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Porokeratosis Treatment & Management

  • Author: Amarateedha H. Prak, MD; Chief Editor: William D James, MD  more...
 
Updated: May 09, 2016
 

Medical Care

The approach to treatment must be individualized, based on the size of the lesion and the anatomical location, the functional and aesthetic considerations, the risk of malignancy, and the patient's preference. Protection from the sun, use of emollients, and watchful observation for signs of malignant degeneration may be all that is needed for many patients. If lesions are widespread and medical treatment is desired, several medications have potential benefit.

Topical 5-fluorouracil

Topical 5-fluorouracil can induce remission in all forms of porokeratosis.[69, 70] Treatment must be continued until a brisk inflammatory reaction is obtained. Enhancement of penetration, which heightens the response, may be achieved by occlusion or the addition of topical tretinoin, tazarotene, or salicylic acid.[71] Recurrences may be seen.

Topical vitamin D-3 analogues

Both calcipotriol and tacalcitol have been shown to be effective after 3-6 months of treatment of disseminated superficial actinic porokeratosis (DSAP).[72, 73, 74]

Immunomodulators

Topical imiquimod cream has been shown to be effective for treating classic porokeratosis of Mibelli (PM).[75, 76]

Ingenol mebutate has shown efficacy in the treatment of porokeratosis of Mibelli (PM).[77]

Calcineurin inhibitors

Tacrolimus (0.1%) was shown to be effective for treating linear porokeratosis. A single case report showed complete resolution of associated pain, pruritus, and paresthesias, as well as cosmetic improvement.[78]

Topical retinoids

Topically applied retinoids (tretinoin, tazarotene) may be beneficial for improving the abnormality in keratinization that causes cornoid lamellation, thereby reducing the hyperkeratosis of the edge of the lesions. It is also thought to improve the percutaneous absorption of other topically applied medications, rendering them somewhat more effective.

Diclofenac gel

Diclofenac gel 3% (Solaraze), may be effective for DSAP.[79]

Oral retinoids

The use of oral retinoids (isotretinoin, etretinate, and acitretin) in patients who are immunosuppressed, who are at higher risk for malignant degeneration, may reduce the risk of carcinoma in porokeratotic lesions.

Oral isotretinoin at 20 mg daily combined with topical 5-fluorouracil is reported to be effective for DSAP and porokeratosis palmaris et plantaris disseminata (PPPD), but it causes burning, itching, and painful erosions.

Prior to the removal of etretinate from the US market, conflicting reports of etretinate efficacy were published. Reports of etretinate efficacy are conflicting. Etretinate at doses of 75 mg/d for 1 week followed by 50 mg/d was shown to be helpful in linear porokeratosis and symptomatic PM. Higher doses of 1 mg/kg/d were reported to exacerbate lesions of DSAP after 4-6 weeks of treatment.[80] Even when etretinate therapy is successful, relapses may occur. Digitate keratoses were reported to develop after the use of etretinate for DSAP.[81]

Acitretin, a second-generation monoaromatic retinoid that is the active metabolite of etretinate, is likely to have results similar to those of etretinate. A case of systematized linear porokeratosis with good response to acitretin has been reported.[82, 83]

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Surgical Care

Surgical treatment is essential for porokeratosis lesions that have undergone malignant transformation. No studies showing the value of prophylactic nonexcisional surgical treatment in reducing the incidence of malignancy within porokeratosis have been reported. Surgical modalities other than excision may improve cosmesis and/or function but are frequently followed by relapses.

Excision is most appropriate when malignant degeneration develops.

Cryotherapy is helpful for porokeratosis lesions with minimally raised cornoid lamellae, such as DSAP and PPPD. It is a minimally invasive method of inducing resolution for large numbers of lesions.

Electrodesiccation and curettage can be used to treat small lesions or when cryosurgery is ineffective.

Diamond fraise dermabrasion has been used with conflicting reports of efficacy. It was effective in improving the appearance of linear porokeratosis in one patient, but a child with a large PM lesion had recurrence after treatment.[84]

Various types of laser therapy have been used. A rapid recurrence reportedly followed carbon dioxide laser ablation. The 585 nm flashlamp-pumped pulsed dye laser was shown to help one patient with linear porokeratosis. Another patient with PM with an underlying hemangioma had good improvement of the hemangioma but no change in the porokeratosis after treatment. The frequency-doubled Nd:YAG laser was shown to be helpful for one patient with disseminated superficial porokeratosis (DSP). Two cases of disseminated superficial actinic porokeratosis were successfully treated with the 1927-nm thulium fiber fractional laser.[85] The Q-switched ruby laser has been reported to be effective in the treatment of DSAP and PM. Benefits of laser therapy include convenience and safety, with nearly no downtime or morbidity associated with pigment or textural changes.[85, 86, 87]

Ultrasonic surgical aspiration was shown to be effective in the treatment of vulvar porokeratosis in one patient.

Photodynamic therapy with methyl aminolevulinate has been reported to be successful for DSAP and linear porokeratosis.[88]

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Complications

The most important complication to watch for is the development of cutaneous malignancy. Functional impairment due to involvement of critical anatomical locations may develop. Prophylactic excision could be considered in appropriate situations.

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Long-Term Monitoring

Regularly monitoring patients for the development of malignant transformation is essential, especially in the setting of immunosuppression. Squamous cell or basal cell carcinomas can be aggressive in patients who are immunosuppressed.

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Contributor Information and Disclosures
Author

Amarateedha H. Prak, MD Naval Flight Surgeon, Marine Corps Air Station Camp Pendleton

Amarateedha H. Prak, MD is a member of the following medical societies: Aerospace Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Kristina Marie Dela Rosa, MD Dermatologist, Naval Hospital Camp Pendleton

Kristina Marie Dela Rosa, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American College of Rheumatology

Disclosure: Received income in an amount equal to or greater than $250 from: XOMA; Biogen/IDEC; Novartis; Janssen Biotech, Abbvie, CSL pharma<br/>Received honoraria from UpToDate for author/editor; Received honoraria from JAMA Dermatology for associate editor and intermittent author; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; for: Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Linda V Spencer, MD Spencer Dermatology Associates, LLC

Linda V Spencer, MD is a member of the following medical societies: American Academy of Dermatology, Dermatology Foundation, American Medical Association, Indiana State Medical Association

Disclosure: Nothing to disclose.

Andrea Leigh Zaenglein, MD Professor of Dermatology and Pediatrics, Department of Dermatology, Hershey Medical Center, Pennsylvania State University College of Medicine

Andrea Leigh Zaenglein, MD is a member of the following medical societies: American Academy of Dermatology, Society for Pediatric Dermatology

Disclosure: Received consulting fee from Galderma for consulting; Received consulting fee from Valeant for consulting; Received consulting fee from Promius for consulting; Received consulting fee from Anacor for consulting; Received grant/research funds from Stiefel for investigator; Received grant/research funds from Astellas for investigator; Received grant/research funds from Ranbaxy for other; Received consulting fee from Ranbaxy for consulting.

Acknowledgements

The view(s) expressed herein are those of the authors and do not reflect the official policy or position of the U.S. Navy Medical Department, the U.S. Navy Office of the Surgeon General, the Department of the Navy, Department of Defense, or the U.S. Government.

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Porokeratosis of Mibelli on the lower leg in a renal transplant recipient.
Disseminated superficial actinic porokeratosis on the lower legs of a female patient.
A 42-year-old woman with multiple lesions on the pretibial aspects of the legs.
A young boy with a linear lesion of porokeratotic eccrine ostial and dermal duct nevus extending onto the nailbed, causing pterygium formation.
 
 
 
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