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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.
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.
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.
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.
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.