Parakeratosis is a heterogeneous group of keratinization disorders classified on the basis of clinical appearance. Parakeratosis is a fairly common reason for visiting a dermatologist and cosmetologist; patients are often women aged 30-40. Symptomatic therapy acts temporarily, as well as methods of destruction of lesions using cryodestruction or a laser. At the moment, more and more specialists are focusing their attention on pathogenetic therapy, including for the treatment of a group of dyskeratosis. This article on estet-portal.com presents data on the effectiveness of pathogenetic therapy with lovastatin and cholesterol for patients with parakeratosis.
Pathogeny of parakeratosis
Parankeratosis options include:
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- disseminated superficial actin parakeratosis;
- disseminated superficial parakeratosis;
- Mibelli's parakeratosis;
- parakeratosis palmar and plantar;
- linear parakeratosis.
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All variants are divided according to the histopathological feature of the stratum corneum.
Lesions appear in open areas as asymptomatic/pruritic pink, brownish papules or plaques with a raised border.
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Parakeratosis is considered a precancerous condition with a malignant transformation rate of 7.5%.
The most common malignant neoplasm is squamous cell carcinoma, and parakeratosis can also transform into basal cell carcinomas and melanomas.
Although all subtypes of parakeratosis have an increased risk of developing skin cancer, linear, large, and long-standing lesions have a higher risk.
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As with other clonal keratinocyte disorders, treatment of parakeratosis is primarily focused on destruction of the lesion using cryotherapy, photodynamic therapy (PDT), and CO2 lasers. Other strategies to reduce the scale and inflammation associated with these lesions include acitretin, corticosteroids, and vitamin D analogues, but these approaches are often ineffective and expensive.
Cholesterol, one of the end products of the mevalonate pathway, is a key component of the extracellular lipid matrix in the stratum corneum, playing an important role in providing and maintaining the barrier function of the skin. Cholesterol depletion has been reported to result in increased sensitivity of keratinocytes to stimuli that induce apoptosis. Premature apoptosis and regulated differentiation of keratinocytes have been identified in several types of parakeratosis. Supporting a simple pathogenesis model in which mutations in function result in cholesterol deficiency in parakeratotic skin, directly leading to the disease phenotype.
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Genetic understanding of the pathogenesis of parakeratosis provides guidance for targeted therapy and correction of metabolic abnormalities resulting from reduced activity of the mevalonate pathway enzyme.
Topical application of lovastatin, an HMG-CoA inhibitor, and cholesterol resulted in significant improvement in skin lesions.
Efficacy of lovastatin/cholesterol for the treatment of parakeratosis
Cholesterol 2%/2% lovastatin ointment or lotion was applied twice daily to the affected skin with occlusion for the first 1-2 weeks depending on the thickness of the skin lesion, therapy continued for 6 weeks to 3 months. All patients were allowed to use emollients. Patients were examined at intervals of 3-4 weeks and up to 3 months for clinical response. Evaluation of clinical response consisted of a baseline photographic protocol and a biopsy of the affected skin. Erythema, scaling, thickness, size, and number of lesions were assessed at each visit.
Response to therapy in disseminated superficial actin parakeratosis:
After 3 months of lovastatin/cholesterol combination therapy, only small erythematous patches were observed on the treated areas.
Reduction in the extent of the lesion was noted already in the first week of treatment, and after 4 weeks of therapy there was a marked decrease in erythema, scaling and the size of visible lesions.
Response to therapy for palmar and plantar parkaretosis:
Treatment for 6 weeks with marked reduction in scaling and moderate reduction in erythema. In patients, improvement in lesion scaling was seen within 4 weeks of therapy and there was no change in the number and size of lesions.
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Response to therapy for linear parakeratosis:
A noticeable reduction in scale was noted 3-4 weeks after the start of therapy. After 3 months of treatment, patients experienced a moderate decrease in thickness and residual deposits over the thicker component of linear plaque. Importantly, all patients tolerated the therapy without side effects. There were no reports of redness, irritation, itching or allergic contact dermatitis in the treated areas.
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