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.

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]

Jakie są przyczyny hiperkeratozy?

Przyczyny hiperkeratozy mogą mieć różnorodne podłoże. Należą do nich:

• tarcie i ucisk,
• problemy hormonalne,
• reumatyzm,
• cukrzyca,
• nadwaga,
• reakcje uczuleniowe,
• niedobory witamin,
• kontakt z silnymi środkami chemicznymi (np. detergentami),
• zbyt sucha skóra,
• dziedziczne choroby genetyczne, np. rybia łuska,
• łuszczyca,
• atopowe zapalenie skóry,
• podrażnienia mechaniczne,
• infekcje grzybicze i bakteryjne.

W przypadku hiperkeratozy na stopach do przyczyn zalicza się również:

• źle dobrane obuwie,
• zdeformowaną budowę stopy,
• konieczność stania przez długi czas,
• długie spacery i marsze,
• biegi długodystansowe,
• zbyt dużą potliwość stóp,
• brak odpowiedniej higieny stóp.

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.

A Word From Verywell

A skin condition can be challenging to deal with, especially if it causes painful symptoms. The good news is that dealing with most forms of hyperkeratosis is manageable with the proper treatment. In most cases, this condition is not severe or life-threatening.

The best thing you can do if you have hyperkeratosis is to speak to a dermatologist (a medical doctor specializing in conditions of the skin, hair, and nails) about your condition and any concerns you have. They will be able to determine the next steps to address your condition.

Frequently Asked Questions

The treatment for hyperkeratosis will depend entirely on its type and the underlying cause. Treatment isn't always necessary because some forms of hyperkeratosis are either asymptomatic or present with mild cosmetic symptoms. The most common forms of treatment include keratolytics, moisturizers, emollients, and retinoids.

Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.

1. Jakeman A. The effective management of hyperkeratosis.Wounds Int. 2012,1:65-73.
2. National Human Genome Research Institute. Genetic disorders.
3. Tian Y, Li XX, Zhang JJ, Yun Q, Zhang S, Yu JY, Feng XJ, Xia AT, Kang Y, Huang F, Wan F. Clinical outcomes and 5-year follow-up results of keratosis pilaris treated by a high concentration of glycolic acid.World J Clin Cases. 2021 Jun 26,9(18):4681-4689. doi:10.12998/wjcc.v9.i18.4681
4. Harvard Health Publishing Harvard Medical School. Hyperkeratosis.
5. National Organization for Rare Disorders. Lamellar Ichthyosis.

By Angelica Bottaro
Bottaro has a Bachelor of Science in Psychology and an Advanced Diploma in Journalism. She is based in Canada.

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