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Wyprysk z hiperkeratozą - Objawy, Diagnoza i Leczenie
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.
NADMIERNE ROGOWACENIE I ZESPÓŁ PĘKAJĄCYCH PIĘT
Przerośnięta żółto-szara warstwa rogowa pięt jest zazwyczaj sucha, łuszczy się i często pęka. Pęknięcia mogą być rysami, szczelinami, bądź nawet głębokimi rozpadlinami w suchym przerosłym naskórku.
W zależności od postaci klinicznej wyróżniamy:
PĘKNIĘCIA WILGOTNE wiążą się z maceracją na skutek nadpotliwości lub długotrwałego kontaktu z wodą. Każde pęknięcie skóry staje się wrotami infekcji. Zakażenie rany noże być przyczyną, a także skutkiem wysięku.
SUCHE PĘKNIĘCIA są następstwem przesuszenia (uszkodzony płaszcz hydrolipidowy) i utraty elastyczności skóry. Suche pęknięcia z małych rys mogą przechodzić w głębokie, krwawiące rany.
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.
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.
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.