Phrynoderma is a rare skin pathology associated with a lack of retinol in the body against the background of violations of its consumption or absorption in the intestine. It is clinically manifested by the process of keratinization in the area of hair follicles, resembling the hyperkeratotic “grater phenomenon”, which eventually turns the patient’s skin into a rough “toad shell”. The process involves the mucous membranes of the oral cavity, which lose their shine and moisture. Phrynoderma is diagnosed taking into account anamnesis, clinic, histology and blood serum analysis for carotene, vitamin A. Systemic pathology requires consultation of specialized specialists. Treatment of phrynoderma is carried out with retinol in large doses: both medicinally and by increasing its intake with food.
Phrynoderma – alimentary vitamin deficiency A with the phenomena of follicular keratosis. The dryness of the dermis, the formation of horny follicular and perifollicular nodules on it the size of a millet grain make the skin look like the skin of a toad, which gave rise to the name of the pathological process phrynoderma. American dermatologists consider phrynoderma to be an analogue of Crocker’s or Piccardi’s awl lichen, however, the connection of these dermatoses with lichen, and not with beriberi, refutes this hypothesis. The pathological process practically does not occur in highly developed in USA and is common in third world countries, where hunger, unsanitary conditions, poor living and social conditions are factors provoking the development of phrynoderma. The urgency of the problem in modern dermatology is associated with the tendency to increase the incidence of drug-induced phrynoderma due to uncontrolled medication intake, the development of dysbiosis.
The trigger of the phrynoderm is obvious – retinol deficiency as a result of exogenous (lack of vitamin A in foods, incorrect culinary processing of food that contains retinol) and endogenous (malabsorption in the small and large intestines, hemodialysis) factors that cause an imbalance of metabolism.
Retinol (vitamin A) is one of the central links of metabolic processes occurring in the epidermis and dermis. With its lack, trophic disorders and inflammation occur, which activates the T-lymphocyte system and reticular tissue cells. The latter stimulate the proliferation of horn cells. At the same time, due to metabolic disorders, the composition of the secretion of the sebaceous glands changes, which glues the excess of horn cells at the mouth of the follicles. There is a corneal plug that blocks the mouth of the hair exit to the skin surface, causing perifollicular inflammation, aggravating the proliferation of cells of the upper layer of the epidermis, forming foci of follicular hyperkeratosis. So there is a phrynoderm.
Clinical manifestations of the pathological process may have different degrees of severity. Phrynoderma of the first degree of severity is characterized by widespread hyperkeratosis on the background of dry skin; the second is the appearance of lenticular papules; phrynoderma of the third degree of severity is characterized by the addition of vegetative papules, erosions.
The onset of pathological changes is visually manifested by a change in the color of the dermis, which turns pale, becomes dry. It loses moisture, and along with it – elasticity, begins to peel off, at the same time the work of the skin glands is disrupted. The mucous membranes are involved in the process, they fade, become dry, cracks appear on them. Follicular hyperkeratosis is formed – one of the main symptoms of phrynoderma, the foci of which are depigmented along the perimeter. Later, with the progression of the phrynoderm, secondary, perifollicular nodules appear next to the follicular nodules, the skin becomes rough, like a toad, the glandular apparatus of the dermis atrophies.
Deep cracks form in the corners of the mouth. The process with a small nodular rash on the extremities extends to the face, back, buttocks. Papules transform into plaques that begin to vegetate, ulcerate. The mucous membrane of the red border of the lips with phrynoderm gradually becomes keratinized, becomes dry, cracks. The pathology accompanying the disease manifests itself: tartar is deposited, conjunctivitis, keratitis (Bito spots) occurs, vision worsens, especially in the dark and twilight. There is a typical manifestation of vitamin deficiency A, known as a symptom of “night blindness”.
Diagnosis and treatment
The clinical diagnosis of phrynoderma is made by a dermatologist taking into account the anamnesis, clinical dynamics of the pathological process, the results of histological examination, the conclusions of narrow specialists (gastroenterologist, ophthalmologist, dentist). The concentration of carotene and retinol in the blood serum is determined. In the biopsy from the focus of the phrynoderm, a near-follicular infiltrate with the phenomena of hyperkeratosis, atrophy of the glandular apparatus of the dermis is noticeable. There is a clear hyalinization of collagen and elastic fibers, the absence of subcutaneous fat. Phrynoderma is differentiated with styloid lichen, lichen planus, ichthyosis, red hair bran-like lichen, nodular pruritus, Darye’s disease, lichenoid tuberculosis of the skin, psoriasis, keratoses, oil folliculitis (acne), chronic ulcerative pyoderma.
The therapy of the pathological process is long-term, based on the introduction of large doses of vitamin A into the patient’s body, which is associated with its epithelial-plastic properties. The introduction of high-calorie foods rich in vitamin A into the diet improves tissue trophism, minimizes skin manifestations of phrynoderma. Externally, salicylic, keratolytic ointments, aniline dyes, products containing fish oil and vitamin A are used. In parallel, they correct the pathology of the digestive tract, review the expediency of drug therapy previously prescribed for indications other than phrynoderma. Prevention consists in regular full nutrition. The forecast is relatively favorable.