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Wyprysk z hiperkeratozą - Objawy, Diagnoza i Leczenie
HYPERKERATOZY – rodzaje i różnicowanie cz.2
- odciski
- modzele
- nadmierne rogowacenie i zespół pękających pięt
- rogowiec
Zmiany będące reakcją obronną skóry na bodźce zewnętrzne. Powstają na skutek nadmiernego wytwarzania komórek warstwy rogowej naskórka. Powstaje bariera uniemożliwiająca fizjologiczną migrację nowych komórek, a co za tym idzie dochodzi do pozostawania korneocytów w niższych warstwach skóry.
Odciski są wyniosłymi zgrubieniami naskórka o kształcie okrągłym, podłużnym lub nieregularnym. Cechą wyróżniającą odciski jest obecność rdzenia, czyli twardego czopu rogowego, zlokalizowanego najczęściej centralnie.
Trzpień odcisku często sięgając głęboko (nawet do okostnej), drażni zakończenia nerwowe dając uczucie bólu.
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.
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.
History and Physical
Hyperkeratosis is a histopathological term defining a thickened stratum corneum and may be present in many different skin conditions, with many possible overlaps. History and clinical evaluation are key, and the main goal is to collect as much information as possible and discern which cases require a histopathological diagnosis to direct the most appropriate treatment.
The history comprises the age of the patient, family history, exposure to toxic substances, drugs, occupational duties, anamnesis of the current lesion, concomitant pathologies, and treatments. In those patients where the diagnosis was already established, it is appropriate to reevaluate it, monitor progression and complications following the treatment.
The physical examination must be thorough to exactly understand the extent of the disease. Except for localized disease, it is important to inspect the entire skin surface, including scalp, eyelids, ears, perineum and genital mucosa, hair, and nails. The lesion should be described in terms of color, texture, shape, and distribution. Surrounding skin should be examined as well to detect the presence of generalized xerosis (dryness), seborrhea, hyper or hypohidrosis (sweating), texture, photoaging such as lentigines, actinic purpura, rhytides.
Small folliculocentric keratotic nodules can be found in cases of keratosis pilaris, where papules are centered on small hair follicles, and it can be associated with erythema. On close examination, it is possible to recognize a small coiled hair beneath the papule formed by a keratin plug.
Scaling is an important finding in cases of hyperkeratosis. Scales may be described as soft, rough, greyish, bran-like, and so on. Crusts should not be confused with scale as it is the result of dried fluid on the epidermis (serum, blood, pus, or a combination of those) and not thickening of the epidermis. Lichenification is a thickening of the skin and results from chronic injuries such as repetitive scratching. It is present in most chronic eczematous or neurogenic processes.
