Introduction
Actinic keratosis (AK) is one of the most common dermatological diseases. It is a benign intraepidermal proliferation that is a precancerous condition known as squamous cell carcinoma in situ (SCC in situ). It affects around 25% of the adult population, especially elderly people with a prevalence of 4.6% and 14.57% in the age group of 60–69 years and in those older than 80 years, respectively [1, 2]. Clinically, AKs are characterized by the presence of hyperkeratosis and erythema. The main triggering factor of AK is chronic UV-light exposure, thus, it is commonly located on chronically sun-exposed areas such as the face, scalp, neck, and dorsum of the hands [3, 4]. The literature reports that the risk of progression of AK to invasive SCC (iSCC) varies between 0.025% and 16% per year [5, 6] and about 40.7% within 5 years in case of previous cutaneous SCC (cSCC) [5–7]. Lesion induration, bleeding, pain, and enlargement of the lesion in thickness and diameter suggest transforming AK into iSCC [8]. AK lesions are also accompanied by “field cancerization”, an area of tumorigenesis defined as an area of subclinical changes in the periphery of clinically visible AKs that display genetic changes similar to those found in AK lesions [9]. Since AK is a precancerous condition, it is important to implement treatment early enough to prevent cancer progression.
Treatment methods for actinic keratosis
The treatment of AK should be individualized, taking into consideration patient safety, treatment efficacy, the number of AK lesions, comorbidities, patient preferences, and physician experience [10]. Primary prevention, including patient education, sun protection, and patient supervision, is essential in preventing AK and non-melanocytic skin cancers (NMSC). AK treatment can be categorized as lesion-directed or field-directed. Lesion-directed treatments target individual AKs, while field-directed treatments address multiple, widespread, and subclinical AKs within “field cancerization” [3, 11]. Lesion-directed therapy is suitable for fewer than five AK lesions, mild to moderate photodamage, and a low risk of developing NMSC. Field-directed therapy is recommended for more than five AK lesions, severely UV-damaged skin, and a high risk of developing NMSC. Both approaches include topical treatments (imiquimod, 5-fluorouracil, diclofenac) and physical methods (cryotherapy, photodynamic therapy, chemical peels, laser therapy, electrocoagulation, curettage).
Sun protection
All relevant existing guidelines, including those from the Polish Society of Dermatology (2014), the British Association of Dermatology (BAD, 2017), and the American Academy of Dermatology (AAD, 2021), emphasize the significant role of sun protection in preventing AK and NMSC [4, 12–15].
Topical treatment methods
Imiquimod
Imiquimod (IMI) is a toll-like receptor-7 agonist (TLR-7) that acts as a topical immune response modifier. According to the European Guidelines from 2024, 5% or 3.75% IMI should be offered for the treatment of single or multiple AKs, particularly non-hyperkeratotic, non-hypertrophic, palpable AKs located on the face and scalp, along with field cancerization [3]. Overall, IMI has a clearance rate ranging from 56.3% for the 5% concentration over 4 weeks to 63.3% for the 5% concentration over 16 weeks. The 3.75% concentration is associated with a lower clearance rate; two 2-week cycles separated by a 2-week break resulted in a complete clearance rate of 35.6%, with a median percentage of lesion reduction of 81.8% [16].
5-fluorouracil
5-fluorouracil (5-FU), a fluorinated pyrimidine derivative, is an anti-metabolite drug that inhibits DNA synthesis by blocking thymidylate synthase and uracil phosphatase, leading to RNA with abnormal structure. This mechanism impairs growth, causes damage, and induces apoptosis, especially in rapidly dividing cells located in the bone marrow, skin, and mucous membranes. According to European guidelines, topical 5-FU should be offered for the treatment of single or multiple AK lesions and field cancerization [3, 4, 11]. The available 5-FU formulations include 5% 5-FU cream, 4% fluorouracil in aqueous cream, 0.5% fluorouracil in a 10% salicylic acid solution (10% SA), and 5% fluorouracil plus 0.005% calcipotriol cream [3]. The largest placebo-controlled randomized trial demonstrated that treating AKs on the face with 5% 5-FU, applied twice daily for 4 weeks, is more effective than a placebo in achieving complete AK clearance at 6 months (38% vs. 17%; p < 0.01) [17]. Four placebo-controlled randomized controlled trials (RCTs) evaluated the efficacy and safety of 0.5% 5-FU, indicating that the lower concentration of 5-FU is more effective than a placebo for the complete clearance of AKs [18–21].
A new development in topical treatment involves the combination of 5% 5-FU with 0.005% calcipotriol. In a randomized, double-blind clinical trial involving 131 participants, Cunningham et al. compared the effectiveness and safety of 5% 5-FU combined with 0.005% calcipotriol ointment to 5% 5-FU alone. The drug was applied topically twice daily for 4 consecutive days for the field treatment of AKs and the treatment resulted in a mean reduction in the number of AKs by 87.8% (5-FU + calcipotriol) versus 26.3% (5-FU alone) on the face, 76.4% vs. 5.7% on the scalp, 68.8% vs. 9.6% on the right upper extremity, and 79% vs. 16.3% on the left upper extremity by week 8 (p < 0.0001 for all anatomical sites) [22].
Another topical combination is 0.5% 5-FU with 10% SA. Field-directed therapy of AKs on the face and scalp areas with 0.5% 5-FU plus 10% SA once daily for 12 weeks led to higher complete clearance rates in 188 subjects in a randomized, vehicle-controlled phase III trial (49.5% vs. 18.2%, respectively) [23].
Interestingly, Gupta et al. performed a network meta-analysis of the outcome of ‘participant complete clearance’ in non-immunosuppressed participants for eight interventions for AK. According to the study, the best ‘participant complete clearance’ rates were achieved with 0.5% or 5.0% 5-FU. This was followed by ALA-PDT, which showed similar results to 5% IMI, ingenol mebutate (IMB) 0.015–0.05%, and MAL-PDT. Cryotherapy came next, followed by diclofenac 3% in 2.5% hyaluronic acid [24].
Diclofenac
Diclofenac is a nonsteroidal anti-inflammatory drug (NSAID) that inhibits the cyclooxygenase-2 enzyme (COX-2), which is often overexpressed in cancerous tumours. This inhibition results in decreased synthesis of prostaglandin E2, exerting anti-inflammatory, anti-angiogenic, and pro-apoptotic effects [25]. Diclofenac 3% gel with 2.5% sodium hyaluronate (2.5% HA) is approved for treating clustered AK and field cancerization associated with AK. Nelson et al. reported a complete clearance response of 41% in patients treated with diclofenac 3% gel applied twice daily for 90 days [26, 27]. Kose et al. conducted a randomized comparative open-label study with 49 patients diagnosed with AK [28]. Of these, 24 patients applied 3% diclofenac gel once daily to their lesions, while the remaining 25 patients were treated with 5% IMI cream three times a week for 12 weeks and there were no significant differences between the two groups (p > 0.05) with a good tolerance and safety profile [29, 30]. The drug is generally safe for elderly patients. However, caution is advised for patients using NSAIDs in combination with systemic corticosteroids due to a higher risk of upper gastrointestinal bleeding thus it is contraindicated in cases of peptic ulcer disease or in patients with a history of gastrointestinal bleeding [31].
Other topical drugs
Ingenol mebutate (IMB), a drug of plant origin that was once effectively used to treat AKs in the West, had its marketing authorization withdrawn by the European Medicines Agency’s (EMA) Pharmacovigilance Risk Assessment Committee in the European Union. Reports indicated that after 3 years, the incidence of skin cancer in areas treated with IMB was more than three times higher compared to treatment with IMI (6.3% vs. 2%, respectively). The drug was completely removed from the market in the US by the end of 2020 [9, 30].
Tirbanibulin is a non-adenosine triphosphate competitive inhibitor of Src kinase, which inhibits tubulin polymerization in actively dividing cells. Src kinase is increasingly expressed in AK and appears to play a crucial role in its progression to cSCC [31]. Tirbanibulin 1% cream was approved for the topical treatment of AK on the face or scalp in adults in the EU in July 2021. However, it is not yet available in Poland. European specialists recommend tirbanibulin 1% ointment for the treatment of both single or multiple AKs and for field cancerization treatment of the face and scalp [3, 4, 11].
Resiquimod is a TLR7/8 agonist that activates dendritic cells and promotes cytokine release. It is cited in European guidelines as a promising option for the topical treatment of AK [3]. Resiquimod is available in four concentrations, with the highest efficacy observed when applied three times weekly for 4 weeks. According to a study by Stockfleth et al. involving 217 participants, complete clinical clearance was achieved in 56% to 85% cases [32].
Physical methods of treatment
Cryotherapy
Cryotherapy is a popular outpatient treatment for AK due to its cost-effectiveness, widespread availability, and patient tolerance. According to the 2024 European Guidelines, it should be regarded as a first-line standard treatment for solitary AK [3]. There are two methods of cryotherapy: contact and spray (which is generally more effective for AK). AK grade I-II lesions typically undergo a single freeze-thaw cycle with a freezing time ranging from 5 to 20 s [33, 34]. For larger and hypertrophic AK lesions, two freeze-thaw cycles of 10 s each are recommended. Before cryotherapy, it is advisable to remove hyperkeratotic scales through gentle curettage or by applying keratolytic agents (urea or salicylic acid) at least 2 weeks prior to the procedure [35]. Cure rates for cryotherapy as a standalone treatment for AK range from 39% to 83%, and may be improved when combined with other topical therapies [36].
Heppt et al. reported in their meta-analysis that cryosurgery combined with other topical drugs showed significantly higher complete clearance rates compared to cryosurgery alone (RR = 1.74, 95% CI: 1.25–2.43) [37]. The AAD strongly recommends combining cryotherapy with 5-FU or IMI [11].
Photodynamic therapy
Photodynamic therapy (PDT) is a field-directed treatment for AK that leverages the toxic reaction of reactive oxygen species with highly proliferative, inflammatory, and cancerous cells. PDT uses light-sensitizing substances known as “photosensitizers”, such as 5-aminolevulinate (5-ALA) or its ester methyl-aminolevulinate (MAL), which selectively accumulate in these cells. In the USA, a 20% ALA solution is approved for use with blue light, while in Europe, a nanoemulsion equivalent to a 10% ALA preparation (BF-200 ALA) is widely available. Additionally, a self-adhesive ALA patch facilitates direct and highly standardized application without prior lesion preparation [38, 39].
Two types of PDT are distinguished: conventional PDT (c-PDT) and daylight PDT (dl-PDT). The European Consensus recommends both c-PDT and dl-PDT using 5-ALA and/or MAL for treating single or multiple AKs and field cancerization [3].
For c-PDT, the procedure typically involves applying the photosensitizer (usually 5-ALA) to the AK lesion under occlusion for about 3 h. After removing the occlusive dressing and cleansing the lesion, the AK area is exposed to an appropriate light source, usually red light with a wavelength of 650–670 nm for BF-200 ALA what activates reactive oxygen species that lead to the chemical destruction of targeted cells [40]. Inflammation induced by the treatment promotes healing and remodelling of AK lesions. Typically, 2–3 treatments are administered at 4–8 week intervals, although this can be extended if significant inflammation occurs after irradiation. Clearance rates for c-PDT in randomized controlled trials range from 50% to 94.3% for cALA-PDT/ALA-c-PDT and from 31.4% to 90.3% for MAL-PDT [3, 4]. A head-to-head trial showed that ALA-PDT demonstrated slightly higher clearance rates compared to MAL-PDT [41]. A recent network meta-analysis indicated that c-PDT with BF-200 ALA offers the most favourable long-term lesion clearance rates compared to other interventions, underscoring its high efficacy [42].
Various c-PDT protocols exist, but detailed analysis and listing are beyond the scope of this article. They are summarized in the Table of the European Dermatology Forum (EDF) guidelines on topical photodynamic therapy, prepared by Morton et al. [38].
Systematic reviews have compared PDT to other therapies. Gupta et al.’s review, covering 83 RCTs with 10,036 participants, significantly favoured PDT for individual lesions compared to placebo-PDT with the following photosensitizers: ALA-PDT (blue light: RR = 6.22, 95% CI: 2.88 to 13.43; 1 study with 243 participants), ALA-PDT (red light: RR = 5.94, 95% CI: 3.35 to 10.54; 3 studies with 422 participants), and MAL-PDT (red light: RR = 4.46, 95% CI: 3.17 to 6.28; 5 studies with 482 participants). ALA-PDT also showed significant efficacy compared to cryotherapy (RR = 1.31, 95% CI: 1.05 to 1.64) [43]. Some studies have demonstrated promising results of combining PDT with other topical therapies for AK among others 4 studies combined PDT with IMI, 3 with 5-FU, and one each with ingenol mebutate (IMB) gel, tazarotene gel, and calcipotriol ointment. These combinations showed significantly higher clearance rates compared to monotherapy. Among all therapies, topical IMI used before or after PDT showed higher participant complete clearance rates than monotherapy (RR = 1.57, 95% CI: 1.09–2.25, p = 0.02) [44]. Additionally, Steeb et al. reported significantly higher lesion clearance rates after laser-assisted PDT compared to PDT alone (RR = 1.33, 95% CI: 1.24–1.42, I2 = 25%, p < 0.01) [45]. Promising results were also observed with PDT combined with pre-treatment using microneedling [46]. Each case should be assessed individually to determine the most appropriate treatment approach.
Daylight PDT (dl-PDT) involves applying an organic sunscreen followed by ALA or MAL to AK lesions, without occlusion. After 30 min, patients are exposed to sunlight for 2 h [38, 40]. Dl-PDT tends to result in reduced local discomfort compared to c-PDT. In most European countries, dl-PDT can be performed from April to September when outdoor temperatures exceed 10°C, even on cloudy days. The AAD suggests that ALA-dl-PDT is less painful but equally effective as ALA-red light PDT (moderate quality of evidence) [11]. Additionally, pretreatment with topical 5-FU cream, applied twice daily for 6–7 days before PDT, or microdermabrasion prior to the procedure, have resulted in greater improvement in AK lesions [47–49].
Chemical peels
Reports indicate that chemical peels, such as those using trichloroacetic acid (TCA), a-hydroxy acids (AHA), and glycolic acid, combined with 5-fluorouracil (5-FU), demonstrate greater efficacy compared to 5-FU alone. Only the German Dermatological Society (DDG) recommends chemical peelings for the treatment of single or multiple AKs and field cancerization [50, 51].
Laser therapy
Laser therapy involves inducing damage and remodelling of the epidermis and dermis to treat individual AK lesions. All of the cited guidelines mentioned laser therapy as an AK treatment option (Table 1) [3, 4, 11, 13]. The DDG specifically suggests ablative laser methods, such as CO2 and Erbium lasers, which demonstrate effectiveness ranging from 72.4% to 91.91%. Depending on the clinical response, multiple treatments may be necessary.
Table 1
Treatment algorithm for actinic keratoses (adapted from the European consensus-based interdisciplinary guideline for diagnosis, treatment and prevention of actinic keratoses) [3]
| Diagnosis of AK | ||
| Primary prevention | ||
| Effective sun protection | Use sunscreen | Choose a sunscreen that offers broad-spectrum protection (against both UVA and UVB rays) with an SPF of 30 or higher, preferably 50. Apply the sunscreen generously 20 min before sun exposure, and reapply every 2 h, or more often if swimming or sweating. Select a water-resistant sunscreen if you’re swimming or sweating. |
| Wear protective clothing | Wear long-sleeved shirts and long pants to cover as much skin as possible. Choose clothing made of tightly woven fabrics for better protection. Consider wearing clothing specifically designed to block UV rays, often labelled with an ultraviolet protection factor (UPF). | |
| Use accessories | Wide-brimmed hats: A hat with at least a 2–3 inch brim all around can protect your face, neck, and ears. Sunglasses: Wear sunglasses that block 100% of UVA and UVB rays to protect your eyes and the surrounding skin. | |
| Avoid the peak UV hours (10 a.m. – 3 p.m.) | ||
| Do not use tanning beds | ||
| Stay hydrated | ||
| Regular skin checks | Self-examinations and periodic dermatological examinations. | |
| Assesment of AK lesions (If hyperkeratotic lesions are present, consider gentle curettage or the use of keratolytic agents containing urea or salicylic acid, starting at least 2 weeks prior to the procedure.) | ||
| Topical treatment | ||
| 5-fluorouracil (5-FU) | 5% 5-FU cream | Apply topically to AK lesions once or twice daily until erosion forms, typically within 2 to 4 weeks, with a maximum treatment duration of 12 weeks. |
| 0.5% 5-FU* | Apply topically once daily for 1–4 weeks. | |
| 0.5% 5-FU in salicylic acid 10% solution (10% SA)* | Apply topically once daily until the lesions have completely healed, or for up to a maximum of 12 weeks. | |
| 4% 5-FU* | Apply topically once daily for 4 weeks. | |
| Imiquimod (IMI) | 5% IMI cream | Apply in a thin layer to the AK lesion 6 h before bedtime, 3 times a week for 4 weeks. After completing the treatment, a follow-up is recommended to assess the treated AK lesions. If partial clearance is achieved, an additional treatment cycle can be considered, with a maximum treatment duration of 16 weeks. This treatment is not recommended during the summer period. |
| 3.75% IMI cream* | Apply topically once daily for 2 weeks, followed by a 2-week break from treatment. This cycle may be repeated one or two times. | |
| 2.5% IMI cream* | Apply topically once daily for 2 weeks, followed by a 2-week rest period. This cycle may be repeated once or twice. | |
| Diclofenac | 3% gel with 2.5% sodium hyaluronate (2.5% HA) | Apply topically twice daily directly to AK lesions for 60–90 days, with a maximum daily dose of 8 g. Initial effects may be observed within 30 days after completing the treatment. |
| Ingenol mebutate (IMB)* | 0.015% IMB | For the face and scalp. Apply once daily on 3 consecutive days. |
| 0.050% IMB | Trunk, extremities. Apply once daily on 2 consecutive days. | |
| Tirbanibulin* | 1% tirbanibulin | Apply topically once daily to AK lesions for 5 consecutive days. |
| Resiquimod* | Apply topically three times a week for 4 weeks. | |
| Physical treatment | ||
| Cryotherapy | AK grade I–II lesions | Single freeze-thaw cycle with a freezing time of 5 to 20 s. |
| Larger and hypertrophic AK lesions | Two freeze-thaw cycles, each lasting 10 s. | |
| For hyperkeratotic lesions, use gentle curettage or apply keratolytic agents containing urea or salicylic acid for at least 2 weeks prior to the procedure. Immediately after cryotherapy, blister formation and erosion at the treatment site may occur. | ||
| Curettage | Administer once, with the possibility of repeating up to two additional times. | |
| Chemical peels | Trichloroacetic acid (TCA), a-hydroxy acids (AHA), and glycolic acid | Apply once, repeat up to two times. |
| Laser therapy | Ablative laser devices (e.g., carbon dioxide (CO2) laser, erbium-YAG (Er:YAG) lasers) | Apply once, repeat up to several times. |
| Non-ablative laser devices (e.g., Nd:YAG laser, fractional lasers [1,540 nm]) | Apply once, repeat up to several times. | |
| Photodynamic therapy (PDT) | ALA-c-PDT (conventional PDT with aminolevulinic acid) | Remove scales/crusts, gently roughen surface, degrease skin. Apply a layer of cream approx. 1 mm thick and surrounding 5 mm of skin or entire cancerized fields of about 20 cm2. Cover with occlusive dressing for 3 h or patch for 4 h (before applying the patch there is no need to remove the scales/crusts). After 3 h, remove dressing, wipe clean, then illuminate using red light either with a narrow spectrum (~630 nm, light dose 37 J/cm2) or a broad spectrum (570–670 nm, 75–200 J/cm2). If necessary, repeat after 4–12 weeks. |
| MAL-c-PDT (conventional PDT with methyl aminolevulinic acid)* | The same procedure as in ALA-c-PDT. After removing the occlusive dressing, illuminate the lesion, using red light of spectrum 570–670 nm, total dose 75 J/cm2 (red light with narrower spectrum, giving the same activation, can be used: ~630 nm, light dose of 37 J/cm2). | |
| ALA-dl-PDT (daylight PDT aminolevulinic acid) | Apply sunscreen to the treatment areas. Once the sunscreen is dry, wipe the area with a cotton pad soaked in ethanol or isopropanol. Remove scales and crusts, and roughen the skin surface. The patient can go outdoors within 30 min, dry day with temperature > 10°C, for 2 h. Sky may be cloudless or overcast but with no rain. Use one treatment, reassess after 3 months. | |
| MAL-dl-PDT (daylight PDT with methyl aminolevulinic acid)* | The same procedure as in ALA-dl-PDT. | |
| Reassessment | ||
| Follow-up visit | Typically scheduled 12 weeks after initial treatment. | |
| Evaluation of response (clinical assessment, dermatoscopic assessment, non-invasive imaging techniques (if necessary)) | Complete response: No further treatment needed, regular skin checks. | |
| Partial response or recurrence: Consider repeat or alternative treatment. | ||
| Poor response: Reevaluate diagnosis and consider biopsy. | ||
Other invasive methods
Curettage is a less commonly employed technique for treating isolated AK lesions. Recent evidence from a meta-analysis by Steward et al. suggests that combining curettage with destructive treatments such as electrodesiccation or cryosurgery may be more effective than PDT, 5-FU, or IMI for managing SCC in situ or superficially iSCCs [52].
Combined methods
The latest guidelines of AAD emphasize the evaluation of treatment outcomes and the efficacy of combination therapies for AK. Cryotherapy combined with topical treatments (5-FU and IMI) is prominently featured (grade B). Additionally, combinations of cryotherapy with diclofenac (grade C), IMI (grade C), and adapalene (grade C) are mentioned. The guidelines also highlight the need for further research into the efficacy and safety of combining 5% 5-FU with 0.005% calcipotriol [11].
New promising therapeutic options
In 2024, Bernal Masferrer et al. published a comprehensive review on topical immunotherapy for AK and field cancerization. This review highlights new immunotherapies, such as ingenol disoxate, N-phosphonacetyl-L-aspartate (PALA), and anti-PD1 agents, which have shown promising results. However, further research is needed to standardize their clinical use [40].
Additionally, gene therapy emerges as a potential therapeutic option. Genomic studies have identified genetic aberrations in AK, including common mutations in genes such as TP53, NOTCH1, and NOTCH2. The progression from AK to cSCC involves chromosomal aberrations and alterations in oncogenes and tumor suppressor genes. Although the functional relationships among these genes are not yet fully understood, network analysis offers valuable insights into their potential mechanisms [53].
Treatment algorithm
The wide array of therapeutic options for treating AK can make it challenging for clinicians to select the most appropriate treatment for their patients. To aid in decision-making, clinicians may find the therapeutic algorithm modified by Gupta et al. and the practical treatment algorithm for office-based dermatology proposed by Dirschka et al. particularly useful [8, 54]. These algorithms provide structured approaches to treatment, helping to streamline decision-making and tailor therapy to individual patient needs. For the purpose of this review, we created our algorithm for the treatment of AK according to the data available in the literature and guidelines (Table 1) [3]. In addition, we have compiled data on the strength of recommendations for AK treatment methods available in current guidelines of dermatological societies (Table 2) [3, 4, 11, 13].
Table 2
Summary of actinic keratoses (AK) treatment methods (strength of recommendations, level of evidence strength of consensus) according to current guidelines of the European Academy of Dermatology and Venerology (EADV) 2024; German Dermatological Society (DDG) 2023; American Academy of Dermatology (AAD) 2021; British Association of Dermatology (BAD) 2017; European Dermatology Forum (EDF) 2015 [3, 4, 11, 13, 15]
[i] According to nomenclature used in guidelines, the strength of recommendations was classified as follows:
[iii] B: Weak recommendation for the use of an intervention – “It should be offered/We conditionally recommend”.
[viii] According to nomenclature used in guidelines, the level of evidence was classified as follows:
[ix] 1: Systematic review AND/OR meta-analysis AND/OR network meta-analysis AND/OR prospective multicentre study AND/OR randomized controlled trials AND/OR open label single arm trial AND/OR trials with active comparator arm
[xii] High strength of evidence; Moderate strength of evidence; Low strength of evidence; Very low strength of evidence; Good Practice Statement
Follow up
According to European guidelines, treatment response for AK should be assessed 3 months after the completion of therapy. The evaluation should include:
Clinical assessment: Visual and physical examination of the treated area.
Dermatoscopic assessment: Use of a dermatoscope to detect any residual or recurrent lesions.
Non-Invasive imaging techniques (if necessary): Employing methods such as optical coherence tomography (OCT) or confocal microscopy for a detailed analysis if clinical and dermatoscopic evaluations are inconclusive.
If any signs of recurrent AK lesions are observed, either retreatment or a biopsy is recommended to confirm the diagnosis and assess further treatment options [3].
Summary
With growing awareness of the detrimental effects and long-term complications associated with chronic UV exposure, the diagnosis of AK is becoming increasingly common. This heightened awareness has led more patients to seek medical consultation. Therefore, it is essential for physicians across various specialties, especially family practitioners who are often the first point of contact, to be well-informed about the diagnosis of AK and make appropriate referrals to dermatologists when necessary. Education on effective sun protection is critical for patients, medical students, and healthcare professionals from other specialties. Preventing skin cancer through sun protection is more socio-economically advantageous than treating it.
In terms of treatment, field-directed therapies such as PDT are considered highly effective for AK. Cryotherapy, whether used alone or in combination with topical treatments, remains a widely utilized method. Nevertheless, due to the unique nature of each case, individualized treatment plans and thorough assessments are crucial for optimal patient care.
