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Experts don't completely understand what causes a seborrheic keratosis. This type of skin growth does tend to run in families, so there is likely an inherited tendency. If you've had one seborrheic keratosis, you're at risk of developing others.


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An actinic keratosis (ak-TIN-ik ker-uh-TOE-sis) is a rough, scaly patch on the skin that develops from years of sun exposure. It's often found on the face, lips, ears, forearms, scalp, neck or back of the hands.

Also known as a solar keratosis, an actinic keratosis grows slowly and usually first appears in people over 40. You can reduce your risk of this skin condition by minimizing your sun exposure and protecting your skin from ultraviolet (UV) rays.

If treated early, actinic keratosis can be cleared up or removed. If left untreated, some of these spots might progress to squamous cell carcinoma. This is a type of cancer that usually isn't life-threatening if detected and treated early.

For many people, keratosis pilaris goes away with time, even if you opt not to treat it. Clearing tends to happen gradually over many years. There is no way to know who will see keratosis pilaris clear.

In most cases, a dermatologist can tell if your skin growth is a seborrheic keratosis by looking at it. Sometimes, a seborrheic keratosis can look like a skin cancer. If it does, the dermatologist will remove the growth so that it can be looked at under a microscope. This is the only way to tell for sure whether a growth is skin cancer.

Cryosurgery: The dermatologist applies liquid nitrogen, a very cold liquid, to the growth with a cotton swab or spray gun. This destroys the growth. The seborrheic keratosis tends to fall off within days. Sometimes a blister forms under the seborrheic keratosis and dries into a scab-like crust. The crust will fall off.

After removal of a seborrheic keratosis, the skin may be lighter than the surrounding skin. This usually fades with time. Sometimes it is permanent. Most removed seborrheic keratoses do not return. But a new one may occur elsewhere.

Actinic keratosis develops slowly. It most likely appears on areas of skin often exposed to the sun. These can include the face, ears, bald scalp, neck, backs of hands and forearms, and lips. It tends to lie flat against the skin of the head and neck, but appears as a bump on arms and hands. The base of an actinic keratosis may be light or dark, tan, pink, red, or a combination of these. Or it may be the same color as the skin. The scale or crust may be horny, dry, and rough. In some cases, it may itch or have a prickly or sore feeling.

Healthcare providers can often diagnose an actinic keratosis by looking at and feeling the area on your skin. But sometimes an actinic keratosis can be hard to tell apart from skin cancer. Your healthcare provider might remove the area of skin to have it checked under a microscope. This is known as a skin biopsy.

Actinic keratosis (AK) is a chronic skin disease in which clinical and subclinical cutaneous lesions coexist on sun-exposed areas such as the head and neck region and the extremities. The high prevalence of AK means the disease burden is substantial, especially in middle-aged and elderly populations. Evidence indicates that AK may progress into invasive cutaneous squamous cell carcinoma, so the European guidelines recommend treatment of any AK regardless of clinical severity. Given the aging population and therefore the increasing incidence of AK and cutaneous field carcinogenesis, further updates on the long-term efficacy of current therapies and new investigational agents are critical to guide treatment choice. Patients often have difficulty adequately applying topical treatments and coping with adverse local skin reactions, leading to less than optimum treatment adherence. The development of associated local skin symptoms and cosmetic outcomes for the area of interest are also relevant to the choice of an appropriate therapeutic strategy. Treatment is always individually tailored according to the characteristics of both patients and lesions. This review focuses on the therapeutic approaches to AK and illustrates the currently available home-based and physician-managed treatments.

EMA has completed its review of Picato (ingenol mebutate), a gel for treating the skin condition actinic keratosis, and concluded that the medicine may increase the risk of skin cancer and that its risks outweigh its benefits.

The review looked at results of a study comparing Picato with imiquimod (another medicine for actinic keratosis). After 3 years, 6.3% of patients treated with Picato (15 out of 240 patients) developed skin cancer, particularly squamous cell carcinoma, in the treated skin area compared with 2% of patients treated with imiquimod (5 out of 244 patients).

Picato was available as a gel which was applied to skin areas affected by actinic keratosis. It was used when the outer layer of the affected skin was not thickened or raised. Actinic keratosis is caused by too much sunlight exposure and can turn into skin cancer.

There are no specific tests for keratosis pilaris. The doctor will be able to make a diagnosis based on the typical appearance. There are other conditions that can sometimes look similar to keratosis pilaris and a skin biopsy might help the diagnosis.

Actinic keratosis Actinic keratosis is usually considered to be a pre-cancer. It is often treated because it might turn into squamous cell skin cancer. But because this risk is low, treatments are generally aimed at avoiding scars or other disfiguring marks as much as possible.

Actinic keratosis is often treated with either cryotherapy or topical creams or gels such as fluorouracil (5-FU), imiquimod, or diclofenac. These treatments destroy the affected area of the epidermis, the outermost layer of the skin, which usually cures actinic keratosis.

The cause of keratosis pilaris is not fully understood, but it is thought to have a genetic association with autosomal dominant inheritance. Correlations have been made with mutations in filaggrin (a key protein in skin barrier function).

Keratosis pilaris may occasionally be associated with redness and pigmentation of the skin of the cheeks (erythromelanosis folllicularis facei et coli and keratosis pilaris rouge), loss of eyebrow hair (ulerythema ophryogenes), and small atrophic areas over the cheeks (atrophoderma vermiculatum).

There is no cure for keratosis pilaris, however, it often clears up during adult life. This is because adults tend to be better at managing the skin condition with the measures discussed above. Any atrophy or scarring with hair loss may be permanent.

Keratosis pilaris is a common, mostly harmless skin condition that causes small, rough, white or reddish bumps or patches on the skin. While it can occur at any age, keratosis pilaris most commonly affects children and adolescents. The symptoms often improve and then disappear entirely early in adult life.

The term actinic keratosis (AK) was coined in 1958 and means literally thickened scaly growth (keratosis) caused by sunlight (actinic). The condition is also known as solar keratosis.

Actinic keratosis is seen most commonly in fair-skinned people in areas of long-term sun exposure caused by UV rays - for example, using tanning beds. Although the condition is very similar to Bowen's disease or carcinoma in situ, most lesions do not progress to malignancy. However, recognition and simple treatment help to prevent progression.

Diagnosis of actinic keratosis is usually clinical, ideally with the help of a dermatoscope. Confocal laser microscopy and optical coherence tomography can also help in diagnosis. Skin biopsy is used where there are features which are high risk for malignant change.

PPKS2 is characterized by linear hyperkeratosis of the palms, which is particularly evident in affected individuals who perform manual labor. Hyperkeratosis of the soles primarily involves pressure points, and diffuse background palmoplantar thickening may also be present. (Armstrong et al., 1999; Whittock et al., 1999).

Whittock et al. (1999) studied a 45-year-old male construction worker with a 20-year history of dry flaking skin on his palms and soles that gradually became thicker, exacerbated by heavy manual labor. Examination revealed hyperkeratosis with a marked linear appearance on his right palm, whereas the hyperkeratosis was more diffuse on his left palm and was more focal on the soles of his feet. The proband's mother had signs of focal plantar keratoderma, but her palms showed only mild skin dryness, and the proband's 8-year-old son showed some hyperkeratosis on the plantar aspect of the right great toe. The proband had 3 unaffected sibs and an unaffected 14-year-old daughter. Light microscopy of lesional palmar skin showed acanthosis and hyperkeratosis, with widening of keratinocyte intracellular spaces throughout the spinous layer. Ultrastructurally, desmosomes were smaller and fewer compared to site-matched control skin, and the attachment of the keratin filament network to the plasma membrane was perturbed. In addition, the keratin filaments were condensed and compacted in a perinuclear distribution. 041b061a72


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