an electrosurgery device to control bleeding. Cut the PG off with a blade and send to pathology. Curetting the base will also help stop the bleeding and prevent recurrence. The base is curetted and electrodesiccated until the bleeding stops. SOR C
• Both cryosurgery and laser surgery often require more than one treatment and rates of scarring may be high (12% to 42% and 44%, respectively).1,7 SOR C
• In one case series, sclerotherapy was reported to leave no scarring or recurrence.7 SOR C

• PG develops over weeks and growth typically stabilizes over several months.1 Eventually, it shrinks to become a fibrotic “angioma.” Some nodules spontaneously infarct and involute. In one pediatric retrospective case series with telephone follow-up, 4 untreated patients had spontaneous resolution within 6 to 18 months with no recurrences.8
• Congenital PG is an uncommon disseminated variant that presents with multiple lesions, is similar in appearance to the cutaneous form, and is present at birth. The condition appears to follow a benign course, with spontaneous resolution over 6 to 12 months.1

• Explain to patients that lesions may resolve spontaneously and that multiple successful treatments are available (note that most patients will be grateful to have treatment that day as the lesion tends to be a great nuisance by bleeding easily and having an undesirable appearance).
• Once treated, if the lesion begins to recur, patients should follow-up quickly before the lesion gets larger and harder to treat.

In 2 weeks to receive the result of the pathology and to check wound healing.

Patient Resources

• http://www.nlm.nih.gov/medlineplus/ency/article/001464.htm.
• http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002435/.

Provider Resources

• http://emedicine.medscape.com/article/910112.
• http://emedicine.medscape.com/article/1077040.
• Usatine R, Pfenninger J, Stulberg D, Small R. Dermatologic and Cosmetic Procedures in Office Practice. Philadelphia, PA: Elsevier; 2012. The book has many photographs and descriptions that provide details of how to surgically treat PGs. It is also available as an electronic application with video included: www.usatinemedia.com.