1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results and discussion: expert opinions on the management of actinic keratoses
  6. Conclusions
  7. Acknowledgements
  8. References


Actinic keratoses (AK) are common photo-induced cutaneous lesions that may progress to invasive squamous-cell carcinoma and serve as a risk marker for skin cancer. Although numerous studies present the various therapeutic options for AK, publications that can be used to pragmatically guide dermatologists in their daily practice are limited. National and international guidelines have been published, however, they are based on clinical trials with highly selected patient populations and do not always capture the range of patients seen in everyday practice.


The objective of this expert panel of French dermatologists was to present an analysis of AK geared towards everyday practice, to express an informed opinion about most recent treatments, and to propose a treatment algorithm for AK for daily practice in France.


Over a 12 month period, six expert dermatologists in the field of AK (AKTeamTM expert panel) met regularly to formulate an opinion about treatment in everyday practice compared with the analysis of the literature and guidelines published since 1990.


Definitions, terminology, diagnosis and risk factors were summarized. Data from the literature and current practices related to the initial evaluation, indications for biopsy, therapeutic indications, therapeutic options and effectiveness, monitoring and prevention were discussed. A pragmatic treatment algorithm was formalized according to current data available. This practical algorithm distinguishes between different clinical situations depending on the number of AK, their hyperkeratotic or suspicious nature, and includes cryotherapy, curettage-electrocoagulation, 5% 5-fluorouracil, 3% diclofenac sodium, 5% imiquimod, 150 and 500 μg/g ingenol mebutate, lasers, photodynamic therapy and surgery.


This up-to-date expert opinions about AK and its treatment provide a management strategy and practical treatment algorithm for AK for French dermatologists to use.


  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results and discussion: expert opinions on the management of actinic keratoses
  6. Conclusions
  7. Acknowledgements
  8. References

Actinic keratoses (AK), also called solar keratoses, are photo-induced chronic cutaneous lesions that are frequently observed in adults. They occur on repeatedly sun-damaged areas and are one of the clinical signs of skin photo-ageing. This photo-ageing is most often characterized by actinic lentigines (sunspots) or wrinkles before AK onset. Histologically, AK are atypical areas of keratinocyte proliferation and differentiation. They are prone to transform into invasive cutaneous squamous-cell carcinomas (SCC). Their presence is also considered as a risk marker for skin cancer.

Actinic keratoses are frequent, with a prevalence of 15.4% and 34% in men and 5.9% and 18.2% in women in 40- and 70-year old adults, respectively.[1] In the southern hemisphere, the prevalence can reach 40–60% in elderly populations with a light skin phototype.[1-5] This prevalence dramatically rises with age, particularly in predisposed populations with a light skin phototype, and due to accumulation of sun exposure over a person's lifetime.[6] In France, AK prevalence is unknown but its frequency is estimated as being 5% of patients consulting in dermatology practice.[7] AK management, due to population ageing and the risk of AK transformation to SCC, may eventually become a public health issue.

National and European management guidelines for AK are largely based on analyses of clinical trials with highly selective inclusion criteria.[8-18] These guidelines and systematic reviews provide the reader with an evaluation of the evidence level of the different therapeutic options, but it may be difficult for the dermatologist to transfer these options to their daily therapeutic strategy, which includes a much broader range of patients with often other illnesses and treatments and often poor treatment adherence.

Given this background, the objective of this report was to provide a practical algorithm for the treatment of AK taking in account the most recent therapeutics.


  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results and discussion: expert opinions on the management of actinic keratoses
  6. Conclusions
  7. Acknowledgements
  8. References

Six experts, all clinicians and dermatologists, with significant experience in dermato-oncology, dermatological surgery or dermatopathology, met to form an expert panel (AKTeamTM panel). Panel members were from various French regions (west, southwest, southeast, east, Ile-de-France), and from either hospitals, university hospitals and/or private practice. All members are well recognized in the field of AK and cutaneous cancer management.

During successive meetings, these experts worked on the formalization and writing of this report, based mainly on their own practice, and guidelines, including those of the French Society of Dermatology of 2009[8] and the European guidelines of 2011.[10]

The topics discussed were based on definitions and terminology, diagnosis of AK, risk factors for AK, initial evaluation, indications for biopsy, therapeutic options, clinical results and relapses. A practical therapeutic algorithm was developed based on this information as well as on the practical clinical experience of the panel. Proposals were only selected if there was consensus among the expert panel or if the opinion was adopted by the majority. A meeting in 2011 and four successive meetings in 2012 have resulted in the expert opinions presented below.

Results and discussion: expert opinions on the management of actinic keratoses

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results and discussion: expert opinions on the management of actinic keratoses
  6. Conclusions
  7. Acknowledgements
  8. References

Definitions and term inology

Actinic keratoses (AK) are precancerous cutaneous lesions that rarely occur as a single lesion, but most often occur as multiple lesions. This chronic condition is also considered to be a risk marker for cutaneous malignancies.

Cutaneous SCC include primitive cutaneous malignant epithelial tumours that show squamous transformation and that differ from basal-cell carcinomas. SCC can develop de novo or after progression of precursor lesions such as AK. Only SCC arising from AK are considered in this expert opinion report. Indeed, de novo SCC or SCC caused by burns, chronic ulcers or chronic skin infections differ epidemiologically and biologically from SCC arising from AK.

In the literature, the advocates of a unicist theory consider that AK are already in situ SCC.[19] The expert opinion is that AK are an in situ form of carcinoma that does not require the same management as invasive SCC. Indeed, although histological images and data based on the molecular biology of AK show that they are intra-epidermal carcinomas, evolutionary clinical data show that the risk of transformation to invasive SCC of any given AK is low and the outcome is variable.

Actinic keratoses can evolve following three major directions: the apparent spontaneous disappearance, persistence without progression to invasive SCC, or progression to invasive SCC. The spontaneous regression rate of AK, determined over a 1-year period, has been estimated as being 15–25% in the literature.[8, 20, 21] Some authors therefore highlight the potential importance of the spontaneous disappearance and emergence of new AK lesions. The occurrence rate of invasive SCC in patients with AK is evaluated in the literature as being 5–20% over follow-up periods of 10–25 years.[22, 23] The transformation rate from AK to SCC is much lower, ranging between 0.1% and 0.24% in 1 year.[20, 24] Remarkably, 82.4–100% of patients with invasive SCC on sun-exposed areas have a history of AK.[21, 25, 26]

Overall, experts agree that the progression rate from AK to SCC is low, spontaneous regression can occur but is difficult to assess, and a clinicopathological continuum of transformation from AK to invasive carcinoma exists but there is an element of uncertainty. No clinical, histological or biological criterion can, to date, be used to predict, with certainty, the type of AK progression. However, some AK are clinically more suspicious than others. These suspicious clinical signs are defined below (see ‘Initial evaluation: when to biopsy?’).

The ‘field of cancerization’ is defined as an area of subclinical changes in the periphery of visible AK lesions that can be highlighted histologically or using molecular biology or by imaging (reflectance confocal microscopy).[27, 28] Clinically, this risk field of cancerization is defined as a chronically photo-exposed anatomical area in which multiple and/or recurrent AK appear. Other histological and clinical photo-ageing signs (solar elastosis, wrinkles, sunspots, lentigines, telangiectases) can often appear in this risk area as well. Most affected skin areas include the forehead, temples, nose, scalp, ears, neckline, back of hands and forearms. Experts agreed with these definitions.

Diagnosis of actinic keratoses

The diagnosis of AK is essentially clinical. Most often, they occur in individuals with a fair skin phototype, on sun-exposed areas (face, dorsum of hands, and scalp in patients with alopecia). Signs of heliodermia are often associated (wrinkles, freckles, sunspots). On visual examination, the AK lesions are keratotic, of variable thickness, poorly delimited, with a diameter of 1 cm or less, a variable degree of erythema, and sometimes pigmented (Fig 1). They can also have a cutaneous horn shape. Lesions are keratotic and rough on palpation.


Figure 1. Multiple actinic keratoses on a field of cancerization. Example of the scalp in a 75-year-old man.

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When analysing the literature, some semantic difficulties have appeared, such as whether to use the term ‘hyperkeratotic AK’ or ‘hypertrophic AK’, and whether to use the term ‘AK recurrence’ or to use ‘new lesion’ when a lesion re-occurs on a treated area. Expert opinion on these issues is summarized in Table 1.

Table 1. Semantic issues
Hyperkeratotic or hypertrophic actinic keratoses?
Hypertrophic actinic keratoses show infiltration unlike hyperkeratotic actinic keratoses. The experts have retained the term ‘hyperkeratotic actinic keratoses’ for the treatment algorithm.
Recurrence or new lesion on treated areas?
In a given area, the interpretation of the term ‘recurrence’ should be modulated as it is not always possible to determine whether it is a recurrence or a new lesion.

Clinically, differential diagnosis of AK mainly includes seborrheic keratoses, actinic lentigines (sunspots), flat warts, melanocytic lentigines, but also sometimes SCC, Bowen's disease, basal-cell carcinoma, melanocytic nevus or melanoma. The examination of patients with AK must be carried out primarily by a dermatologist searching for other AK or even skin carcinomas that may already be associated. In the screening setting, it is essential to educate other health professionals who are likely to examine patients with AK (e.g. transplanters, rheumatologists, general practitioners, geriatricians, occupational physicians) about AK risk and advise them to refer the patient to a dermatologist for regular follow-up.

Risk factors for actinic keratoses

Risk factors for AK recognized by the experts are presented in Table 2.

Table 2. Medical conditions that predispose patients to a risk of actinic keratosis

Organ transplantation

Long-term immunosuppressive treatments (chemotherapy or biotherapy)

Exposure to skin carcinogens

Sun exposure or phototherapy

Light skin phototype (I/II), especially if other risk factors are associated

Personal history of cutaneous squamous-cell carcinoma

Some hemopathies

Initial evaluation: when to biopsy?

The initial evaluation is clinical; no paraclinical examination is justified. It must include at least the examination of photo-exposed areas to search for other AK lesions and possibly associated SCC. The physician must also assess the phototype of the patient and markers of chronic sun exposure (wrinkles, sunspots). In clinical practice, a biopsy for histological analysis is not necessary in typical cases in order to confirm the diagnosis of AK. However, a biopsy may be performed in the following cases to exclude or confirm invasive SCC, the management of which would be different: in cases where the skin is thickened, size >1 cm, induration, inflammation, ulceration, bleeding, rapid expansion or pain on palpation;[29] in cases of rapid recurrence (2–3 months) (see Table 1) or persistence of the treated lesion after standard treatment; and in cases located on a risk zone (lip, back of hand, ear).

Treatment: when and who to treat?

The need for systematically treating all AK to reduce the risk of skin cancer has not been demonstrated. However, treatment can be justified depending on the clinical characteristics of AK, but also cutaneous history (previous skin carcinomas). And subjective signs as patient request, impact of lesions on quality of life, and when requested, regular monitoring of the patient should be undertaken to detect a SCC as early as possible.

Physical treatment options


This approach destroys the tissue surface by vaporization of liquid nitrogen on a lesion to freeze it. Cell freezing and thawing cause tissue necrosis. Cryotherapy is simple, rapid and inexpensive. There is no standard protocol in terms of freezing duration of the lesion, number of cycles or treatment frequency. The approach is thus highly dependent on the operator. It is, however, the most frequently used treatment for isolated AK in France. It is a ‘gold standard’ in current practice of AK.


Complete clearance rates are around 68–75% at 3 months, with one and two applications, and 82.5–88% at 24 weeks (with two applications).[30-34] The progression and recurrence (see Table 1) rates of treated lesions have not precisely been assessed at 1 year. In only one study, the maintenance rate of clearance at 1 year was 28% (with two applications of 20–40 s).[30]

Adverse events

The main adverse events were related to pain during and immediately after treatment. There is also a risk of hyper- or hypopigmented scars occurring.

Expert opinion: Cryotherapy is the first-line standard treatment for isolated or small numbers of AK.

Surgical procedures

Surgical excision of the lesion, including the minimum margin, is considered as the standard treatment for suspicious isolated AK that may progress to invasive SCC. Rarely, surgical excision of an entire cutaneous area (scalp, back of hand) is performed in very specific cases of multiple AK that are unmanageable with local treatments and when there are multiple suspicious areas of transformation to SCC.

Expert opinion: Resection is indicated for suspicious isolated AK. Surgery with large exeresis of suspicious multiple AK that are unmanageable with local treatments is rare and must rely on a multidisciplinary decision.

Curettage and electrocoagulation

Mechanical curettage of the AK lesions with a curette followed by electrocoagulation is reported in the literature and can be an alternative to cryotherapy for first-line therapy. The procedure is rapid and ensures haemostasis, including in patients receiving anticoagulants. This treatment is mentioned in the English and Italian guidelines for AK.[12, 13] This technique is rarely used in France. No data on its effectiveness have been published.

Expert opinion: Curettage and electrocoagulation can be an alternative for AK treatment. It is indicated for isolated or small numbers of hyperkeratotic (see Table  1 ), non-suspicious and well-delimited AK.

Laser therapies

Ablative ultrapulse Er:Yag and CO2 lasers are indicated for isolated or small numbers of AK,[8] but clearance rates have not been evaluated in double-blind, randomized clinical trials.[13] The thermal effect and non-selective tissue vaporization, with loss of substance and coagulation necrosis of the margins, lead to a healing phase that results in erythema, pain, irritation, pruritus, oedema, and sometimes secondary infection.

Non-ablative fractional lasers (Er:Yag and CO2) are used to create microtunnels that optimize the penetration of topical treatments[35] or chromophores, and therefore the effectiveness of photodynamic therapy (PDT).[36] As their action targets the dermis, they are not particularly effective on AK. Finally, although non-ablative fractional lasers do not significantly reduce the number of AK, they could improve skin quality.[37]

Expert opinion: Multiple AK on large surfaces are the target of ultrapulse Er:Yag and CO2 lasers. However, no randomized study has objectively compared these treatments to other lasers and to other treatment options.

Photodynamic therapy (PDT)

Photodynamic therapy relies on the application of a topical photosensitizer that, after illumination using an appropriate light, will selectively destruct the tumour cells.[38] One other interest of PDT is to identify the limits of field cancerisation.[39] In most studies, a heme precursor is used as the photosensitizer – for example, methyl-aminolevulinate or amino-levulinic acid. In terms of dosage, one PDT session should be performed. The treated lesions should then be assessed at 3 months and a second session can be performed if needed.

In most studies, two sessions spaced 1 week apart have been carried out, explaining the high clearance rates observed. European guidelines on the use of PDT for AK, Bowen's disease, basal-cell carcinoma or other emerging indications have recently been published.[40] At a practical level, office dermatologists rarely own red/blue lamps, which is one of the limits of this treatment.


A complete clearance rate of treated lesions, ranging from 59% to 91% at 3 months, after two treatment sessions has been obtained.[31, 32, 41, 42] The recurrence rate (see Table 1) of lesions that were in clearance after a 12-month follow-up was 17%.[43] The best results were obtained in studies using two PDT sessions.

Adverse events

A total of 60–80% of patients showed a transient local reaction after treatment, with burning sensation, cutaneous pain, crusting and erythema. The treatment itself is painful when the light is applied to photosensitized areas. PDT is an effective but painful technique. Reduced discomfort has been observed with novel protocols, including shorter photosensitizer application times and in daylight PDT (using the photosensitizer and natural daylight).[40] Three recent randomized controlled trials have highlighted the effectiveness of daylight PDT for AK treatment.[44] This technique seems simpler and better tolerated than conventional PDT.

Expert opinion: PDT is indicated for thin/non-hyperkeratotic (see Table  1 ), multiple AK of the face and scalp. It can also be used on other locations. Pain is the major limiting factor of this treatment.

Topical treatment options


Emollients improve patient comfort by reducing skin dryness and roughness. In the literature, two studies compared the use of an emollient alone (control arm) to groups treated with masocroprol or diclofenac gel.[45, 46] In these studies, the emollient alone resulted in partial improvement in 44% of patients, without monitoring the follow-up data available. These results are insufficient to reliably assess their effectiveness.

Topical keratolytics containing urea or salicylic acid are indicated for hyperkeratotic forms of AK (see Table 1) and induce an exfoliation of the superficial layers of the epidermis by cleavage of the corneodesmosomes.

DNA-repair enzyme photolyase

Photolyase is a photoreactive DNA repair enzyme that specifically converts dimerized pyrimidines back into their original monomeric form. In order to induce DNA repair in the epidermis of skin treated with photolyase, exposure to 300–500 nm light is needed to photoreactivate the enzyme. In the manuscript by Stege et al., data show that after exposure to UVB radiation, the application of topical photolyase followed by photoreactivation decreased the number of dimers and prevented radiation-associated immunosuppression and erythema formation.[47]


5-fluorouracil (5-FU) is an antimetabolite cytotoxic agent belonging to the antipyrimidine group.[48] It interferes with DNA synthesis and, to a lesser extent, inhibits RNA transcription. In France, 5% 5-FU cream has been used for the treatment of AK since the 1960s. The 0.5% 5-FU cream is not available in France. It is most commonly applied once- to twice-daily according to tolerance, for 3–4 weeks on average. For better penetration, an occlusive dressing may be used. The treated surface must not be larger than 500 cm2 per treatment. In practice, use patterns are highly variable.


After 3–4 weeks, the complete clearance rate varied from 43% to 96%.[30, 49, 50] In about 65% of patients, lesions were recurrent 12 months after treatment.[30]

Adverse events

Pain, pruritus, burning sensation and hyperpigmentation may occur at the application site. The application on healthy skin causes an erythematous inflammatory reaction that may require temporary treatment discontinuation.[48]

Expert opinion: 5-FU can be used to treat thin or hyperkeratotic (see Table 1), multiple AK on large areas when lesion number or size limits the efficacy and/or tolerance of cryotherapy.

5-fluorouracil+salicylic acid

This combined therapy is not used in France.


Imiquimod is an imidazoquinoline-derivative, the main mechanism of action of which is through activation of the innate immunity.[51] In France imiquimod is indicated in immunocompetent patients and should be used with caution in patients taking immunosuppressants.[51] It induces activation of the Toll-like Receptor 7 and stimulates cytokine synthesis and release (e.g. interferon-alpha, IL-12). It has an indirect antineoplastic action and is used to treat both AK and the field of cancerization by stimulating the cutaneous innate immunity. It is used as 5% cream in 250 mg sachets on 25 cm2 contiguous treatment surfaces. The maximum recommended dose is one sachet per application for 8 weeks maximum. The imiquimod treatment scheme for AK is one cycle of three applications per week for 4 weeks, with an assessment at 4 weeks after treatment cessation. The cycle can be repeated once. In Europe, 3.75% imiquimod cream received market authorization in August 2012. This latter formulation is not marketed in France and could not be evaluated in practice by the experts.


With the dosage regimen used in France, between 26.8% and 55% of complete clearance are reported after one and two cycles, respectively.[52-57] The recurrence (see Table 1) rate at 1 year is 17.4–39% in treated areas.[30, 53]

Adverse events

Local reactions such as pruritus, burning, erythema, pain, oedema, dryness, crusting, erosions and ulcerations may occur. Systemic reactions (myalgia, fatigue, nausea) are rarer. Reactions occur less during a second treatment cycle.

Expert opinion: 5% imiquimod is recommended to treat non-hyperkeratotic (see Table  1 ), multiple AK of the face or scalp. The experts also recommend its use in other locations, although they have not been evaluated. It must be used with caution if an immunosuppressive therapy is ongoing, especially in organ transplant patients.

3% Diclofenac, 2.5% hyaluranic acid.

3% diclofenac gel is a non-steroidal anti-inflammatory drug that is used to treat AK in combination with hyaluronic acid.[58] It inhibits the cyclooxygenase pathway, resulting in decreased prostaglandin E2 (PGE2) synthesis. The recommended dosage is twice-daily applications for 8–12 weeks (60–90 days). The maximum dose is 8 g of gel/day.


Note that the maximum therapeutic effect is seen 30 days after treatment cessation. The complete clearance rate is 31% and 47% after 2 and 3 months of follow-up, respectively.[48, 59] The recurrence rate at 1 year is 21% (recurrence of treated lesions that had disappeared).

Adverse events

Local reactions such as contact eczema, cutaneous dryness, oedema, pruritus, scaly rash, ulcerations and vesiculobullous rash are frequent.[58]

Expert opinion: Diclofenac gel is well-tolerated but seems to be less effective than 5-FU or imiquimod. Its use is recommended for non-hyperkeratotic (see Table  1 ) superficial AK.

Ingenol mebutate

Ingenol mebutate is a biological compound that is derived from the surge sap (Euphorbia peplus).[60] Its mechanism of action in AK is not completely understood. In vitro and in vivo models have shown a dual mechanism: immediate cytotoxicity with occurrence of mitochondrial oedema and dissolution of cytoplasmic membranes; and delayed immunomodulation of innate immunity through production of inflammatory cytokines (IL-8 and TNF-alpha) and recruitment of neutrophils. Ingenol mebutate 150 μg/g gel is used on the face and scalp and applied once-daily for 3 consecutive days; 500 μg/g gel is used on the trunk and extremities and applied once-daily for 2 consecutive days.[60]


In a pooled analysis of two trials involving the face and scalp and two other trials involving the trunk and extremities, a complete clearance was observed after 2 months of treatments in 42% and 34% of patients, respectively.[61] After 12 months, a recurrence rate of 54% (see Table 1) was observed on the face and scalp, and 56% on the trunk and extremities.

Adverse events

Only local and not systemic adverse events occurred. They included erythema, scaling, crusting, oedema, vesicles/pustules and erosions/ulcerations. Local cutaneous reactions resolved within 2–4 weeks, depending on location.

Expert opinion: Ingenol mebutate is the first topical treatment with a short duration of application. It is indicated for the treatment of multiple non-hyperkeratotic AK (see Table 1), located in a field of 25 cm² on the face and scalp but also on the trunk and extremities.

Treatment algorithm

A treatment algorithm has been determined by the experts, who took into account both the literature and their own clinical experience. In this algorithm, criteria for choosing a treatment are based on daily practice and selection of the literature: the number of lesions, their non-hyperkeratotic nature (see Table 1) and their non-suspicious clinical appearance (Fig 2). Physical destruction methods (cryotherapy or curettage and electrocoagulation) are indicated as first-line treatments for isolated or small numbers of AK, surgery or laser being then proposed as second-line treatment in cases of recurrence (see Table 1) or treatment resistance. Any suspicious AK must be biopsied or excised.


Figure 2. Treatment algorithm proposed by the experts for actinic keratosis management, depending on lesion number and appearance.

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First-line topical treatments for multiple AK include 5% 5-FU, 3% diclofenac, 5% imiquimod, and 150 μg/g (face and scalp) or 500 μg/g (trunk and extremities) ingenol mebutate. The treatment choice will depend on factors such as patient adherence to treatment, quality of life, other illnesses and treatments associated and adverse events that may occur. Physical treatments can then be considered, especially for elderly and lonely patients for whom topical application can be difficult.

The management of patients with AK is often long as AK is a chronic disease and may require the use of sequential treatments or combined approaches. However, to date, the literature does not support a particular order for sequential therapy, nor the interest of maintenance therapy and did not conclude the most effective combined approaches.

Local inflammatory reactions: What should be done at the practical level?

An inflammatory skin reaction may be induced by some topical drugs and could cause an early cessation of treatments. Patients with inflammatory reactions are recommended to use a gentle cleanser gel that is compatible with skin pH. Depending on the severity of the painful, inflammatory and/or oedematous lesions induced, analgesic intake associated with thermal water sprays should be recommended. When lesions are erosive or crusted, a healing dermo-cosmetic may be applied twice-daily. An emollient can be combined when skin dryness occurs. When the inflammatory reaction is strong, a break from treatment can be considered. Corticosteroid prescription should be avoided because the anti-inflammatory action could inhibit the local inflammatory reactions necessary for agent effectiveness.

Photoprotection is needed on treated areas, especially during the spring or summer, to avoid photosensitivity damages and the risk of post-inflammatory pigmentation. It is sometimes better to wait until the autumn or winter to medically treat AK.

Particular situation: organ transplant patients

Organ transplant patients are a population at elevated risk of skin cancer. In these patients, AK incidence is extremely high and SCC incidence is nearly 100 times higher than that of the general population having the same age and phototype.[62] The risk is variable, and is related to the degree of immunosuppression, its duration, and the type of transplanted organ (higher risk for cardiac transplant than for kidney transplant patients). Existing data suggest that AK progress more rapidly to SCC in these patients. However, the greater SCC aggressiveness in transplant patients described in the literature is currently questioned. Usual treatments for AK are often less effective than in non-transplant patients and result in resistance or frequent recurrence.[63] A close monitoring and more rigorous treatment approach are necessary in these patients. AK treatment should be considered before organ transplantation. A regular clinical follow-up is carried out by the dermatologist for early detection and treatment of these lesions. In addition, patient education on skin self-examination is fundamental and allows delaying the development of potential cancerous lesions in transplant patients.[64]

Monitoring and secondary prevention

Patients with AK should be monitored regularly because of the chronic nature of lesions and an invasive SCC should be detected as early as possible.

In patients at risk, the monitoring rate proposed is at least a yearly consultation. During these consultations, the patient should be educated on the need for reconsulting earlier if any lesion changes rapidly or in case of recurrence after treatment. Organ transplant patients must be managed in a particular way, especially in terms of personalized monitoring.

Sun protective clothing and behaviour, and the use of sunscreen products (chemical or mineral filters), should be recommended to patients to minimize the worsening of photo-induced skin damage and to prevent skin cancer. It has been demonstrated that sunscreen is an effective AK prevention method. Applying sunscreen (greater than SPF-15 applied every 2–3 h) reduces the risk of AK lesions by up to 24% over time, even compared with beta-carotene and topical tretinoin cream 0.05%. The AAD (Amercian Association of Dermatology) states that selecting a sunscreen with broad-spectrum cover (UVB/UVA) is vital and that daily use of an SPF-30 product is recommended on all exposed skin before daylight exposure.[65-68]


  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results and discussion: expert opinions on the management of actinic keratoses
  6. Conclusions
  7. Acknowledgements
  8. References

The objective of this expert panel report was to provide a pragmatic solutions for dermatologists in terms of diagnosis, monitoring and a treatment algorithm that they could use in their daily practice, based on data from the literature and former guidelines.


  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results and discussion: expert opinions on the management of actinic keratoses
  6. Conclusions
  7. Acknowledgements
  8. References

We would like to thank Dr Maxime Battistella, Service de Pathologie de l'Hôpital Saint Louis in Paris, for his help in the writing of this article.


  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results and discussion: expert opinions on the management of actinic keratoses
  6. Conclusions
  7. Acknowledgements
  8. References
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