Keratosis Treatment Side Effects
Actinic keratoses (AK) are malignant cutaneous cellular structures which are evolving. They also are called keratinocytic intraepidermal neoplasia or in situ squamous cell carcinoma of solar keratotic kind. Two general methods are in use for treating actinic keratosis, which are topical therapies and destructive/physical ones. A number of therapeutic options have yielded significant results in keratosis treatment. These include imiquimod, 5-Fluorouracil, retinoids, colchicine and diclofenac.
Topical 5-Fluorouracil has been a prime focus of treating actinic keratosis for long. It thus has undergone many intensive studies to date. The action mechanism involved in the working of this drug is well understood and all leads to reduced DNA synthesis. This arises from low consequential levels of the chemical thymidine, which precipitates selective cell death in actinic lesions rather than normal skin. It is however unclear if regular cells only absorb less fluorouracil, in contrast to AK cells. Researchers neither have established whether absorption is similar for both cases, without generating equal parallel effects.
Imiquimod is another FDA approved medication in use for treating actinic keratosis. A large number of scientific reports support the efficacy of this drug in AK therapy, when topically applied in off-label conditions. Being an immunomodulator, imiquimod triggers a chemical release series of cytokines that sensitize and activate the local system of cellular immunity. This includes, yet is not limited to cytotoxic T-cells, which kill naturally. The cascade propagated here effects localized immune response that acts against abnormal cells in the activation area.
Diclofenac is a Non-steroidal Anti-inflammatory Drug (NSAID), which also has undergone comprehensive evaluation in AK treatment. Scientists are nonetheless yet to verify its action against precancerous tissue cells. Current research focuses on the possibility of cyclooxygenase enzyme inhibition as the cause of Diclofenac’s clinical action. Metabolism products of Arachidonic acid are thought to reduce downstream as a result of this. A portion of these by-products will control apoptosis inhibition, upward regulation of tumor cell invasive ability, together with overall immunosurveillance.
Colchicine is an alkaloid plant extract which is prominent as gout topical treatment. Since 1968 when it was first indicated as useful in actinic keratosis therapy, it has been verified through various studies as an effective drug on keratotic lesions. Colchicine is UV sensitive and works by down-regulating leucocytes affected by keratosis treatment.
Retinoids exhibit potential for inducing differentiation and antiproliferation. In consequence of this, they have been demonstrated as capable of improving damage effects precipitated by UV light on skin of patients. Retinoids have been associated with Keratosis treatment since 1962. Since then, significant progress has been made along this line, mainly involving tretinoin and retinoin use.
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