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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.
Types of Hyperkeratosis
"Hyperkeratosis" is an umbrella term for skin conditions that develop from excess amounts of keratin. There are various types of hyperkeratosis, each marked by its cause.
Hereditary Types of Hyperkeratosis
Some types of hyperkeratosis develop due to a hereditary component. Examples include:
- Epidermolytic hyperkeratosis
- Multiple minute digitate hyperkeratosis (MMDH)
- Focal acral hyperkeratosis
- Lamellar ichthyosis
- X-linked ichthyosis (XLI)
- Keratosis pilaris, otherwise known as follicular hyperkeratosis
Acquired Hyperkeratosis
Other forms of hyperkeratosis are acquired later in life. It’s not always clear what the cause of each type is. Some acquired hyperkeratosis conditions include:
Acquired vs. Hereditary
Hereditary conditions are passed down through families. Often if a person is related by blood to someone with a genetic disorder, their risk of getting it is a lot higher. Acquired conditions, on the other hand, develop for many reasons unrelated to genetics.
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.
ROGOWIEC
Choroba genetyczna cechująca się hyperkeratynizacją skóry i paznokci. Jest to pogrubienie ograniczone do powierzchni dłoniowych i podeszwowych, pojawiające się zwykle z powodu mutacji.
GŁÓWNE OBJAWY ROGOWCA:
- nadmiernie zrogowaciały naskórek
- żółte lub woskowe zabarwienie skóry
- zgrubiałe i przerosłe płytki paznokciowe
Odmiany rogowca
Unna-Thost pojawia się ok. 1-2 roku życia. Zmiany rogowe są symetryczne, występuje nadpotliwość dłoni i stóp.
Keratoma disseminatum pojawia się po 20 roku życia. Charakteryzuje się drobnymi, rozsianymi wykwitami. Z wiekiem może ich przybywać.
Keratoma trnsgrediens et progrediens pojawia się w pierwszych miesiącach życia. Ogniska hyperkeratotyczne występują poza dłońmi i stopami i najczęściej znajduję się na łokciach i kolanach.
Lokalizacje odcisku:
- palce stóp (okolica grzbietowa stawy międzypaliczkowe, boczna i przyśrodkowa powierzchnia palców w miejscu stykania się skóry Clavus mollis, okolica podeszwowa palca – Clavus appex)
- przodostopie (głowy kości śródstopia)
- wały paznokciowe (clavus sulcus)
- przestrzenie podpaznokciowe (clavus subungualis)
Clavus durus (Cd) – zbudowany jest ze zwartej i twardej masy ułożonej warstwowo (nawet do 200 warstw), zawierający jądro.
Clavus mollis (Cm) – to inaczej odcisk miekki.
Clavus vascularis (Cv) – to odcisk z zawartością drobnych naczyń krwionośnych.
Clavus neurovascularis (Cnv) – odcisk nerwowo – naczyniowy.
Clavus neurofibrosis (Cnf) – odcisk nerwowo – włóknisty.
Clavus papilaris (Cp) – to odcisk brodawkowy. Często się powtarza.
Clavi miliares (Cmil) – odciski mnogie.