At his 2020 Winter Clinical Dermatology Conference presentation “New Therapies for Benign Skin Lesions,” Neal D. Bhatia, MD, took attendees through a lesson on the latest weapons available in the therapeutic war against warts.
Dr Bhatia started off by detailing the similarities between the two benign lesions. “They have the same abnormal turnover, both have [human papillomavirus, HPV,] as part of the pathogenesis, they both grow and don’t have roots,” said Dr Bhatia, “and dermatologists treat them the same way—they freeze and go.” Among other similarities include the lack of prevention strategies that are either adhered to, are approved, or actually work, as well as the topical management strategies being painful, expensive, and complicated to have covered by insurance. Notably, both actinic keratoses and warts are able to resist host apoptosis and defenses.
When considering the pathogenesis of warts and actinic keratoses, HPV is a double agent. While multiple phenotypes of warts are linked to HPV, HPV strains 21, 23, and 38 are linked to actinic keratoses and squamous cell carcinoma.
In his presentation, Dr Bhatia asked the crowd, given the similarities in pathogenesis and treatment, if there are “subclinical warts” just like there are subclinical actinic keratoses. This notion of the subclinical or precursor wart can be commonly seen in the genital or cervical presentation. If innocent lateral skin does not show clinical change despite histological presence of HPV, then this “innocent” skin does contain infected keratinocytes, and koilocytosis is simply delayed after the initial infection.
When it comes to treatment, Dr Bhatia discussed the similar therapeutic options for the treatment of actinic keratoses and warts. He noted that some destructive- and immune-bsed therapies currently approved for actinic keratoses have been studied as off-label treatments for warts, such as combination therapy with cryotherapy (including topical 5-FU, tazarotene, imiquimod, ingenol mebutate, sinecatechins, ALA-PDT) and Imiquimod, IM gel, and sinecatechins for genital warts. However, costs, tolerability, and compliance are limiting factors. More studies are needed to elucidate the efficacy of combination therapy.
Patients may be pursuing “Dr Google” treatments instead of visiting their dermatologist for the treatment of warts, choosing options such as:
- Banana peels
- Duct tape
- Vicks Vaporub or Robitussin
- Teatree oil
- Apple cider vinegar
These options are ineffective at best. Instead, dermatologists need to get patients comfortable with some more effective, though painful, options.
The first wart therapy to consider is cryonecrosis with liquid nitrogen. As suggested by Adam Friedman, MD, dermatologists should get close and get mean with their cryotherapy application. Roughly 10 seconds of cryonecrosis can induce destruction of the wart. The sensation of the treatment may last for a short period following application.
Other options for the treatment of warts include zinc sulfate (10 mg/kg/day for up to 3 months), 5-FU cream, 28.5% salicylic acid extended release antiviral film-forming solution, thermal pad exposure (though only studied in a proof of concept study, N = 3), sinecatechins 15% ointment, and phototherapy with 20% ALA with 3-5 hours of incubation. Future treatments on the horizon include A-1010 45% topical solution (Aclaris Therapeutics) and CLS006 furosemide topical gel 0.125% (Cutanea Lifesciences Inc). Dr Bhatia also mentioned the use of cantharidin 0.7%. This treatment is applied topically in the office.
To conclude, Dr Bhatia offered a two final pearls for the treatment of warts: wait at least a week following cryotherapy to initiate topical use, and encourage callus reduction between destructive therapies.
Reference
Bhatia ND. New Therapies for Benign Skin Lesions. Presented at: 2020 Winter Clinical Dermatology Conference; Kohala Coast, HI; January 18, 2020.
