Keratoderma climactericum is a chronic keratodermatitis of the menopausal period caused by a lack of estrogens in the body. Symptomatically manifested by spontaneously arising foci of hyperkeratosis on the palms and soles, significantly reducing the quality of life, interfering with walking and homework due to the appearance of cracks on the skin. The primary element is a flat papule, which tends to merge and peripheral growth. Rashes are accompanied by itching, which increases at night. The diagnosis is clinical, confirmed by histological studies. Therapy is pathogenetic (HRT) and symptomatic (keratolytics, regeneration stimulants, local baths).
Climacteric keratodermia (Haxthausen syndrome) is a hypoestrogenic climacteric dermatitis with a predominant violation of keratinization processes in the stratum corneum of the epidermis. Pathology has a bright gender coloring. About 20% of women over the age of 45 are ill. The first dermatologist who described the clinic of this form of keratodermia and associated its beginning with menopause was the Englishman Henry Brooke in 1891. He devoted most of his life to the study of “keratin dermatoses”, discovering in 1886 follicular keratosis, and then an unusual epithelial nevus. In 1934, Haxthausen described in detail 10 clinical observations of menopausal women with keratotic lesions of the palms and soles, who had deep cracks in the skin, bringing them real suffering. He also suggested a connection between hyperkeratosis and ovarian pathology. But it was only in 1943 that Peter Lynch identified the leading factor in the development of this pathology – estrogen deficiency. The relevance of the problem today is determined by the possible relationship of climacteric keratoderma with chronic neoplastic processes in the body of patients.
Modern dermatology considers keratoderma climactericum to be one of the components of menopause symptoms associated with age-related depletion of ovarian function. Since neuroendocrine regulation of skin trophism is carried out through ovarian hormones “working” in close contact with the thyroid gland under the control of the central nervous system, the general condition of the skin directly depends on the hormonal background of the patient. In the process of physiological aging, there is a restructuring of this background. The level of estrogens naturally decreases, and the transport of proteins, fats, and carbohydrates necessary for the construction of normal tissue structures immediately decreases. The hypothalamus tries to compensate for this lack by the increased work of other systems controlled by it, as a result of which such phenomena as hyperhidrosis and tachycardia occur, vasoconstriction occurs, and the protective properties of the skin increase.
One of the mechanisms to enhance such protection is the minimal desquamation (peeling) of the cells of the stratum corneum, the surface layer of the epidermis, directly in contact with external factors. In this case, with the development of hyperkeratosis, the cells of the epidermis do not just begin to divide at a double rate, as with other keratoses, but degenerate as a result of a violation of metabolic processes in the skin. Proteins responsible for keratinization are produced prematurely, disrupting the ratio of components involved in keratinization processes. The cells of the epidermis do not have time to get the necessary nutrients due to the violation of the trophic skin, their enzyme systems work with minimal energy costs, lipid metabolism is disrupted, the cytoplasm is overflowing with keratin, which displaces the nucleus and organelles from the cell and appears on the surface in the form of horny scales.
At the same time, inflammation occurs around pathologically developing cells, a substance is produced that cements the horn cells. These are myelin-type lipid inclusions. Normally, there is a dynamic balance on the surface of the skin between the exfoliating cells of the stratum corneum and the living cells of the basal layer that replace them. This determines the thickness of the epidermis and stratum corneum. With a decrease in the synthesis of estrogens, cell proliferation decreases, their desquamation decreases, and the thickness of the epidermis increases due to the cells of the stratum corneum remaining on the surface. An excess of dead cells forms foci of keratodermia on the surface of the skin.
The primary element of keratoderma climactericum is inflammatory erythema, against which papular elements of small size are poured out, which tend to merge and diffuse spread over the entire surface of the palms and soles, on which the pathological process is most often localized. Papules are covered with silver scales. The rash occurs in a dehydrated version, so the skin is dry, flaky. Over time, hyperkeratotic layers thicken the surface of the skin, due to dryness in the thickness of keratous foci, deep cracks appear, causing severe pain. The lesion of the skin is symmetrical, cracks are localized more often in places of pressure on the skin, that is, on the edges of the palms, soles, but they can affect the flexor surfaces of the elbow and knee joints, other areas of the skin.
Subjective symptoms correspond to menopause: hot flashes, sweating, chills, palpitations, increased blood pressure. Patients suffer from severe itching, more at night. The primary rashes are joined by combs, secondary infection, the clinical picture resembles “dry” eczema. Nails are involved in the process. They become cloudy, thicken, become brittle, the periarticular bed becomes inflamed, burrs appear along the perimeter. Relief of menopause symptoms leads to self-resolution of skin manifestations. However, if keratoderma developed against the background of an existing latent or obvious tumor process, its malignancy is possible.
Diagnosis and treatment
The clinic of keratoderma climactericum is typical, there is no doubt about the diagnosis. Histological examination is rarely resorted to. Histopathology is nonspecific: hyper- and parakeratosis phenomena with lymphoid infiltration, degeneration of collagen and elastic fibers of the dermis. Microscopy of the scraping from the hearth on mushrooms and consultation of a gynecologist-endocrinologist is mandatory. Differentiate the disease with other forms of local hyperkeratosis, the “dry” form of idiopathic eczema, psoriasis, lichen planus, rubromycosis, keratodermal syphilis.
The therapy is pathogenetic, aimed at replenishing the lack of estrogens. In parallel, thyroidin, vitamin therapy (A, E), keratolytic ointments, wound healing drugs are used. A good effect is given by warm soda baths, baths with chamomile, sage. The prognosis is relatively favorable, taking into account frequent relapses and violations of the quality of life.