Real-World Treatment for Actinic Keratosis: Practical Dermatology Office-Based Treatment Algorithm

María Romero^*
*Correspondence: María Romero, Department of Materials, National Polytechnic School, Quito, Ecuador, Email:

Introduction

Multiple clinical and subclinical lesions coexist over large areas of sunexposed skin in actinic keratosis (AK), a chronic skin disease that leads to field cancerization. Because they have the potential to develop into invasive squamous cell carcinoma, lesions require treatment. In order to supplement existing evidence-based guidelines, the purpose of this article is to provide straightforward guidance on AK treatment in daily clinical practice for dermatologists and general practitioners who practice out of offices. Differentiating patients based on whether they have isolated scattered lesions, lesions clustered in small areas, or large affected fields without reference to specific absolute numbers of lesions is one of the novel aspects of the proposed treatment algorithm. Perceiving that total sore leeway is seldom accomplished, in actuality, practice and that AK is a persistent illness, the proposed treatment objectives are to diminish the quantity of sores, to accomplish long haul infectious prevention and to forestall sickness movement to obtrusive squamous cell carcinoma [1]. In the clinical setting, doctors should choose AK treatments based on their patients' presentation, needs and local availability. The proposed AK treatment algorithm is simple to use and has a lot of real-world application in dermatology offices.

Description

Retinoids have been linked to cancer since the 1920s, when rats with vitamin A deficiency developed cancer. In 1962, Von Stuttgen used vitamin A acid to treat three patients with AKs. Biochemical studies in the 1970s and 1980s suggested that epithelial cancers may be associated with a relative deficiency of retinoid. An important study utilizing oral isotretinoin for chemoprevention of skin cancer in high-risk patients was published in 1982 by Peck and colleagues. In 1988, Kraemer demonstrated that oral isotretinoin at high doses (2 mg/kg/ day) prevented skin cancer in five xeroderma pigmentosum patients. Retinoids' mechanism of action in treating and preventing skin cancer is still poorly understood. It is known that they:have anti-apoptotic and pro-proliferative properties; control keratinocyte growth and differentiation; hinder the process of tumor development; reduce proto-oncogene regulation; raise the expression of p53 and caspases that promote apoptosis; and make keratinocytes more sensitive to apoptosis. Retinoids target the B-Raf/Mek/Erk signaling pathway in murine skin cancer models. They may act as an antioxidant, decreasing the number of sunburn cells, according to some theories. They might protect against the HPV, which is considered a co-carcinogen [2,3].

The dosage of the active ingredient and the frequency of application determine the severity of LSRs. Additionally, a number of studies have implications for environmental and patient-associated risk factors. Light pigmentation is primarily a risk factor for both AK and the severity of LSRs caused by treatment. a study involving IngMeb. showed that patients with fair skin (phototypes I–II) had stronger LSRs at day 4 and more erosions than patients with phototypes III–IV with a standard patient-applied regimen of once daily IngMeb for three consecutive days. In addition, only an albino patient experienced moderate erythema after two hours of exposure to the outdoors, despite the fact that DL-PDT does not typically result in severe LSRs. The following are additional potential risk factors for more severe LSRs with IngMeb:the female gender, patients who are younger than 70 years old and Koreans. The disparity in skin thickness and race was thought to be related to this final observation. It has been suggested that environmental factors are important. during the months of September and October in Italy. Specifically, high outside temperature was related with seriousness of LSRs and treatment adequacy of DL-PDT [4,5].

Conclusion

The technique's efficacy can range from 69% of lesions clearing up completely after more than 5 seconds of freezing to 83% after more than 20 seconds. There is a decrease in keratinocyte atypia, epidermal and stratum corneum thickness and lymphocytic infiltrate following a single 10-s cryotherapy cycle. The effectiveness of photodynamic therapy (PDT) and single-cycle or double-cycle freezing cryotherapy was compared in the available studies; One study found that 85% of patients treated after 12 months had a complete response after receiving single-cycle (10') sessions of cryotherapy. These sessions were repeated every three months until each patient received complete clearance. When comparing MAL-photodynamic therapy (PDT) vs. cryotherapy (double cycling) in actinic keratoses, at 12 months of follow-up, the complete response with photodynamic therapy (PDT) was 89. 1% vs. 86. 1% with cryotherapy, with no statistical difference between the groups. 186 Another study used a double cryotherapy cycle in a single session (freezing time not reported) and achieved complete response in 88% of treated cases.

Acknowledgement

None.

Conflict of Interest

There are no conflicts of interest by author.

References

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