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Wyprysk z hiperkeratozą - Objawy, Diagnoza i Leczenie
Histopathology
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.
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]
Treatment / Management
Basic skincare measures are important to prevent excessive dryness and to encourage exfoliation. Those remedies include soaps with skin-specific pH, soap-free cleansers, and avoidance of hot baths. Emollients and topical keratolytic agents (lactic acid, salicylic acid, urea) should be advised to be applied over affected areas at the appropriate times.
Surgical procedures have limited relevance in the treatment of hyperkeratosis. In cases of untreatable plantar keratosis with significant daily limitation, skin grafts with rotation skin flap have been demonstrated effective.[25][26]
Corticosteroids are the treatment of choice for inflammation-driven diseases such as lichen planus or psoriasis. Topical application is the best choice for localized disease. Topical applications should last one to two weeks.
Immunosuppressant or immunomodulators (cyclosporin, hydroxychloroquine, mycophenolate mofetil, sulfasalazine, alefacept, efalizumab) can be used in severe recurrent cases.
Topical calcineurin inhibitors (tacrolimus or pimecrolimus) can also be used.
Retinoids, topical or oral-based, are used in disorders of keratinization such as ichthyoses, keratosis folliculitis, and psoriasis. Topical administration is variable and must be evaluated in the appropriate clinical context, treatment usually lasts 8 to 12 weeks.
Combination treatments with lasers (e.g., pulsed-dye laser, 755-nm alexandrite laser, 810-nm diode laser, 1064-nm Nd:YAG laser) and microdermabrasion are noninvasive techniques currently under approval for different hyperkeratotic diseases.
Introduction
Hyperkeratosis refers to the increased thickness of the stratum corneum, the outer layer of the skin. Stratum corneum is composed of multiple layers of keratinocyte bodies that, during maturation, produced keratin and subsequently have lost their nucleus and cytoplasmic organelles. The result is a basketweave appearance of anucleate keratinocytes that protect the underlying cells during maturation.
Hyperkeratosis is subclassified as orthokeratotic or parakeratotic. Orthokeratotic hyperkeratosis refers to the thickening of the keratin layer with preserved keratinocyte maturation, while parakeratotic hyperkeratosis shows retained nuclei as a sign of delayed maturation of keratinocytes. Hyperkeratosis can be associated with dyskeratosis. It represents a premature (keratinocytes that are located below the granular cell layer) or abnormal keratinization of individual keratinocytes.
Hyperkeratosis, associated with other abnormalities in the skin biopsy, can be a key to the final histological diagnosis. Epidermal hypertrophy is a benign alteration of the skin that presents with acanthosis (increased thickness of the keratinocyte layers) and hyperkeratosis.
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