1. Actinic Keratosis: New Solutions for the Primary Care Physician
Actinic Keratosis: New Solutions
for The Primary Care Physician
Marcie Ulmer MD FRCPC FAAD
Clinical Instructor
Department of Dermatology & Skin Science
University of British Columbia

2. Actinic Keratosis: New Solutions for the Primary Care Physician
Faculty/Presenter Disclosure
• Faculty: Marcie Ulmer MD FRCPC FAAD
• Relationships with commercial interests:
– Speakers Bureau/Honoraria: Valeant Canada, Leo
Pharma, Inc.
– Consulting Fees: Valeant Canada, Leo Pharma, Inc.

3. Actinic Keratosis: New Solutions for the Primary Care Physician
Disclosure of Commercial Support
• This program has received financial support from Leo Pharma, Inc.
in the form of an educational grant
• This program has received in-kind support from Leo Pharma, Inc. in
the form of logistical support
• Potential for conflict(s) of interest:
– Dr. Marcie Ulmer has received funding from Leo Pharma, Inc. and
Valeant Canada whose products are being discussed in this program.
– Leo Pharma, Inc. and Valeant Canada benefit from the sale of products
that will be discussed in this program: ingenol mebutate, 5-fluorouracil
and Imiquimod.

4. Actinic Keratosis: New Solutions for the Primary Care Physician
Mitigating Potential Bias
• Information will be presented supporting multiple
therapeutic options for the treatment of actinic keratoses

5. Case 1: Denise
Diagnosis and Treatment of
Actinic Keratosis Lesions

6. Learning Objectives
After attending this session, participants will be able to:
• Explain the link between actinic keratosis (AK) and
non-melanoma skin cancers (NMSC)
• Identify the clinical signs and symptoms of actinic
keratosis lesions
• Describe current treatment options for actinic keratosis

7. Patient Profile
• Female, age 63 years
• Non-smoker
• Spends time outdoors gardening, swimming, and golfing
in the summer, cross-country skiing in the winter
• History of sunburn as both a child and adult
• Conscientious about using sunscreen and wearing a hat
for past 10+ years

8. Prior Medical History
• History of AK lesions 12 months ago (2 on
back of right hand, 2 on right forearm)
– Treated successfully with cryosurgery by family physician
• History of basal cell carcinoma over past 15 years (3 on
chest, 2 on back)
– Excised/biopsied by dermatologist

9. Discussion Question
1. True or false: There is a link between actinic keratosis
and non-melanoma skin cancer.
A. True
B. False

10. Actinic Keratoses and
Non-melanoma Skin Cancer
• AK is pre-cancerous skin lesion1,2
• Non-melanoma skin cancer (NMSC) includes squamous
cell carcinoma (SCC) and basal cell carcinoma (BCC)
– NMSC is the most common type of cancer3
– A history of NMSC increases the risk for malignant
melanoma and other types of cancer, including colon, lung,
and breast cancer4
1. Criscione VD, et al. Cancer. 2009;115(11):2523-30.
2. Lober BA, et al. South Med J. 2000;93:650-5.
3. Rogers HW, et al. Arch Dermatol. 2010;146(3):283-7.
4. Chen J, et al. J Natl Cancer Inst. 2008;100:1215-22.

11. Actinic Keratoses and NMSC
SCC
• AK lesions may progress to
SCC1-3
– Progress less often to
BCC4
• AK lesions and SCC are
frequently contiguous as
they share the same
genetic alterations and
morphology5,6
1. Marks R, et al. Lancet. 1988;1:795-7.
2. Mittelbronn MA, et al. Int J Dermatol. 1998;37:677-81.
3. Dinehart SM, et al. Cancer. 1997;79:920-3.
4. Criscione VD, et al. Cancer. 2009;115(11):2523-30.
5. Berman B, et al. J Fam Pract. 2006;55(5):suppl 1-8.
6. Feldman SR, et al. Cutis. 2011; 87:201-7.
© Diepgen TL, Yihune G, et al. Dermatology Online Atlas.
AK

12. Natural History of AK Lesions
• Natural course of AK lesions is unpredictable1-5
– Estimates of 40 to 80% of cutaneous SCCs arise from, or
near, an AK lesion2-5
• AK lesions may persist, regress, or progress1,3
– Some lesions that regress will recur, from 32% within
1 year to 92% within 5 years
– Progression identified as hypertrophic AK, SCC in situ
(Bowen’s disease), and/or invasive SCC
1. Criscione VD, et al. Cancer. 2009;115(11):2523-30.
2. Feldman SR, et al. Cutis. 2011;87(4):201-7.
3. Marks R, et al. Lancet. 1988;1(8589): 795-7.
4. Mittelbronn MA, et al. Int J Dermatol. 1998;37:677-81.
5. Dinehart SM, et al. Cancer. 1997;79:920-3.

13. Discussion Question
2. Which of the following is not a risk factor for
development of actinic keratosis lesions?
A.
B.
C.
D.
E.
F.
G.
Male gender
Light-coloured eyes and hair
Cumulative exposure to UV radiation
Excessive/habitual alcohol consumption
Fair skin
Immunosuppression
All of the above are risk factors

14. General Risk Factors for AK
•
•
•
•
High intensity or cumulative exposure to UV radiation1,2
Use of tanning beds or sunlamps3
Prior history of AKs or other skin cancer4
Clinical signs of photodamage, such as solar/senile
lentigines, facial telangiectasia, and actinic elastosis of
the neck4
• Immunosuppression5
• Human papillomaviruses may play a role in etiology
of AKs5
1. Diepgen TL, et al. Br J Dermatol.2002;146(suppl 61):1-6.
2. Berman B, et al. J Fam Pract. 2006;55(5):suppl 1-8.
3. Hemminki K, et al. Arch Dermatol. 2003;139:885-9.
4. Feldman SR, et al. Cutis. 2011;87(4):201-7.
5. Goldberg LH, et al. J Drugs Dermatol. 2010;9(9):1125-32.

15. Red or
blond hair
Male gender
Light-coloured eyes
Fair skin
Older age, especially
those age 50 years and
older
… But also seen in
individuals aged 20 to
50 years
Individual Susceptibility Factors for AK
Salasche SJ. J Am Acad Dermatol. 2000;42(1 Pt 2):4-7.

16. Individual Susceptibility Factors for AK
1
1
2-4
Classification
Response to UV rays
Skin colour
I
Never tans, always burns
White
II
Tans with difficulty, usually burns
White
III
Average tanning, sometimes burns
White
IV
Easily tans, rarely burns
Moderate Brown
V
Very easy to tan, very rarely burns
Hispanic, Latin, African, Asian, Indian
VI
Never burns
Black
1. Fitzpatrick TB. J Med Esthet. 1975;2:33034. 2. Sng J, et al. J Am Acad Dermatol. 2009;61(3):426-32.
3. Ahluwalia J, et al. J Drugs Dermatol. 2012;11(4):484-6. 4. Davis SA, et al. J Drugs Dermatol. 2012;11(4):466-73.

17. Denise’s Recent History
• 2 months ago, Denise returned to her
physician because she found a “suspicious
spot” on her forehead
• The lesion had the appearance of an AK lesion
• The physician also noted a small rough patch next to
the more visible lesion that he concluded was also an
AK lesion

18. Discussion Question
3. Which of the following is not a clinical sign or symptom
of actinic keratosis lesions?
A. Lesions are usually less than 1 cm in diameter
B. Lesions are generally found on sun-exposed areas of the
body
C. Visible lesions are usually brown to dark brown
D. Lesions may be rough and/or scaly to the touch

19. Clinical Signs
of Actinic Keratosis Lesions
• Visible/detectable lesions
are reddish to reddish
brown, rough, scaly patches
less than 1 cm in diameter1
• Non-visible, non-palpable
lesions occur up to 10 times
more often than visible
lesions, particularly in sundamaged skin2
– >80% of all AK lesions are
found on sun-exposed
areas of the body3
1. Ulrich M, et al. Dermatology. 2010;220(1):15-24.
2. Berman B, et al. Expert Opin Pharmacother. 2009;10(18):3015-31.
3. Salasche SJ. J Am Acad Dermatol. 2000;42(1 Pt 2):4-7.
4. Berman B, et al. J Fam Pract. 2006;55(5):suppl 1-8.
Courtesy of Dr. Kirk Barber .
When one AK is seen,
assume that other,
perhaps non-visible,
AK lesions exist4

20. Clinical Signs
of Actinic Keratosis Lesions
• Lesions can often be felt
more easily than seen1
• Red, rough, scaling spots2
• White scale over a pink
macule or papule1
• Pinhead to 4–5 mm in
diameter1
• Distribution: solitary,
clustered, or disseminated1
• Generally asymptomatic1,2
© DermNet NZ; dermnetnz.org.
1. Stulberg D, et al. Am Fam Physician. 2004;70(8):1481-8.
2. Canadian Dermatology Association. Actinic keratoses fact sheet. 2012.

21. Examples of AK Lesions
Photos: © DermNet NZ; dermnetnz.org.

22. Differential Diagnosis of AK Lesions
Bowen’s disease (SCC in situ)
Keratoacanthoma
BCC
Invasive SCC
Duncan KO, et al. In: Wolff K, et al. Fitzpatrick's Dermatology in General Medicine: 7th ed. 2008:Chapter 113.
Photos, top and bottom left, top and bottom right, © Danderm; www.danderm-pdv.is.kkh.dk. Photo, centre, © DermNet NZ; dermnetnz.org.
Lentigo maligna

23. The Differential Diagnosis
of AK Lesions
Verruca vulgaris
Solar lentigo
Seborrheic keratosis
Lichen planus
Discoid lupus erythematosus
Duncan KO, et al. In: Wolff K, et al. Fitzpatrick's Dermatology in General Medicine: 7th ed. 2008:Chapter 113. Photos: Top left, bottom right,
© Danderm; www.danderm-pdv.is.kkh.dk. Top centre and right, © DermNet NZ; http://dermnetnz.org. Bottom left, © DermAtlas; www.DermAtlas.org.

24. Discussion Question
4. Which of the following factors should be considered
when selecting treatment for actinic keratosis lesions?
A. Number of lesions
B. Location of lesions
C. Potential for presence of subclinical (non-visible,
non-palpable) lesions
D. All of the above
E. A and B only

25. Actinic Keratosis Is a
Field Disease
•
Field of cancerisation surrounds
clinical AK lesions and is partially or
completely clinically invisible –
multifocal, paraneoplastic,
subclinical changes1
•
Histopathology of AKs is found in
surrounding skin2
•
Clinical lesions
Subclinical (non-palpable, nonvisible) AK lesions occur ~10 times
more often than clinical AK lesions
in sun-damaged skin3
Subclinical lesions
1. Vatve M, et al. Br J Dermatol. 2007;157(Suppl 2):21-4.
2. Berman B, et al. Exp Opin Pharmacother. 2009;10(18):3015-31.
3. Braakhuis BJM, et al. Cancer Res. 2003;63(8):1727-30.

26. Is Field Treatment the Necessary
Approach?
• It is impossible to know which AK lesions will progress to invasive
SCC, so it is recommended that all AK lesions be treated1
• The ultimate goal of treatment is to clear the entire actinically
damaged field2
– Addressing both clinical and non-visible lesions may significantly
reduce recurrence rates of AK2
• Early diagnosis and treatment of the field of actinic damage
decreases overall disease burden and helps to prevent development
of invasive SCC1,2
1. Martin G. J Clin Aesthet Dermatol. 2010;3(11):20-5.
2. Ulrich M, et al. Exp Opin Emerg Drugs. 2010;15(4):545-55.

27. Discussion Question
5. Which of the following topical medications is not
indicated for field-directed treatment of AK lesions?
A.
B.
C.
D.
E.
Imiquimod 3.75%
Tretinoin cream 0.025%
Ingenol mebutate 0.015%
5-fluorouracil
B and C

28. Field-directed Topical Treatment
Options
Treatment
Dosing
Duration of treatment
5-fluorouracil (5-FU)1
Twice daily
Usual duration: 2-4 weeks
Imiquimod 3.75% (face, balding
scalp)2
Up to 2 packets once daily
6 weeks (2 treatment cycles of 2
weeks, separated by a 2-week
no-treatment period)
Imiquimod 5% (face, balding scalp)3
Twice weekly
16 weeks
Ingenol mebutate 0.015% (face,
scalp)4
Once daily
3 consecutive days
Ingenol mebutate 0.05% (trunk,
extremities)4
Once daily
2 consecutive days
Aminolevulinic acid5 or methyl
aminolevulinate6 with PDT
Agents applied a day5 or a few
hours6 before light treatment
15 to 26 treatment cycles
May be retreated 8+ weeks5 or
3+ months6 after initial treatment
1. EFUDEX® product monograph, 2004. 2. ZYCLARA® product monograph, 2012.
3. ALDARA® product monograph, 2012. 4. PICATO® product monograph, 2013.
5. Levulan Kerastick® product monograph, 2004. 6. METVIX™ product monograph, 2009.

29. Efficacy of Field-directed Topical
Therapies
Treatment
Complete
clearance,
% patients
Follow-up
period
Patients with
sustained
clearance, %
Follow-up
period
5-FU
48–58%1-3
4 weeks
54%4
12 months
Imiquimod 3.75%*
36%5
8 weeks
41%6
12 months
Imiquimod 5%7*
45%
8 weeks
43%
12-18 months
Ingenol mebutate 0.015%*8
42%
57 days
46%
12 months
Ingenol mebutate 0.05%8
34%
57 days
50%
12 months
47–82%9-11
1–3 months
40%9
12 months
Photodynamic therapy
(PDT)
Between-study comparisons are not intended due to differences in patient demographics and other study parameters.
*Indicated for face and scalp only.
1. Jorizzo J, et al. Cutis. 2002;70(6):335-9. 2. Weiss J, et al. Cutis. 2002;70(2 Suppl):22-9. 3. Tanghetti E, et al. J Drugs Dermatol. 2007;6(2):144-7.
4. Krawtchenko N, et al. Br J Dermatol. 2007;157(Suppl 2):34-40. 5. ZYCLARA® product monograph, 2012. 6. Hanke CW, et al. J Drugs Dermatol.
2011;10(2):165-70. 7. ALDARA® product monograph, 2012. 8. Lebwohl M, et al. New Engl J Med. 2012;366(11):1010-9. 9. Tschen EH, et al. Br J
Dermatol. 2006;155(6):1262-9. 10. Piacquadio DJ, et al. Arch Dermatol. 2004;140(1):41-6. 11. Pariser DM, et al. J Am Acad Dermatol. 2003;48(2):227-32.

30. Lesion-directed Treatment Options
• Physically destructive methods
– Cryosurgery
– Laser ablation
• Surgical removal
– Shave excision
– Curettage
– Electrodessication
de Berker D, et al. Br J Dermatol. 2007;156:222-30.

31. Combination/Sequential Therapy
• Cryosurgery to treat visible AK lesions + topical
treatment to treat underlying field cancerisation:
– 5-FU followed by cryosurgery1
– Cryosurgery followed by 3.75% imiquimod2
1. Jorizzo J, et al. Arch Dermatol. 2004;140:813-6.
2. Jorizzo J, et al. J Drugs Dermatol. 2010;9:1101-8.

32. Denise’s Recent Treatment
• Because of concerns about field cancerisation
and Denise’s desire for a non-surgical
treatment on her forehead, her physician
prescribed ingenol mebutate 0.015%, once daily
for 3 days

33. Treatment Follow-up
• Two months later, Denise returns for a
follow-up appointment to check on clearance
of forehead lesions
• At this appointment, she points out another “suspicious
spot” located near the scar from removal of an earlier
AK lesion on her right hand
– Her physician diagnoses it as an AK lesion

34. Discussion Question
6. What treatment would you recommend for
this new AK lesion on Denise’s hand?
A.
B.
C.
D.
E.
Cryosurgery ± 5-FU
5-FU monotherapy
Imiquimod 5%
Ingenol mebutate 0.05%
Other

35. Summary
• Actinic keratoses are pre-cancerous skin lesions that may
progress to SCC; progression is unpredictable
• Risk factors for development of AK lesions include:
–
–
–
–
–
Amount of cumulative/prolonged exposure to UV
Fair skin
Light-coloured hair/eyes
Older age
Male gender
• AK lesions may be visible or non-visible/non-palpable
• Effective treatment of AK lesions may help to prevent
recurrence and/or progression to SCC

36. Case 2: Frank
Treating Actinic Keratosis Lesions
and Counselling Patients

37. Learning Objectives
After attending this session, participants will be able to:
• Describe the expected local skin reactions for various
topical, field-directed treatment options for actinic
keratosis (AK)
• Identify other potential adverse effects of topical AK
therapies
• Discuss key messages when counselling patients about
the application of topical AK therapies and potential local
skin reactions

38. Patient Profile
• Male, age 58 years
• Non-smoker (quit 15 years ago)
• Sedentary lifestyle; doesn’t participate in outdoor
activities or sports
• History of sunburn as both a child and adult
• Freckled skin on torso, arms, legs, face, and scalp
• “Never” remembers to wear sunscreen unless his wife
reminds him

39. Frank’s Recent History
• During a routine physical, Frank’s family
physician noticed reddish lesions on Frank’s
scalp, some of which had white scaling
• Upon further examination, the physician noted 2 lesions
that were palpable (rough to the touch, like grains of salt)
but not readily visible, for a total of 7 lesions

40. Prior Medical History
• No prior history of non-melanoma skin cancer
(squamous cell carcinoma and basal cell
carcinoma) or AK lesions
• Family history of melanoma (father, age 72 years)

41. Frank’s Risk Factors
for AK Lesions
• Sun-damaged skin as evidenced by number
and distribution of lentigines
• Tans with difficulty, usually burns
• History of sunburn
• Male gender
• Age (over 50 years)
• Fair skin
• Light-coloured eyes

42. Discussion Question
7. What is the recommended strategy for treatment of
multiple AK lesions?
A. Lesion-directed therapy (cryosurgery, shave excision,
curettage, etc.)
B. Field-directed topical therapy
C. Sequential/combination therapy (e.g., topical 5-FU
followed by cryosurgery)
D. Any of the above
E. B or C only

43. AK Treatment Strategies
• Primary treatment decision point: is it a single AK lesion
vs. multiple lesions?
• Single lesion:
– Consider lesion-directed therapy
– If there is evidence of extensive photodamage, consider
field-directed therapy to treat potential subclinical AK
lesions
• Multiple lesions:
– Consider sequential/combination therapy
– If there are a significant number of AK lesions in an area,
consider field-directed therapy
Berman B, et al. J Fam Pract. 2006;55(5):suppl 1-8.

44. Other Factors to Consider When
Selecting Treatment
•
•
•
•
•
Size of lesions1
Typical vs. atypical lesions1
Well defined vs. poorly defined lesions1
Location of lesions1
The potential for field cancerisation (non-visible
lesions)2,3
• Patient’s desire to improve appearance of photoaged
skin4
1. de Berker D, et al. Br J Dermatol. 2007;156:222-30.
2. Martin G. Clin Aesthet Dermatol. 2010;3(11):20-5.
3. Ulrich M, et al. Exp Opin Emerg Drugs. 2010;15(4):545-55.
4. LEO Pharma. Market research data on file. 2011.

45. Discussion Question
8. What treatment would you recommend for
the 7 AK lesions on Frank’s scalp?
A.
B.
C.
D.
E.
F.
5-FU monotherapy
Imiquimod 3.75%
Imiquimod 5%
Ingenol mebutate 0.015%
Ingenol mebutate 0.05%
Other

46. Field-directed Treatments:
Local Skin Reactions
Treatment
Local skin reactions
5-FU1
• Erythema, erosion, crusting, ulceration
• Significant erythema, burning, erosion, crusting, and/or ulceration can
occur during treatment and may require treatment interruption
Imiquimod 3.75%, 5%2,3*
• Erythema, flaking/scaling/dryness, scabbing/crusting
• Intense local skin reactions including erythema, scabbing/crusting, and
erosion/ulceration can occur after a few applications, and may require
treatment interruption
Ingenol mebutate 0.015%*, 0.05%4
• Erythema, flaking/scaling, crusting, swelling, vesiculation/pustulation
• Typically occur within 1 day of treatment initiation and peak in intensity up
to 1 week following completion of treatment
• Usually resolve within 2 weeks on face and scalp and within 4 weeks on
trunk and extremities
Aminolevulinic acid or methyl
aminolevulinate with PDT5,6
Erythema, edema, crusting
Between-study comparisons are not intended due to differences in patient demographics and other study parameters.
*Indicated for face and scalp only.
1. EFUDEX® product monograph, 2004. 2. ZYCLARA® product monograph, 2012.
3. ALDARA® product monograph, 2012. 4. PICATO® product monograph, 2013.
5. Levulan Kerastick® product monograph, 2004. 6. METVIX™ product monograph, 2009.

47. Additional Question
• How will you explain the time course of LSRs (topical
agents) with your patients?

48. Examples of LSRs
This LSR comprises erythema,
vesiculation, and mild swelling.
This LSR comprises more pronounced
swelling and erythema.

49. Field-directed Treatments:
Other Adverse Events
Treatment
Other adverse events
5-FU1,2
Application site pain, pruritus, burning, dermatitis, soreness, tenderness,
hyperpigmentation, scarring
Insomnia, stomatitis, suppuration, scaling, swelling, irritability, medicinal taste,
photosensitivity, and lacrimation
Laboratory abnormalities (leukocytosis, thrombocytopenia, toxic granulation,
eosinophilia)
Imiquimod 3.75%, 5%3,4*
Target site pain, tenderness, bleeding, itching, stinging, burning, tingling, irritation,
photosensitivity
Flu-like symptoms, including malaise, fever, nausea, myalgias, and chills
Exacerbation of inflammatory skin conditions
Ingenol mebutate 0.015%*, 0.05%5
Administration site pruritus, irritation, pain, infection
Periorbital pain
Headache
Eyelid edema
Aminolevulinic acid or methyl
aminolevulinate with PDT6,7
Stinging and burning during light therapy
Application site itching, photosensitivity
Between-study comparisons are not intended due to differences in patient demographics and other study parameters.
*Indicated for face and scalp only.
1. EFUDEX® product monograph, 2004. 2. Cheigh NH. In: DiPiro JT, et al., eds. Pharmacotherapy: A Pathophysiologic Approach. 2008:1584-5.
3. ZYCLARA® product monograph, 2012. 4. ALDARA® product monograph, 2012. 5. PICATO® product monograph, 2013.
6. Levulan Kerastick® product monograph, 2004. 7. METVIX™ product monograph, 2009.

50. Frank’s Treatment
• Frank asked his physician if he could just
“zap” off the lesions to get rid of them quickly
• Because of the number of AK lesions (7) and the
potential for non-visible lesions, Frank’s physician
prescribed 5-FU twice daily for 21 days

51. Setting Treatment Expectations
• It is important that your patients…
–
–
–
–
Understand the importance of field therapy
Know all treatment options available
Know the direct effects of treatment options
Know that local skin reactions are a normal and expected
part of topical therapy
– Understand the side effects associated with every option
and how to manage them
– Recognize that new/additional AKs can recur after initial
treatment

52. Counselling Tips for Topical
AK Therapies
• Wash hands before and after applying treatment
• Use care if applying the medication near the eyes,
nostrils, or mouth
• Some local skin reactions may become visible and/or
cause discomfort
EFUDEX® product monograph, 2004. ZYCLARA® product monograph, 2012.
ALDARA® product monograph, 2012. PICATO® product monograph, 2013.

53. Patient Counselling Tips: 5-FU
• Before applying, wash the area to be treated with soap and
water and dry carefully1
• Apply a thin layer of medication only to the affected area1
• Apply with cotton-tipped applicator or suitable glove1
• Do not cover treated area with a bandage or other dressing 1
• If the area being treated becomes painful with continued use,
stop treatment for 1–3 days1
– An over-the-counter steroid may help to alleviate swelling and
soreness2
• During treatment and for 1 to 2 months after treatment has
ended, stay out of direct sunlight1
1. EFUDEX® product monograph, 2004.
2. Cheigh NH. In: DiPiro JT, et al., eds. Pharmacotherapy: A Pathophysiologic Approach. 2008:1584-5.

54. Patient Counselling Tips: Imiquimod
•
Apply a thin layer of medication only to the affected area
•
Avoid washing or getting the area wet for 8 hours; after 8 hours, wash the
area with mild soap and water
•
Stop treatment and contact the office if:
– You have a severe local skin reaction; wash off the medication with mild soap
and water
– Skin breaks down
– Sores develop during the first week of treatment
– You have any skin reactions that affect your daily activities or do not go away
– Your develop flu-like signs and symptoms, such as malaise, fever, nausea,
muscle pain, and chills
•
Non-visible lesions may become visible during treatment
•
During treatment, avoid exposure to sunlight, a sunlamp, or a tanning bed
ZYCLARA® product monograph, 2012.
ALDARA® product monograph, 2012.

55. Patient Counselling Tips:
Ingenol Mebutate
•
•
•
•
Apply gel gently with the fingertip to the treatment area
Allow to dry for 15 minutes
Avoid washing or touching the treated skin for 6 hours
Avoid applying immediately after taking a shower or less than
2 hours before bedtime
• Do not cover the treated area with a bandage or other type of
dressing
• If a local skin reaction does not improve, contact the office
• Put medication in a refrigerator (2°C to 8°C) as soon as
possible after picking it up from the pharmacy and always
store it in the fridge
PICATO® product monograph, 2013.

56. Discussion Question
9. How often would you follow-up with Frank
after cessation of treatment?
A.
B.
C.
D.
8 weeks initially, then twice a year
4-8 weeks initially, then twice a year
8 weeks initially, then once a year
2 weeks initially, then once a year

57. Summary
• When there is a significant number of AK lesions in one
area, consider field-directed therapies to help ensure
adequate treatment of both visible and non-visible
lesions
• Set treatment expectations with patients, including
potential for adverse effects/local skin reactions
• Follow-up/monitor patients for recurrence or malignant
transformation