About Hemangioma of Infancy

Hemangioma of infancy,caused by a proliferation of endothelial cells (which line blood vessels), is the most common tumor of infancy. Hemangioma of infancy ranges in color from red to purple, and are soft and compressible. Lesions are usually solitary, favoring the head and neck.  Girls are affected more often than boys. Hemangioma of infancy is not present at birth but appears postnatally.

Hemangioma of infancy goes through three stages: proliferation, involution, and involuted.  The proliferation stage usually occurs during the first year of life, during which the hemangioma can enlarge rapidly.  The hemangioma then gradually involutes over the two to six years, and is usually completely involuted by the fifth year. Ulceration may occur in the course of regression. Hemangioma of infancy usually resolves without scarring, but atrophy, depigmentation and scarring sometimes occur.

Variations of hemangioma of infancy include deep hemangioma, multiple hemangiomas of infancy and congenital hemangiomas.  Deep hemangiomas are located deep in the dermis or subcutaneous fat and are typically bluish in color, possibly with overlying telangiectases or a superficial hemangioma of infancy. Multiple hemangiomas of infancy are small papular lesions that can affect either skin alone (termed benign cutaneous hemangiomatosis) or skin and internal organs (termed diffuse neonatal hemangiomatosis). Congenital hemangiomas are present at birth, unlike hemangioma of infancy. They are divided into rapidly involuting congenital hemangiomas (RICH) and non-involuting congential hemangiomas (NICH).

Hemangiomas of infancy may interfere with vital functions such as vision or breathing during the proliferation stage. Specific subtypes (tufted angiomas and Kaposiform hemangioendothelioma) may give rise to the Kasabach-Merritt syndrome, in which platelets get entrapped in the hemangioma leading to thrombocytopenia.

Infantile hemangiomas that do no interfere with vital functions are best observed for resolution. Treatment options, if necessary, include: pulse dye laser, cryosurgery, intralesional or systemic glucocorticoids, interferon alpha, and most recently propanolol. Deep hemangiomas rarely regress and may warrant surgery.

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About malignant melanoma

Malignant melanoma is a malignant neoplasm comprised of melanocytes and nevus cells, both of which are pigment-producing. It is typified by irregularity in shape and color, and eventually a palpable papule or plaque. There are four types of malignant melanoma: superficial spreading, lentigo maligna, nodular, and acral lentiginous.

Lentigo maligna melanoma. This form usually occurs in sun-exposed areas, such as the head and neck, and most frequently occurs in the elderly (median ~70 yrs old). It is multicolored and variably elevated in some areas. It is preceded by  in situ melanoma, or lentigo maligna.

Superficial spreading. This is the most common form of melanoma. It is not associated with sun-exposed surfaces, and can often be found on the back or legs. Median age of onset is ~50 years. It is irregular in color, border, and surface texture.

Nodular. This form occurs on all skin surfaces, with a median age of onset of ~50 years. It is a rapidly growing, blue-black nodule, that may be eroded.

Acral lentiginous. This form occurs on the palms and soles and, in contrast to the other forms, occurs most frequently in Blacks and Asians. It has a median onset of ~60 years of age. It has irregular borders and a black color.

With what can malignant melanoma be confused?

Lentigo maligna melanoma can be confused with actinic lentigo or, sometimes, seborrheic keratosis. A superficial spreading melanoma can resemble pigmented basal cell carcinoma or a nevus or, less often, seborrheic keratosis or angioma. Nodular melanoma can be confused with blue nevus (a blue nodule that begins in childhood), pyogenic granuloma, angioma, or dermatofibroma. The acral lentiginous variety can mimic a nevus or a rare fungal infection termed tinea nigra palmaris.

How is malignant melanoma diagnosed?

A new pigmented lesion, or one that increases in size or changes color, areworrisome signs that often prompt patients to seek medical care. Other suspicious signs are bleeding or itching of a pigmented lesion. Some patients have a family history of melanoma, prompting increased scrutiny. Your dermatologist may examine the lesion with a special lens called a dermatoscope to aid in diagnosis. The classic ABCDEs of melanoma detection are asymmetry, border irregularity, color variegation, diameter greater than 6 mm, and evolving, or changing in size, shape or color. However, not all malignant melanomas follow the ABCDE rules; any suspicious pigmented lesion should be examined by biopsy, excisional when possible, with 2 to 3 mm margins. If the lesion is large, such as often occurs with lentigo maligna melanoma, incisional biopsy is acceptable.

How is malignant melanoma treated?

Excision is the treatment of choice when melanoma is detected early. The required margin is determined by the depth of cancer invasion, with deeper lesions requiring wider margins. The surgeon may perform sentinel lymph node mapping, in which a tracer is injected in to the lesion to determine the first draining lymph node. This node can then be examined to determine whether malignant cells have spread. The potential benefit of lyphadenectomy is determined by the stage of the cancer. If the melanoma has metastasized, chemotherapy and/or immunotherapy is required; excision will not be curative. Melanoma is treated by specialists including a surgeon and an oncologist. Frequent follow-up is required. Melanoma vaccines are still in the research and development stage.

What is the prognosis for malignant melanoma?

The lentigo maligna, superficial spreading and acral lentiginous types of melanoma have a “horizontal” growth phase, during which the lesion is flat or slightly raised. The lesion is completely curable by excision during this phase, and prognosis is directly related to the thickness of the tumor, ranging from a 5 year survival of 99% to 22% . Therefore, early detection is crucial. Nodular melanoma unfortunately only has a “vertical” growth phase.

How is malignant melanoma prevented?

Sunlight is likely a risk factor in some types of melanoma, as is family history. A large number of small nevi, large nevi, or dysplastic nevi are also risk factors. Prudent avoidance of sunlight irradiation is always recommended. Close physician follow-up for patients with risk factors is recommended, with the exact frequency determined by the risk factors and prior duration of follow-up.

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About squamous cell carcinoma

Squamous cell carcinoma is a commonly occurring malignant growth derived from epidermal keratinocytes. It appears as an indurated (hard), scaling or crusted plaque or nodule that may ulcerate or bleed. A number of risk factors contribute to the development of squamous cell carcinoma, including exposure to ultraviolet radiation and chemical carcinogens. It is more common in light-skinned people with frequent sun exposure, such as farmers and outdoor laborers. The incidence of the disease increases with proximity to the equator. Not surprisingly, it occurs most often on sun-exposed areas such as the head, neck, and arms. It also can arise in sites of damaged skin or mucous membranes, such as burn injuries. The lower lip is frequently involved as a result of chronic injury from smoking or sun damage. Squamous cell carcinoma can be very locally invasive, and also harbors the capacity to metastasize to distant sites.

With what can squamous cell carcinoma be confused?

Squamous cell carcinoma must be distinguished from basal cell carcinoma, actinic keratosis, warts, keratoacanthoma, seborrheic keratosis, and Bowen’s disease and, on the penis, from erythroplasia of Queyrat.

How is squamous cell carcinoma diagnosed?

Any ulcer that fails to heal should undergo biopsy to rule out squamous cell carcinoma.

How is squamous cell carcinoma treated?

Excision is the preferred therapy. Small lesions can be effectively destroyed with cryotherapy, curettage or electrodessication, but it is often preferable to obtain a tissue sample. Larger tumors and those on cosmetically sensitive areas, such as the face, may be removed using the Mohs micrographic surgery technique. Sun protection with sunscreen, protective clothing, and sun avoidance is necessary to reduce the risk of further tumors.

What is the prognosis for squamous cell carcinoma?

Only about 2% of squamous cell carcinomas metastasize. Large, poorly differentiated, deeply invading carcinomas and those arising in scars or mucous membranes are more likely to do so.

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About basal cell carcinoma

Basal cell carcinoma (BCC) is a cancer arising from the basal cell layer of the epidermis. It is the most commonly occurring human cancer. Despite only rarely metastasizing, these aggressive tumors can cause profound local tissue destruction. The majority of basal cell carcinomas are caused by exposure to ultraviolet radiation in the form of sunlight. It occurs most frequently in fair-skinned, light-eyed individuals with other evidence of sun-damage to their skin.

There are four subtypes of BCC: nodular, pigmented, superficial, and sclerotic. The nodular type is most common, appearing as the classic “pearly papule” with a central depression, associated telangiectasia (small blood vessels), and a rolled, waxy border. It is often found on the face, especially the nose. The pigmented type, as the name suggests, is a blue or black nodule, papule, or plaque, often speckled, with a rolled border. Superficial BCC appears similar to eczema, and is often found on the trunk. It is red, scaly, well-demarcated, and has a pearly border. The scarring type appears as a white atrophic plaque that can be confused with a scar. It is the most aggressive and, fortunately, least common, subtype of BCC. Another type is the Pinkus type, also known as fibroepithelioma. It is distinguished by its unique reticulated appearance on histology. The Pinkus type of BCC is most frequently found in the lumbrosacral area.

With what can basal cell carcinoma be confused?

Nodular BCC can resemble squamous cell carcinoma, non-pigmented nevus, molluscum contagiosum, and sebaceous hyperplasia. Pigmented BCC can be confused with other pigmented lesions such as pigmented nevus and, importantly,malignant melanoma. Seborrheic keratosis is also in the differential. Superficial BCC can be confused with eczema,dermatitis, psoriasis, and Bowen’s disease. Scarring BCC, as the name suggests, can be confused with a scar or sometimes a squamous cell carcinoma.

How is basal cell carcinoma diagnosed?

A BCC might be suspected after a routine skin exam. A new growth that does not heal and bleeds easily is suspicious for BCC, especially in fair skinned persons with a history of sun exposure and evidence of actinic (sun) damage. This suspicion will be confirmed with a skin biopsy, either punch or shave, which is interpreted by a dermatopathologist. As the cancer’s name suggests, its cells resemble the basal cells of the epidermis. The tumor extends from the epidermis into the dermis with various morphologies such as nodules, cysts, buds, and strands.

How is basal cell carcinoma treated?

Possibilities include scalpel excision, curettage and electrodessication, cryotherapy, radiation therapy, and 5-fluorouracil, a topical chemotherapeutic agent. Treatment depends on various parameters such as size, location, whether it is a recurrence, histopathologic type, and age and general health of the patient. Excision with suture closure is the most common modality. A special form of surgery, Mohs’ micrographic surgery, is sometimes performed. In this procedure, the surgeon examines the excised tissue in real time to ensure that it is free of cancerous cells. It enables the surgeon to remove only as much tissue as is necessary to ensure tumor-free margins.

What is the prognosis for basal cell carcinoma?

These tumors rarely metastasize (spread to a remote location), with an estimated rate of 0.003%. However, they can be aggressive locally. If not treated in a timely fashion, a BCC can result in significant deformity. Annual follow-up is recommended; up to 35% of patients will develop a second BCC within five years.

How is basal cell carcinoma prevented?

Avoidance of further sun damage is critical. This includes the daily use of sunscreens with a minimum SPF of 15 to 30, depending on skin type, protective clothing such as a wide-brimmed hat and long sleeved shirt, and sun avoidance, especially midday when the sun is strongest.

More about basal cell carcinoma

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About dysplastic nevus

A dysplastic nevus, or atypical mole, is irregular in color and border, is larger than 5 mm in diameter, and often has an erythematous (red) background. In certain families, dysplastic nevi indicate an increased risk of developing a familial form of malignant melanoma. This is the Dysplastic Nevus Syndrome, also known as Familial Atypical Mole and Melanoma Syndrome. Affected members in these families invariably develop malignant melanoma. However, most individuals with a dysplastic nevus that do not have a family history of Dysplastic Nevus Syndrome will never develop malignant melanoma. The precise risk is uncertain.

With what can dysplastic nevus be confused?

Malignant melanoma is the main differential diagnosis.

How is dysplastic nevus diagnosed?

A dysplastic nevus is diagnosed clinically by your dermatologist. Your doctor will perform a biopsy to confirm the diagnosis.

How is a dysplastic nevus treated?

Depending on how many lesions are present, excisional biopsy is the treatment of choice. When many nevi are present, at least two should be biopsied. The rest are followed closely with frequent dermatologist skin exams, total skin photography, patient education, and patent self-examination. The exact physican follow-up schedule depends on whether or not the patient has a family history of Dysplastic Nevus Syndrome, and for how long the patient has already been followed.

What is the prognosis for dysplastic nevus?

Virtually all patients with dysplastic nevi who have a family history of Dysplastic Nevus Syndrome will develop malignant melanoma. Close physican follow-up and excisional biopsies are required.

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About tinea versicolor

Tinea versicolor is the fungal form of the yeast organism Pityrosporum ovale (the fungal form was previously known as Malssezia furfur until it was demonstrated that it was the hyphal form of Pityrosporum ovale.) It is a common fungal infection of the superficial layers of the stratum corneum. The lesions are round, have a fine scale, and can be white, pink or tan, with white being most frequently observed. They may become confluent. The neck, trunk, and upper arms are most often affected; the face and extremities are usually spared. The condition is usually asymptomatic, but may be associated with mild pruritus (itching). Patients usually seek care for cosmetic concerns. In winter months, the lesions appear darker that the surrounding skin, while in the summer months they typically appear as white spots. The lesions do not tan and therefore become more noticeable following sun exposure. There is also a hyperpigmented variety. Although immunosuppression can be a risk factor, most patients with the condition are otherwise in good health.

Is tinea versicolor contagious?

The yeast form of the organism is a frequent skin colonizer. It is only with conversion to the hyphal form that infection occurs. Conjugal cases are not common. Not everyone exposed to, or colonized by, the organism develops the disease. For unknown reasons, some individuals are susceptible.

With what can tinea versicolor be confused?

The differential diagnosis includes vitiligo and pityriasis alba. If the lesions are tan or pink with scale they may be confused with seborrheic dermatitis.

How is tinea versicolor diagnosed?

A KOH preparation of scraped scale is the mainstay of diagnosis. A “spaghettis and meatball” appearance of short hyphae and spores is characteristic. The organism cannot be cultured using typical fungal culture medium. Under Wood’s light examination the lesions will appear white but not “chalk white”.

How is tinea versicolor treated?

Topical selenium sulfide—found in anti-dandruff shampoos (e.g. Selsun)—is often effective when applied and left on for 10 minutes and then rinsed. When lesions are present, this should be repeated for three days, and then weekly for a month, though other regimens are possible (e.g. two times a week for 2-4 weeks). The entire area from the neck to the knees should be treated. Recurrence can be prevented with periodic application (e.g. every three months). Zinc pyrithione shampoo (Head & Shoulders), topical ketoconazole, and terbinafine spray (Lamisil) are also effective. A single 400 mg dose of oral ketoconazole (Nizoral) is very effective and easy to comply with.

What is the prognosis for tinea versicolor?

The tinea versicolor organism is eradicated rapidly with treatment, but pigmentation takes months to return to normal. The recurrence rate is high (approximately 50%), but prophylactic treatment with topical selenium sulfide or oral ketoconazole (400 mg every three months) can reduce this.

More on tinea versicolor

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About tinea unguium (onychomycosis)

Tinea unguium, also known as onychomycosis, is infection of the nail—usually the distal nail bed—with a dermatophytic fungus. The usual culprits are Tricophyton rubrum and Tricophyton mentagrophytes, with T. rubrum being the most common cause of distal subungual onychomycosis. The nail appears discolored with areas of yellowish-brown or white. Involvement of the nail undersurface results in debris buildup and nail separation. Infection of the top surface leads to a brittle white surface. Involvement of the proximal nail plate is a sign of HIV infection.

Tinea unguium is a common problem, with prevalence increasing with age. The toenails are affected more frequently that the fingernails. The most common complaint is regarding the thickened unsightly appearance of the nail, but the condition can also cause pain or discomfort.

With what can tinea unguium be confused?

Nail disease is difficult to diagnose by appearance alone. The nail plate appearance of tinea unguium can be confused with the changes caused by psoriasis, trauma, or aging. Psoriasis will usually have other skin findings, and trauma can usually be identified by history.

How is tinea unguium diagnosed?

A KOH preparation and fungal culture confirms the diagnosis. Sometimes, a nail biopsy is required.

How is tinea unguium treated?

As is the case for tinea capitis, fungal infection of the nail cannot be eradicated with topical therapy; oral anti-fungal agents such as terbinafine (e.g. Lamisil) or itraconazole (e.g. Sporanox) are required for weeks to months, during which time the drug accumulates in the nail. Systemic antifungal agents have side-effects and the risk-benefit must be considered. Monitoring of hepatic enzymes and hematologic parameters is recommended. Since these drugs remain in the nail for months, retreatment should not be considered for six months for fingernails and 12 months for toenails.  Recently, some have proposed laser treatment as an option.

What is the prognosis for tinea unguium?

After a course of treatment, nails will still not appear completely normal. Tinea unguium is difficult to cure, and recurrence is common, especially for toenails.

More on tinea unguium (onychomycosis)

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What is Tinea Pedis?

Tinea pedis, more commonly known as “athlete’s foot,” is a dermatophytic infection of the feet. It occurs in three forms:

Interdigital. This appears as scaling and maceration between the toes. It is the type frequently seen in patient’s with sweaty feet.

Diffuse plantar scaling. This appears as general scaling of the soles and sides of the feet in what has been called a “moccasin’ distribution. It is common in elderly patients. Nail involvement may be present as well.

Vesiculopustular. This form manifests as vesicles and pustules on the insteps of the feet. It is often misdiagnosed, since vesicles and pustules are an uncommon presentation of dermatophytic infections.

With what can tinea pedis  confused?

Maceration alone, without dermatophytic infection, can occur in patient’s with sweaty feet and be confused with interdigital tinea pedis. Diffuse plantar scaling secondary to tinea pedis may be mistaken for dry skin. Contact dermatitis, dyshidrotic eczema, and pustular psoriasis of the palms and soles can mimic vesiculopustular tinea pedis.

See: Tinea Diagnosis, Treatment and Prognosis

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What is Tinea Manuum?

Tinea manuum is dermatophytic infection of the palm. It is relatively uncommon, and almost always occurs in patient’s that also have tinea pedis (athlete’s foot). It usually only involves one hand, giving rise to the “one hand, two feet” syndrome of tinea manuum plus tinea pedis. It appears as diffuse scaling of the palm, usually with a well-demarcated border..

With what can tinea manuum be confused?

Chronic irritant contact dermatitis can also cause scaling of the palm; however, this condition is usually bilateral. Psoriasis can also effect the palms.

See: Tinea Diagnosis, Treatment and Prognosis

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What is Tinea Faciale?

This dermatophytic infection of the face appears typically as a serpiginous, erythemetous rash with a sharply demarcated border.

With what can tinea faciale confused?

Chronic irritant contact dermatitis can also cause scaling on the face, as can seborrheic dermatitis. Tineal faciale may occasionally mimic the rash of a photodermatitis or the butterfly rash of systemic lupus erythematosus.

See: Tinea Diagnosis, Treatment and Prognosis

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