Actinic keratosis (AK): Dr Sarma s simple guide

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Actinic keratosis (AK): Dr Sarma s simple guide Actinic keratosis is a very common lesion that you will see in your day-to-day practice. First, let me explain the name Actinic keratosis. It means keratosis resulting from actinic damage to skin. Skin lesions appear as scaly or crusty patch on the sun-exposed skin. The scale is composed of keratin. Keratosis means abnormal keratin or keratinocytic lesion and Actinic radiation (ultraviolet light from sun or indoor tanning) induces the disease, together is Actinic keratosis (AK). Another common name that is used for actinic keratosis is Solar keratosis, a good name because it means that the keratosis is caused by solar or sun damage. But, there is some problem with this name! Indoor tanning is widely popular, many AK s are may be induced by UV radiation to the skin from tanning. Solar keratosis will be an inappropriate name. Second problem with a name as Solar keratosis is, you may shorten the name as SK, causing a common confusion with Seborrhic keratosis which is commonly called SK. My personal suggestion, stay with Actinic keratosis as the only name and do not use the name Solar keratosis!

It s easy to understand some specifics of AK. Q. Which parts of your body get the most sun? - Face, lips, ears, dorsal hands, forearms, scalp or neck. Most of the AK s are seen in these sites. The sun has several types of ultraviolet (UV) rays. UVA damages the dermal soft tissue leading to wrinkles (solar dermal damage). UVB damages the DNA of the basal keratinocytes leading to mutation and neoplasia. Q. What about people who were exposed to a lot of indoor tanning? - AK can develop in all various site that is exposed to UV rays. Q. What about people with dark skin vs. fair skin? Are they equally prone to develop AK? - No, AK (as well as basal cell carcinoma, squamous cell carcinoma and melanoma) occurs more commonly in the fair-skinned persons exposed to a lot of sun. Higher concentration of melanin in the epidermis of the dark-skinned people offers significant protection from the damage caused by UV radiation reducing incidence of all sun-induced skin cancers including AK. Q. AK s should be multiple lesions. Right? Also, in old people? - Yes, skin is exposed to actinic radiation, so multiple lesions are common. Once you get one AK, usually more will follow. As far as age goes, yes it takes exposure to sun for years before you develop AK. Most of the patients with AK are old. Q. Does bald-headed people gets more AK on head? - Yes, hair protects the scalp from sun. No hair.more sun exposure..more AK! WEAR HAT!! Q. Is AK malignant? - AKs are premalignant lesion. Untreated actinic keratosis may progress to become squamous cell carcinoma in 10-15% cases.

Single or mostly multiple scaly, hyperkeratotic patches or plaques Compact hyperkeratosis, dysplastic basal cells, dermal actinic change

Compact hyperkeratosis, dysplastic basal cells, dermal actinic change

Compact hyperkeratosis

Dysplastic basal cells

Dysplastic squamous cells making abnormal compact keratin on top. Actinic keratosis is a suninduced dysplastic epidermal lesion. Dysplasia starts at the basal layer. Look at the dysplastic basal cells. Dysplastic squamous cells making abnormal compact keratin on top. Dermis shows solar degeneration (solar elastosis) Look at the dysplastic basal cells. Solar degeneration (Bluish color of the upper dermis with irregularly thickened elastic fibers)

Actinic keratosis: Diagnostic findings Compact hyperkeratosis Dysplastic basal cells Actinic dermal change REMEMBER: Do not make a diagnosis of actinic keratosis if hyperkeratosis and actinic dermal change are absent. YOU MUST HAVE ACTINIC DERMAL CHANGE AND ABNORMAL KERATIN (IN THE FORM OF COMPACT HYPERKERATOSIS) BEFORE YOU MAKE A DIAGNOSIS OF ACTINIC KERATOSIS. No hyperkeratosis and no actinic dermal change = No actinic keratosis

Various types of actinic keratosis Hypertrophic: AK with marked hyperkeratosis with acanthotic epidermis. Atrophic: AK with slight hyperkeratosis with atrophic epidermis. Acantholytic: AK with intercelleular clefts or lacunae in the lower epidermal layer due to disrupted intercellular bridges between the dysplasic keratinocytes. Bowenoid: AK with full-thickness dysplasia of the keratinocytes. It essentially means an in-situ or intraepidermal squamous cell carcinoma arising in actinic keratosis. Pigmented: AK with significant melanocytic pigmentation of the keratinocytes. Clinically it may appear as a pigmented skin lesion. Lichenoid: AK with a band-like lymphocytic infiltrate in the papillary dermis.

Actinic keratosis, hypertrophic type Marked hyperkeratosis overlying papillomatous dysplastic epidermal keratinocytes. Actinic dermal degeneration.

Actinic keratosis, atrophic type Thin epidermis with loss of rete ridges (epidermal atrophy). Hyperkeratosis Atypical keratinocytes mostly in the basal layer. Actinic dermal change

Actinic keratosis, acantholytic type Clefts and lacunae between the dysplastic keratincytes near the basal layer due to loss of intercellular bridges between the keratinocytes

Actinic keratosis, Bowenoid type The entire thickness of the epidermis is composed of dysplastic keratinocytes, mimicking the histologic appearance of Bowen's disease or squamous cell carcinoma in situ

Actinic keratosis, lichenoid type In addition to dysplastic keratinocytes there is liquefaction along the basal layer with necrotic keratinocytes and dense bandlike chronic inflammation in the upper dermis

Actinic cheilitis and Cutaneous horn This is actinic keratosis of lip, usually called actinic cheilitis. This is cutaneous horn (cornu cutaneum), a hard keratinous projection above the skin surface. Most commonly, it arises from hypertrophic actinic keratosis.

Let me tell you one more story. We have talked about six different types of actinic keratosis. During my years of practice, I came across another interesting histologic type of AK that is not in any book. So, I decided to call it by a very logical name, Bullous solar keratosis. The Internet Journal of Dermatology ISSN: 1531-3018 Bullous Solar Keratosis Deba P. Sarma M.D. Department of Pathology, Creighton University Medical Center Omaha, NE USA Poonam Sharma M.D Department of Pathology, Creighton University Medical Center Omaha, NE USA Citation: D.P. Sarma, P. Sharma: Bullous Solar Keratosis. The Internet Journal of Dermatology. 2006 Volume 4 Number 1 Keywords: Solar keratosis variant, Bullous actinic keratosis, Bullous solar keratosis, Rare type of actinic keratosis Abstract Two cases of a rare variant of solar keratosis showing subepidermal bulla formation occurring in two elderly males are reported. Various histologic types of solar keratosis are reviewed. Introduction Solar keratoses are common lesions occurring among the middle-aged and older fair-skinned people usually caused by prolonged exposure to sun over many years (1). The lesions are located over the sun-exposed areas, such as, face, scalp, ears, and distal upper extremities. Clinically, several types of solar keratoses have been described, such as, hypertrophic, pigmented, and lichenoid variants. Histologically, at least six variants have been described: hypertrophic, atrophic, Bowenoid, acantholytic, pigmented, and lichenoid. Recently we observed two cases of solar keratoses that on histologic examination revealed subepidermal bulla along with typical epidermal dysplasia and dermal elastosis. We could not uncover any report of such a bullous variant of solar keratosis in the English literature.

Reports of Cases Case 1 A 74-year-old Caucasian man presented with an ill-defined 1-cm keratotic lesion of his forehead. A shave biopsy showed (Figs.1 and 2) hyperkeratosis, parakeratosis, and moderate dysplasia of the keratinocytes. Dermis showed solar elastosis and nonspecific focal chronic inflammation. The epidermis was raised upward by a subepidermal bulla containing eosinophilic acellular fluid. The basal lamina if the epidermis was intact. The epidermal cells overlying the bulla did not show any acantholysis. We interpreted the lesion as a bullous variant of solar keratosis. Figure 1: Epidermis shows hyperkeratosis, parakeratosis, and dysplasia of. keratinocytes. Note the subepidermal bulla. Dermis shows solar elastosis and chronic inflammation.

Figure 2: Higher magnification shows dysplastic keratinocytes and subepidermal bulla containing acellular eosinophilic material. Additional clinical history did not disclose any other bullous disease or any history of recent topical treatment of the lesion prior to biopsy.

Case 2 A shave biopsy of a 5mm keratotic lesion of the right distal arm of a 72-year-old Caucasian man showed an acellular subepidermal bulla along with epidermal dysplasia and marked solar elastosis. There was no clinical evidence of any bullous disease. Discussion Clinically, solar keratoses may be diagnosed as a hypertrophic, pigmented, lichenoid, or cutaneus horn type. Histologically, at least six variants of solar keratoses have been observed (2). In hypertrophic solar keratosis, there is marked hyperkeratosis and parakeratosis overlying papillomatous dysplastic epidermal keratinocytes. Atrophic solar keratosis shows thin epidermis with loss of rete ridges, minimal hyperkeratosis, and atypical keratinocytes mostly in the basal layer. In the Bowenoid type of solar keratosis, the entire thickness of the epidermis is composed of dysplastic keratinocytes, mimicking the histologic appearance of Bowen's disease or squamous cell carcinoma in situ. In acantholytic type of solar keratosis, there are clefts and lacunae between the dysplastic keratincytes near the basal layer due to loss of intercellular bridges between the keratinocytes. The pigmented type of actinic keratosis, the basal as well as atypical keratinocytes show large amount of melanin pigment. In lichenoid type of solar keratosis, in addition to dysplastic keratinocytes there is liquefaction along the basal layer with necrotic keratinocytes and dense band-like chronic inflammation in the upper dermis. We are documenting the two cases of bullous variant of solar keratosis, where each lesion shows the histologic appearance of a solar keratosis along with a subepidermal bulla formation. This picture is different from the acantholytic variant of solar keratosis because there is no acantholysis, clefts, or lacunae observed in the epidermis in our cases. Subepidermal bulla seen in bullous pemphigoid usually shows eosinophils and lymphocytes in the bulla and in the dermis. Clinically, the lesions appear as multiple tense bullae of varying size in the elderly. The patients with subepidermal bullae of dermatitis herpetiformis present with intensely pruritic lesions. The skin biopsy usually shows acute neutrophilic papillitis and subepidermal bulla containing neutrophils. The patients with porphyria cutanea tarda may have subepidermal bulla with no inflammation, intact dermal papillae at the base of the bulla, and hyalinization of the dermal capillary walls. Our patients did not have any clinical evidence of any bullous disease. We believe that our two cases represent a rare histologic variant of solar keratosis that may be called bullous solar keratosis. References 1. Weedon D. Skin Pathology, 2nd Ed, Edinburgh: Churchill Livingstone, 2002, pp 761-762. 2. Elder DE, Editor. Lever's Histopathology of the Skin, 9th Ed, Philadelphia: Lippincott Williams and Wilkins, 2005, pp 820-824. D. P. Sarma & P. Sharma : Bullous Solar Keratosis. The Internet Journal of Dermatology. 2006 Volume 4 Number 1.