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Wyprysk z hiperkeratozą - Objawy, Diagnoza i Leczenie
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.
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.
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.
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.
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]