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Wyprysk z hiperkeratozą - Objawy, Diagnoza i Leczenie
Lokalizacje modzeli:
- palce stóp (okolica grzbietowa i podeszwowa oraz boczna)
- pięta
- przodostopie
- boczna krawędź stopy
ODCISK
BRODAWKA WIRUSOWA
Często występują u dzieci
Dr n.med. Danuta Nowicka ”Dermatologia. Ilustrowany podręcznik dla kosmetologów”, Wrocław 2014
Toxicokinetics
BCR-ABL inhibitors (mainly nilotinib and dasatinib) are commonly used for ontological target therapy, and the cutaneous side effects are only second to the hematologic sequelae. They are usually transitory and not severe. The most common dermatological side effect is a pruritic skin rash, while chronic dermatological side effects include psoriasis, lichenoid hyperkeratosis, pityriasis, and others.[14][15][16]
Multikinase-inhibitors (VEGF, PDGFR, EGFR, KIT, RET, Flt3, and RAF) affect the skin homeostasis and give rise to many different cutaneous manifestations, mainly with hyperkeratosis in the form of hyperkeratotic hand-foot skin reaction.[14] Hyperkeratosis occurs in the sites of friction or pressure, mainly soles, causing pain and limitation of the daily activities.[17][18]
Pathophysiology
The skin is composed of three layers: the epidermis, the dermis (composed of the superficial papillary and deeper reticular dermis), and the hypodermis. The skin has structural differences among the different areas of the body in terms of epidermal and dermal thickness, distribution of appendages, and pigmentation. The epidermis is composed of multiple layers of maturing keratinocytes: the basal layer (stratum basale), the squamous layer (stratum spinosum), the granular layer (stratum granulosum), and the cornified layer (stratum corneum). This stratified epithelium is in a constant process of self-renewing and exfoliation that takes 20-40 days to complete. The cells in the outer layer are the most differentiated in the keratinocyte line, composed almost entirely of keratin lamels of high molecular weight, and those are the ones that undergo desquamation, completing the maturation cycle.
When the epidermis is exposed to repetitive injury, it usually elicits an increased proliferative rate of the keratinocytes and accelerates their maturation. Keratinocytes also tend to produce more keratin, thus increasing the stratum corneum's thickness.
Genetic mutations resulting in hyperkeratosis is seen in ichthyoses and keratoderma. There are several damages in keratin-encoding genes such as KRT1 and KRT10, which cause defects in keratin structure. Defective keratin causes irregular aggregates of intermediate filaments, which leads to cellular collapse and blistering. The barrier function is then compromised, and the skin reacts with compensatory hyperproliferation, which leads to hyperkeratosis.
Treatment
Hyperkeratosis is, for the most part, highly manageable through various courses of treatment. The most effective treatment options for the varied types of hyperkeratosis include:
- Keratolytics are designed to break down the outer layer of thick skin.
- Moisturizers help combat dry and rough skin.
- Corticosteroids can reduce inflammation.
- Retinoids are designed to encourage a more regulated level of skin cell growth.
That said, each type will have its own treatments. They can include:
When to Call a Healthcare Provider
Make an appointment with your healthcare provider to discuss symptoms and treatment. Your provider will investigate your condition and advise you on which treatment will work best for you. In some cases, treatment is unnecessary.
