Syphilitic leukoderma, alopecia, tonsillitis and other manifestations of secondary syphilis. Leucoderma is light spots on the skin due to depigmentation that arise for various reasons. Physical examination results

Leucoderma is not independent disease, but a characteristic sign of several diseases that are accompanied. This term comes from two Greek words: leukos and derma (translated as White skin). It is used to indicate a pigmentation disorder, which is accompanied by a decrease in the level or complete disappearance of (coloring pigment) and the appearance of multiple white spots of various shapes and outlines on the skin. Sometimes dermatologists use the following terms to refer to such pathological changes: hypopigmentation, hypochromia, hypomelanosis or leukopathy.

Leucoderma is observed with equal frequency in both men and women. This pathology can develop at any age, but more often its first signs are detected in children under 12 years of age (sometimes already at the time of birth).

Such pigmentation disorders may appear suddenly and without any visible reasons on any part of the body. Sometimes their formation is provoked by various factors (for example, inflammatory skin diseases). In any case, such an unpleasant aesthetic defect of the skin always causes a person to feel awkward in front of others and a lot of inconvenience. Why do white spots appear on the skin? How can they manifest themselves and what to do with such pigmentation disorders? You will get answers to these questions that concern every person who is faced with this problem in this article.

Causes

Skin tone is determined by the level of melanin, which is synthesized in special cells - melanocytes. The starting material for the formation of this pigment is the amino acid tyrosine.

This substance enters the body with food, but under the influence of pineal gland hormones and an enzyme such as phenylalanine-4-hydroxylase, it can be synthesized from the amino acid L-phenylalanine, found in muscle tissue proteins.

If any malfunction occurs in this complex biochemical process, which is regulated by the endocrine and nervous systems, then skin cells stop accumulating melanin, and a pigmentation disorder occurs - skin dyschromia. One of the manifestations of such a disorder is leukoderma.

There is no consensus among dermatologists on the classification of the causes of leukoderma. This is explained by the fact that many of them have not yet been sufficiently studied, and research continues.

Some dermatologists conditionally divide the causes of leukoderma into two groups:

• unknown etiology;
• infections.

Most dermatologists identify the following main reasons for the appearance of leucoderma:

• inflammatory;
• pathologies of the nervous system;
• pathologies of the endocrine system.

Leukoderma can accompany various infectious diseases (for example, tuberculosis, leprosy, etc.) and becomes a consequence of such skin lesions as pityriasis, red flat, multi-colored, white, scaly lichen, etc. Sometimes this pigmentation pathology is inherited or caused by exposure to toxic or medicinal substances on the body.

Some experts believe that hypomelanosis is a secondary skin dyschromia. Others divide leukoderma into primary and secondary, congenital and acquired.

The most common types of leukoderma are:

• infectious (syphilitic leukoderma, leprosy leukoderma, leukoderma with white, red flat, multi-colored or scaly lichen) - develops in infectious diseases;
• post-inflammatory leukoderma - develops with burns and skin diseases accompanied by inflammatory processes (psoriasis, eczema, etc.);
• medicinal and occupational (or toxic) leukoderma - develops as a result of exposure to toxic substances on the body (for example, at work) or certain medications;
• congenital leukoderma (10 forms of albinism, Bloch-Sulzberg melanoblastosis) – develops with congenital Ziprovsky-Margolis, Wulff, Waardenburg syndromes, pigment incontinence;
• immune leukoderma (Halo-nevus, scleroderma) - caused by complex, during which one’s own the immune system destroys melanocytes.

Special attention should be paid to the reasons for the development of such a disease, accompanied by the appearance of white spots on the skin, as vitiligo. This pathology is observed in approximately 5% of people and can begin to manifest itself both from the moment of birth and in adulthood.

Many dermatologists believe that its development is caused by complex autoimmune reactions, but there is an assumption that the disease is congenital and caused by a gene mutation. Scientists have not yet identified this carrier gene. The exact causes of the development of vitiligo are still unknown, and this pathology is still classified as immune leukoderma.

Symptoms

The appearance of white (or discolored) spots, the main symptom of leukoderma, depends on the disease that caused them. They can be of different sizes, shapes, shades and located on different parts of the body.

White spots may be flat or raised above the surface of the skin. With age, their size may increase, they may merge with each other, forming areas of hypo- or depigmented skin.

The color of the spots can be completely white or approaching pale pinkish and yellowish tints. In some diseases, the edges of hypopigmentation have a border of a darker color (sometimes red), and with Halo-nevus, areas of pinkish or brown pigmentation appear on the skin, surrounded by a white border.

Most often, white spots appear on the upper and lower extremities, torso or in the groin folds and armpits. Sometimes they are scattered throughout the body and can.

A characteristic arrangement of areas of depigmentation is observed in syphilitic leukoderma. 3-6 months after infection, a “necklace of Venus” appears on the posterolateral part of the patient’s neck (less often on the back, abdomen or side of the chest), which is a cluster of white spots.

In some diseases, in addition to white spots, the patient exhibits leukotrichia (congenital gray hair) or leukonychia (complete or partial discoloration of the nail plates or white spots on them), and in some forms of albinism, a very light color of the iris is observed: it can be light blue, very light and acquire reddish or pink shades in bright light.

A disease such as tuberous sclerosis is accompanied not only by the appearance of areas of depigmentation, but also leads to the growth of tumors in many internal organs (heart, kidneys, brain, retina, etc.), the development of mental retardation and epilepsy.

With albinism, patients often experience pathologies of the visual organs: nystagmus, a sharp decrease in visual acuity and photophobia.

In some diseases, white spots may disappear on their own or after treatment. These types of leukoderma include depigmentation that appears after inflammatory diseases skin, leprosy, burns, scleroderma or lichen. And with other pathologies, white spots remain for life and can steadily progress.

Diagnostics

If white or light spots appear on the skin, you should consult a dermatologist. The doctor will carefully examine the skin, study the medical history and family history, find out what medications the patient took and whether he had contact with certain chemicals. After this, the specialist will conduct a differential diagnosis and prescribe additional laboratory and instrumental studies. If necessary, the patient will be assigned consultations with highly specialized specialists: geneticist, ophthalmologist, cardiologist, etc.

Treatment

Treatment tactics for leukoderma depend on the cause that caused the underlying disease and led to pigmentation disorders. For some types of lichen (white and red flat) and post-inflammatory leukoderma, treatment is not prescribed, since areas of depigmentation are eliminated on their own. If the appearance of white spots was caused by toxic substances or medications, then the patient is recommended to completely eliminate the provoking factor that caused their appearance.

For infectious or some types of immune leukoderma, therapy is aimed at treating the underlying disease. Congenital forms of pigmentation disorders and vitiligo are much more difficult to correct. The prognosis for the treatment of such forms of leukoderma is not very encouraging, because effective ways Scientists and doctors have not yet been able to find a normalization of pigmentation.

Treatment tactics in such cases are determined individually for each patient. This may include:

• medications for internal or external use: glucocorticosteroids, furocoumarins, synthetic analogues of phenylalanine and tyrosine amino acids, tranquilizers, digestive enzymes and etc.;
• vitamins A, B, E, C and PP;
• drugs;
• copper preparations;
• PUVA therapy.

In some cases, to eliminate leukoderma, surgical operations are performed to transplant autologous melanocytes and transplantation of one's own skin or donor samples.

• seafood and sea fish;
• meat;
• liver;
• dairy products;
• eggs;
• vegetable oils;
• cereals (especially oats, millet, buckwheat);
• legumes;
• vegetables (carrots, beets, radishes, tomatoes, pumpkin, spinach, cauliflower);
• avocado;
• parsley;
• bananas;
• blueberries;
• raisin;
• nuts (almonds, peanuts, hazelnuts, pistachios);
• seeds (sesame, flax, sunflower, pumpkin).

The appearance of white spots on the skin is a reason to contact a dermatologist. Their occurrence always signals a malfunction in the body.

– a polyetiological dermatological condition, which is characterized by a violation of the formation and accumulation or accelerated destruction of pigment in certain areas of the body. It is manifested by the presence of discolored areas of the skin. The size, number and location of areas depend on the causes of the disorder. Diagnosis of leukoderma is based on the results of an examination by a dermatologist and a general examination of the patient’s body, carried out to identify hidden pathologies. In some cases, a tissue biopsy from the affected area may be required. Treatment tactics depend on the etiology of this condition; both specific therapy for the provoking disease and supportive measures in the form of vitamin therapy and UV irradiation are possible.

General information

Leukoderma is not a separate skin disease; it is a symptom indicating a general or local disorder of pigment metabolism. The condition has been known since ancient times, and in some cultures, patients with such skin changes were recognized as marked by the gods. Leukoderma is a very common dermatological pathology; according to some data, 5 to 8% of the planet's population suffers from its various forms. It can be an acquired condition that arises as a result of a certain lifestyle of a person or exposure to various factors on his body external environment, and congenital, genetically determined. The latter type is characterized by particular difficulty in the treatment process and often bothers the patient already in early childhood. The sexual distribution of leukoderma depends on the type and form of the pathology. Some conditions occur only in men (X-linked hereditary variants), others may affect both sexes equally often or occur slightly more often in women.

Causes of leukoderma

The shade of human skin depends on the presence of several pigments, the main one of which is melanin. The rate of formation of this compound depends on two factors - the presence of tyrosine in the body, which serves as a substrate for the formation of melanin, and the processing enzyme tyrosinase. In albinism, which is considered by some dermatologists as an extreme variant of leukoderma, there are defects in the structure of tyrosinase. The enzyme does not work, which causes a lack of melanin synthesis. In some forms of leukoderma, a similar process is observed - the enzyme is disrupted, pigment is not synthesized, and as a result, discolored areas of the skin appear.

There is another mechanism for hypopigmentation in this dermatological condition. Melanin must not only be synthesized, but deposited in special cellular inclusions - melanosomes. There are factors of exogenous and endogenous nature that complicate this process. Under their influence, with normal or even increased melanin synthesis, pigment is not deposited in certain areas of the skin, which leads to the appearance of foci of leukoderma. A variant of this process may be the selective death of skin melanocytes caused by infectious agents, immunological disorders or exposure to certain chemicals. Due to the increased rate of decay of pigment cells, their timely replacement does not occur, which also provokes the occurrence of symptoms of leukoderma.

The above described violations can lead to great amount various pathological conditions and unfavorable factors. Most often, leukoderma occurs as a result of certain infectious diseases (syphilis, leprosy, certain dermatomycosis), autoimmune conditions (systemic lupus erythematosus, scleroderma), genetic pathologies (Wolff's disease, Vaanderburg, etc.). In addition, there are forms of the so-called occupational leucoderma, provoked by exposure to certain industrial chemicals on the body. Separately, vitiligo and idiopathic forms of pathology are usually distinguished. In addition, some helminthic infestations, immune disorders and endocrine disorders.

Classification of leucoderma

The modern classification of leukoderma in dermatology is based on the etiology of this condition. However, even a generally accepted list of varieties cannot cover absolutely all forms of pathology. Because of this, idiopathic leukoderma is classified as a separate type, classifying all forms and varieties of the condition with an unknown cause. This classification most completely and objectively separates the various groups of leukoderma according to the reasons for their appearance. The convenience of classification also lies in the fact that leukodermas included in a certain group are characterized by similarity clinical symptoms– this allows the dermatologist to roughly determine the list of possible etiological factors based only on the patient’s appearance. Most often, patients are diagnosed with the following types of leukoderma:

1. Infectious leucoderma– hypochromia, caused by the influence of various microorganisms on the skin, which can either directly affect melanocytes or disrupt local metabolism in tissues so much that the synthesis and accumulation of pigment in them becomes difficult. This type includes syphilitic and leprosy leukoderma, as well as hypopigmentation due to various forms of lichen.
2. Immune leucoderma– in this group, researchers include vitiligo and some other autoimmune conditions (scleroderma, lupus), which may be accompanied by impaired skin pigmentation. Immune leukoderma is also caused by immunological disorders that occur against the background of helminthic infestations. The unifying factor is the defeat of melanocytes by their own immune system.
3. Toxic leucoderma caused by local or general exposure to certain chemicals, including medications. This group includes the so-called occupational hypochromia, which occurs in employees of certain chemical production plants with prolonged exposure to industrial toxins.
4. Congenital leukoderma has genetic causes or (less commonly) caused by intrauterine lesions. Characterized by a variety of symptoms, often in addition to skin disorders Patients have developmental defects and other disorders.
5. Post-inflammatory leucoderma often occurs against the background of scar changes after burns, as well as with long-term skin diseases inflammatory in nature(for example, with eczema).
6. Idiopathic leukoderma includes all forms of pathology with unidentified or unclear causes.

Symptoms of leucoderma

The main manifestation of leukoderma is a violation of pigmentation of the skin in various parts of the body. The nature of pigmentation disorders varies depending on the form and causes of the condition. Thus, with infectious syphilitic leukoderma, skin discoloration occurs mainly on the neck, torso, and sometimes the face and can have three clinical forms: reticular, marbled and spotted. In the first case, areas of depigmentation consist of many small fibrous foci resembling lace, in the second - of whitish dots with unclear contours that tend to merge. Spotted syphilitic leukoderma is characterized by the formation of individual round foci of hypochromia with clear contours and almost the same size.

Leprosy leukoderma often occurs on the arms, thighs, back and buttocks. Its peculiarity is the formation of round lesions with clear boundaries. After their appearance, lesions can remain unchanged for many years. Immune forms of hypochromia, developing with systemic lupus erythematosus, scleroderma and helminthic infestation, are often accompanied not only by focal loss of pigment, but also by peeling or atrophy of the skin. With proper treatment of infectious or autoimmune leukoderma, the severity of skin manifestations decreases, since the factor that has a negative effect on melanocytes or pigment metabolism disappears. A similar picture is observed in the case of chemical or toxigenic hypochromia - often the central element of the treatment of these forms is the elimination of the provoking factor, which in itself makes it possible to reduce the severity of skin manifestations.

Congenital forms of leukoderma have a variety of symptoms, which are largely determined by the underlying disease. Skin manifestations (foci of depigmentation of various sizes and shapes) can be combined with disorders of other organs and systems. Post-inflammatory leukoderma is characterized by the appearance of hypochromia in those areas of the skin that have been subjected to burns, psoriasis or seborrhea. Often in the center of a lesion with reduced pigmentation one can find scar changes. The localization of pigment disorders depends on the location of previous inflammatory lesions skin. With these forms of leukoderma, as well as with vitiligo, restoration of normal skin color can be very difficult, and the disorders persist for many years.

Diagnosis of leukoderma

Leukoderma is quite easy to identify during a routine examination of the patient’s skin, but to determine its causes may require a whole range of different clinical studies. When examining the patient's skin, areas of depigmentation of various shapes, sizes and localization are revealed; in some cases, the lesions are surrounded by a rim of hyperpigmentation (a compensatory reaction of the body). If the infectious nature of leukoderma is suspected, general analysis blood, in which they can be determined nonspecific signs inflammation (leukocytosis, increase in ESR). Eosinophilia may indicate the presence of helminthic infestation. To determine the causative agent, serological tests can also be prescribed: the Wasserman reaction, a test for the presence of leprosy, and others.

By examining the patient's vital blood counts and some diagnostic tests It is possible to identify not only inflammatory, but also immune leukoderma. For example, in lupus, the presence of antinuclear antibodies is determined. An important role in the diagnosis of leukoderma is played by interviewing the patient and a thorough study of the medical history, since in toxigenic and post-inflammatory forms of this dermatological condition it is the previous diseases that most often cause pigmentation abnormalities. For a more accurate determination of leucoderma and its differentiation from some forms of lichen, a Wood's ultraviolet lamp is used.

In controversial cases, skin biopsy from areas of decreased pigmentation and histological examination may be resorted to. Depending on the form and cause of leukoderma, lesions may show signs of inflammation, scar tissue, swelling of the dermis, or changes in the epidermis. In the most common cases of depigmentation, abnormalities of melanocytes are usually noted - they are either completely absent or have structural changes (low number of melanosomes, deformed processes). For some congenital forms of leukoderma, genetic tests are used.

Treatment of leucoderma

Therapy for leukoderma comes down to eliminating the causes that led to impaired skin pigmentation. For infectious forms, antibiotics are used, for autoimmune pathology, immunosuppressive and cytostatic agents are used, for helminthic infestations, they are prescribed anthelmintic drugs. For toxic leukoderma special treatment may not be necessary; in some cases, it is sufficient to ensure that the patient ceases contact with the toxic substance. This is possible by changing the type of activity (when working in chemical plants) or eliminating (replacing) certain medications. The most difficult forms of leukoderma to treat are those caused by hereditary factors, as well as vitiligo - with the latter, some specialists practice transplanting the patient’s normally pigmented skin, taken from another part of the body, onto areas of hypochromatosis.

Maintenance therapy can significantly improve the condition of the patient's skin and accelerate the restoration of normal pigmentation. General and local forms of vitamins A, E, PP and group B, vitamin and mineral complexes containing zinc and copper are prescribed. According to some data, enriching the diet with tyrosine also helps reduce the symptoms of leukoderma, so patients’ diets should include eggs, seafood, liver, oatmeal and buckwheat. Of the specific techniques used in dermatology, PUVA therapy is used - treatment of the skin with special photoactive substances followed by ultraviolet irradiation. It is important to consider that some forms of leukoderma respond to UV irradiation by increasing the degree of depigmentation, so such techniques should be prescribed with caution.

Prognosis and prevention of leukoderma

The prognosis for leukoderma regarding the patient’s life is always favorable - this dermatological condition never poses a threat fatal outcome or severe complications, only concomitant developmental defects in congenital forms and syndromes are capable of this. Regarding recovery and restoration of normal pigmentation of the skin, the prognosis is often uncertain, even in the case of relatively mild toxigenic forms of the disease. Congenital and immune varieties of leukoderma, as well as vitiligo, are extremely difficult to treat. Prevention includes eating foods rich in tyrosine, protecting the skin from ultraviolet radiation and avoiding contact with chemicals that can cause depigmentation.

SYPHILITIC LEUCODERMA

Syphilitic leukoderma (syphilide pigmentosa) is pathognomonic for secondary (usually recurrent) syphilis and is more common in women. Its predominant localization is the lateral and posterior surfaces of the neck ("necklace of Venus"). The chest may often be affected, shoulder girdle, back, stomach, lower back, sometimes limbs. The affected areas first appear as gradually increasing diffuse hyperpigmentation. Subsequently, hypopigmented round spots the size of a fingernail appear against its background. Distinguish spotted And lace syphilitic leucoderma, when there are a lot of spots and they almost merge with each other, leaving only small stripes of the hyperpigmented background. It exists for a long time (sometimes for many months and even years), its development is associated with damage to the nervous system (there are no treponema pallidums in the affected tissue).

In the presence of leukoderma, patients usually experience pathological changes in the cerebrospinal fluid.

Polyadenitis considered one of the most important symptoms secondary syphilis. It is characterized by multiple lesions of the lymph nodes; always develops in many groups of lymph nodes, and affects both subcutaneous ones, accessible to direct palpation, and deep ones, right down to the mediastinal and retroperitoneal ones, which is detected by special research methods.

In the secondary period, almost all organs and systems may be involved in a specific process, although this is observed, however, not too often. The main significance is damage to bones and joints, the central nervous system and some internal organs. Bone damage occurs in 5% of patients in the form of diffuse periostitis, manifested by painful doughy swellings and night pain in the bones. Osteoperiostitis is less common. The most commonly affected bones are the skull and tibia. Damage to the joints usually occurs as polyarthritic synovitis with the formation of effusion in the joint cavity (hydrarthrosis): the joint appears swollen, enlarged in volume, and painful when pressed. The appearance of pain when trying to move and the disappearance of pain in the joint during movement are very typical. The most important specific visceritis of the secondary period includes syphilitic hepatitis (enlarged and painful liver, increased body temperature, jaundice), gastritis, nephroso-nephritis, myocarditis. Syphilitic visceritis quickly disappears after specific treatment. Damage to the nervous system in the secondary period of syphilis is usually called early neurosyphilis. Characteristic damage to the mesenchyme, i.e. meninges and vessels. A neurological examination, as well as an analysis of cerebrospinal fluid, reveals syphilitic meningitis (often asymptomatic), sometimes complicated by hydrocephalus, as well as syphilis of the brain vessels (meningovascular syphilis), rarely - syphilitic neuritis and polyneuritis, neuralgia. The percentage of positive classical seroreactions in the secondary period of syphilis is extremely high - positive reaction Wasserman with secondary fresh syphilis is observed in 100% of cases, with secondary recurrent syphilis - in 98-100%.

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TERTIARY SYPHILIS

Tertiary syphilis develops in approximately 40% of patients in the 3rd-4th year of the disease and continues indefinitely.

The transition of the disease into the tertiary period is facilitated by inadequate treatment or its absence in the previous stages of syphilis, severe concomitant diseases, poor living conditions, etc. Manifestations of the tertiary period are accompanied by the most pronounced, often indelible disfigurement of the patient’s appearance, severe disorders in various organs and systems, leading to disability, and often to death. Distinctive features of the tertiary period are the appearance of powerful inflammatory infiltrates in the form of tubercles and gummas, prone to decay, followed by extensive destructive changes in the affected organs and tissues; productive nature of inflammation with the formation of infectious granuloma; limited lesions (single elements); ubiquity of lesions; wavy, intermittent flow. This shows similarities with the secondary period (manifestations of tertiary syphilis, having usually existed for several months, undergo spontaneous regression, followed by a period of relative dormancy of the infection). In the presence of clinical manifestations, tertiary active syphilis is diagnosed; in the absence of such, tertiary latent syphilis is diagnosed. Relapses of tertiary lesions are observed infrequently and are separated from each other by long (sometimes many years) latent periods; The duration of existence of tertiary syphilides is calculated not in weeks, but in months and years, so that attacks of tertiaryism are very long; in tertiary syphilides an extremely small number of pale treponema is found, and therefore studies for the presence of the pathogen are not carried out and the low infectiousness of these manifestations is characteristic; tendency to develop specific lesions in areas of nonspecific irritation (primarily in areas mechanical injuries); classical serological reactions in 1/3 of patients with tertiary syphilis are negative, which does not exclude its diagnosis; the intensity of specific immunity in the tertiary period gradually decreases (this is due to a decrease in the number of pale treponema in the patient’s body), and therefore true resuperinfection becomes possible with the development of hard chancre at the site of new introduction of pallid treponema. Transition syphilitic infection in the tertiary period is explained by further changes in the immunobiological reactivity of the body towards an increase in the state of infectious allergies, so that the manifestations of tertiary syphilis are infectious-allergic in nature. Most often, the skin, mucous membranes and bone skeleton are involved in the gummous process.

Skin lesions are represented by two syphilides - tuberculate And gummous.

TUBEROUS SYPHYLIDE

The main element of tubercular syphilide is a small dense tubercle located in the thickness of the skin, hemispherical in shape, the size of a cherry pit, dark red or bluish-red in color. Its surface is smooth and shiny. After a few weeks or months, the tubercle softens and ulcerates to form a round, rather deep ulcer with ridge-like, steeply cut edges. Gradually, the bottom of the ulcer is cleared of decay, covered with granulations and turns into an atrophic scar pigmented along the periphery, on which new rashes never appear. The group of scars has a mosaic appearance.

GUMMA

Gumma is a ball the size of a walnut, densely elastic consistency, with sharp boundaries, covered with purple-red skin, limited mobility.

Subjective sensations are insignificant or absent. Subsequently, softening and disintegration of the gumma is observed with the formation of a deep ulcer, the bottom of which is covered with the remains of the disintegrating infiltrate (“gummy core”). The ulcer has a rounded outline, a deep bottom and very characteristic roller-shaped thick, densely elastic, bluish-red edges. Gradually, the ulcer scars, leaving a discolored scar with a zone of hyperpigmentation along the periphery. Sometimes there is irradiation of gumma - the spread of gummous infiltrate to neighboring tissues (from the skin to the periosteum, bone, blood vessels), which can not only aggravate the disfigurement of the patient’s appearance, but also lead to death. Gummas of the mucous membranes are quite common. First of all, the mucous membrane of the nasal cavity is affected, then the pharynx. Gummous lesions of the tongue, hard and soft palate, nose, pharynx, larynx lead to severe and often irreparable disorders of speech, swallowing, breathing, changes appearance patient ("saddle" nose, complete destruction of the nose, perforation of the hard palate). Among gummous lesions of other organs, tertiary syphilides of the periosteum, bones and joints are more common. The bones of the legs, forearms, skull, knee, elbow and ankle joints are most often affected. Changes in other organs and systems are described in special manuals.

CONGENITAL SYPHILIS

Congenital syphilis is transmitted to the offspring by a sick mother during pregnancy through a placenta affected by syphilis.

The social significance of congenital syphilis is aggravated by the high mortality rate of children with congenital syphilis: the mortality rate is higher, the younger the child is.

Transmission of syphilis through the placenta can occur in two ways: 1) more often, treponema pallidums are introduced into the child’s body as emboli through the umbilical vein; 2) less often, treponema pallidums penetrate into lymphatic system fetus through the lymphatic slits of the umbilical cord. A healthy placenta is a perfect filter for Treponema pallidum. In order for the causative agent of syphilis to penetrate the fetus’s body, it is necessary to first infect the placenta with syphilis, followed by disruption of the placental barrier. Transmission of syphilis to offspring occurs mainly in the first 3 years after infection of the mother; in the future, this ability gradually weakens, but does not fade away completely (“Kassovich’s law”). The effect of syphilis on pregnancy is expressed in disruption of its course in the form of late miscarriages and premature birth, and there are often stillbirths (premature or at term), and the birth of sick children. Depending on the period of syphilitic infection in a child, the following periods of congenital syphilis are distinguished: fetal syphilis, early congenital syphilis (infant syphilis and early syphilis are distinguished). childhood) and late congenital syphilis (after 4 years). The division of congenital syphilis into early and late is due to clinical manifestations, and early congenital syphilis mainly corresponds to secondary, and late to tertiary acquired syphilis.

Defeat Fetal syphilis occurs in the 5th month of pregnancy and is accompanied by changes in the internal organs, and somewhat later in the skeletal system. Primary and predominant liver damage in such fetuses confirms the placental theory of transmission of syphilis to offspring. Specific lesions of the internal organs of the fetus are mostly of a diffuse inflammatory nature and are manifested by small cell infiltration and proliferation of connective tissue. Widespread and severe lesions of the visceral organs of the fetus often make it nonviable, which leads to late miscarriages and stillbirths. There is no organ or system that could not be affected by syphilis in infancy. The most commonly observed lesions are the skin, mucous membranes and bones.

Early manifestation syphilis at children infancy is syphilitic pemphigus. The rashes are localized on the palms, soles, forearms and legs. Bubbles the size of a pea and a cherry, initially serous, then purulent, sometimes hemorrhagic, are located on an infiltrated base and are surrounded by a zone of specific papular infiltrate of a bluish-red color. Diffuse infiltration of Hochsinger usually localized on the soles, palms, face and scalp. The lesion is sharply demarcated, has at first a smooth, shiny, bluish-red surface, then a cracked brownish-red surface, and has a dense elastic consistency, which leads to the formation of cracks that have radial directions around the mouth and leave so-called radiant Robinson-Fournier scars for life. Also observed widespread or limited roseolous, papular and pustular rashes in all their varieties, similar to those in the secondary period of syphilis. A feature of roseola in infants is its tendency to coalesce and peel. Papular rashes tend to erode and subsequently pustulate. Skin rashes are often preceded by an increase in body temperature. Hair loss may be of the nature of both diffuse and small focal syphilitic alopecia. Damage to the mucous membranes most often occurs in the form of syphilitic runny nose, which is a specific erosive-papular hyperplastic anterior rhinitis. There is a narrowing of the nasal passages, mucopurulent discharge, shrinking into crusts. Breathing through the nose becomes extremely difficult, which makes the act of sucking impossible. As a result of ulceration of the papular infiltrate of the nasal septum, its destruction with deformation of the nose (in the form of a saddle or blunt, “goat”) is possible. Syphilitic papules prone to ulceration may be observed on the mucous membrane of the mouth and pharynx. Lesions of the skeletal system in the form of osteochondritis, sometimes ending in pathological fractures of the limb bones (Parro's pseudoparalysis). In children over 4 months of age, manifestations on the skin and mucous membranes are often limited; in the bones, periostitis predominates; damage to internal organs and the nervous system is less common. With congenital syphilis of early childhood, limited large-papular (usually weeping) rashes such as condylomas lata are more often observed on the mucous membranes.- erosive papules; Bones are often affected (syphilitic periostitis of long bones).

Manifestations of late congenital syphilis occur between the ages of 5 and 17 years and correspond to damage to various organs and systems in acquired tertiary syphilis. In addition, there are constant persistent signs resulting from syphilis suffered in infancy, or appearing later due to the influence of a syphilitic infection on the developing skeletal system and some other organs. It is the combination of these signs that makes it possible to distinguish late congenital syphilis from tertiary syphilis.

Signs of late congenital syphilis are divided depending on the degree of specificity into absolute, or unconditional; relative, or probable(observed more often with late congenital syphilis, but also occurs with other diseases), and dystrophy(can be a consequence of both congenital syphilis and other diseases).

To unconditional signs applies Hutchinson's triad: Hutchinson teeth (barrel-shaped or chisel-shaped incisors, hypoplasia of the chewing surface with a semilunar notch along the free edge); parenchymal keratitis (uniform milky-white opacification of the cornea with photophobia, lacrimation and blepharospasm); labyrinthine deafness (inflammatory phenomena and hemorrhages in inner ear in combination with degenerative processes in the auditory nerve).

Possible signs have less diagnostic value and require additional confirmation; they are assessed in conjunction with other manifestations. These include syphilitic chorioretinitis (a characteristic “salt and pepper” pattern in the fundus); saber-shaped shins are the result of diffuse osteoperiostitis with reactive osteosclerosis and anterior curvature of the shin bones; saddle-shaped or “goat” nose (the result of a syphilitic runny nose or gumma of the nasal septum); buttock-shaped skull (sharply protruding frontal tubercles with a groove located between them); “kidney-shaped (purse-shaped) tooth”, Myna’s tooth (underdevelopment of the chewing cusps of the first molars); Fournier’s “pike tooth” (a similar change in the fang with thinning of its free end); glad paired Robinson-Fournier scars (in the circumference of the mouth after Gochsinger infiltration); syphilitic gonitis (Cletton's synovitis), occurring as chronic allergic synovitis (differing in the absence of sharp pain, fever and joint dysfunction); damage to the nervous system (speech disorders, dementia, etc.). Dystrophies in congenital syphilis: Ausitidian sign (thickening of the sternal end of the clavicle due to diffuse hyperostosis); “Olympic forehead” (enlarged frontal and parietal tubercles); high (“gothic”) sky; infantile (shortened) little finger Dubois - Hissar (hypoplasia of the fifth metacarpal bone); Keir's axiphoidia (lack of xiphoid process); Gachet's diastema (widely spaced upper incisors); Carabelli cusp (additional cusp on the chewing surface of the first molar upper jaw); Tarnovsky hypertrichosis (overgrowth of hair from the forehead almost to the eyebrows). All of the listed dystrophies do not each have diagnostic value individually. Only the presence of several dystrophies in combination with other signs of syphilis and medical history can, in unclear cases, help make a diagnosis of congenital syphilis.

The diagnosis of syphilis must be clinically substantiated and laboratory confirmed (detection of Treponema pallidum, positive serological tests for syphilis). Of primary importance is the complex of serological reactions (CSR), including the complement fixation reaction (type of Wasserman reaction) with cardiolipin and treponemal antigens and the glass reaction (express method). Positive results are expressed by crosses (from + to ++++). In the case of a sharply positive reaction, an additional study is carried out with various dilutions of serum (from 1: 10 to 1: 320). The most diagnostic results are sharply positive results of the complement fixation test with high dilutions of serum. The CSR becomes positive from the middle of the primary period in almost all patients with syphilis, remains positive in the secondary period, but in the tertiary period it can become negative in "/ 3 -1/2 patients. The most specific reaction is the immobilization of pallidum treponema (RTI). It has special diagnostic value in recognizing false-positive results of seroreactions to syphilis. It is positive later than the CSR and is assessed as positive when 50-100% of pallidum treponema is immobilized, as weakly positive - at 30-50%, as doubtful - at 20-30% and as negative - when immobilized less than 20% of pale treponema. RIBT remains positive in late forms of syphilis. The most sensitive immunofluorescence reaction (RIF), which becomes positive in the majority of patients with syphilis even in the primary seronegative period (sometimes at the end of the incubation period). Its results are assessed in the positive (from + to ++++) RIF is positive in all periods of syphilis (including late forms) in almost all patients. It is necessary to remember the possibility of biologically false-positive seroreactions to syphilis in a number of diseases and conditions accompanied by dysglobulinemia (malaria, tuberculosis, leprosy, hepatitis, systemic lupus erythematosus, metastatic tumors, leukemia, and also during pregnancy). In these cases, seroreactions, as a rule, are not sharply positive. Based on sharply positive results of seroreactions performed twice in two different laboratories, the doctor can make a diagnosis of latent seropositive syphilis. The microreaction on glass (express method), although the simplest, is the least specific, and therefore is used in isolation only as a screening method for mass examinations. Persons who have had sexual or close household contact with patients with contagious forms of syphilis, but who do not show signs of the disease during examination, are considered to be in the incubation period of syphilis and are subject to preventive (protective) treatment. The differential diagnosis of primary syphilis is carried out with a number of erosive and ulcerative dermatoses, in particular with a boil in the ulceration stage, erosive and ulcerative balanoposthitis and vulvitis, herpes simplex, spinocellular epithelioma. Syphilitic roseola is differentiated from manifestations of typhus and typhoid fever and other acute infectious diseases, from toxic roseola; in case of allergic medicinal toxidermia, in case of localization of rashes of the secondary period in the pharynx area - from a common sore throat. Papular syphilides are differentiated from psoriasis, lichen planus, parapsoriasis, etc.; wide condylomas in the anus - from genital warts, hemorrhoids; pustular syphilides - from pustular diseases skin; manifestations of the tertiary period - from tuberculosis, leprosy, skin cancer, etc.

Treatment of syphilis is carried out in accordance with the methodological recommendations "Treatment and Prevention of Syphilis", which are created on the basis of the experience of the country's leading venereological institutions, are reviewed and clarified every 3-5 years and are necessarily approved by the Ministry of Health of the Russian Federation. Specific treatment for a patient with syphilis is prescribed after diagnosis, which must be clinically justified and laboratory confirmed. Exceptions to this general rule include preventive treatment; preventive treatment (carried out to pregnant women who had syphilis, but were not removed from the register, in order to prevent congenital syphilis in the child, as well as to children born to mothers who did not receive preventive treatment during pregnancy); trial treatment (for late active tertiary syphilis with a negative complex of seroreactions for additional diagnostic purposes). Since the treatment of syphilis is carried out almost exclusively with antibiotics, before starting treatment it is necessary to collect an allergic history regarding their tolerance, and before the first injections of soluble penicillin and its durant drugs, prescribe antihistamines. Exist various techniques and patterns of use of penicillin and other antibiotics for syphilis. Water-soluble penicillin preparations are considered the most effective, treatment of which is carried out in a hospital in the form of round-the-clock intramuscular injections. For outpatient treatment, bicillin (1, 3 and 5) is usually used. The volume and duration of treatment depend on the duration of the syphilitic infection. In late forms, along with antibiotics, bismuth preparations (biyoquinol, bismoverol) are used, as well as nonspecific therapy. Preventive treatment is often carried out on an outpatient basis (for example, bicillin-5 is administered intramuscularly at 1,500,000 units 2 times a week, 4 injections in total). In a hospital setting, it is more advisable to administer penicillin (400,000 units intramuscularly every 3 hours around the clock for 14 days). Patients with primary and secondary fresh syphilis are treated according to the same regimens, but in the case of using bicillin, the number of injections is increased to 7. Sometimes used novocaine salt benzylpenicillium (600,000 units intramuscularly 2 times a day for 14 days). In the treatment of patients with secondary recurrent and early latent syphilis, the number of bicillin injections is increased to 14, and water-soluble penicillin or its novocaine salt is administered for 28 days. Specific antisyphilitic drugs are used in combination with nonspecific stimulating methods. For the treatment of early forms, extencillin and retarpen are successfully used (2,400,000 units intramuscularly with an interval of 8 days, only 2-3 injections. Treatment of patients with late latent, tertiary, visceral and neurosyphilis begins with the preparation of bioquinol (2 ml every other day before doses of 14 ml), then penicillin therapy is carried out (400,000 units intramuscularly every 3 hours for 28 days), after which the course of bioquinol is completed (up to a total dose of 40-50 ml). In case of contraindications to bismuth drugs, 2 courses of penicillin therapy are carried out. Specific agents are combined with non-specific ones, the latter including pyrotherapy (pyrogenal, prodigiosan), biogenic stimulants(aloe extract, vitreous, splenin), immunomodulators (decaris, methyluracil). Patients with late forms are observed by a therapist and a neurologist. In cases of intolerance to penicillin drugs, reserve antibiotics can be used: erythromycin, tetracycline, oletethrin, doxycycline. They are prescribed in increased daily doses for 14-40 days (depending on the stage of syphilis), as well as cefamizine, which is administered intramuscularly at 1 g 6 times a day for 14-16 days. In early forms, treatment with sumamed (azithromycin) is also recommended. - 0.5 g 1 time per day for 10 days. Treatment of pregnant women and children has a number of features presented in the guidelines. The prognosis for syphilis in the case of timely and qualified treatment can be considered very favorable in the vast majority of cases. At the end of treatment, all patients remain under the clinical and serological supervision of a medical specialist for different periods: after preventive treatment- for 3 months (in some cases up to 1 year), for primary seronegative syphilis - 6 months, for primary seropositive and secondary fresh syphilis - 1 year (for delayed negative seroreactions - up to 2 years). For late forms, latent, visceral and neurosyphilis, an observation period of 3 years was established. During the observation period at the end of treatment, patients are periodically (every 3-6 months) subjected to a thorough clinical examination and serological tests are performed. After the end of the observation period, patients are subject to a comprehensive clinical examination (with the involvement of a therapist, radiologist, ophthalmologist, neurologist, otolaryngologist), after which the issue of deregistration is decided.

The criteria for curing syphilis are: complete treatment (in accordance with the latest Guidelines); a favorable observation period (absence of clinical and serological signs of syphilis within the prescribed period); absence of manifestations of syphilis during a detailed final examination before deregistration.

Prevention of syphilis is divided into public and individual. Methods of public prevention include free treatment from qualified specialists at dermatovenerological clinics, active identification and involvement in treatment of sources of infection and contacts of patients with syphilis, provision of clinical and serological control over patients before deregistration, preventive examinations for the presence of syphilis in donors, pregnant women, all inpatients, workers of food enterprises and child care institutions. According to epidemiological indications, so-called risk groups in a given region (prostitutes, homeless people, taxi drivers, etc.) may also be involved in the examination. Health education plays an important role, especially in youth groups. A network of 24-hour centers for individual prevention of syphilis and other sexually transmitted diseases has been deployed at dermatovenerological dispensaries. Personal (individual) prevention of syphilis is based on the exclusion of casual sexual intercourse and especially promiscuity, the use of condoms when necessary, as well as the implementation of a set of hygienic measures after suspicious contact both at home and at an individual prevention point. The traditional preventive complex carried out in dispensaries consists of immediate urination, washing the genitals and perigenital areas with warm water and laundry soap, wiping these places with one of the disinfecting solutions (sublimate 1: 1000, 0.05% solution of chlorhexidine bigluconate, cidipol), instillation into the urethra 2-3% solution of protargol or 0.05% solution of chlorhexidine digluconate (gibitan). This treatment is effective within the first 2 hours after possible infection when the causative agents of sexually transmitted diseases are still on the surface of the skin and mucous membrane. 6 hours after contact it becomes useless. Currently, immediate autoprophylaxis of sexually transmitted diseases is possible in any situation using ready-made “pocket” prophylactic agents, sold in pharmacies (cidipol, miramistin, gibitan, etc.).

CHANCROID

Soft chancroid (syn.: venereal ulcer, chancroid) is an acute venereal disease.

Cases of non-sexual infection are extremely rare. Distributed in Southeast Asia, Africa, America. More often observed in men. Often associated with other sexually transmitted diseases.

Etiology and pathogenesis. The causative agent is Streptobacillus Ducray - a gram-negative rod. Contagiousness is high - the disease is detected in 50% of sexual partners. Chancroid does not provide lasting immunity. The incubation period ranges from 3 to 10 days (average 2-3 days).

Clinical picture. At the site of entry of the pathogen, a small inflammatory spot appears, on which a papule forms, transforming into a pustule, and after its opening an ulcer appears. In classical cases it has irregular shape, diameter from several millimeters to several centimeters, undermined and jagged edges, the bottom is covered with necrotic exudate. Around the large ulcer there are small “daughter” ulcers. A characteristic feature of ulcers is a soft consistency and pain, only sometimes bleeding is noted. Ulcers are most often localized on the foreskin, frenulum of the penis, labia, and perianal area. Varieties of chancroid include elevated, serpiginous, follicular, diphtheritic, gangrenous, phagedenic, etc. Mixed chancroid, which occurs during simultaneous or sequential infection with streptobacilli and treponema pallidum, is also distinguished. Lymphangitis is also characteristic - inflammation of the lymphatic vessels as a result of their damage by streptobacilli. In men, it develops on the dorsal surface of the penis, in women - on the pubis and the outer surface of the labia majora. It can be felt as a dense, clearly thickened cord. The skin over it turns red and swells. Involutions spontaneously or undergoes purulent melting involving the overlying skin and the formation of an ulcer. Bubo is a consequence of the penetration of the pathogen into The lymph nodes, develops acutely 3-4 weeks after the appearance of a chancre ulcer. The inguinal lymph nodes are usually affected. Periadenitis develops, the lymph nodes become fused with each other and with the skin, which becomes bright red. There is a general malaise, body temperature rises, and sharp pain occurs in the affected area. Subsequently, the lymph nodes soften and open, releasing a large amount of purulent-bloody contents. As a result, an ulcer of soft chancre is formed - chancroid bubo. Histological examination reveals that the base of the ulcer is formed by necrotic tissue with a pronounced perivascular infiltrate of polymorphonuclear leukocytes, erythrocytes and fibrin. The underlying infiltrate consists of plasma cells and newly formed blood vessels with endothelial proliferation and blood clots. Ulcerations exist for about 3-4 weeks, then their bottom is cleared, covered with granulations, and after 1-2 months healing occurs with the formation of a scar. Complications such as phimosis, paraphimosis, and gangrene of the penis are possible. The diagnosis is made based on clinical picture and bacterioscopic examination - streptobacilli are detected in the discharge of an ulcer or bubo. Differential diagnosis is carried out with syphilis, donovanosis, lymphogranulomatosis venereum, tuberculosis.

Treatment: trimethoprim - 320 mg, sulfamethoxazole (Bak-Trim) - 600 mg or erythromycin - 2 g per day for a week. Xeroform (iodoform) powder and epithelializing ointments are used locally. Prevention is mandatory dispensary observation, examination of sexual partners and their treatment. After completion of treatment, all patients are observed for 6 months with blood testing for CSR, RIBT, RIF. Personal prevention consists of using condoms, and if infection is suspected, washing the genitals and rubbing sulfonamide emulsions or ointments into the skin, as well as taking sulfonamide drugs orally during the first 3 hours after sexual intercourse.

Secondary syphilis develops 6-7 weeks after the first symptoms of syphilis; if it has not been carried out, it lasts 2-4 years, it proceeds in waves: active manifestations are replaced by hidden ones, and therefore they are distinguished as secondary fresh syphilis, secondary recurrent and hidden, latent.

In secondary syphilis, generalization of the syphilitic infection occurs; At the same time, the blood and especially the rashes contain a large number of spirochetes, so the manifestations are very contagious (the contagiousness of erosive elements is especially high).

Secondary syphilis symptoms:

Clinically characterized by predominant damage to the skin and mucous membranes; to a lesser extent - changes in internal organs and the nervous system (sometimes at a subclinical level). The rashes of the secondary period are polymorphic in nature: spotted (spotted, roseolous syphilide), papular (papular syphilide); Vesicles and pustules (pustular syphilides) are observed much less frequently.

There are no acute inflammatory changes in the area of ​​the rash (the rash is not brightly colored; its color or shade is compared to copper or ham). The rashes have rounded outlines and do not merge; there is no tendency towards peripheral growth. The elements can appear on any part of the skin and have a dense infiltrate at the base (with the exception of roseola).

Erotic papule

Characteristic is the absence of subjective sensations (pain, itching, burning) in the area of ​​secondary syphilides. Changes in the secondary period are characterized by relative benignity - the rashes disappear even without treatment, leaving no trace (scars remain only after deep pustular syphilides), are not accompanied by an increase in body temperature and significant violation general condition. The rash quickly regresses under the influence of antisyphilitic treatment.

Rashes of the secondary period are accompanied by positive CSR (Wasserman river and sedimentary - in 98-100%).

Syphilitic roseola.

Syphilitic roseola (spotted syphilide) is one of the common manifestations of the secondary period. This is a dim, round spot of pinkish-bluish color with unclear boundaries, without peeling. The spots do not merge, do not tend to grow peripherally, there are no signs of acute inflammation or subjective sensations.

Roseola is most often localized on the lateral surfaces of the body; disappear spontaneously after a few days (less often - 2-3 weeks), without peeling, leaving no trace. In atypical cases, roseola is observed: with peeling, confluent, edematous (or urticarial), granular (follicular; sometimes visually and palpably determined in the form of perifollicular compactions - in weakened individuals with tuberculosis).

Syphilitic roseola may be similar to manifestations of toxicoderma, rashes with acute infections, spots from insect bites, as well as “marbled” skin. After the first administration of antibiotics (penicillin), roseola becomes brighter - “flames”, can transform into atypical (as a manifestation of the Herxheimer-Lukashevich reaction; “endotoxic shock” - due to the release of endotoxins during the massive decay of spirochetes).

Papular syphilide.

Another characteristic manifestation of secondary syphilis is papular rashes. Varieties are traditionally described papular syphilides, differing in size (miliary, lenticular, numular, condylomas lata), characteristics of desquamation (seborrheic, psoriasiform), localization (palmoplantar), type of grouping of elements (corimbiform), relief (frambesiform), etc.

With all the variety of descriptions, you should pay attention to the following: papules of regular shape, with a dense infiltrate, no tendency to peripheral growth, ham-like hue. Characteristic is peeling along the periphery of the papules (“Biette’s collar”) and the absence of subjective sensations. Papules can erode, turning into weeping syphilide (especially typical for condylomas lata - in folds); bright red papules without epithelium are often observed in the oral cavity. It should be noted that when syphilis is combined with any dermatosis, a kind of “layering” of clinical symptoms is possible.

For example, we observed manifestations of secondary syphilis in a patient who had suffered from psoriasis for a long time; his syphilides were psoriasiform, but with a bluish tint; many papules had a mixed type of peeling - with silver-white scales and the “Biette collar” type; against the background of specific treatment, a rapid regression of “psoriatic” elements was noted. Sometimes isolated syphilitic papules appear on the soles, resembling manifestations of mycosis, resembling calluses (we observed single papules in the interdigital folds of the feet).

Pustular syphilide.

Pustular syphilides are particularly “diagnostic insidious”, reminiscent of manifestations of banal pyoderma and other infections (hence the names - impetiginous, acne), but having a bluish tint, greater density (there may be a copper-red ridge along the periphery, often called a “Biette collar”) .

Syphilitic leucoderma.

Syphilitic leukoderma (“necklace of Venus”) - occurs more often 4-6 months after infection (classified as a manifestation of secondary recurrent syphilis). It is most often localized on the back and side of the neck (however, it can also affect larger areas of the skin - the upper back, area shoulder joints). Depigmented spots appear on the affected areas, surrounded by a zone of hyperpigmentation. The spots have a round shape and vary in size and quantity in different patients. Pigmentary syphilide can persist for a long time (many months); its manifestations are classified as trophic disorders (a kind of neurodystrophic process).

When studying the cerebrospinal fluid in patients with leukoderma, changes were revealed (pathology of neurocytes, etc.). It is believed that disorders of the autonomic and central nervous system play an important role in the development of leukoderma, and therefore, in the presence of a “Venus necklace”, attention should be paid to the neurological status; according to indications, involve a neurologist - with the prescription of neurotropic therapy and drugs that improve the penetration of antisyphilitic drugs into the cerebrospinal fluid (ethamide, prodigiosan, systemic polyenzymes, Cavinton, Sermion, cinnarizine, piracetam, etc.). At differential diagnosis secondary leukoderma should be kept in mind (occurs after regression of some skin rashes, for example, with lichen versicolor).

Syphilitic alopecia.

Syphilitic alopecia - also appears more often in patients with secondary recurrent syphilis; manifests itself in forms: small-focal, diffuse and mixed. In this case, bald spots appear (“moth-eaten fur”) or general thinning of the hair is observed; the skin is not changed. It is believed that hair loss is due to vasculitis, the formation of specific perivascular and perifollicular infiltrates, which leads to trophic disorders; Moreover, by their severity one can partially judge the degree of vascular discorrelations. Although this process is benign (hair grows back), rheologically active and trophic-improving drugs (nicotinic acid, complamin, etc.), vitamins C, rp.B, P, A, E should be additionally prescribed. Patients with syphilitic alopecia should refrain from walking in cold weather without a hat, because this aggravates trophic disorders and hair loss. The syphilitic nature of baldness is established on the basis of other manifestations of syphilis, as well as positive serological reactions.

Of great practical importance features secondary fresh and recurrent periods of syphilis. With secondary fresh syphilis, residual manifestations of primary syphilis may be observed (ulcerative chancroid, regional scleradenitis, polyadenitis); there is no leukoderma or alopecia. With secondary recurrent syphilis, there are no manifestations of primary lues; the appearance of leukoderma and alopecia are characteristic of this period.

With secondary fresh syphilis, the rashes are abundant, widespread, scattered, small in size and brighter in color. With secondary recurrent syphilis, it is more often observed a small amount of rash, tendency to group it; At the same time, the elements are larger and their color is faded. However, the difficulty of differentiating fresh and recurrent syphilis has now been noted; at the same time, their clinical differences are “erased” - so symptoms characteristic of recurrent syphilis can occur with fresh syphilis and, vice versa (for example, a bright, abundant, small rash - with recurrent syphilis). More often, rashes with itching, burning, and monopalm (or plantar) syphilide are recorded (in the absence of a rash in other places); sometimes papules have a “waffle” symptom, similar to that of parapsoriasis. The “updated”, “modern” features of secondary syphilis include an increase in the number of patients with damage to the mucous membranes (erythematous-papular rashes, manifestations such as tonsillitis, etc.). When it is difficult to distinguish between fresh and recurrent syphilis, sometimes the designation appears: “secondary fresh-recurrent syphilis” (treatment is prescribed in the “interests of the patient” - according to schemes for the relapse period).

Palmar syphilide
Plantar syphilide

As noted, after the rash of secondary fresh syphilis, a latent period begins; after some time (varies in different patients) it is replaced by new active manifestations, i.e. with the development of secondary recurrent syphilis. In this case, relapses of the secondary period can last for 2-4 years (they are replaced by latent manifestations). Secondary latent syphilis is characterized by the absence of clinical symptoms that would allow one to suspect the presence of syphilis in the patient. However, blood tests reveal positive CSR.

We can once again note the social significance of secondary syphilis - due to the long course of this period and its high infectiousness. In this regard, the following data for making the diagnosis of secondary syphilis are of great practical importance:

1. Clinical manifestations: the appearance of rashes (usually roseola, papules) on the skin and mucous membranes, without a bright inflammatory color and subjective sensations. The peculiarity of the morphology and location of the rash reflects the stage of the disease - multiple, bright, small rashes in combination with remnants of ulcerative chancre and polyadenitis indicate secondary fresh syphilis; in case of relapse - the rash is not numerous, less bright, but larger, with a tendency to cluster; additional signs recurrent cases are neurotrophic disorders (leukoderma, alopecia).
2. Visualization of a pale spirochete in the discharge of erosive syphilides (especially condylomas lata, elements in the oral cavity).
3. An important diagnostic criterion is the results of immunological tests (DSR, RIBT, RIFT). With secondary fresh syphilis KSR is positive in 100%, with secondary relapse - 98%.
4. “Venerological alertness” is necessary - even when examining patients who seemingly “cannot have syphilis,” including those suffering from dermatoses; It is possible to avoid mistakes if the rule is followed - all patients with spotty, papular (“parapsoriasis”), pustular rashes (abundant or localized, especially unknown origin) must be carried out serological test, because if overlooked, the secondary period can go into .

Among all skin diseases, a condition in which white (discolored) spots appear on the body is common. This pathology is associated with a general or local (directly in the skin) disorder of pigment metabolism and is called leukoderma.

Leucoderma: description and types

Leukoderma is not an independent dermatological disease, but one of the symptoms that manifests itself various pathologies. Leukoderma is also called leukopathy, hypomelanosis, hypochromia, hypopigmentation. Discolored spots appear on the skin due to a disorder in the synthesis and deposition of the substance melanin, the main of the four pigments that color the skin. The reason may also be increased destruction of pigment.

Leukoderma, or leukopathy, is white patches on the skin

White spots are a fairly common occurrence. According to statistics, up to 8% of the entire world population suffers from various forms of leukopathy. In this case, a violation of normal skin coloring can be either acquired or caused by genetic abnormalities or congenital. Latest form It is most often observed at a very early age and presents serious difficulties in getting rid of the disease. The gender distribution of hypochromia depends on the type of pathology: some conditions occur predominantly in women or only in men, which is associated with hereditary factors, while others can be observed in both sexes equally often.

Leukopathy is manifested by multiple depigmented spots of different shapes and locations. The prevalence of the process depends on the cause of hypopigmentation. On etiological factors the modern classification of pathology is also based.

Dermatologists divide hypochromia into several main types:

• primary leukoderma. This category includes:
  • a congenital form that has genetic causes or occurs in utero. Such patients most often also have other disorders and malformations, for example:
    • Ito hypomelanosis, or achromatic melanin incontinence;
    • albinism or partial albinism (piebaldism);
    • tuberous sclerosis (multisystem disease);
  • chemical (toxic) leukopathy, which affects people who interact with harmful substances due to professional activity. For example, with hydroquinone and its varieties, which are used in the industrial production of various dyes, plastics and rubber products;
  • drug hypochromia, which develops under the influence of any medication;
• secondary, or acquired, leukopathy. Is a consequence or manifestation of another disease. Among this category are:
  • infectious form:
    • syphilitic leukoderma - a condition that develops with secondary syphilis and includes 3 subspecies: spotted leucoderma, marbled, reticulate (lace);
    • leprosy leukopathy (including the tuberculoid form with the formation of pigmented lepris), which occurs as a resolution of the infectious process;
    • hypopigmentation against the background different types lichen (pink, red, scaly -), parapsoriasis, trichophytosis;
  • post-inflammatory form (pseudo-leukoderma), which occurs against the background of post-burn skin changes, as well as as a consequence of some long-term dermatological diseases of an inflammatory nature (eczema,);
  • immune leukopathy, in which pigment cells are destroyed by one’s own immunity. This category includes:
    • autoimmune diseases - systemic lupus erythematosus, scleroderma with hypochromatosis;
    • hypochromia due to infection with worms;
    • vitiligo;
• idiopathic leukopathy, which includes all cases of hypochromia with an unknown cause.

Some experts attribute the infectious form of the pathology (syphilitic and leprosy) to primary hypochromia.

In terms of prevalence, hypochromia can be local (several spots in certain places) or diffuse (generalized), that is, the lesions are located almost throughout the body.

Causes of the disorder

Several mechanisms may underlie the development of hypochromia. Normally, melanin, the main skin-coloring pigment, is synthesized from the amino acid tyrosine, which enters the body with food, and can also be produced under the influence of liver enzymes and hormones from the amino acid l-phenylalanine, found in muscle tissue protein molecules. Tyrosine is converted into melanin under the action of the enzyme tyrosinase in special pigment cells - melanocytes. Such complex biochemical reactions lead to the fact that melanin is synthesized and deposited in specific cellular structures - melanosomes, and the skin acquires an even shade.

Failure at one of the stages of this complex process, be it tyrosine deficiency, tyrosinase deficiency, or the inability to accumulate pigment in melanosomes due to the influence of external or internal factors, leads to the appearance of leukodermic lesions on the skin. Thus, with albinism, which some experts assess as an extreme variant of hypochromia, there are defects in the structure of the enzyme tyrosinase, which is why melanin synthesis does not occur.

With other types of leukoderma, selective death of pigment cells is observed under the influence of viral or bacterial agents, toxic substances or immune disorders. Melanocytes do not have time to be replaced in time, which leads to hypochromia.

Diseases and factors that provoke the appearance of white spots:

• infections - leprosy, syphilis, trichophytosis ( fungal infections skin);
• autoimmune pathologies - scleroderma, lupus erythematosus;
• inflammatory processes - psoriasis, eczema, neurodermatitis;
• genetic diseases - Wolf's disease, Waardenburg syndrome, Ziprovsky-Margolis syndrome, albinism and others;
• the effects of drugs and chemicals on the body;
• helminthiases and endocrine diseases;
• immune disorders.

Video: what causes white spots on the skin

Manifestations of hypochromia

The main symptom is the appearance of depigmented spots on various parts of the body - limbs, torso, in skin folds, on the face. Their shape, color shades and quantity, as well as accompanying manifestations depend on the type of leukopathy and the reasons that caused it.

The color of hypochromic lesions can be of different shades - from completely white, pearl to light yellow and pale pink. In some pathologies, the spots may be surrounded by a border of a darker shade or red; areas of brownish or pink pigmentation may also be observed, surrounded by a wide discolored border (with Setton's nevus). Hypo- or depigmented areas are most often completely flat, or may be slightly protruding. Over time, the size of the lesions can grow, and individual spots merge with each other.

Interestingly, under the influence of solar radiation in normal skin melanin synthesis is enhanced, but this is not observed in discolored areas remaining after healing of psoriasis or eczematous elements (solar leukoderma).

Some diseases, in addition to hypochromic spots, are accompanied by discoloration of skin appendages - leukonychia (white spots on the nails or complete absence pigment) or leukotrichia (hair lacking color), with certain forms of albinism there is a very light color of the iris.

Features of manifestations of individual forms of leukoderma - table

Photo gallery - manifestations of leukopathy

Post-inflammatory leukoderma - white spots form on the skin as a result of inflammatory rashes Specific white spots on the neck - characteristic manifestation secondary syphilis (lace syphilitic leucoderma) After healed psoriatic rashes, residual effects are observed (infectious leukoderma) Chemical leukoderma - discoloration of areas of the skin in contact with toxic substances
Autoimmune processes in the body can manifest themselves in the formation of areas of hypochromia The most common type of immune leukopathy is vitiligo.

Diagnosis of pathology

A dermatologist diagnoses and treats the patient. A specialist can easily make a diagnosis by examining the skin of the person who contacts him, but a comprehensive examination may be necessary to establish the causes of leukopathy.

The dermatologist evaluates the localization, color, shape of hypochromic lesions, determines whether there is a compensatory skin reaction in the form of rims of hyperpigmentation around colorless spots. An important diagnostic point is the collection of anamnesis: associated symptoms, whether there was contact with harmful substances, what medications the patient took, whether there is hypochromia in relatives.

From laboratory research apply:

• a clinical blood test, which can indicate the infectious nature of the pathology if nonspecific indicators of the inflammatory process are present (acceleration, increased level of leukocytes) or indicate helminthic infestation if eosinophils are increased;
• a blood test for syphilis (RW - Wasserman reaction or PCR diagnostics), as well as a specific skin test for leprosy, can determine the root cause of the infectious form of leukopathy;
• enzyme immunoassay of blood if the autoimmune nature of the pathology is suspected (lupus or scleroderma).

To differentiate non-infectious leukopathy from different forms of lichen, luminescent diagnostics are used - examination of the skin using ultraviolet lamp Wooda.

In cases that are difficult to diagnose, a biopsy of an area of ​​hypopigmented skin is used, followed by microscopic analysis. Depending on what caused hypochromia, the study may reveal connective (scar) tissue, swelling of the dermis, changes in the cells of the epidermis, and signs of an inflammatory reaction. Most often, abnormal melanocytes are present - structurally altered, or they may be completely absent.

Differential diagnosis consists of determining the form of leukoderma, distinguishing skin manifestations in secondary syphilis, psoriasis, eczema, lichen, neurodermatitis, vitiligo, congenital syndromes with hypochromia.

Treatment of leucoderma

Therapy comes down to eliminating the causes that caused skin discoloration. Apply medications, physiotherapy, sometimes - surgery. Additionally, herbal medicine can be used. Diet plays an important role in the fight against leukopathy.

Medicines

The choice of medications depends on the form of the pathology:

• infectious leukoderma is treated with antibiotics:
  • syphilis - with Penicillin preparations;
  • leprosy - Dapsone or Rifampicin;
  • mycoses - antifungal agents - Clotrimazole, Lamisil;
• autoimmune pathologies require the prescription of cytostatics and immunosuppressants (under strict medical supervision):
  • vitiligo is treated with topical (external) corticosteroids, calcineurin inhibitors are used - Tacrolimus, Pimecrolimus, furocoumarin preparations to stimulate melanogenesis - Beroxan, Ammifurin, Meladinin, pulse therapy with Dexamethasone is used;
• for helminthic diseases, antihelminthics are prescribed - Dekaris, Albendazole, Pirantel, Vermox.

In certain cases, the use of medicinal analogues tyrosine and phenylalanine. Complexes with vitamins A, E, C, PP, copper and zinc are prescribed.

With toxic leukoderma, special therapy may not be required; as a rule, it is enough to stop the patient’s contact with chemical or stop taking the drug.

Diet

A balanced diet is beneficial for every person. A patient with pigmentation disorders must constantly adhere to the principles of a healthy diet: exclude excessively fatty, fried foods, fast food, alcohol, products with harmful food additives, preservatives. During the day, it is advisable to drink up to two liters of liquid in the form of pure water, teas, and natural juices.

It is very important to include tyrosine-rich foods in your diet:

• valuable varieties of sea fish and seafood;
• beef liver, veal tongue;
• meat - turkey, rabbit, goose;
• dairy products;
• vegetable oils;
• cereals - buckwheat, oatmeal and millet;
• legumes;
• vegetables, fruits and berries, preferably fresh - pumpkin, tomatoes, spinach, avocado, parsnip root, eggplant, cauliflower, potatoes, beets and carrots, blueberries, bananas, strawberries, papaya;
• nuts and seeds - pistachios, hazelnuts, almonds, peanuts, sesame seeds, sunflower and pumpkin seeds.

Photo gallery: foods rich in the amino acid tyrosine

It is recommended to include legumes in the diet in boiled or stewed form.
In addition to tyrosine, dairy products contain a large amount of vitamins and microelements
If you have leukoderma, it is recommended to include cereals in your diet every day.
A certain amount of tyrosine, as well as polyunsaturated compounds beneficial to the body fatty acid found in seafood Nuts are beneficial for the body not only due to the presence of tyrosine in them, but also high content microelements and vitamins Fresh juices must be present on the table of a patient with leukopathy Beef liver contains 0.73 g of tyrosine per 100 g of product By including a sufficient amount of fruits and vegetables in your diet, you can provide the body not only with tyrosine, but also with many useful vitamins

Physiotherapy

Physiotherapeutic methods are especially effective for hypomelanosis associated with autoimmune reactions, such as vitiligo.

Ultraviolet radiation has an immunosuppressive effect, helping to stop the process of destruction of pigment cells and stimulate their recovery.

The following methods are used:

1. Phototherapy using a UVB lamp (narrow band).
2. PUVA therapy (phototherapy with UVA and psoralen). The method is based on taking Methoxalen or another photosensitizing agent 2 hours before treating the skin with long-wavelength ultraviolet rays. Local PUVA therapy can be used in adults and children over 2 years of age.
3. Monochromatic excimer light using a special lamp or laser. The use of the technique is justified for localized forms of leukopathy.

Ultraviolet treatment is not used for all forms of hypochromia. The medical approach to prescribing physiotherapy should be strictly individual.

Surgery

The most difficult to treat are hereditary forms of hypochromia and vitiligo. In the latter case, the patient may be offered surgical treatment.

The method of melanocyte transplantation is used, as well as transplantation of one’s own areas of healthy skin or donor samples.

The essence of the pigment cell transplant operation is as follows: healthy melanocytes are isolated from an area of ​​pigmented skin (most often from the gluteal region), they are processed and injected into hypochromic areas. Before transplantation, the old epidermis is removed from the hypopigmented area using laser or dermabrasion. After the operation, the treated area is covered with a special sterile bandage for a week.

Repigmentation occurs 1.5–3 months after the procedure. Approximately 3–4 weeks after transplantation, the skin is irradiated with ultraviolet light for a course of about 3 months. Additionally, a course of corticosteroids is prescribed. The maximum effect after surgery can be seen no earlier than six months later.

Folk remedies

Can't be underestimated healing properties medicinal plants that are recommended for use as an additional remedy in the treatment of hypochromia. Particularly useful are herbs that contain furocoumarins, which increase skin sensitivity to ultraviolet radiation and stimulate melanogenesis.

Of these plants, the most commonly used for leukopathy are cumin (in the form of oil), parsnip root, aromatic rue, St. John's wort, and white ash. Aloe juice, honey and herbal preparations are recommended as biostimulants. In some cases, excluding the infectious form, bleaching agents (juice of sauerkraut, lemon, cucumber) are used to smooth out the boundaries of discolored areas.

Recipes for the treatment of leukopathy

1. Ready-made oil can be purchased at a pharmacy.
2. A few drops of the product should be rubbed daily into the affected areas of the skin.
3. It is permissible to mix in equal proportions with St. John's wort, sesame or linseed oil.

Cumin is a treasure trove active substances regulating the functioning of skin cells, including pigment cells. It contains essential amino acids, vitamins A, F, E, antibacterial substances, microelements - sulfur, iron, phosphorus, calcium. Such a rich composition allows the plant to be used not only as a stimulating and regenerative agent, but also as an antifungal and anti-inflammatory for various trichophytosis and dermatoses.

Aloe as a stimulating, regenerative and anti-inflammatory agent:

1. Cut an aloe leaf (at least three years old) and keep it in the refrigerator on the bottom shelf for at least a week.
2. Rinse thoroughly, remove the skin, chop finely and squeeze out the juice.
3. Store the juice in the refrigerator for no more than three days.
4. Take a teaspoon before meals three times a day. Can be mixed with a tablespoon of fresh honey.
5. Aloe juice can be applied externally to affected areas.

Turmeric to stimulate melanogenesis:

1. Chopped raw turmeric (300 g) should be mixed in a glass container with grated ginger root (approximately 100–150 g), add the juice of 2 lemons.
2. Place the mixture in the refrigerator.
3. Take 2 teaspoons before meals. The drug is contraindicated for diseases of the gastrointestinal tract.

Turmeric infusion (at the rate of 1 tablespoon per glass of water) can be used externally, applying wipes soaked in the product to hypopigmented areas.

Parsnip root infusion for skin repigmentation:

1. Finely grate fresh root, pour a glass of boiling water, leave for an hour.
2. Take half a glass of medicine, mixed with a tablespoon of honey three times a day, half an hour before meals.
3. The course of treatment is at least a month.

Infusion sweet rue to enhance melanin production:

1. Pour boiling water (400 ml) over a teaspoon of chopped herbs and leave for 6 hours.
2. Take the infusion one third of a glass 4 times a day before meals.
3. The course of treatment is 30 days.

Alcohol tincture of rue leaves:

1. Mix fresh juice (1 part) with medical alcohol (6 parts).
2. Leave in a dark place for 10 days, filter.
3. Take 10 drops three times a day.

Infusion of white ash (photosensitizing, anti-inflammatory, immunomodulatory and antitoxic agent):

1. A teaspoon of crushed dry raw materials should be brewed with a glass of boiling water and left for an hour.
2. Strain and drink half a glass in the morning and evening.

Decoction of ash roots:

1. Boil crushed dry roots (a teaspoon) in 0.5 liters of water for 5 minutes.
2. Leave until cool and strain.
3. Take a third of a glass of the decoction three times a day before meals, and also use externally in the form of compresses.

The use of sauerkraut brine for whitening, stimulation of metabolic processes, saturation of the body with vitamins and microelements:

1. Cabbage juice (2 tablespoons) should be mixed with yogurt (the same amount) and a teaspoon of lemon juice.
2. Apply to skin for no more than 10 minutes.

Such compresses smooth out the boundaries of hypopigmented areas.

Prognosis, complications and consequences

Regarding the patient’s life, the prognosis for leukopathy is always favorable, since this dermatological condition does not pose a threat of death or serious complications - only severe defects accompanying congenital forms of hypochromia and infectious diseases can lead to this.

As for the possibility of restoring pigmentation in damaged areas, the prognosis is usually uncertain even with mild forms of pathology. With a toxic form, the chances of a complete recovery are much greater than with leukopathy caused by autoimmune diseases. Vitiligo is extremely difficult to treat.

It is worth remembering that some forms of the disease can only have consequences in the form of emotional distress due to a cosmetic problem, while in other cases, severe infections accompanied by hypochromia can lead to extremely serious complications (for example, syphilis).

Prevention of leukopathy

Due to the fact that there is no specific prevention of pathology, preventive measures include:

• adequate protection of the skin from solar radiation;
• avoiding contact with toxic substances;
• taking medications as prescribed by a specialist;
• timely consultation with a doctor in case of infectious, viral infections and dermatological diseases;
• eating foods rich in tyrosine.

There are many reasons for the development of pigmentary disorders, so make a correct diagnosis and prescribe correct treatment Only an experienced dermatologist can. Therapeutic tactics are always determined individually. Do not self-medicate and be healthy!