Follicular hyperkeratosis: symptoms
Follicular hyperkeratosis is a medical term, popularly known as “goose bumps”. This is a condition in which the following symptoms appear:
- roughness and roughness of the skin;
- dryness;
- the formation of small beige, pink or red nodules.
This dermatitis is based on thickening of the stratum corneum and impaired exfoliation of keratinized epithelial cells. Due to the fact that the stratum corneum grows and the scales clog the pores, tubercles appear. This leads to the skin becoming covered with microcomedones.
Publications in the media
Skin papillomas - see Warts, Human papillomavirus infection. Trichoepithelioma multiple familial (*601606, 16q12–q13 and 9p21, MFT, TEM, Â genes) is a benign skin tumor originating from hair follicles, a relatively common inherited dermatosis with many small tumors, more often on the face.
Cysts are fluid-filled cavities • Epidermal cysts; treatment - excision • Sebaceous cysts are the result of blockage of the excretory ducts of the sebaceous glands. Treatment is excision (prevents recurrence). For infected cysts, they are limited to opening and draining the abscess with subsequent excision in a planned manner (they often recur when part of the capsule is left) • Dermoid cysts arise as a result of a violation of embryogenesis; when localized in the midline (glabella, nose), it is necessary to exclude communication of the cyst with the cranial cavity (cerebral hernia); treatment - excision • Synovial cyst - a cyst with fibrous walls containing a thick clear fluid rich in mucopolysaccharides; usually associated with underlying tendons; usual localization - palms and feet; Treatment is excision; with incomplete resection of the pedicle and walls of the cyst, relapse is possible.
ICD-10. L72.0 Epidermal cyst.
Vascular birthmarks are classified according to location and cellular composition. • Hemangioma (strawberry spot) - a soft red formation with a raised surface; characterized by the presence of proliferating mast cells and rapid growth during the first year of life; localization - head, neck, torso and limbs. Spontaneous recovery is possible; Surgery or steroid therapy is indicated for hemangiomas that cause functional impairment (if localized in the eyes, ears, or pharynx).
• Vascular malformations are divided into capillary, venous and lymphatic •• Capillary hemangiomas (“port wine stains”) are most often localized on the face, chest and limbs, observed in Sturge-Weber and Klippel-Trenaunay-Weber syndromes. These are clusters of dilated capillaries in the papillary, dermal and subdermal layers. For small tumors, the method of choice is excision. Laser therapy and sclerotherapy are also effective. • Venous malformations (cavernous hemangiomas) often affect deep structures, including muscles. Platelet sequestration is possible. Treatment is excision, possibly introducing a sclerosing agent into the cavity. •• Lymphatic malformations (lymphangiomas, cystic hygromas) cause hypertrophy of the affected soft tissues. Treatment is excision. A common complication is seroma. •• Arteriovenous aneurysms can suddenly increase in volume, causing compression of surrounding tissue. The treatment method is excision.
ICD-10. Q82.5 Congenital non-neoplastic nevus
Vascular tumors • Pyogenic granuloma (bothryomycomoma) is a tumor-like formation of red or brown skin on a stalk, which is a proliferation of granulation tissue with a large number of capillaries, localized on the face, chest and fingers, and can bleed. Surgical excision or cryodestruction is indicated • Stellate nevi (telangiectasia) occur at any age on the face, chest and limbs. They consist of a central arteriole with radiating vessels similar to venules. An increase in nevi is possible during pregnancy and liver failure. Bleeding is rare. Treatment: laser destruction, electrocoagulation, cryotherapy, sclerotherapy.
Seborrheic keratosis is characterized by light and dark brown papules. If malignancy is suspected, a biopsy is necessary. Treatment is electrocoagulation.
ICD-10. L82 Seborrheic keratosis
Keloids are growths of fibrous tissue in areas of injury and scarring. Treatment is excision. Sometimes auxiliary local GC therapy, electrophoresis or lidase injections, and laser irradiation are indicated.
ICD-10. L91.0 Keloid scar.
How does follicular hyperkeratosis develop?
It is considered normal that when the lumen of the follicular canal contains a thin layer of corneocytes, its rejection occurs quite easily. But if microcomedones form - blockage of the follicles - this process slows down. Impaired desquamation can lead to retention hyperkeratosis, the formation of dense plugs of keratin, sebum and bacteria in the orifices.41
The structure of the follicle suggests the presence of an acroinfundibulum (its upper part) and an infrainfundibulum. With hyperkeratosis of the first, open comedones are formed, when increased keratinization concerns the second - closed comedones. 41
In closed comedones, the level of oxygenation is very low, and the drainage of metabolites of propionibacteria and sebum is blocked. The dark color of open comedones is associated with the accumulation of melanin. 41
Symptoms
Symptoms of actinic keratosis appear as a white scaly lesion, within which there is redness and roughness of the epidermis. In a small area of skin there may be many lesions of actinic keratosis, which can have different diameters from a few millimeters to even 3 centimeters. Discoloration of the skin, thickening of the epidermis, deep wrinkles, elastosis, lenticular spots, dry skin and telangiectasias are also common in the lesions.
Actinic keratosis is divided into the following categories:
- 1st degree - changes are clearly visible, tender to the touch;
- 2nd degree - changes are clearly visible and palpable;
- 3rd degree - the changes are very noticeable, hyperkeratotic.
Symptoms of actinic keratoses may remain unchanged for several years, disappear spontaneously, or develop into squamous cell carcinoma.
Causes of follicular hyperkeratosis on the face
Scientists cannot yet say unequivocally what is the initiator of increased proliferation of keratinocytes and their adhesion, but it is assumed that the following factors may have an influence41:
- decrease in linoleic acid levels;
- androgens;
- increased interleukin-1 activity.
If we compare epidermal and follicular keratinocytes, then in the latter 17-HSD and 5 reductase are more active. This leads to an increase in DHT in the body, and it is one of the main initiators of the proliferation of keratinocytes and an increase in sebum production. 41
Linoleic acid regulates the proliferation of follicular keratinocytes. With acne, its level drops significantly, which can cause an increase in the proliferation of follicular keratinocytes and the synthesis of pro-inflammatory cytokines. 41
Treatment
Treatment of actinic keratosis is limited to local destruction of the lesions or the area that may be affected by the tumor. The type of method depends on the number of lesions and the presence of signs of photoaging on the surrounding skin.
One of the most commonly used methods for treating single lesions is cryotherapy. It is characterized by speed, efficiency and low financial costs. In addition, CO2 ablation laser and Erbium Yag laser can be used. However, they do not show greater advantage over cryotherapy due to high cost and the high operator experience required.
Photodynamic therapy, chemical peels, tretinoin, and topical immune response modifiers are used to treat symptoms suggestive of squamous cell carcinoma.
Follicular hyperkeratosis: treatment
It is impossible to get rid of follicular hyperkeratosis once and for all, as it is a chronic condition. However, it does not require and does not have specific treatment. Nevertheless, follicular keratosis is one of the links in the pathogenesis of acne, a common dermatological disease. You can reduce the appearance of goose bumps by including the following products in your care256:
- Acid peels. To combat follicular hyperkeratosis, it is necessary to include in your care products with lactic, salicylic, and citric acids, which help exfoliate dead skin particles. This will help make the surface of the skin smoother and also softer.
- Products with urea. Urea perfectly moisturizes the skin. Products with it can be used throughout the body. But it is important to take into account its percentage in a cosmetic product: at 10% it acts as a moisturizer, at 20-50% it acts as a keratolytic. If the concentration is 50% or more, the product can only be used on rough skin, for example, for calluses and corns, but for other areas, including hyperkeratosis of the facial skin, it is not suitable.
- Products with retinol. This component, unlike urea and acid peels, does not cause exfoliation. Retinol does not react to dead horny scales, but to living cells of the basal layer of the skin. Under its action, they divide faster and move towards the epidermis, pushing out the dead cells located on top, which is expressed in the form of peeling.
Also, for acne, hardware or injection procedures can be used to eliminate follicular hyperkeratosis. They should be selected by a specialist.
Follicular keratosis (parafollicular keratosis, Kirle disease - CD) is a rare skin disease from the group of perforating dermatoses, which is based on a violation of keratinization with intradermal invagination of the epidermis [1] (synonyms: follicular and parafollicular hyperkeratosis, penetrating the skin, follicular and parafollicular hyperkeratosis with penetration into the skin (hyperkeratosis follicularis et parafollicularis in cutem penetrans), penetrating hyperkeratosis [2, 3]).
The disease was first described in 1916 by the Austrian dermatologist J. Kyrle, who observed this dermatosis in a patient with diabetes mellitus [3-5].
Epidemiology.
The disease is rare. The age of patients is 20-70 years. Women get sick more often, children - very rarely. Concomitant diseases: often - diabetes mellitus and chronic renal failure, less often - heart failure, hypothyroidism, type II hyperlipoproteinemia (increased blood levels of cholesterol and triglycerides) [1, 3-6].
Etiology and pathogenesis
have not been fully studied. The previously assumed role of a viral or bacterial infection, a violation of vitamin A metabolism in the development of this dermatosis is only of historical interest [4]. A certain significance in the development of the disease, in addition to impaired carbohydrate metabolism, is attributed to liver damage (chronic hepatitis) with the development of secondary vitamin A deficiency [5].
The genetic predisposition to the development of CD has not been conclusively proven, although cases of the disease among relatives in the same family with consanguinity (first-degree relatives) have been described [1, 3-5].
According to the original definition by J. Kirle [7], this is a disease in which an atypical clone of keratinocytes penetrates through the epidermis into the dermis. It is believed that the basis of the pathological process is a violation of keratinization, differentiation and keratinization of keratinocytes (formation of dyskeratotic foci and acceleration of the keratinization process). This leads to the formation of keratotic plugs with areas of parakeratosis. Keratification begins already at the border of the epidermis and dermis. The rate of differentiation and keratinization exceeds the rate of cell proliferation, therefore the parakeratotic cone partially penetrates deeper into the damaged epidermis and causes its perforation into the dermis [1, 3-6].
Unified classification
There are no follicular keratoses. Among the independent nosological forms, papular, atrophying and vegetative follicular keratoses are distinguished [8]. A number of authors [4, 6] draw attention to the similarity of CD with lenticular persistent hyperkeratosis of Flegel and consider the latter as a variant of CD, although the clinical manifestations differ. Other authors [5, 8] classify CD as vegetative follicular keratoses, and persistent keratosis follicularis (Flegel's disease) as papular.
The concept of reactive perforative keratinization disorder against the background of kidney, liver, and diabetes mellitus is considered. A concept has emerged - perforating skin diseases; it includes a group of diseases in which the elimination of altered skin components occurs through the epidermis (a process called transepidermal elimination). Some authors dispute CD as an independent nosological entity [7].
In the International Classification of Diseases, 10th revision, in class XII (diseases of the skin and subcutaneous tissue), heading L87 is allocated - transepidermal perforated changes, in which CD is assigned a separate subheading L87.0.
Pathomorphology
very characteristic and has diagnostic significance. The recesses of the epidermis and the dilated openings of the hair follicles are filled with hyperkeratotic plugs. Under the plugs in the epidermis, the growth of the granular layer is pronounced, and in places where there is no hypergranulosis, there is parakeratosis, penetrating the entire epidermis to the dermis. Subsequently, thinning of the epidermis occurs and penetration of horny masses into the dermis with the formation of inflammatory infiltrates such as granulomas from lymphocytes, leukocytes, histiocytes and giant cells of foreign bodies in the dermis. Death of the sebaceous glands in the area of the affected follicles, degeneration of collagen fibers, and hyperelastosis are observed [1, 2, 5, 6].
Clinical picture.
The onset of the disease is gradual, new rashes appear as old elements disappear. Follicular or parafollicular papules are characteristic, first the color of healthy skin, and subsequently grayish or brownish-red in color, with a diameter from a pinhead to 1 cm. In the center of the elements there is a horny plug, when removed, a crater-shaped depression is formed. Papules tend to grow peripherally and merge with the formation of dry polycyclic plaques covered with layers of scales and crusts. The consistency is dense, the surface is uneven, warty. Fresh rashes are accompanied by mild itching (more often in patients with diabetes) or do not bother the patient. Older, larger lesions are painful, especially when pressed. In the places of calculations there is a linear arrangement, which indicates the possibility of the occurrence of the Koebner phenomenon. A secondary infection may occur. Localization of rashes - extensor surfaces of the limbs, torso, buttocks. The mucous membranes are not affected [1-6]. Rashes in the mouth, palms, soles, and genitals are rare [4].
Flow
CD is chronic, relapsing. The disease is difficult to treat. The prognosis largely depends on the underlying disease.
Diagnostics
based on anamnesis, clinical and histological picture of the disease. Differential diagnosis of CD should be carried out with Devergy's lichen pilaris, Darier's follicular dyskeratosis, Mibelli's porokeratosis, transepidermal perforated skin changes (perforating creeping/serpiginous elastosis, reactive perforating collagenosis), Flegel's disease [8].
Flegel's disease
(hyperkeratosis lenticularis perstans), like CD, is a rare form of keratosis pilaris. It is believed that the basis of this disease is a hereditarily determined (autosomal dominant type) pathology of keratinization, expressed in a violation of the synthesis of keratin 55K, the content of which is sharply reduced in the lesions of Flegel's disease, while in normal skin this type of keratin dominates. Histologically, thinning of the epidermis, follicular orthokeratosis with foci of parakeratosis, and spongiosis in places are revealed; a band-like lymphocytic (mainly T-helper) infiltrate is expressed in the dermis. The previously attached great importance in the pathogenesis of dermatosis to the absence or disruption of the structure of Odland bodies [4] is now being questioned. Odland's granules appear in the upper rows of the spinous layer in keratinocytes, occupy a peripheral position and release their contents by exocytosis into the intercellular space, where it takes on a lamellar structure (intercellular cement) - a component of normal keratinization. Unlike CD, this dermatosis appears more often in adolescence and middle age, and is characterized by the formation of disseminated, smaller (1–5 mm) and more superficially occurring horny papules (without a tendency to form plaques). In CD there is no impairment of keratin 55K [6].
Treatment:
vitamin A, long-term aevit, retinoids (neotigazone, etretinate, acitretin at the rate of 0.5 mg/kg per day). Externally - keratolytic ointments, 2% sulfur salicylic ointment, retinoid cream, 0.1% tigazone cream, 5% fluorouracil cream (for an area of no more than 500 cm2 at a time), electro-, cryo- and laser destruction (carbon dioxide laser) of individual lesions, ultraviolet irradiation . The effect of treatment is temporary. After removal of the horny plug, an atrophic, unevenly pigmented scar remains; relapse may occur nearby. Correction of visceral pathology is necessary [3-6].
We present our own clinical observation.
Patient B., 57 years old, retired (military orchestra musician), was admitted to the purulent surgery department on September 13, 2010 for surgical treatment for osteomyelitis of the left foot. The attending physician prescribed a consultation with a dermatologist due to skin rashes.
Anamnesis.
The first rash on the skin of the front chest appeared about 20 years ago. The rashes practically did not bother me; minor itching was rarely noted; I was more “worried” about the cosmetic aspect. Diagnoses were made: dermatitis, xerosis, keratosis. There was no effect from the recommended salicylic ointment, creams with chamomile, string, or taking vitamin A orally, which was explained by the “peculiar structure of the patient’s skin.” According to the patient, the best effect was noted from the use of cindol (“the chatter dries well and peels off the plugs” on the skin). The rashes did not disappear completely, no seasonality was noted.
Since 1995, he has been suffering from type 2 diabetes mellitus and has been taking oral hypoglycemic drugs (diabetes). In 2009, he received inpatient treatment at his place of residence for diabetic foot syndrome, a purulent-necrotic wound on the left foot; healing by secondary intention. Since the summer of 2010, the rashes have increased significantly, which the patient associated with extreme heat. In July, I received a puncture wound in my left foot (I stepped on a nail at the dacha), which did not heal for a long time, and my blood sugar level increased. Due to worsening severe pain, the patient was hospitalized.
Skin status.
On the skin of the body there are multiple follicular and parafollicular papules of a red-brown color, in places grouped into small plaques covered with dense scales. In the center of the papules there are horny plugs. Where the plugs have come off, there are crater-shaped depressions filled with the previously applied zindol. In place of the resolved elements there are small scars. On palpation, the rashes are dense, the skin resembles a “grater”, and is moist. Several intradermal nevi are round, dome-shaped, soft in consistency, and brown in color (Figure a-c).
Figure 1. Patient B., 57 years old: manifestations of CD.
The patient suffers from diabetes mellitus and diabetic nephropathy. a—c—many pinkish-red and grayish-colored papules and nodules with horny plugs. In those places where the patient scratched the skin, the elements of the rash are located linearly (Koebner's symptom). Several intradermal nevi. Skin of the head, limbs, visible mucous membranes without rashes, physiological coloring. Results of special examinations.
Clinical blood test: hemoglobin - 124 g/l, erythrocytes - 4.0 1012/l, leukocytes - 6.7 109/l (upon admission 12.8 109/l), neutrophils - 67%, segmented - 65 %, band - 2%, eosinophils - 3%, lymphocytes - 23%, monocytes - 9%, erythrocyte sedimentation rate - 35 mm/h (on admission 53 mm/h). ASTL-0 titer and rheumatoid factor were not detected. PSA -10 mg/l. Urinalysis upon admission: specific gravity - 1020, protein - 0.132‰, sugar - 0.3 mg/l, acetone - no, leukocytes - 3-5 in the field of view, erythrocytes - 4-5 in the field of view, cylinders - 4 in drug. Upon discharge, urine analysis was normal.
Radiography
chest organs - without pathology. X-rays of the left foot show complete destruction of the head of the third metatarsal bone, partial destruction of the second metatarsal joint. Electrocardiogram - sinus rhythm, heart rate 76 per minute; changes in the myocardium; phenomenon of early ventricular repolarization.
Endocrinologist.
Diabetes mellitus type 2, severe, insulin-requiring, decompensated. Diabetic angiopathy of the vessels of the lower extremities. Diabetic nephropathy. CRF-0.
Ophthalmologist.
Proliferative diabetic retinopathy. Initial cataract of the right eye.
Surgeon.
Flaccid granulating wounds of the plantar surface of the left foot. Osteomyelitis of the II-III metatarsal bones of the left foot.
Dermatologist.
Keratosis follicular and parafollicular, penetrating (KK). Intradermal nevi. There are no contraindications to surgical treatment.
On September 20, 2010, the patient underwent transmetatarsal resection of the head of the third metatarsal bone. Amputation of the third toe of the left foot. Received antibacterial therapy, humulin, lantus; Dressings with dimexide, water-soluble ointments, and physiotherapy were carried out. The skin of the body was treated with cindol once a day.
Recommendations for discharge.
Observation by an endocrinologist or surgeon at the place of residence; humulin 18 units 3 times a day before the main meal, lantus at 22:00 16 units. Dressing of residual wounds with betadine ointment. Laser coagulation of the retina after normalization of sugars in a separate hospitalization, then see a dermatologist.
Discussion
Every dermatologist encounters strange patients. This is especially true for rare dermatoses, some of which a doctor may encounter only once during his practice. “It’s better to see once than to hear a hundred times,” says Russian folk wisdom. “The main tool of a dermatologist is his eyes” [3].
The fact that our patient had severe symptoms of hyperkeratosis of the trunk was obvious, but we had not encountered either CD or Flegel’s disease before. Only on the basis of anamnestic data, a characteristic clinical picture and information obtained from literature sources (the patient refused the proposed skin biopsy) was the final diagnosis made. Our patient suffers from diabetes mellitus and diabetic nephropathy. If the recommended screening of all patients with hyperkeratoses to detect latent diabetes [4] had been done earlier, the diagnoses might have been made earlier. This is precisely the purpose of this publication.
What links in pathogenesis are affected by Clindovit®?
Clindovit® is a topical antibiotic that is active against most strains of propionibacteria6. When applied to the skin, it reduces free fatty acid levels from approximately 14 to 2%6. The main active ingredient of the drug is clindamycin6. The base also contains auxiliary components: emollient and allantoin6.
Since Clindovit® is an antibiotic, it is recommended to combine it with other drugs, for example, benzoyl peroxide or azelaic acid (Azelik®)12. In particular, azelaic acid normalizes keratinization processes and helps eliminate follicular hyperkeratosis40.
What is keratosis
Actinic keratosis of the skin (actinic keratosis) is a dysplastic skin lesion limited to the layers of the epidermis. They are located in areas where the skin is overexposed to ultraviolet rays or on aging skin. As a result, noticeable foci appear that determine the characteristics of tissue damage, which are called the tumor threat zone. It should be emphasized that these areas can progress to non-melanoma skin cancer, especially squamous cell carcinoma (SCC).
The disease most often occurs in people of the Caucasian race with skin phototype I or II, prone to sunburn, constantly exposed to phototherapy, with genetic tendencies (albinism, pigmented skin), very often in men without hair on the head.
Actinic keratosis and the possibility of its progression to squamous cell carcinoma result from damage to the DNA of keratinocytes by solar radiation, which leads to mutation of suppressor and regulatory proteins. The most dangerous wavelength is radiation in the UVB range (280–320 nm). This disease was first described by Christian Neumann in 1869.
Prevention
Photoprotection plays an important role in the prevention of actinic keratosis. Sunscreens should be selected based on skin color, radiation intensity, and the amount of time the skin is exposed to the sun. The factor that determines the effectiveness of this type of product is the sun protection factor (SPF).
The SPF index determines the multiple of time after which solar erythema occurs on the skin protected by the product in relation to the unprotected area of the body under the same conditions.
It should be emphasized that sunscreens, in addition to protecting against UVB, must also contain ingredients that protect against UVA rays. The ability of a cosmetic product to provide such protection is determined by the abbreviation PPD (persistent pigment darkening) or IPD (intermediate pigment darkening).
The key to effective photoprotection is proper application of sunscreen. It is recommended to apply them 20 minutes before putting on clothes. A time relationship between product application and product contact with clothing has been demonstrated, indicating an impact on actual SPF value. In addition, the amount of product used is very important. It should cover 2 mg/cm2 of skin. The effectiveness of sunscreen cosmetics is reduced by contact with moisture, so application should be repeated every 2-3 hours and after each skin contact with water.
An important part of sunscreen is to avoid sun exposure between 11am and 3pm. Remember to gradually increase your tanning time, cover your body with light clothing, use a protective hat and sunglasses.
Protecting your skin from sun damage is a key part of your daily skin care routine. Skin prevention with photoprotection can prevent the development of squamous cell carcinoma of the skin (SCC) or its early form.
