ICD-10-CM Diagnosis Code L57.0 - Actinic keratosis (original) (raw)

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  6. 2026 ICD-10-CM Code L57.0

Actinic keratosis

ICD-10-CM Code:

L57.0

ICD-10 Code for:

Actinic keratosis

Is Billable?

Yes - Valid for Submission

Chronic Condition Indicator: [1]

Not chronic

Code Navigator:

L57.0 is a billable diagnosis code used to specify a medical diagnosis of actinic keratosis. The code is valid during the current fiscal year for the submission of HIPAA-covered transactions from October 01, 2025 through September 30, 2026.

  1. Code Information
  2. Approximate Synonyms
  3. Clinical Classification
  4. Clinical Information
  5. Tabular List of Diseases and Injuries
  6. Index to Diseases and Injuries References
  7. Diagnostic Related Groups Mapping
  8. Convert to ICD-9 Code
  9. Patient Education
  10. Other Codes Used Similar Conditions
  11. Code History

The following list of clinical terms are approximate synonyms, alternative descriptions, or common phrases that might be used by patients, healthcare providers, or medical coders to describe the same condition. These synonyms and related diagnosis terms are often used when searching for an ICD-10 code, especially when the exact medical terminology is unclear. Whether you're looking for lay terms, similar diagnosis names, or common language alternatives, this list can help guide you to the correct ICD-10 classification.

Clinical Classifications group individual ICD-10-CM diagnosis codes into broader, clinically meaningful categories. These categories help simplify complex data by organizing related conditions under common clinical themes.

They are especially useful for data analysis, reporting, and clinical decision-making. Even when diagnosis codes differ, similar conditions can be grouped together based on their clinical relevance. Each category is assigned a unique CCSR code that represents a specific clinical concept, often tied to a body system or medical specialty.

CCSR Code: SKN007

Inpatient Default: Y - Yes, default inpatient assignment for principal diagnosis or first-listed diagnosis.

Outpatient Default: Y - Yes, default outpatient assignment for principal diagnosis or first-listed diagnosis.

an autosomal dominantly inherited skin disorder characterized by warty malodorous papules that coalesce into plaques. it is caused by mutations in the atp2a2 gene encoding serca2 protein, one of the sarcoplasmic reticulum calcium-transporting atpases. the condition is similar, clinically and histologically, to benign familial pemphigus, another autosomal dominant skin disorder. both diseases have defective calcium pumps (calcium-transporting atpases) and unstable desmosomal adhesion junctions (desmosomes) between keratinocytes.

group of mostly hereditary disorders characterized by thickening of the palms and soles as a result of excessive keratin formation leading to hypertrophy of the stratum corneum (hyperkeratosis).

an autosomal dominant disorder characterized by a widely distributed, well-demarcated hyperkeratosis of the palms and soles. there is more than one genotypically distinct form, each of which is clinically similar but histologically distinguishable. diffuse palmoplantar keratoderma is distinct from palmoplantar keratoderma (keratoderma, palmoplantar), as the former exhibits autosomal dominant inheritance and hyperhidrosis is frequently present.

an autosomal dominant hereditary skin disease characterized by epidermolytic hyperkeratosis that is strictly confined to the palms and soles. it has been associated with mutations in the gene that codes for keratin-9.

any horny growth such as a wart or callus.

white or pink lesions on the arms, hands, face, or scalp that arise from sun-induced dna damage to keratinocytes in exposed areas. they are considered precursor lesions to superficial squamous cell carcinoma.

benign eccrine poromas that present as multiple oval, brown-to-black plaques, located mostly on the chest and back. the age of onset is usually in the fourth or fifth decade.

a white patch seen on the oral mucosa. it is considered a premalignant condition and is often tobacco-induced. when evidence of epstein-barr virus is present, the condition is called hairy leukoplakia (leukoplakia, hairy).

rare, autosomal recessive disorder occurring between the first and fifth years of life. it is characterized by palmoplantar keratoderma with periodontitis followed by the premature shedding of both deciduous and permanent teeth. mutations in the gene for cathepsin c have been associated with this disease.

a group of disorders which have in common elevations of tyrosine in the blood and urine secondary to an enzyme deficiency. type i tyrosinemia features episodic weakness, self-mutilation, hepatic necrosis, renal tubular injury, and seizures and is caused by a deficiency of the enzyme fumarylacetoacetase. type ii tyrosinemia features intellectual disability, painful corneal ulcers, and keratoses of the palms and plantar surfaces and is caused by a deficiency of the enzyme tyrosine transaminase. type iii tyrosinemia features intellectual disability and is caused by a deficiency of the enzyme 4-hydroxyphenylpyruvate dioxygenase. (menkes, textbook of child neurology, 5th ed, pp42-3)

a type ii keratin found predominantly expressed in the terminally differentiated epidermis of palms and soles. mutations in the gene for keratin 9 are associated with keratoderma, palmoplantar, epidermolytic.

a rare autosomal dominant disorder with high penetrance that affects the limbal conjunctiva. it is almost exclusively encountered in native americans belonging to the haliwa-saponi tribe of northeastern north carolina and is caused by a duplication in chromosome 4q35. it is characterized by the presence of frequently bilateral, elevated epithelial dyskeratotic plaques in the limbal conjunctiva. there is prominent inflammation in substantia propria. epithelial dysplasia is absent.

abnormal cell keratinization.

actinic keratosis that develops in the skin of the eyelid.

a benign eyelid tumor that presents with asymptomatic papules and is characterized by the proliferation of squamous and basaloid cells of the follicular infundibulum.

limiting self-care adls or severe impact on age-appropriate normal daily activity (pediatric)

a rare autosomal dominant disorder with high penetrance that affects the limbal conjunctiva or oral mucosa. it is almost exclusively encountered in native americans belonging to the haliwa-saponi tribe of northeastern north carolina and is caused by a duplication in chromosome 4q35. it is characterized by the presence of elevated epithelial dyskeratotic plaques in the limbal conjunctiva or oral cavity. epithelial dysplasia is absent.

a rare skin disorder with brownish-purple, thick scaly papules or small nodules arranged in a linear or reticulate pattern on the trunk and limbs. many cases are associated with seborrhoeic dermatitis- or rosacea-like lesions on the face. it is distinguished from lichen planus by the absence of pruritus, a lack of response to a topical or systemic corticosteroid and the presence of focal parakeratosis in histological samples.

a rare autosomal dominant disorder with high penetrance that affects the oral mucosa. it is almost exclusively encountered in native americans belonging to the haliwa-saponi tribe of northeastern north carolina and is caused by a duplication in chromosome 4q35. it is characterized by the presence of elevated epithelial dyskeratotic plaques in the oral mucosa. epithelial dysplasia is absent.

a rare genetic skin keratinization disorder with an autosomal dominant mode of inheritance. it is characterized by numerous flesh-colored warty papules on the back of the hands, medial aspect of the feet, knees, and elbows.

a precancerous lesion of the skin composed of atypical keratinocytes. it is characterized by the presence of thick, scaly patches of skin. several histologic variants have been described, including atrophic, acantholytic, and hyperkeratotic variants.

a hyperkeratotic skin lesion that occurs in patients who have been exposed to arsenic.

an autosomal dominant inherited chronic skin disorder caused by mutations in the atp2a2 gene. it is characterized by the development of yellow-brown keratotic skin papules in the neck, ears, forehead, chest, back and groin. it is associated with fragility of the free margins of the nails.

human dkc1 wild-type allele is located in the vicinity of xq28 and is approximately 15 kb in length. this allele, which encodes h/aca ribonucleoprotein complex subunit 4 protein, plays a role in the stabilization and maintenance of telomerase and h/aca small nucleolar rna ribonucleoprotein biogenesis. mutation of the gene is associated with both hoyeraal-hreidarsson syndrome and x-linked dyskeratosis congenita.

dyskeratosis congenita caused by autosomal dominant mutation(s) in the terc gene, encoding telomerase rna component.

dyskeratosis congenita caused by mutation(s) in the tert gene, encoding telomerase reverse transcriptase.

dyskeratosis congenita caused by autosomal dominant mutation(s) in the tinf2 gene, encoding terf1-interacting nuclear factor 2. mutations in tinf2 may also lead to another phenotype known as revesz syndrome (dyskeratosis congenita, autosomal dominant 5).

dyskeratosis congenita caused by mutation(s) in the acd gene, encoding adrenocortical dysplasia protein homolog.

dyskeratosis congenita caused by autosomal recessive mutation(s) in the nop10 gene, encoding h/aca ribonucleoprotein complex subunit 3.

dyskeratosis congenita caused by autosomal recessive mutation(s) in the nhp2 gene, encoding h/aca ribonucleoprotein complex subunit 2.

dyskeratosis congenita caused by autosomal recessive mutation(s) in the wrap53 gene, encoding telomerase cajal body protein 1.

dyskeratosis congenita caused by mutation(s) in the rtel1 gene, encoding regulator of telomere elongation helicase 1.

dyskeratosis congenita caused by autosomal recessive mutation(s) in the parn gene, encoding poly(a)-specific ribonuclease parn.

a rare genetic disorder characterized by nail dystrophy, reticulated skin pigmentation especially on the neck and chest, and oral leukoplakia. in about half the cases mutations in the tert, terc, dkc1, or tinf2 genes are identified. patients are at an increased risk of developing bone marrow failure, myelodysplastic syndrome, leukemia, or cancer, especially in the head and neck region.

an autosomal dominant inherited skin disorder caused by mutations in the krt1 and krt10 genes. it is manifested at birth and is characterized by generalized erythema, skin blisters and skin fragility.

actinic keratosis that develops in the skin of the external ear.

a benign skin neoplasm that arises from the eyelid. it is characterized by the intraepidermal proliferation of basaloid keratinocytes, acanthosis, hyperkeratosis, and cysts formation.

present

limiting self-care adls

a rare genetic disorder with an autosomal dominant pattern of inheritance with variable penetrance. it was initially described among native americans belonging to the haliwa-saponi tribe of northeastern north carolina. it is caused by a duplication of chromosomal dna at 4q35. clinical signs present in early childhood and include asymptomatic plaques of the epibulbar conjunctivae and oral mucosa. clinical progression of the plaques to malignancy has not been reported.

an autosomal dominant inherited disorder characterized by thickened and spongy oral mucosa with a white tint. it may affect other anatomic sites as well.

a disorder characterized by a thickening of the outer layer of the skin.

hypertrophy of the outermost layer of the epidermis. it may be caused by physical or chemical irritants, irradiation, infection, or neoplastic processes.

a morphologic finding indicating increased keratin formation, preservation of the nuclei in the superficial cells, and absence of the stratum granulosum in a skin or squamous mucosa sample.

a finding that generally has features of hyperplasia and hyperkeratosis.

seborrheic keratosis that arises from follicular structures in the skin. it presents as a solitary nodule in the skin and is characterized by the presence of prominent squamous eddies.

keratin, type i cytoskeletal 10 (584 aa, ~59 kda) is encoded by the human krt10 gene. this protein plays a role in the structure of intermediate filaments.

excessive growth of keratin on the skin.

a very common, non-neoplastic dermatologic disorder characterized by keratinization of hair follicles of the skin. it manifests as small, rough folliculocentric keratotic papules, usually in the outer-upper arms and thighs. it affects children and adolescents and usually improves with age.

human krt1 wild-type allele is located within 12q12-q13 and is approximately 6 kb in length. this allele, which encodes keratin, type ii cytoskeletal 1 protein, plays a role in the regulation of epidermal development. mutation of the gene is associated with bullous congenital ichthyosiform erythroderma, ichthyosis hystrix curth-macklin type, palmoplantar keratoderma non-epidermolytic, ichthyosis annular epidermolytic and palmoplantar keratoderma striate type 3.

human krt10 wild-type allele is located in the vicinity of 17q21 and is approximately 4 kb in length. this allele, which encodes keratin, type i cytoskeletal 10 protein, is involved in the intermediate filament structure of terminally differentiated epidermal cells. mutations in this gene are associated with epidermolytic hyperkeratosis, ichthyosis with confetti, and cyclic ichthyosis with epidermolytic hyperkeratosis.

a premalignant pathologic process that affects the mucosal epithelium of the larynx. it appears as a localized or diffuse white patch on the laryngeal mucosa. morphologically it is characterized by the pathologic production of keratin in the mucosal epithelial surface with or without epithelial atypia. it may progress to or co-exist with invasive squamous cell carcinoma.

a benign intraepidermal squamoproliferative neoplasm characterized by irregular acanthosis, hyperkeratosis, parakeratosis, and prominent chronic inflammation.

an epithelial hyperplasia of the oral cavity mucosa associated with epstein-barr virus and found almost exclusively in persons with hiv infection. the lesion consists of a white patch that is often corrugated or hairy.

a white patch or plaque on the oral mucosa that cannot be characterized clinically or pathologically as any other disease. the diagnosis of leukoplakia is one of exclusion; other conditions such as candidiasis, lichen planus, leukoedema, etc., must be ruled out before a diagnosis of leukoplakia can be made. leukoplakia may be a premalignant condition.

the formation of an epidermal layer which lacks nuclei during normal keratinization.

abnormal retention of nuclei, and the resulting incomplete keratinization, of epithelial cells in the stratum corneum layer of the skin.

a clonal proliferation of abnormal keratinocytes characterized by the development of localized or multiple atrophic skin patches surrounded by an annular keratotic ring called cornoid lamella.

a hyperkeratotic skin lesion that occurs in patients with a history of prolonged exposure to psoralen and ultraviolet a (puva) therapy.

an autosomal dominant form of dyskeratosis congenita, caused by mutation(s) in the tinf2 gene, encoding terf1-interacting nuclear factor 2. it is a fatal disease associated with exudative retinopathy and bone marrow failure.

a common benign neoplasm usually affecting older individuals. the lesions usually arise in the trunk, head and neck, but they can occur on any skin surface other than the palms, soles, and mucosal surfaces. they appear as flat-based papules or plaques. histologically, there is intraepidermal proliferation of basaloid keratinocytes, acanthosis, hyperkeratosis, and cysts formation.

a premalignant pathologic process that affects the oral mucosa. it is associated with the use of smoked tobacco. it appears as white lesions on the oral mucosa. morphologically it is characterized by the pathologic production of keratin in the mucosal epithelial surface with or without epithelial atypia. it may reverse with the cessation of tobacco use.

hyperparakeratosis of the oral mucosa caused by chronic tobacco use. it manifests as oral leukoplakia.

an inherited disorder characterized by the development of keratotic lesions on the palms and soles. it appears in childhood as redness on the palms and soles which progresses to well demarcated, thickened, yellowish and waxy lesions.

seborrheic keratosis that arises from follicular structures in the vulva. it is characterized by the presence of prominent squamous eddies.

a benign squamous neoplasm that arises from the vulva. it is characterized by the proliferation of the basal cells in the squamous epithelium, acanthosis, hyperkeratosis, and cysts formation.

a rare, usually solitary, benign epithelial tumor of the skin that appears to arise from a hair follicle. it usually develops in the head and neck region as a nodular lesion with a central keratotic plug.

dyskeratosis congenita inherited in an x-linked recessive pattern. it is caused by mutations in the dkc1 gene.

actinic keratosis characterized by the presence of acantholysis of the dysplastic keratinocytes.

a precancerous lesion of the skin composed of atypical keratinocytes. it is characterized by the presence of thick, scaly patches of skin. several histologic variants have been described, including atrophic, acantholytic, hypertrophic, proliferative, lichenoid, bowenoid, and pigmented variants.

actinic keratosis characterized by the presence of marked epidermal atrophy.

actinic keratosis characterized by the presence of usually focal, nearly full-thickness squamous atypia.

actinic keratosis characterized by the presence of epidermal hyperplasia, parakeratosis, and orthokeratosis.

actinic keratosis characterized by the presence of a band-like chronic inflammatory infiltrate in the papillary dermis and vacuolar changes in the basal keratinocytes.

human mbtps2 wild-type allele is located in the vicinity of xp22.12 and is approximately 46 kb in length. this allele, which encodes membrane-bound transcription factor site-2 protease protein, is involved in intramembrane proteolysis of membrane bound transcription factors, such as sterol regulatory element-binding proteins (srebps). mutation of the gene is associated with x-linked olmsted syndrome, x-linked keratosis follicularis spinulosa decalvans, osteogenesis imperfecta 19 and ifap (ichthyosis follicularis, atrichia, and photophobia) syndrome 1 with or without bresheck (brain anomalies, retardation, ectodermal dysplasia, skeletal malformations, hirschsprung disease, ear/eye anomalies, cleft palate/cryptorchidism, and kidney dysplasia/hypoplasia) syndrome.

a benign epithelial proliferation with papillary formations that arises from the distal nail matrix. in some cases, multinucleated keratinocytes are present. it is usually located in fingernails.

actinic keratosis characterized by the presence of increased melanin pigmentation in the basal keratinocytes.

actinic keratosis characterized by the presence of dermal projections of nested atypical keratinocytes and dense dermal inflammation.

The following annotation back-references for this diagnosis code are found in the injuries and diseases index. The Index to Diseases and Injuries is an alphabetical listing of medical terms, with each term mapped to one or more ICD-10-CM code(s).

References found for this diagnosis code in the External Cause of Injuries Index:

Below are the ICD-9 codes that most closely match this ICD-10 code, based on the General Equivalence Mappings (GEMs). This ICD-10 to ICD-9 crosswalk tool is helpful for coders who need to reference legacy diagnosis codes for audits, historical claims, or approximate code comparisons.

ICD-9-CM: 702.0

This is a direct match with no additional mapping qualifiers. The absence of a flag generally means the mapping is considered exact or precise. In other words, the ICD-10 code maps cleanly to the ICD-9 code without qualification, approximation, or needing multiple codes.

Skin Conditions

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Ultraviolet (UV) rays are an invisible form of radiation. They can pass through your skin and damage your skin cells. Sunburns are a sign of skin damage. Suntans aren't healthy, either. They appear after the sun's rays have already killed some cells and damaged others. UV rays can cause skin damage during any season or at any temperature. They can also cause eye problems, wrinkles, skin spots, and skin cancer.

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Check your skin regularly for changes in the size, shape, color, or feel of birthmarks, moles, and spots. Such changes are a sign of skin cancer.

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