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Wyprysk z hiperkeratozą - Objawy, Diagnoza i Leczenie
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Psoriasis and psoriasiform dermatitis: It shows perivascular aggregates of lymphocytes in the dermal-epidermal junction with focal migration of leukocytes (neutrophils, lymphocytes) into the epidermis. There is increased epidermal proliferation and elongation of rete ridges giving an undulating appearance to the epidermis (papillomatosis) with or without spongiosis. The altered differentiation of keratinocytes results in hyperkeratosis with parakeratosis. Psoriasis also shows the formation of microabscesses by small aggregates of neutrophils in the upper epidermis (pustules) or in the stratum corneum (Munro microabscesses).
Interface and lichenoid dermatitis: Dense aggregates of lymphocytes along the dermal-epidermal junction associated with vacuolation of basal keratinocytes.[6] There is dyskeratosis, hyperkeratosis, and is sometimes associated with hypergranulosis.
Verrucae vulgaris and plana are characterized by marked hyperkeratosis, papillomatosis, and acanthosis. A typical feature is the presence of koilocytes, cells infected with papillomavirus which have structural changes like perinuclear halos and keratohyalin granules. Koilocytes can be absent in older lesions, but when present, are located in the upper stratum spinosum or granulosum. Parakeratosis may be present.
Seborrheic keratosis features marked hyperkeratosis, papillomatosis, and acanthosis. Pseudo-cysts and horn cysts are frequently present. There may be lymphocytic infiltrate and pigmentation as secondary features when irritated or inflamed.
The ichthyoses are a group of diseases caused by altered keratinization. The most common forms are ichthyosis vulgaris, X-linked, congenital, and epidermolytic hyperkeratosis.[7] They can be hereditary or acquired during life.[8][9] All of the forms show a defective epidermal barrier that induces hyperkeratosis, skin scaling, and inflammation.
Squamous cell carcinoma (SCC) is a neoplastic proliferation of atypical keratinocytes, restricted only to the epidermis (SCC in situ or Bowen's disease) or infiltrating the dermis (infiltrative SCC). Classic features are hyper-parakeratosis and loss of the granular layer.
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.
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]
