INTRODUCTION — Individuals may acquire a multitude of benign skin lesions over the course of a lifetime. Many of these lesions are easily visible, and patients often ask clinicians to confirm that new growths on the skin are benign.
An overview of the clinical features, diagnosis, and treatment of some acquired benign skin lesions is presented here. Dermatofibroma is discussed separately. Benign lesions in the newborn and infant are also discussed separately.
APPROACH TO DIAGNOSIS — Most benign skin lesions are diagnosed based on clinical appearance (morphology, distribution) and history. (See "Approach to the clinical dermatologic diagnosis".)
Dermoscopy, a skin examination technique performed with a handheld instrument called a dermatoscope that allows the visualization of subsurface skin structures, is a helpful adjunct to the clinical examination of a variety of pigmented and nonpigmented lesions. (See "Dermoscopic evaluation of skin lesions".)
If the diagnosis of a lesion is uncertain or if a lesion has exhibited unexpected or rapid changes in appearance or symptoms, a diagnostic procedure (eg, biopsy, excision) is indicated for a precise diagnosis. (See "Skin biopsy techniques".)
Acrochordon (skin tag) — Acrochordon, commonly known as a skin tag, is an outgrowth of normal skin. It appears as a pedunculated lesion on a narrow stalk (picture 1A-E).
Acrochordons are common in adult individuals, and the risk of developing them increases with age . They are frequently seen in obese patients and in patients with diabetes mellitus [2,3]. Observational studies suggest that acrochordons may be a skin sign of insulin resistance and metabolic syndrome [4-6] (see "Insulin resistance: Definition and clinical spectrum"). Skin tags also appear with increased frequency during the second trimester of pregnancy and may regress postpartum .
Acrochordons usually occur in sites of friction, particularly the axilla, neck, inframammary, and inguinal regions. They become symptomatic when traumatized (eg, caught on jewelry, rubbed by clothing). An infarcted acrochordon, resulting from torsion of its peduncle, appears as a red or black lesion (picture 1F).
Perianal skin tags are common in patients with Crohn's disease . Acrochordons, together with fibrofolliculomas and trichodiscomas, are seen in Birt-Hogg-Dubé syndrome, an inherited condition characterized by cutaneous adnexal tumors, lung cysts, spontaneous pneumothorax, and increased risk of kidney cancer  (see "Perianal Crohn disease" and "Birt-Hogg-Dubé syndrome"):
●Diagnosis – The diagnosis of acrochordons is usually based upon clinical appearance. They must be differentiated from neurofibromas, which are usually larger and firmer than acrochordons (picture 2), and from pedunculated dermal nevus (picture 3). The latter sometimes can only be differentiated histologically. (See "Neurofibromatosis type 1 (NF1): Pathogenesis, clinical features, and diagnosis", section on 'Peripheral neurofibromas'.)
●Treatment – Treatment is indicated if lesions are irritating or the patient desires removal for cosmetic reasons. Local anesthesia with 1% lidocaine with epinephrine may be required in larger lesions. Treatment options include (see "Office-based dermatologic diagnostic procedures"):
•Removal with forceps and fine-grade scissors; larger lesions may require suturing.
•Cryosurgery with liquid nitrogen.
Lesions often bleed freely after surgical removal. Thus, aluminum chloride, silver nitrate sticks, or electrosurgery should be readily available for coagulation; however, silver nitrate may cause permanent skin pigmentation . Lesions are unlikely to recur after removal, but new lesions develop in predisposed skin areas.
Dermatofibroma — Dermatofibroma, also called benign fibrous histiocytoma, is one of the most common cutaneous soft-tissue lesions. It represents a benign dermal proliferation of fibroblasts and typically presents as a solitary, firm, often hyperpigmented nodule 0.3 to 1 cm in diameter (picture 4A-B). The pathogenesis, clinical presentation, diagnosis, and management of dermatofibroma are discussed in detail separately. (See "Dermatofibroma (benign fibrous histiocytoma)".)
Cutaneous neurofibroma — Cutaneous neurofibroma is a benign nerve sheath tumor composed of cells of neuromesenchymal origin, including Schwann cells, fibroblasts, perineurial cells, and mast cells. Multiple cutaneous neurofibromas and their variants (ie, plexiform, dermal) may occur in the setting of neurofibromatosis. (See "Neurofibromatosis type 1 (NF1): Pathogenesis, clinical features, and diagnosis", section on 'Peripheral neurofibromas'.)
Most commonly, cutaneous neurofibroma occurs as a sporadic, solitary lesion in healthy adults. It typically presents as a asymptomatic, soft, skin-colored or hyperpigmented papule or nodule <2 cm in diameter (picture 2). Applying direct pressure to some neurofibromas may make them seem to retract into the skin, a finding that has been described as the "buttonhole" sign.
The clinical differential diagnosis for neurofibromas often includes dermal melanocytic nevi (picture 3) and acrochordon (picture 1A). (See "Acquired melanocytic nevi (moles)" and 'Acrochordon (skin tag)' above.)
Treatment is not necessary for solitary cutaneous neurofibromas. Surgical excision can be used to remove lesions when the diagnosis is in question or when removal is desired due to discomfort or cosmetic concerns.
Seborrheic keratosis — Seborrheic keratosis is a common epidermal tumor consisting of a benign proliferation of immature keratinocytes . It is most commonly seen in middle-aged individuals, but it can also develop in young adults. There is a genetic predisposition to develop a high number of seborrheic keratoses, although the precise inheritance pattern is unknown. The pathogenesis is incompletely understood. Evidence for a role of cumulative ultraviolet (UV) radiation exposure or human papillomavirus (HPV) infection is inconsistent . Somatic activating mutations in the fibroblast growth factor receptor 3 (FGFR3) and PIK3CA oncogenes have been found in seborrheic keratoses, but their pathogenetic role is uncertain [13-16].
Clinical features — Seborrheic keratosis presents as a well-demarcated, round or oval lesion with a dull, verrucous surface and a typical stuck-on appearance (picture 5A-D). It is generally asymptomatic, but chronic irritation due to friction trauma may occasionally cause pruritus, pain, or bleeding. Seborrheic keratosis may vary in color, from skin colored to light brown, dark brown, or black.
The number of seborrheic keratoses can vary from an isolated lesion to literally hundreds. A "Christmas tree" pattern may be seen on the back, due to lesion distribution along the Blaschko lines (picture 6). The sign of Leser-Trélat, which refers to the sudden appearance of multiple seborrheic keratoses in association with skin tags and acanthosis nigricans, has been associated with a variety of malignancies, including gastrointestinal and lung cancers. Inflammation of preexisting seborrheic keratoses may occur during chemotherapy, in particular with cytarabine or docetaxel (pseudo-sign of Leser-Trélat) [17,18]. (See "Cutaneous manifestations of internal malignancy", section on 'Sign of Leser-Trélat' and "Cutaneous manifestations of internal malignancy", section on 'Acanthosis nigricans'.)
Clinicopathologic variants of seborrheic keratosis include dermatosis papulosa nigra (picture 7A-C), stucco keratosis (picture 8), large cell acanthoma (picture 9), clonal seborrheic keratosis, and irritated seborrheic keratosis. (See 'Dermatosis papulosa nigra' below.)
Diagnosis and differential diagnosis — The diagnosis of seborrheic keratosis is usually based on the clinical appearance of "stuck on," warty, well-circumscribed, often scaly hyperpigmented lesions located most commonly on the trunk, face, and upper extremities (picture 5A, 5E-F). Close inspection with a hand lens often will demonstrate the presence of horn cysts or dark keratin plugs (picture 10). Examination with a dermatoscope shows multiple milia cysts, comedo-like openings, and fissures and ridges forming a cerebriform pattern (picture 11).
Biopsy may be necessary if the diagnosis is uncertain and there is concern for malignancy. Rare cases of seborrheic keratoses with associated basal cell carcinomas or melanomas (collision tumors) have been reported [19-23]. (See "Office-based dermatologic diagnostic procedures" and "Skin biopsy techniques".)
Histologically, seborrheic keratosis typically shows a well-demarcated proliferation of keratinocytes, with characteristic small keratin-filled cysts. A dermal lymphocytic infiltrate is often present in inflamed or irritated lesions.
Seborrheic keratoses should be differentiated from other benign and malignant lesions, including:
●Acrochordon (see 'Acrochordon (skin tag)' above)
●Verruca vulgaris (see "Cutaneous warts (common, plantar, and flat warts)")
●Epidermal nevus (see "Epidermal nevus and epidermal nevus syndrome")
●Melanocytic nevus (see "Acquired melanocytic nevi (moles)")
●Basal cell carcinoma (see "Epidemiology, pathogenesis, clinical features, and diagnosis of basal cell carcinoma")
●Squamous cell carcinoma (see "Cutaneous squamous cell carcinoma (cSCC): Clinical features and diagnosis")
●Melanoma (see "Melanoma: Clinical features and diagnosis")
It is important that lesions with atypical clinical and dermoscopic features (eg, large lesions, history of rapid change or growth, ulcerated lesions) be biopsied for histopathologic examination .
Treatment — Because seborrheic keratoses are benign and slow-growing lesions, treatment is generally not required. However, lesions that are symptomatic or that cause cosmetic concerns can be removed. Treatments commonly used in clinical practice include (see "Minor dermatologic procedures"):
●Cryotherapy – Cryotherapy is the treatment most commonly used, particularly for flat or thin lesions. Cryotherapy should only be used if the clinical diagnosis is not in doubt.
●Curettage/shave excision – Curettage or shave excision, with submission of specimen for pathology, can be performed with a no. 15 scalpel blade after anesthesia with 1% lidocaine.
●Electrodesiccation – Electrodesiccation alone or followed by curettage usually requires anesthesia with 1% lidocaine.
A variety of lasers, including pulsed carbon dioxide (CO2) laser, erbium yttrium aluminium garnet (YAG) laser, 755 nm alexandrite laser, and 532 nm diode laser, have been also used for the treatment of seborrheic keratosis [25-27]. However, none of the above treatments has been adequately evaluated in randomized trials. The choice of therapy is generally based upon the lesion size and thickness, patient's skin type, and clinical experience.
In a small study of 25 patients, treatment of seborrheic keratoses with either cryotherapy or curettage with a no. 15 scalpel provided similar cosmetic improvement as rated by patients . However, most patients preferred cryotherapy over curettage due to the minimal postoperative wound care required with cryotherapy.
Postinflammatory hypo- or hyperpigmentation and scarring may occur with healing. Postinflammatory hypopigmentation following cryotherapy is particularly frequent in individuals with darkly pigmented skin. (See "Postinflammatory hyperpigmentation".)
Dermatosis papulosa nigra — Dermatosis papulosa nigra is characterized by the presence of multiple hyperpigmented papules measuring from 1 to 5 mm on the face of individuals with darkly pigmented skin (picture 7A, 7D). There is a genetic predisposition to dermatosis papulosa nigra, with over 50 percent of patients reporting the condition in other family members . Typically, lesions are symmetrically distributed on the face; less frequently, they can occur on the neck and trunk.
Histologically, dermatosis papulosa nigra lesions show acanthosis, papillomatosis, and hyperkeratosis and are considered a variant of seborrheic keratosis. However, in contrast with seborrheic keratosis, horn pseudocysts are usually absent.
The treatment of dermatosis papulosa nigra may be particularly challenging due to the high risk of post-treatment pigmentary alterations in patients with darkly pigmented skin. Treatment options include snip excision, curettage, electrodesiccation, and laser vaporization . Light electrodesiccation using low power settings is most commonly used. The application of a petrolatum-based ointment after the procedure may alleviate subjective symptoms of burning and pain and promote healing .
Cryotherapy should be avoided due to the high frequency of postinflammatory hypopigmentation in patients with darkly pigmented skin.
APPENDAGEAL (ADNEXAL) TUMORS — Benign appendageal tumors are relatively uncommon neoplasms that exhibit morphologic eccrine, apocrine, follicular, or sebaceous differentiation (table 1). They typically present as pink, skin-colored, or slightly bluish papules or nodules ranging in size from a few millimeters to several centimeters (picture 12A-E).
Benign and malignant cutaneous adnexal tumors are discussed separately. (See "Cutaneous adnexal tumors".)
CYSTS — A cutaneous cyst is a sac-like lesion lined by an epithelium that presents as a dermal or subcutaneous papule or nodule. Several cyst subtypes can be distinguished based on the nature of the lining epithelium and cyst content. Common cutaneous cysts, including milia and epidermoid cysts, are lined by stratified squamous epithelium. Some cysts, including mucocele and digital myxoid cyst, are not lined by an epithelium.
Milium — Milia are minute subepidermal keratin cysts that arise from the pilosebaceous units or eccrine sweat ducts. They present as firm, white papules, 1 to 2 mm in diameter, most frequently located on the face (picture 13). Milia are common lesions; they occur at all ages and are a common finding in newborns.
In adults, when milia are small, they may at times be confused with other common lesions, such as flat warts or syringoma (picture 14) (see "Cutaneous adnexal tumors", section on 'Syringoma'). Milia are reported to fluoresce bright yellow under Wood's lamp, and this may be used in cases of diagnostic uncertainty . (See "Skin lesions in the newborn and infant".)
Milia may develop spontaneously or as secondary lesions during the healing process of second-degree burns, blistering diseases (eg, epidermolysis bullosa, porphyria cutanea tarda), dermabrasion, and ablative laser resurfacing. They may also be an adverse effect of tyrosine kinase inhibitors . The so-called "milia en plaque" is an unusual lesion consisting of a cluster of milia occurring on an erythematous and edematous base, typically located in the retroauricular area and associated with autoimmune skin disorders.
Histologically, the milial cyst consists of a wall of several layers of stratified squamous epithelium and a central keratinous material, similar to epidermoid cysts.
Milia can be treated for cosmetic reasons by incision of the overlying epidermis and expression of the content. Smaller lesions may respond to topical retinoids applied daily for several weeks. Recurrence is uncommon [34,35].
Clinical features — Epidermoid cyst, also called epidermal cyst, epidermal inclusion cyst, or, improperly, "sebaceous cyst," is the most common cutaneous cyst. It can occur anywhere on the body and typically presents as an asymptomatic, skin-colored dermal nodule (picture 15C), often with a clinically visible central punctum (picture 15A-B). The size ranges from a few millimeters to several centimeters in diameter. The cyst wall consists of normal stratified squamous epithelium derived from the follicular infundibulum.
Epidermoid cysts unusual in number and location (extremities rather than face, base of ears, and trunk) may be seen in the setting of Gardner syndrome, a rare, inherited condition characterized by familial adenomatous polyposis of the colon associated with a number of extracolonic abnormalities. (See "Gardner syndrome".)
Epidermoid cysts may be primary or may arise from the implantation of the follicular epithelium in the dermis, as a result of trauma, or from a comedo. Lesions may remain stable or progressively enlarge. Spontaneous inflammation and rupture can occur, with significant involvement of surrounding tissue (picture 16). There is no way to predict which lesions will remain quiescent and which will become larger or inflamed.
Epidermoid cysts may become secondarily infected by the normal skin flora. Infected, fluctuant cysts tend to be larger, more erythematous, and more painful than sterile, inflamed cysts, although an intense, inflammatory response to cyst rupture may also occur in the absence of infection.
Diagnosis and differential diagnosis — The diagnosis of epidermoid cyst is usually clinical, based upon the clinical appearance of a discrete cyst or nodule, often with a central punctum, that is freely movable on palpation (picture 15B-C). The diagnosis can be confirmed by histologic examination. The cyst wall consists of stratified squamous epithelium similar to skin surface or infundibulum of hair follicles. The cavity is filled with laminated layers of keratinous material. In ruptured cysts, a foreign-body inflammatory granulomatous reaction due to the release of the cyst content into the dermis may result in the formation of a keratin granuloma (picture 17).
The differential diagnosis of epidermoid cysts includes:
●Pilomatricoma (picture 12B, 12F) (see "Cutaneous adnexal tumors", section on 'Pilomatricoma').
●Abscess (see "Acute cellulitis and erysipelas in adults: Treatment").
●Ganglion cysts (picture 19A-B) (see "Ganglion cysts of the wrist and hand", section on 'Definition').
●Steatocystoma multiplex (see 'Steatocystoma multiplex' below).
●Dermoid cyst – In infants and young children, a dermoid cyst is another possible confusing diagnosis. Dermoid cysts are congenital lesions that present as subcutaneous nodules seen along embryonic fusion lines on the face, scalp, and spine and contain epidermal and dermal tissues. The most common locations include the anterior fontanelle, the upper lateral region of the forehead near the eyebrow (picture 20), and the submental region. Nasal dermoids, resulting from congenital fusion abnormalities at the nasal root, present as noncompressible masses over the nasal dorsum with an associated midline pit or punctum (picture 21). (See "Cutaneous developmental anomalies in the newborn and infant" and "Congenital anomalies of the nose", section on 'Nasal dermoids'.)
Treatment — Treatment of stable, uninfected epidermoid cysts is not necessary, unless desired by the patient. Inflamed, ruptured cysts that are not infected may resolve spontaneously without therapy, although they tend to recur. Injection of triamcinolone acetonide (3 mg/mL for the face and 10 mg/mL for the trunk) into the inflamed lesion can hasten the resolution of inflammation and may prevent infection and the need for incision and drainage. Only small amounts (enough to slightly distend the cyst) should be injected, since injection of larger amounts can result in rupture and scarring. If the lesion is fluctuant, incision and drainage is indicated rather than injection.
Excision is best accomplished when the lesion is not inflamed; when the cyst is acutely inflamed the cyst wall is very friable, complete excision usually is not possible, and recurrence is likely. Thus, it is reasonable to wait until the inflammation has resolved before attempting excision. A description of cyst excision can be found separately. (See "Minor dermatologic procedures", section on 'Epidermoid cysts'.)
The punch incision technique and minimal incision technique are alternative methods to remove uncomplicated epidermoid cysts [36-39]. A small incision is made on the cyst with a no. 11 surgical blade or 4 mm punch; the cyst content is then expressed by exerting a vigorous lateral pressure on the cyst (figure 1). With this procedure, the cyst wall is usually released from the surrounding tissues and can be extracted through the small incision. The minimal incision technique provides better cosmetic results than the standard excision and is particularly useful for cysts in cosmetically sensitive areas. Recurrence rates of approximately <1 to 8 percent have been reported with the minimal incision technique [36,37,39].
Fluctuant cysts require incision with a no. 11 blade and drainage of the purulent material after anesthesia with 1% lidocaine. Anesthesia should be injected around the lesion rather than into the lesion in order to avoid rupturing the cyst wall with the pressure of the anesthetic agent. (See "Techniques for skin abscess drainage".)
The presence of significant surrounding cellulitis or cysts that have not responded to drainage may require oral antibiotic therapy, although in most cases the lesions are sterile. However, the drained contents should be sent for culture. Pending culture results, empiric antibiotic therapy can be started with agents active against methicillin-resistant Staphylococcus aureus (MRSA) in areas of high MRSA prevalence (table 2). (See "Acute cellulitis and erysipelas in adults: Treatment".)
Pilar (trichilemmal) cysts — A pilar cyst (trichilemmal cyst) resembles an epidermoid cyst, as it presents as a firm, slow-growing subcutaneous nodule. It is derived from the root sheath of the hair follicle and is most commonly located on the scalp (picture 22A-B). Pilar cysts can occur sporadically or in the setting of a hereditary predisposition with autosomal dominant transmission . Patients with familial pilar cysts are often younger and often present with multiple lesions at the same time. Hereditary trichilemmal cysts appear to result from a two-hit mechanism involving germline and somatic variants of the phospholipase C Delta 1 gene (PLCD1) .
Removal of pilar cysts is usually easier than removing epidermoid cysts, since the cyst wall is firm and tends not to rupture as easily. Enucleated cysts typically appear as firm, smooth, white nodules. Histologic examination of the removed lesion can confirm the diagnosis.
Vellus hair cyst — Eruptive vellus hair cyst is a benign condition occurring in children and young adults characterized by a sudden appearance of small, follicular, dome-shaped papules, usually on the trunk (picture 23) . The disorder is due to a developmental abnormality of the vellus hair follicle at the infundibular level and may be inherited in an autosomal dominant fashion. The diagnosis is based upon the histologic finding of a cystic structure located in the mid-dermis lined by squamous epithelium containing laminated keratinous material and numerous vellus hairs.
Eruptive vellus hair cysts are usually asymptomatic and may slowly regress over several years. However, patients may require treatment for cosmetic reasons. Treatment modalities include incision and extraction, carbon dioxide (CO2) laser or erbium-doped yttrium aluminium garnet (Er:YAG) laser vaporization, and topical retinoids [43-45].
Steatocystoma multiplex — Steatocystoma multiplex is an uncommon disorder characterized by multiple dermal, sebum-containing cysts measuring from less than 3 mm in diameter to 3 cm or more (picture 24) . Lesions usually appear during adolescence or early adulthood and can occur anywhere on the body, including the scalp, intertriginous areas, and genitalia, but show a predilection for the chest.
Steatocystoma multiplex is caused by mutations in the KRT17 gene, which also cause a subtype of pachyonychia congenita , and is a sporadic disorder in most cases, although it may be inherited as an autosomal dominant trait (see "Pachyonychia congenita"). Histopathologically, lesions consist of dermal cyst lined by a thin wall of stratified squamous epithelium containing small sebaceous gland lobules and sebum.
Treatment is difficult, due to the high number of lesions. Options include surgical excision, incision and expression of the cyst content followed by extraction of the cyst wall, and carbon dioxide laser therapy [48-50].
Mucocele — A mucocele is a common cystic lesion most frequently found in the lower lip mucosa. It results from mucin leakage from a disrupted salivary duct, in most cases as a consequence of an intraoral trauma (eg, repetitive lip biting). They are variable in size, contain a gelatinous fluid, and typically appear as pink/blue, soft papules or nodules (picture 25).
Digital myxoid cyst — A digital myxoid cyst or myxoid pseudocyst (also called mucous or mucoid cyst) typically presents as a translucent nodule on the dorsum of the digit between the distal interphalangeal joint and the proximal nail fold (picture 26). It results from mucoid degeneration of the connective tissue and/or joint fluid leaking from an osteoarthritic distal interphalangeal joint by way of a communicating canal. The diagnosis and treatment of digital myxoid cysts are discussed separately. (See "Principles and overview of nail surgery", section on 'Digital myxoid cyst' and "Overview of nail disorders", section on 'Digital myxoid cyst or myxoid pseudocyst'.)
Infantile hemangioma — Infantile hemangiomas are benign tumors of vascular endothelium and the most common tumors of childhood (picture 27). The clinical presentation, diagnosis, and management of infantile hemangiomas are discussed separately. (See "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications" and "Infantile hemangiomas: Evaluation and diagnosis" and "Infantile hemangiomas: Management".)
Cherry angioma — Cherry angiomas, also known as Campbell de Morgan spots, are mature capillary proliferations that are common in middle-aged and older adult patients. They tend to be less conspicuous in individuals with darkly pigmented skin. They usually occur as multiple lesions, most commonly on the trunk, and bleed profusely with any traumatic rupture. The pathogenesis is incompletely understood. Oncogenic mutations in GNAQ and GNA11, similar to those found in port wine stains and Sturge-Weber syndrome, have been found in 50 percent of tissue samples .
Cherry angiomas are often dome shaped, typically 0.1 to 0.4 cm in diameter, and do not usually blanch with pressure (picture 28A-B).
The diagnosis is based on the clinical appearance of the lesions. Examination with a dermatoscope shows characteristic red, purple, or blue-black lagoons (picture 29). (See "Dermoscopic evaluation of skin lesions", section on 'Other benign lesions'.)
Cherry angiomas may be confused with amelanotic melanomas, which are usually friable lesions that may have recently changed in size or configuration (picture 30). If there is any concern for malignancy, the lesion should be excised and sent for histopathologic examination.
Treatment of cherry angiomas is only necessary for patients who are bothered by the lesions. Patients should be advised, however, that new lesions are likely to develop and there is no known way to prevent them.
The following modes of treatment may be used :
●Small lesions can be electrocauterized after local anesthesia with 1% lidocaine.
●Shave excision and electrocauterization of the base is useful for larger lesions.
●Laser therapy can also be used to remove superficial lesions. (See "Laser and light therapy for cutaneous vascular lesions".)
Pyogenic granuloma — Pyogenic granuloma or lobular capillary hemangioma is a benign vascular tumor of the skin (picture 31A-D) or mucous membranes (picture 32) characterized by rapid growth and friable surface that bleeds profusely after minor trauma. Pyogenic granuloma occurs in patients of all ages, with a peak incidence in the second and third decade of life and during pregnancy. The cause of this is unknown. Reported trigger factors include trauma and medications.
Pyogenic granuloma is discussed in detail separately. (See "Pyogenic granuloma (lobular capillary hemangioma)".)
TUMORS OF SUBCUTANEOUS FAT
Lipoma — Superficial subcutaneous lipomas are the most common benign soft-tissue neoplasms. They consist of mature fat cells enclosed by thin fibrous capsules. Lipomas can occur on any part of the body and usually develop superficially in the subcutaneous tissue. Rarely, they may involve fascia or deeper muscular planes.
Lipomas present as soft, painless subcutaneous nodules ranging in size from 1 to >10 cm. They occur most frequently on the trunk and upper extremities and can be round, oval, or multilobulated (picture 18A-B). Frequently, patients may have more than one lipoma, and occasionally they may have a genetic condition (familial multiple lipomatosis) characterized by the development of multiple lipomas in several family members (picture 33). Malignant transformation of a lipoma into a liposarcoma is rare.
The diagnosis of lipoma is usually made clinically. Ultrasound examination can be helpful to distinguish a lipoma from an epidermoid cyst or a ganglion cyst . If a suspected lipoma causes symptoms (pain or restriction of movement), is rapidly enlarging, or is firm rather than soft, a biopsy is indicated.
The treatment of lipomas, if needed because of pain, cosmesis, or concerns over diagnosis, is surgical removal of the fat cells and fibrous capsule. Recurrence of an excised lipoma is not common.
Side effects of surgery include scarring, seroma, and hematoma formation. In areas that are cosmetically sensitive, a surgical technique with segmental extraction and minimal surface incision may limit the scar size . Alternative treatment modalities include liposuction and injection with low concentrations of deoxycholate [55,56]. Deoxycholate injections led to improvement in a small study of six patients [56,57]. However, further studies are necessary before this agent can be routinely recommended.
Angiolipoma — Angiolipoma is a benign tumor of adipocytes typically occurring in adolescents and young adults. Angiolipoma presents as a soft subcutaneous nodule of 0.5 to 2 cm in diameter, usually located on the forearm and chest wall (picture 34). Lesions are frequently multiple. Angiolipomas have been reported in individuals infected with human immunodeficiency virus (HIV) after starting antiretroviral therapy .
Clinically, angiolipomas closely resemble lipomas, although angiolipomas are usually painful and tender. Histopathologic examination is necessary for diagnosis. Macroscopically, angiolipoma appears as a small, well-circumscribed, subcutaneous tumor (picture 35); histology reveals a circumscribed, encapsulated tumor composed of an admixture of mature adipose cells and capillary vessels. Fibrin thrombi are typically seen. Occasionally, a predominance of blood vessels can be seen (cellular angiolipomas). The vascular proliferation component is not seen in lipomas.
Single, painful lesions can be excised. The treatment of multiple lesions is difficult. Liposuction has been used in a few cases [59,60].
GLOMUS TUMOR — Glomus tumor is a rare, benign neoplasm composed of cells resembling the modified smooth muscle cells of the normal glomus body . It is usually located in areas of the skin that are rich in glomus bodies (eg, the subungual regions of digits or the deep dermis of the palm, wrist, forearm, and foot). Glomus tumors of the fingers and toes occur in approximately 5 percent of patients with neurofibromatosis type 1 (NF1) and are considered NF1-associated neoplasms [62-64].
Glomus tumor presents as a pink or purple vascular papule or nodule associated with paroxysmal pain, cold sensitivity, and tenderness. Subungual glomus tumors are particularly painful. Nail dystrophy and/or a bluish-red flush are typically seen (picture 36A-C).
The diagnosis is suspected on the basis of the clinical appearance and history of paroxysmal pain and cold sensitivity. Histopathologic examination of the excised tumor is necessary to confirm the diagnosis.
Histologically, glomus tumor is a well-circumscribed dermal nodule composed of glomus cells, vasculature, and smooth muscle cells (picture 37). Solid glomus tumor, with scarce vasculature and scant muscle component, is the most common variant . Less common variants include glomangioma, with prominent vascular component, and glomangiomyoma, with prominent vascular and smooth muscle components.
Treatment is surgical excision. For subungual tumors, preoperative imaging studies with color Doppler ultrasonography and magnetic resonance may provide information on tumor size, shape, and precise anatomic location . (See "Principles and overview of nail surgery", section on 'Glomus tumors'.)
Melanocytic nevus — Melanocytic nevi (moles) are common neoplasms that result from the proliferation of cutaneous melanocytes. Nevi frequently present as pigmented macules, papules, or plaques but may also be skin colored or pink. (See "Acquired melanocytic nevi (moles)" and "Congenital melanocytic nevi".)
Solar lentigo — Solar lentigo, most commonly known as liver spots, "old age spots," or "sun spots," is a proliferation of normal melanocytes secondary to chronic solar damage. These lesions occur most commonly in individuals with lightly pigmented skin who have a history of chronic sun exposure. Hyperpigmentation may vary from light to dark brown but is uniform within an individual lesion. (See "Benign pigmented skin lesions other than melanocytic nevi (moles)", section on 'Solar lentigo'.)
Diagnosis is based on the clinical appearance of flat, oval, evenly pigmented macules in areas of chronic sun exposure, particularly the face, dorsa of the hands, shoulders, and back (picture 38A-B). However, lesions that are reported to have changed color, variability in color, irregular margins, or developed a papular or nodular component should be biopsied to exclude malignancy.
The differential diagnosis of solar lentigines includes:
●Seborrheic keratosis – Early, macular seborrheic keratoses may be difficult to differentiate from solar lentigines. Scale and palpable components are features of seborrheic keratoses. (See 'Seborrheic keratosis' above.)
●Lentigo maligna – Lesions have variable pigmentation, irregular borders, and a history of gradual enlargement (picture 39A-C). (See "Lentigo maligna: Clinical manifestations, diagnosis, and management".)
●Lentigo maligna melanoma – Lentigo maligna melanoma has an irregular border, variable pigmentation, and may have a raised papule or nodule within the plaque (picture 40A-B). The history is of gradual change, usually over years. (See "Lentigo maligna: Clinical manifestations, diagnosis, and management".)
No treatment is needed unless the patient desires removal for cosmetic reasons. Liquid nitrogen applied for 5 seconds or less can be used if treatment is desired. Lesions may heal with hypopigmentation.
Patients should be educated on the use of sunscreens and sun protection. Regular use of sunscreens prevents the development of solar lentigines, although it does not lead to regression of current lesions .
Hydroquinone cream 4% or triple combination cream with fluocinolone acetonide 0.01%, hydroquinone 4%, and tretinoin 0.05% plus sun protection can lighten existing lesions and reduce postinflammatory hyperpigmentation after cryotherapy . Thin seborrheic keratoses, which are sometimes mistaken for lentigines, will not respond to topical hydroquinone.
Other — Other benign pigmented lesions, including café-au-lait spots, Becker nevus, and dermal melanocytosis, are discussed separately. (See "Benign pigmented skin lesions other than melanocytic nevi (moles)".)
OTHER BENIGN SKIN LESIONS
Chondrodermatitis nodularis helicis — Chondrodermatitis nodularis helicis is a solitary, firm, painful nodule <10 mm in size, located on the helix or, less frequently, on the antihelix of the ear . It is thought to result from cartilage inflammation that in extreme cases may cause cartilage necrosis and transepithelial elimination of degenerated collagen. Etiologic factors include chronic trauma, chronic sun exposure, low temperature, and prolonged or excessive pressure with compromise of local blood supply. An association with systemic diseases, including connective tissue and cardiovascular disease, also has been suggested .
Chondrodermatitis nodularis helicis most often occurs in middle-aged or older men, is usually unilateral, and typically develops on the same side the patient lies on in bed (picture 41) . The nodule enlarges rapidly over a few months and then remains stable. The surface is frequently covered with a scale or crust that conceals a small ulcer. Pain is initiated by pressure or by changes in the ambient temperature and lasts from a few minutes to a few hours.
Diagnosis is based upon the clinical appearance and history of rapid development of a nodular lesion with associated pain and tenderness. If the diagnosis is in doubt, the lesion should be excised and sent for histopathologic examination. Histology shows a nodule of degenerated collagen surrounded by a lymphohistiocytic infiltrate; a central ulceration through which the degenerated collagen is extruded is often present. The differential diagnosis includes hypertrophic actinic keratosis, basal cell carcinoma (picture 42), keratoacanthoma (picture 43), squamous cell carcinoma (picture 44), and tophus (picture 45).
Conservative treatment includes strategies to relieve pressure and intralesional corticosteroids. Relieving pressure is the most important aspect of managing these lesions. The use of a donut-shaped pillow or foam padding for several weeks may provide resolution of symptoms [70-73]. Intralesional injection of triamcinolone acetonide 10 mg/mL may provide rapid pain relief in most patients and long-term resolution of chondrodermatitis nodularis helicis in some . Monthly treatments may be necessary up to three to four treatments. Other treatments that have been evaluated in small numbers of patients include 2% topical nitroglycerin and photodynamic therapy [75-79].
Surgical approaches include cryotherapy, curettage, carbon dioxide laser ablation, wedge excision, and cartilage removal alone [80-85]. Recurrence after surgical excision has been reported in 10 to 30 percent of patients [72,86].
Venous lake — Venous lakes are lesions of dilated venous capillaries on the face, lips, and ears of older adult patients. The lesions bleed easily following minor trauma.
Diagnosis is based upon the appearance of the blue lesion in characteristic locations that disappear when compressed with a glass slide (picture 46). Venous lakes should be differentiated from blue nevi, which do not disappear with compression and do not usually appear on the face, ears, or lips. Nodular melanomas also can be confused with venous lakes, but do not disappear with compression, remaining a firm nodule.
Electrosurgery after anesthesia with 1% lidocaine can be used if the lesion causes a bleeding problem or is cosmetically unacceptable. Pulsed dye vascular laser may remove lesions without causing a scar .
Calluses and corns — Calluses and corns (clavi) are among the most frequent skin conditions and, by virtue of their location on the feet, may be the source of considerable disability, discomfort, and pain :
●Calluses are a diffuse thickening of the outermost layer of the skin, the stratum corneum, in response to repeated friction or pressure (picture 47).
●Corns develop similarly, but differ by having a central "core" that is hyperkeratotic and often painful (picture 48A-B). Corns typically occur at pressure points secondary to ill-fitting shoes, an underlying bony spur, or an abnormal gait.
These lesions are typically located on the plantar aspect of prominent metatarsals, between toe clefts, or on the dorsal aspect of toe joints.
The diagnosis of calluses and corns is based upon their clinical appearance. They must be differentiated from plantar warts. After paring down, warts will have several dark specks that represent punctate capillary thromboses. Warts also disrupt normal skin markings so that the skin lines are no longer evident. Skin lines are more prominent in callosities.
Treatment of calluses and corns begins with prevention. Patients should be advised to avoid ill-fitting shoes. Consider referring patients with severe, recurrent problems for orthotic consultation to fit inner soles or metatarsal bars.
In most cases, calluses or corns can be treated conservatively with the application of keratolytics, such as salicylic acid (plasters or ointment) or urea-based creams. Scalpel debridement may be an alternative treatment to achieve a more rapid decrease of pain and improvement in function . However, the long-term resolution of callus appears to be similar with both approaches . Referral to podiatry to evaluate for an underlying bony abnormality should be considered for patients with lesions that are recalcitrant or recurrent:
●Salicylic acid plaster – Salicylic acid plaster 40% is available without a prescription and is used as follows:
•Debulk the callus or corn by paring skin with a no. 15 scalpel blade.
•Cut the plaster to the size of the lesion and apply. Tape can be used to keep the patch in place and avoid it slipping onto unaffected areas.
•Leave in place for 48 hours.
•Pare down the remaining skin; replace the plaster patch and let the patient resume proper foot care and continue applying the patch at home.
•Patients should be advised to remove the white, "dead" skin with a metal nail file or pumice stone each night before replacing the patch. Soaking the skin in warm water for five minutes before using a nail file or pumice stone can help in removing the "dead" skin.
•Use of the patch should stop once the lesion has resolved.
•Follow-up if lesions do not resolve within one to two weeks.
•Do not use plaster in patients with peripheral neuropathies. These patients may not notice pain with improper patch placement and can develop damage to normal skin.
●Salicylic acid ointment – Salicylic acid 10 to 20% in petrolatum (available in 30 to 45 g tubes) is available by prescription and compounded by a pharmacist. The ointment is applied in a small amount on the callus under occlusion nightly. Patients with peripheral neuropathies should not use salicylic acid ointments.
●Urea-based creams – Creams containing 40% urea, especially under occlusion overnight, can assist with callus removal similarly to salicylic acid. High-concentration urea creams should be used under medical supervision in patients with peripheral neuropathies and diminished sensation in the feet.
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Diagnostic approach – Most benign skin lesions are diagnosed on the basis of clinical appearance (morphology, distribution) and history (see "Approach to the clinical dermatologic diagnosis"). Dermoscopy, a skin examination technique performed with a handheld instrument called a dermatoscope, is a helpful adjunct to the clinical examination of a variety of pigmented and nonpigmented lesions (see "Dermoscopic evaluation of skin lesions"). If the diagnosis of a lesion is uncertain or if a lesion has exhibited unexpected changes in appearance or symptoms, a diagnostic procedure (eg, biopsy, excision) is indicated to confirm the diagnosis. (See "Skin biopsy techniques".)
●Adnexal tumors – Benign adnexal (appendageal) tumors, including sebaceous hyperplasia (picture 12E), poroma (picture 12A), and pilomatricoma (picture 12B), are discussed separately. (See "Cutaneous adnexal tumors".)
●Cysts – Cutaneous cysts include milium, epidermoid cyst (picture 49A-B), pilar cyst (picture 22A, 22C), vellus hair cyst (picture 23), and digital myxoid cyst (picture 26). Mucocele is a common cystic lesion most frequently found in the lower lip mucosa (picture 25). (See 'Cysts' above.)
●Vascular tumors – Benign vascular tumors include infantile hemangioma (picture 27), pyogenic granuloma (picture 31A-D), and cherry hemangioma (picture 28A-B) (see 'Vascular tumors' above). Infantile hemangioma and pyogenic granuloma are discussed in separate topic reviews. (See "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications" and "Pyogenic granuloma (lobular capillary hemangioma)".)
●Pigmented lesions – Common benign pigmented lesions include acquired and congenital melanocytic nevi and solar lentigines (picture 38A-B). These and other pigmented lesions are discussed in separate topic reviews. (See "Acquired melanocytic nevi (moles)" and "Congenital melanocytic nevi" and "Benign pigmented skin lesions other than melanocytic nevi (moles)".)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Beth G Goldstein, MD, who contributed to an earlier version of this topic review.
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