Questions. Dangerous internal herpes

Blistering agents are poisons developed as highly toxic warfare agents. When absorbed into the blood, these substances cause poisoning of the entire body. By the nature of the damage, they are classified as lethal, along with hydrocyanic acid, sarin and phosgene. Understanding the clinical manifestations and methods of diagnosing intoxication will help you take timely measures if necessary to eliminate it.

What is a blister agent?

Blistering toxic substances are toxins, the effect of which on the human body causes acute inflammatory-necrotic transformations of the mucous membranes and dermatological integuments. This sulfur and nitrogen mustards, as well as lewisite.

These substances have an oily consistency, are characterized by a high boiling point, low water solubility and a high level of miscibility with solvents of organic origin. This indicates the ability of toxic substances to quickly penetrate shoes and clothing and be absorbed into the skin.

Distinctive features of mustard gas damage

Mustard gas looks like a colorless or brick-brown liquid with a garlic or mustard odor. The substance slowly evaporates into the air. It is used in two combat states: aerosol and droplet-liquid. The distribution range of its vapor reaches 20 km in open areas.

The effects of mustard gas can be distinguished from intoxication with other toxic substances by the following characteristics:

No pain or discomfort during contact. The poison has an analgesic effect on the nerve endings, so a person does not feel contact with it and cannot take protective measures in a timely manner. Due to the lack of irritant effects, mustard poisoning is quite difficult to diagnose.
The presence of a period of latent progression of the lesion. The duration of absence of specific symptoms may vary in different situations and depend on the volume of the poison exposed, its condition, the mode of penetration into the body and individual susceptibility. The greater the dose of mustard gas exposed to a person, the faster the first symptoms of damage will appear. The eyes are most sensitive to the toxic substance, the skin is the least sensitive. The rate of manifestation of the reaction also depends on the state of aggregation of the poison: droplet-liquid and fog-like mustard gas are characterized by a short latent period, while vapor mustard has a longer latent period. The maximum duration of absence of signs of damage reaches 24 hours.
Reduced immunobiological resistance. When the body is affected by mustard gas, it becomes infected, caused by a sharp decrease in resistance to the effects of pathogenic factors. A decrease in immune defense contributes to a longer treatment period and a more complex course of the disease. This phenomenon is especially dangerous if the organs of vision and breathing are damaged. To improve the condition in a hospital setting, prophylactic antibiotic therapy is used.
Slow recovery process. Neurotrophic disorders caused by exposure to a toxic substance lead to a slowdown in the healing process of damaged tissues and restoration of impaired functions.
Increasing the body's sensitivity to irritants. If a person is repeatedly exposed to mustard gas, even small doses of the substance can cause serious damage.

The mechanism of influence of nitrogen and sulfur mustard is quite similar. The key difference is that nitrogen mustard causes a stronger irritating effect on the respiratory and visual organs. In this case, the disease is characterized by a milder course of the disease and accelerated recovery.

Course of intoxication with vapor mustard gas

Mustard gas vapors affect humans in many ways: may damage eyesight, respiratory system and skin. The severity of the process depends on the saturation of the toxic substance and the time of its effect on the body.

There are three degrees of damage to the body as a result of exposure to vapor mustard gas:

Mild degree. The first symptoms occur 2-6 hours after contact with the toxin. The eyes begin to hurt, react sharply to light, and their redness is noticeable. After 8-12 hours, there is a feeling of dry mouth, sore throat, runny nose, dry cough, loss of voice. Signs of nasopharyngolaryngitis become more and more noticeable over time. After 15-17 hours, erythema forms on the skin - redness of certain areas of the skin. They affect such areas as the inner thighs, armpits and elbows, and the genital area. Possible redness of the face and neck. When heated, the itching intensifies in the area of erythema. Along with local symptoms of intoxication, general ones appear - nausea, vomiting, headache, fever.
Average degree. The latent period of intoxication ranges from 4 to 6 hours. Against the background of pronounced conjunctivitis, signs of damage to the organs of the respiratory system appear. The person has a severe cough, profuse mucopurulent nasal discharge, and difficulty breathing. When swallowing and talking, a sore throat occurs, the cough intensifies as night falls and when the ambient temperature changes, it becomes wet. Signs of acute tracheobronchitis increase, necrosis of the mucous membrane of the bronchi and trachea occurs, leading to various complications. Body temperature rises to 38 degrees. The duration of moderate mustard gas poisoning is 1-2 months.
Severe degree. The described signs of damage include blueness of the skin and mucous membranes, shortness of breath, and increased coughing. Mustard pneumonia develops, and in some cases pulmonary edema occurs. If heart failure occurs, death may occur. A favorable course of poisoning helps to improve the patient’s condition after 2-3 weeks. In this case, a person’s complete recovery is impossible.

Poisoning with liquid mustard gas

Under the influence of droplet-liquid mustard gas, damage to the skin, eyes and gastrointestinal tract occurs. The severity of the body's reaction depends on the amount of the substance exposed.

Stories from our readers

Vladimir
61 years old

Damage to the organs of vision

Eye damage is most often severe and appears within 1-2 hours after contact with the toxin. The first signs of poisoning are a reaction of the cornea, manifested in photophobia, lacrimation, redness, swelling of the conjunctiva, a feeling of sand in the eyes and pain of varying intensity. On the second day, cloudiness and roughness of the cornea are observed, and ulcers begin to appear in the area of inflammation. There is a possibility of corneal rejection and vision loss.

Severe pain in the eye area is caused by a secondary infection, which is accompanied by the formation of pus in the anterior chamber of the eyeball and inflammation of the iris. The duration of inflammation of the organs of vision reaches 5-6 months.

Skin damage

Skin damage as a result of droplet-liquid exposure to mustard gas occurs in different ways. The process depends on the degree of damage:

Mild damage is reflected in the appearance of erythematous areas of the skin. The first symptoms appear 12-14 hours after exposure to the poison. On days 4-5, erythema gives way to pronounced pigmentation and peeling of damaged skin. After a week, the symptoms of poisoning disappear, leaving only pigmentation.
The average form of the lesion appears after 2-4 hours. The appearance of erythema is accompanied by the formation after 8-10 hours of vesicles, which turn into erosion upon opening. For some time, the blisters increase in size, after which they disappear, leaving pronounced erosive areas that are completely covered with epithelium within 2-3 weeks.
Severe damage causes the development of erythematous-bullous dermatitis. Bubbles begin to form 3-5 hours after contact with the toxic substance. On the third day, they are damaged, resulting in the formation of an ulcerative surface. As a result of infection of the ulcers, necrotizing dermatitis may develop, which recedes after 3-4 months. At the site of the ulcers, white scars form, surrounded by pigmented skin.

Damage to different areas of the skin is characterized by different durations and characteristics of the process:

when facial skin is damaged, accelerated healing of ulcers is observed, without the formation of clearly defined scars;
damage to the scrotum is accompanied by the formation of an extensive erosive surface and serious disruption of the urination process;
When mustard gas comes into contact with the feet and legs, the formation of trophic ulcers is observed, which is characterized by a complex process of occurrence and recovery.

Damage to the digestive system

Ingestion of a toxic substance orally with contaminated water or food causes severe intoxication of the gastrointestinal tract. The first signs of damage appear a quarter of an hour after mustard gas enters the body. A person experiences blood flow to the mucous membranes and gums, and loose, bloody stools occur. General signs of intoxication develop: weakness, slowness of reaction, convulsive phenomena. In some cases, necrotic changes occur in the stomach. From the nervous system, symptoms such as excitement, fear, and a state of passion followed by attacks of depression are observed.

Developing acute heart failure can cause death within 1-2 days. Death is also common on days 7–10 as a result of acute wasting. With a more favorable course of the disease, a person experiences a general weakening of the body and anemia. Cancer is likely to develop in the future.

Lewisite poisoning

Lewisite appears as a thick, dark brown to black oily liquid that smells like geranium.. It is highly soluble in fats and solvents, and easily combines with various toxic substances. Lewisite has a higher toxic effect compared to mustard gas.

Symptoms of lewisite poisoning depend on the method of its penetration into the body:

When the respiratory system is affected, irritation of the mucous membrane is observed, expressed by sneezing, coughing, runny nose, and a sore throat. A mild form of poisoning is often cured within 6-7 days. In case of moderate poisoning, bronchitis develops, difficulty breathing, increased coughing with the removal of purulent sputum. Severe degree is characterized by the development of pulmonary edema. If the disease progresses positively, it is cured within 4-6 weeks.
When the skin is affected by lewisite, a burning sensation and pain occurs at the moment of contact. Erythema develops and bubbles form. The process is accompanied by swelling and hemorrhages. Infection of the affected areas often does not occur.
When lewisite gets into the eyes, it causes tearing and pain. Within an hour, clouding of the cornea, swelling of the eyelids, and hemorrhages appear. With a favorable prognosis, recovery occurs within 2-3 weeks.

Treatment

The degree of poisoning of a person and the level of damage to his organs and systems depend on the timeliness of providing treatment measures.

First aid

To provide first aid to victims who have come into contact with toxic substances of blister action in the contaminated area, the following measures are taken:

washing the eyes with clean water or 2% soda solution;
use of a gas mask;
cleansing uncovered areas of skin and tight clothing with the drug provided in the individual anti-chemical package (IPP);
inhalation of a special anti-smoke composition with clearly defined damage to the mucous membranes of the respiratory organs.

Beyond the border of infection, secondary rinsing of the eyes, mouth and nasopharynx is necessary as first aid. When toxic substances enter the digestive system, you need to lavage the stomach, inducing vomiting.

Health care

Emergency procedures for providing medical care cover the following activities:

fragmented sanitation;
the use of special ointments for eye treatment;
cleansing the stomach using a probe;
taking adsorbent drugs;
the purpose of unithiol - an antidote for lewisite intoxication;
anti-burn measures.

Further steps to provide medical care include symptomatic therapy:

The affected areas of the skin are treated with antipruritic and painkillers. If necessary, existing chemical burns are treated.
Treatment of the affected organs of vision is carried out using conservative methods using antibiotics, anesthetics, and antihistamines.
Poisoning through the digestive organs involves the prescription of antispasmodic and ganglion-blocking agents, anti-shock therapy.

The patient is prescribed medications to prevent the development of secondary infections and inflammatory processes. With the help of antihistamines, multivitamin complexes and biostimulating agents, the body's protective function, damaged as a result of exposure to poison, is enhanced.

Prevention

To avoid intoxication with blister substances It is necessary to use personal protective equipment accurately and promptly. These include protective clothing, gas masks and degassing agents: chloramine solutions, products provided for in the IPP.

Infected uniforms and personal items must be decontaminated to prevent further infection upon contact with them.

It doesn’t matter which type of herpes a person has, it harms internal organs, affecting the covering tissues, and as the infection spreads, the symptoms cause a lot of problems for the patient. If externally the infection manifests itself in the form of rashes on the lips and nose, then internal herpes affects the liver, lungs, vagina, uterine epithelium, gastrointestinal tract, and urethra. Doctors' opinions boil down to the fact that cytomegalovirus lives inside every person, and as soon as favorable conditions appear in the form of a cold or decreased immunity, it quickly becomes active. Most of the population, about 95%, are carriers of internal herpes, but most often it appears after 35-40 years.

Features of infection and routes of infection

When diagnosing an infectious disease of viral etiology or herpes, the doctor determines which of the 8 strains of pathogenic microorganisms it belongs to. Most often, the mucous membranes and surface of the lips are affected, and less often the internal organs of a person.

In modern medicine, the prerequisites for the appearance of herpes are:

Infection with viruses type 1 and 2.
Infection with the microorganism Varicella zoster, causing herpes zoster.
Kaposi's eczema herpetiformis is a severe form of the virus.

The process of cytomegalovirus type 5 spreading through the bloodstream and then throughout the body is called viremia. Viremia can be primary, when the infection immediately spreads through the blood and circulates, and secondary, when the virus, after multiplying throughout the body, enters the blood again and the cycle repeats.

There are three main forms of internal herpes strain 5:

Acute manifestations of hepatitis.
Esophagitis.
All types of pneumonia.

Type 5 virus can be diagnosed by herpetic formations on the vaginal walls, in the larynx, on the bladder, trachea, urethra; it is specifically responsible for damage to internal organs.

If it is not possible to determine when the infection process occurred, then we can say for sure that this requires close or intimate contact with the infected person. The main ways of infection by herpes:

Infection through saliva by airborne droplets when it enters the oral cavity of a healthy person.
Sexual intercourse, after which infection through semen remains on the vagina.
Through mother's milk to her baby.
By blood through a woman's placenta during childbirth.
Blood transfusion.

The herpes virus affects to a greater extent people with suppressed immunity, patients with AIDS or cancer, but may not manifest itself throughout life.

Symptoms

It is difficult to identify signs of cytomegalovirus if a person develops fever, weakness and headache, which do not always indicate that herpes has become more active inside the body. In practice, a person may be bothered by prolonged bronchitis or pathologies of the urinary system, indicating the growth of the virus. Symptoms are manifested by the presence of signs similar to other diseases and manifest in different organs (see table).

Areas affected by herpes	Description of symptoms
Esophagus	In addition to painful sensations when eating and chest pain, it is difficult for a person to swallow. By infecting the esophagus, the virus causes discomfort on the diaphragm, the person quickly loses weight, and feels pain behind the sternum. Only an endoscopic examination will confirm the presence of ulcers on the mucous membrane, covered with a film, which subsequently loosen it. Untimely treatment leads to damage to the intestines and pancreas.
Lungs	Symptoms appear based on reduced immunity. These include severe cough and fever, chest pain accompanied by shortness of breath. General weakness occurs due to fungal or bacterial infection. In severe cases, cytomegalovirus is activated when tracheobronchitis moves into the lung parenchyma. If genital herpes in the face and mouth is not treated promptly, bilateral pneumonia may occur.
Genitourinary system	The patient feels discomfort in the lower abdomen, accompanied by discharge from the genitals. The most common signs are pain when urinating and body flushing.
Anus	The peripheral nervous tissue is damaged by the virus, thereby causing unbearable itching at the entrance to the rectum. The patient experiences severe pain, becomes irritable, insomnia, and constipation. Against this background, the lymph nodes become inflamed and enlarged, and hyperemia is possible. Characteristic is the appearance of small blisters, which then burst and heal, indicating their healing. Herpes from the rectum can spread to the gastrointestinal tract, causing erosive changes in the mucous membranes and the appearance of blood in the stool.
Liver	The inflammatory process in the liver with hepatitis B and C is manifested by yellowness of the white membrane of the eyes, skin, pain under the ribs, radiating to the shoulder blade and shoulder. The size of the patient's liver increases, fever periodically appears, which provokes liver dysfunction due to tissue damage. The patient develops weakness, migraines, the concentration of bilirubin in the blood increases, and DIC syndrome appears less frequently.
Brain	With encephalitis or inflammation of the brain, cytomegalovirus enters its cortex, trunk, and both hemispheres. The patient is worried about fever, convulsions, and in rare cases, coma. A person’s behavior changes, dementia develops, acquired skills are lost, and speech is impaired.
Heart	As a result of infection, heart failure develops; when the muscular lining of the heart is damaged, myocarditis develops.

If symptoms appear progressively over the course of two weeks, then you should consult a doctor for a PCR and ELISA test showing the pathogen and antibodies.

Herpetic infection in a newborn

Herpes of internal organs in infants poses a serious danger, as it immediately affects several organs and the central nervous system. Suspecting cytomegalovirus in a newborn, the doctor focuses on skin color, looks at the size of the liver and kidneys, and whether there are extensive hemorrhages.

After activation of cytomegalovirus in a child’s body, the fatal outcome is 65%, and only one child out of ten with damage to the nervous system is able to develop normally. Comparing primary and secondary infection of a pregnant woman, in the second case the risk of complications in the fetus is less. It is important to prevent activation of the virus in a pregnant woman in the first trimester, when all the organs of the fetus are forming.

The greatest danger for infants is that cytomegalovirus can show the main symptoms at a late stage, when it is already difficult to help. For this purpose, women are recommended to treat herpes of internal organs before the expected pregnancy.

Diagnostics

You can understand what a herpes virus infection is by conducting laboratory and instrumental studies, during which specific antibodies to the virus are detected.

Having made a preliminary diagnosis of cytomegalovirus infection, the following diagnostic methods are carried out:

The PCR method involves detecting virus cells in urine, blood, saliva or genital secretions based on their culture. The results do not provide information about the development activity of the virus; they only confirm its presence or absence.
Cell culture makes it possible to assess the rate of progression of herpes, after which effective therapy is prescribed.
The presence of IgM antibodies indicates the presence of a primary infection, IgG indicates contact with an infected person and infection, after which the person remains a carrier of the virus for life.

When conducting diagnostics, a list of antibiotics that are suitable, the presence or absence of rashes, pregnancy, and temperature are taken into account.

Treatment

If emerging herpes rapidly affects and spreads to internal organs, the first step is to seek help from a doctor. In order to correctly diagnose the symptoms and start treatment immediately, the patient is admitted to the hospital, where antiviral or immunostimulating therapy is prescribed, and in case of fever, additional antipyretics.

To determine which immunomodulators are suitable for the patient, an immunogram is performed. Since it is impossible to completely eliminate the virus from the body, drugs are used that eliminate the outbreak of infection and restore the affected organs.

Cytomegalovirus is treated with the following immunostimulating drugs:

Viferon.
Citrovir.
Citrabin.
Ganciclovir.

Amoxicillin and Amoxiclav are prescribed as antibiotics, and the most popular anti-inflammatory drugs are Acyclovir and Vacaclovir.

The categories of people most susceptible to infection are:

Patients with reduced immunity.
Nursing and pregnant women.
Patients with AIDS and HIV.
Blood donors.
Oncology patients.
Patients with diabetes.

Cytomegalovirus infection, which belongs to herpes type 5, is not completely curable, but research is being conducted on glycyrrhizic acid, which is predicted to be able to defeat the disease. If the virus has no symptoms, it does not require treatment.

Prevention

After herpes of internal organs and the corresponding symptoms are identified, treatment of cytomegalovirus with drugs begins, in combination with the doctor’s prescriptions for nutrition and lifestyle.

The patient should be treated under the supervision of medical staff in a hospital.
If the esophagus is affected by cytomegalovirus, a special diet is prescribed, in which the diet should be healthy and balanced.
The patient should give up alcoholic beverages, smoking, and drinking carbonated drinks.
If the lungs are affected by herpes, it is important to take medications that prevent the spread of infected microorganisms throughout the body. At an advanced stage, additional drugs are prescribed to remove sputum from the lungs, such as ACC or Gerbion, which can be taken by adults and children.
The patient can take Viferon or Zovirax ointments if a herpes infection affects the ear or nose areas.
It is recommended to take vitamin complexes to improve immunity.
Every day a person should consume fresh juices from fruits or vegetables, for example, apple, carrot, beetroot.

When the first symptoms of cytomegalovirus appear, you should decide with your doctor how to treat the infection, undergo an examination, and get tested. Despite the fact that at the moment no medicine has been found that completely cures the disease, drugs can extinguish the inflammatory process and remove painful symptoms. Long-term lack of treatment leads to renal failure, cardiac myocardium, damage to the mucous membranes of the gastrointestinal tract, internal genital organs, etc.

How to treat internal herpes?

4.3 (86.67%) 3 votes

Hair damage. Loss of the lateral part of the eyebrows is one of the early symptoms of leprosy. Hair loss in the beard and mustache area is less common. Hair on the scalp is usually retained.

Damage to mucous membranes. The nasal mucosa is most often affected. In severe cases of leprosy, damage to the nasal mucosa is observed in 90-95% of patients. It is very possible that this is where leprosy begins. Scrapings from the nasal mucosa often reveal leprosy bacilli, even in the absence of other clearly defined symptoms of leprosy. Infiltrates appear on the mucous membrane of the nasal septum and paranasal cavities, nasal discharge intensifies, crusts grow, and symptoms of chronic runny nose develop. Infiltrates in the area of the nasal septum tend to ulcerate; the resulting ulcers often lead to destruction of the septum and retraction of the nose at the border of the bone and cartilaginous parts, as a result of which the tip of the nose rises upward. Therefore, the configuration of the nose in leprosy patients has a characteristic appearance. Damage to the bony part of the nose is less common.

On the mucous membrane of the mouth in the area of the hard and soft palate, as well as on the tongue, diffuse infiltrates are observed, rarely ulcerating. With deep infiltrates in the thickness of the tongue, the latter becomes dense, sharply increases in volume, folding appears on its surface with a particularly pronounced longitudinal median fold.

The mucous membrane of the larynx and epiglottis is affected quite often. When the infiltrate spreads to the vocal cords, hoarseness appears, and subsequently aphonia, which can become persistent due to cicatricial changes in the laryngeal mucosa. In some cases, due to edema, laryngeal stenosis may develop, which leads to the need for tracheotomy.

The lymph nodes, especially the femoral ones, are involved early in the pathological process. They increase to the size of a nut, a pigeon egg, acquire a dense elastic consistency, and are painless on palpation. Examination of punctate from lymph nodes makes it possible to establish an early diagnosis of leprosy even in the absence of other symptoms of the disease.

Damage to the nervous system It is often observed in patients with leprosy, and the corresponding symptoms often dominate the picture of the disease, which has given some authors the basis to identify the nervous form of leprosy. Currently, this has been abandoned, since almost every patient with leprosy shows, to one degree or another, pronounced signs of damage to the nervous system. These changes mainly come down to damage to the peripheral nervous system and the development of polyneuritis. Usually affected are n. ulnaris, n. auricularis magnus, n. peroneus. The affected nerve trunks become dense and thicken, so they can easily be palpated in the form of dense cords, sometimes with distinct thickenings. At first they are painful on palpation, and then with the development of anesthesia the pain disappears.

In addition to damage to large nerve trunks, there is a general damage to the nervous system, which is manifested by various disturbances of sensitivity, trophism and movement disorders.

Sensory impairment caused by neuritis and disease of the central nervous system. Persistent and severe neuralgia that lasts for a long time is often observed. At the same time, hyperesthesia develops in the corresponding areas of the skin, which after some time is replaced by complete anesthesia.

Often anesthesia and analgesia are detected symmetrically in the area of individual segments of the body and in the form of a “belt” in the abdomen and chest. Analgesia is sometimes combined with thermal anesthesia, which often causes burns in patients with leprosy. Impairment of tactile sensitivity is much less common. Sometimes there are inadequate reactions to unconditioned stimuli - heat is perceived as cold, and vice versa, as well as a delay in the reaction to an unconditioned stimulus, for example, when a hot object is applied, a touch is first felt, and then a thermal sensation.

Trophic disorders in patients with leprosy are observed very often. These disorders include depigmentation, reminiscent of vitiligo, but differing in that they have sensory disturbances, while vitiligo does not have these disturbances. Trophic changes lead to mutations of the hands and feet, not as a result of deep infiltrates passing to the bones, but as a result of trophic disorders: gradual softening and resorption of the bone substance occurs without obvious changes in the skin, the hands and feet become soft and resemble the paws of a seal; in this case, of course, disturbances in the motor function of the limb occur. Patients with leprosy often experience dysfunction of the sebaceous and sweat glands: first, a sharp increase in it, and then suppression and even a complete cessation of the secretion of sebum and sweat. The skin of such patients becomes dry, rough, and cracks easily form on it.

Movement disorders. Patients with leprosy often develop muscle atrophy, usually symmetrical, more pronounced damage to the extensors, and the face and limbs are mainly affected.

In the facial area, the orbicularis eyelid muscles often undergo atrophy, resulting in the development of lagophthalmos (lagophtalmus) - loss of the ability to spontaneously close the palpebral fissure. The facial nerve is often affected. With atrophy of the facial muscles, facial expressions are disrupted, and the face becomes sad, motionless, and mask-like.

The muscles of the limbs are also affected, resulting in their atrophy. Especially often, the extensors of the small muscles of the hands and feet are involved in the process, then the forearms and legs. In the upper extremities, atrophy begins with the muscles of the thumb and little finger, then appears on the other fingers. The process leads to the fact that the flexors take advantage of the atrophied extensors, therefore, the fingers take a semi-bent position. Due to the unequal degree of atrophy of the extensors on different fingers, the degree of their flexion is not the same, and as a result, the hand takes on a claw-like, disfigured appearance. A similar condition develops on the feet. On the lower extremities, the muscles of the soles are the first to be affected, as well as the mm. tibiales anteriores et extensores digitorum pedis, which leads to the development of pes eqninovarus.

Patients with leprosy also experience general disorders of the central nervous system. Clinically, they are often reduced to a neurotic state. In different patients, disturbances reach varying degrees - from mild neurotic states to severe neuroses and even psychoses.

Eye damage in patients with leprosy occurs in the form of conjunctivitis and keratitis, which is accompanied by thickening and clouding, and then ulceration of the cornea, which can result in blindness.

Testicles and epididymis are often affected in patients with leprosy in the form of orchitis and epididymitis with the subsequent development of sclerotic processes; As a result of azoospermia, infertility occurs.

Of the internal organs with leprosy, the lungs, liver and spleen are most often affected: they enlarge, become dense, but are slightly painful; other organs can also often be affected by leprosy.

The course of leprosy is usually long-term, the disease lasts for years, in some cases even decades. The exception is the course of the disease with febrile symptoms, increasing cachexia and rapid death (after a few months).

Pathohistology. The most typical changes are observed in lepromas, i.e. tubercle elements. In the dermis, there is an accumulation of cellular infiltrate, which is divided into separate foci by layers of connective tissue running from above from the preserved narrow cavity between the infiltrate and the epidermis. The infiltrate consists of epithelioid cells, lymphocytes, plasma cells, fibroblasts and a small number of histiocytes, located mainly along the periphery of cell accumulations. The most typical are large spherical cells with foamy protoplasm; with special Ziehl-Neelsen staining, a huge number of leprosy bacilli and grains of their decay can be detected in them. These leprosy cells, or "globi" as they are called, leprosy balls, are pathognomonic of leprosy. Leprosy bacilli are located in clusters resembling packs of cigars. A huge number of leprosy bacilli are striking: they are found in the infiltrate both internally and extracellularly, in the lumens of blood vessels, in lymphatic crevices.

The connective tissue stroma of the skin within the infiltrate is significantly sparse. Collagen and elastic fibers are preserved only in the form of fragments, but between the lobules of the infiltrate and in the form of a narrow strip under the epidermis they are well preserved. The sweat and sebaceous glands undergo atrophy and are completely destroyed.

In spotted elements, the pathohistological picture is atypical. In the upper third of the dermis, a perivascular infiltrate is observed, consisting predominantly of lymphocytes, a moderate amount of fibroblasts and histiocytes. There are fewer leprosy bacilli in infiltrates than in typical leprosy. However, in some cases, a huge number of them are found in these affected areas.

In the affected nerves, there is an accumulation of lymphoid infiltrate in the thickening of the nerve trunks. At the same time, a perivascular infiltrate is observed in the dermis, consisting mainly of lymphocytes, a small number of fibroblasts and histiocytes.

Sarcoidosis is a systemic disease that can affect various organs and tissues, but most often affects respiratory system. The first mentions of this pathology date back to the beginning of the 19th century, when the first attempts were made to describe the pulmonary and cutaneous form of the disease. Sarcoidosis is characterized by the formation of specific granulomas, which are the main problem. The causes of this disease are currently unknown, despite the large amount of research done in this area.

Sarcoidosis occurs throughout the world and on all continents, but its prevalence is uneven. It is presumably influenced by both climatic conditions and genetic racial characteristics. Among African Americans, for example, the prevalence of sarcoidosis is about 35 cases per 100,000 population. At the same time, among the light-skinned population of North America, this figure is 2–3 times lower. In Europe, in recent years, the prevalence of sarcoidosis has been approximately 40 cases per 100,000 population. The lowest rates ( only 1 – 2 cases) are celebrated in Japan. The highest data are recorded in Australia and New Zealand ( from 90 to 100 cases).

Sarcoidosis can affect people of any age, but there are certain critical periods during which the incidence is highest. The age from 20 to 35 years is considered dangerous for both sexes. In women, there is a second peak in incidence, which occurs from 45 to 55 years. In general, the likelihood of developing sarcoidosis is approximately the same for both sexes.

Causes of sarcoidosis

As mentioned above, the root causes that give impetus to the development of sarcoidosis have not yet been established. More than a hundred years of research into this disease have led to the emergence of a number of theories, each of which has certain grounds. Basically, sarcoidosis is associated with the influence of certain external or internal factors that were encountered in most patients. However, a common factor for all patients has not yet been identified.

The following theories exist regarding the occurrence of sarcoidosis:

infectious theory;
theory of contact transmission of disease;
exposure to environmental factors;
hereditary theory;
drug theory.

Infection theory

The infectious theory is based on the assumption that the presence of certain microorganisms in the human body can trigger a disease. This is explained as follows. Any microbe entering the body causes an immune response, which consists of the production of antibodies. These are specific cells aimed at fighting this microbe. Antibodies circulate in the blood, so they reach almost all organs and tissues. If a certain type of antibody continues to circulate for a very long time, it can affect some biochemical and cellular reactions in the body. In particular, this concerns the formation of special substances - cytokines, which are involved in many physiological processes under normal conditions. If a person has a genetic or personal predisposition, he will develop sarcoidosis.

The risk of sarcoidosis is thought to increase in people who have had the following infections:

Mycobacterium tuberculosis. tuberculosis. Its influence on the occurrence of sarcoidosis is explained by a number of interesting facts. For example, both of these diseases primarily affect the lungs and pulmonary lymph nodes. In both cases, granulomas are formed ( special clusters of cells of various sizes). Finally, according to some data, antibodies to tuberculosis can be detected in almost 55% of patients with sarcoidosis. This suggests that patients have ever encountered mycobacteria ( have had latent tuberculosis or been vaccinated). Some scientists are even inclined to consider sarcoidosis a special subspecies of mycobacteria, but this assumption does not yet have convincing evidence, despite numerous studies.
Chlamydia pneumoniae. This microorganism is the second most common causative agent of chlamydia ( after Chlamydia trachomatis), which mainly causes damage to the respiratory system. The hypothesis about the connection of this disease with sarcoidosis appeared after special research. It compared the prevalence of chlamydia antigens in average healthy people and in patients with sarcoidosis. The study showed that anti-chlamydial antibodies were almost twice as common in the study group of patients. However, no evidence of Chlamydia pneumoniae DNA was found directly in tissue from sarcoid granulomas. This, however, does not exclude that bacteria only trigger the development of the disease through a hitherto unknown mechanism, without directly participating in the development of sarcoidosis.
Borrelia burgdorferi. This microorganism is the causative agent of Lyme disease ( tick-borne borreliosis). Its role in the development of sarcoidosis was discussed after a study conducted in China. Antibodies to Borrelia burgdorferi were detected in 82% of patients with sarcoidosis. However, live microorganisms were detected in only 12% of patients. This also indicates that Lyme borreliosis may precipitate the development of sarcoidosis, but is not required for its development. This theory is contradicted by the fact that borreliosis has a limited geographical distribution, while sarcoidosis is found everywhere. Therefore, a similar study in Europe and North America showed a lower dependence of sarcoidosis on the presence of antibodies against Borrelia. In the Southern Hemisphere, the prevalence of borreliosis is even lower.
Propionibacterium acnes. Bacteria of this species are conditionally pathogenic and are present on the skin and in the gastrointestinal tract ( gastrointestinal tract) healthy people, without showing themselves in any way. A number of studies have shown that almost half of patients with sarcoidosis have an abnormal immune response against these bacteria. Thus, a theory has emerged about the genetic predisposition of the immune system to the development of sarcoidosis upon contact with Propionibacterium acnes. The theory has not yet received unequivocal confirmation.
Helicobacter pylori. Bacteria from this genus play an important role in the development of stomach ulcers. A number of studies in the United States have found that the blood of patients with sarcoidosis contains increased amounts of antibodies to these microorganisms. This also suggests that infection may trigger immune responses that lead to the development of sarcoidosis.
Viral infections. Similarly with bacterial infections, the possible role of viruses in the occurrence of sarcoidosis is considered. In particular, we are talking about patients with antibodies to rubella, adenovirus, hepatitis C, as well as patients with herpes viruses of various types ( including Epstein-Barr virus). Some evidence even suggests that viruses may play a role in the development of the disease, not just in triggering autoimmune mechanisms.

Thus, many different studies have indicated the possible role of microorganisms in the occurrence of sarcoidosis. At the same time, there is no single infectious agent, the presence of which would be confirmed in 100% of cases. Therefore, it is generally accepted that a number of microbes only make some contribution to the development of the disease, being risk factors. However, other factors must be present for sarcoidosis to occur.

Theory of contact transmission of disease

This theory is based on the fact that a significant proportion of people who develop sarcoidosis have previously been in contact with patients. According to various sources, such contact is present in 25–40% of all cases. Familial cases are also often observed, when within one family the disease develops in several of its members. In this case, the time difference can be years. This fact may simultaneously indicate a genetic predisposition, the possibility of an infectious nature and the role of environmental factors.

The theory of contact transmission itself appeared after an experiment on white mice. During it, several generations of mice were successively reseeded with cells from sarcoid granulomas. After some time, the mice that received a dose of pathological cells began to show signs of disease. Irradiation or heating of cell cultures destroyed their pathogenic potential, and the treated culture no longer caused sarcoidosis. Similar experiments have not been carried out in humans due to ethical and legal regulations. However, the possibility of developing sarcoidosis after contact with pathological cells from a patient is accepted by many researchers. Practical evidence is considered to be cases where sarcoidosis developed after organ transplantation from patients. In the USA, where transplantation is most developed, about 10 similar cases have been described.

Impact of environmental factors

Occupational factors may play a role in the development of sarcoidosis. This mainly concerns air hygiene, since most harmful substances enter the lungs with it. Dust in the workplace is a common cause of various occupational diseases. Because sarcoidosis primarily affects the lungs, a number of studies have been conducted to determine the role of occupational factors in the development of the disease.

It turned out that among people who frequently come into contact with dust ( firefighters, rescuers, miners, grinders, publishing and library workers), sarcoidosis is almost 4 times more common.

Particles of the following metals play a special role in the development of the disease:

beryllium;
aluminum;
gold;
copper;
cobalt;
zirconium;
titanium.

Beryllium dust, for example, getting into the lungs in large quantities, leads to the formation of granulomas, which are very similar to granulomas in sarcoidosis. It has been proven that other metals can disrupt metabolic processes in tissues and activate the immune system.

Among household environmental factors not associated with occupational risk, the possibility of the influence of various molds when they enter the lungs with air is discussed.

Tests more specific for sarcoidosis are:

Angiotensin converting enzyme ( APF). This enzyme is normally produced in various tissues of the body and affects the regulation of blood pressure. The cells that make up granulomas in sarcoidosis have the ability to produce ACE in large quantities. Thus, the level of the enzyme in the blood will be greatly increased. The norm for adults is from 18 to 60 units/l. In children, the test is not informative, since normally the ACE content can fluctuate greatly. Venous blood is taken for analysis, and the patient should not eat for 12 hours before donating it, so as not to distort the results.
Calcium. Granulomas in sarcoidosis are capable of producing large amounts of active vitamin D. This form affects calcium metabolism in the body, increasing its performance in almost all tests. Most often with sarcoidosis, calcium in the urine rises ( norm from 2.5 to 7.5 mmol/day). Somewhat later, the level of calcium in the blood rises ( hypercalcemia greater than 2.5 mmol/l). Similar abnormalities can be detected by testing saliva or cerebrospinal fluid, but they do not occur in all patients. Elevated calcium levels in sarcoidosis are thought to indicate the need for active treatment.
Tumor necrosis factor alpha ( TNF-α). This substance was discovered relatively recently, but its active participation in many pathological processes has already been proven. Normally, TNF-α is produced by monocytes and macrophages. Both of these types of cells work in an enhanced mode in sarcoidosis. Thus, in patients, the analysis will show an increase in the level of this protein in the blood.
Kveim-Siltsbach test. This test confirms the diagnosis of sarcoidosis with a high degree of accuracy. A small amount of lymphatic tissue affected by sarcoidosis is injected into the patient's skin to a depth of 1–3 mm. The drug is prepared in advance from the spleen or lymph nodes. In a patient, the administration of the drug will cause the formation of a small bubble protruding above the surface of the skin. At the injection site, characteristic granulomas quickly begin to form. Despite the high accuracy of the test, it is used extremely rarely these days. The fact is that there is no uniform standard for preparing the drug. Because of this, there is a high risk of introducing other diseases to the patient during the test ( viral hepatitis, HIV, etc.).
Tuberculin test. The tuberculin test or Mantoux test is the most important way to detect tuberculosis infection. It is considered a mandatory test for all patients with suspected sarcoidosis. The fact is that pulmonary forms of tuberculosis and sarcoidosis are very similar in symptoms, but require different treatments. In sarcoidosis, the tuberculin test is negative in more than 85% of cases. However, this result cannot definitively exclude the diagnosis. Carrying out the Mantoux test involves introducing tuberculin, a special drug similar to the causative agent of tuberculosis, into the thickness of the skin. If the patient has tuberculosis ( or he had tuberculosis in the past), then after 3 days a red lump with a diameter of more than 5 mm forms at the injection site. Redness of a smaller diameter is considered a negative reaction. In children under 18 years of age, test results may be distorted due to vaccination against tuberculosis.
Copper. In almost all patients with pulmonary sarcoidosis, copper levels in the blood begin to rise at some stage of the disease ( the norm for men is 10.99 – 21.98 µmol/l, for women – 12.56 – 24.34 µmol/l). At the same time as copper, the level of the protein containing this element, ceruloplasmin, also increases.

Instrumental diagnosis of sarcoidosis

Instrumental diagnosis of sarcoidosis is aimed primarily at visualizing the pathological process. With its help, doctors try to determine as accurately as possible the organs affected by the pathology. There have often been cases where instrumental studies done for other diseases showed the first signs of sarcoidosis even before the first symptoms appeared. Thus, instrumental diagnostics is, to some extent, a method of active detection of pathology.

Instrumental methods for imaging sarcoidosis

Research method	Principle of the method	Applications and results in sarcoidosis
*Radiography*	Radiography involves passing x-rays through human tissue. At the same time, particles pass through denser tissues less easily. As a result of this, pathological formations in the human body can be identified. The method involves dosed radiation and has contraindications. The duration of the study and obtaining the result usually takes no more than 15 minutes.	For sarcoidosis, fluorography is done - an X-ray of the chest. At a certain stage of the disease, some changes appear in 85–90% of patients with tuberculosis. Most often, there is an increase in lymph nodes in the mediastinum or signs of damage to the lung tissue. The localization of lesions in the image is usually bilateral. X-ray examination is important for determining the stage of the disease, although it often does not allow it to be accurately identified. In extrapulmonary forms of tuberculosis, radiography is used relatively rarely, since pathological formations will be less distinguishable against the background of other tissues.
CT scan(CT)	The principle of obtaining an image is similar to that of radiography and is also associated with dosed irradiation of the patient. The difference lies in the possibility of layer-by-layer image acquisition, which greatly increases the accuracy of the examination. Modern tomographs make it possible to obtain two-dimensional and three-dimensional images with visualization of small structures, which increases the chances of diagnostic success. The procedure lasts 10–15 minutes, and the doctor receives its results on the same day.	Nowadays, computed tomography is recommended to be preferred when sarcoidosis is suspected. It allows you to identify smaller formations and recognize the disease at an earlier stage. The main area of application of CT is in patients with pulmonary sarcoidosis. There is a bilateral increase in all groups of mediastinal lymph nodes. In addition, with an intense inflammatory process, some pulmonary complications of sarcoidosis can be detected. In the chronic course of the disease, CT scans sometimes reveal calcifications - inclusions of calcium salts that isolated the pathological focus.
Magnetic resonance imaging(MRI)	MRI involves obtaining a highly accurate three-dimensional image with visualization of very small lesions. The best images are obtained in anatomical areas rich in fluids. The patient is placed inside a huge, powerful magnetic field. The duration of the study is 15 – 30 minutes.	MRI is almost never used in pulmonary forms of sarcoidosis, which relegates it to the background in the diagnosis of this disease ( after CT). However, MRI is indispensable for atypical locations of sarcoid granulomas. This study is used primarily for neurosarcoidosis to determine the exact location of lesions in the brain and spinal cord. MRI also plays a great role in determining damage to the heart and musculoskeletal system.
Radionuclide research(scintigraphy)	This study involves the introduction of a special active substance into the patient’s blood, which accumulates in the lesions. For sarcoidosis ( especially in pulmonary forms) prescribe scintigraphy with gallium-67 ( Ga-67). This research method has certain contraindications and is used relatively rarely.	When gallium is introduced into the blood, it actively accumulates in inflammatory foci in the lung tissue. The most intense accumulation occurs precisely in sarcoidosis. It is important that the intensity of accumulation of the substance corresponds to the activity of the disease. That is, in acute sarcoidosis, lesions in the lungs will be clearly visible on the image. At the same time, during the chronic course of the disease, the accumulation of the isotope will be moderate. Given this feature of scintigraphy, it is sometimes prescribed to check the effectiveness of treatment. With correctly selected drugs and dosage, gallium accumulation practically does not occur, which indicates that the active pathological process has stopped.
Ultrasonography(Ultrasound)	An ultrasound scan sends high-frequency sound waves through body tissue. A special sensor detects the reflection of waves from various anatomical structures. Thus, an image is constructed based on the division of body tissues by density. The test usually takes 10 to 15 minutes and does not involve any health risks ( has no absolute contraindications).	Ultrasound is prescribed for extrapulmonary forms and manifestations of sarcoidosis. The data obtained through this study only allows us to detect a neoplasm in the thickness of the soft tissues. Other examinations will be needed to determine the origin of this formation. Ultrasound can also be actively used in the diagnosis of complications of tuberculosis ( internal bleeding, kidney stones).

In addition to instrumental methods for visualizing sarcoidosis, there are a number of studies that allow assessing the functional state of organs. These methods are less common, since they reflect not so much the stage or severity of the disease, but rather the vital functions of the body. However, these methods are important for determining the success of treatment and timely detection of complications of sarcoidosis.

Additional methods of instrumental examination for sarcoidosis are:

Spirometry. Spirometry is prescribed for pulmonary forms of sarcoidosis in the later stages of the disease. This method helps determine the functional volume of the lungs. A special device records the maximum volume of air that the patient inhales. With the development of complications of sarcoidosis, vital capacity ( vital capacity) can decrease several times. This indicates a severe course of the disease and a poor prognosis.
Electrocardiography. Electrocardiography is used both for cardiac sarcoidosis and for the pulmonary form of the disease. As mentioned above, the functioning of the heart muscle can be impaired in both of these cases. An ECG is the fastest and most accessible way to assess the functional state of the heart. It is recommended to repeat this study several times a year in order to be able to compare the dynamics of changes.
Electromyography. Electromyography is sometimes prescribed to detect problems with skeletal muscle function. The study allows you to evaluate the transmission and spread of nerve impulses to muscle fibers. Electromyography may be ordered to help detect early signs of muscle sarcoidosis and neurosarcoidosis. In both cases, there will be a delay in the propagation of the impulse and muscle weakness.
Endoscopy. Endoscopic methods involve the use of special miniature cameras that are inserted into the body to detect signs of disease. Widespread, for example, FEGDS ( fibroesophagogastroduodenoscopy). This study helps in the search for sarcoidosis in the upper gastrointestinal tract. It is performed on an empty stomach and requires preliminary preparation of the patient.
Fundus examination. Examination of the fundus is a mandatory procedure for the development of uveitis or other types of eye damage in sarcoidosis. All diagnostic procedures related to eye assessment are performed by ophthalmologists.

Treatment of sarcoidosis

Treatment of sarcoidosis is a very difficult task, since at different stages and for different forms of the disease it is necessary to use different drugs. In general, it is believed that it is impossible to completely stop the pathological process. However, in most cases, it is possible to achieve long-term remissions and improve the patient’s life so much that he does not pay attention to his illness.

In the treatment of sarcoidosis, an integrated approach is important. Since no common causes for the development of the disease have been found, doctors try not only to prescribe the correct drug treatment, but also to protect the patient from external factors that can aggravate the course of the disease. In addition, some forms of sarcoidosis and its complications require a separate course of treatment. In this regard, treatment of the disease must be carried out in different directions, depending on the specific clinical case.

systemic drug treatment;
local drug treatment;
surgery;
irradiation;
diet;
prevention of disease complications.

Systemic drug treatment

Systemic drug treatment for sarcoidosis is usually carried out initially in a hospital setting. The patient is hospitalized to confirm the diagnosis and undergo a thorough examination. In addition, some drugs used to treat sarcoidosis have serious side effects. In this regard, it is recommended that blood be taken again for analysis and that doctors monitor the basic functions of the body. After selecting an effective treatment regimen, patients are discharged if there is no threat to life.

Drug treatment of sarcoidosis requires adherence to some basic principles:

Patients without obvious symptoms of the disease in whom sarcoidosis is detected at an early stage do not require drug treatment. The fact is that due to limited knowledge about the development of the disease, it is impossible to predict how quickly the process will develop. It is possible that the risk from intensive treatment will exceed the possible risk from developing sarcoidosis itself. Sometimes spontaneous remissions of the disease are observed in the second stage of the disease. Therefore, a course of treatment is not always prescribed even to patients with minor impairments of pulmonary function.
Treatment usually begins with high doses of drugs to reduce the acute symptoms of the disease and thereby improve the patients' standard of living. Subsequently, the dose is reduced in order to only control the onset of symptoms.
The mainstay of treatment is corticosteroid drugs given orally ( in tablet form). It is believed that they have a good effect at almost any stage of the disease.
Long-term use of corticosteroids can cause osteoporosis ( softening of bone tissue due to metabolic disorders). In this regard, it is necessary to simultaneously prescribe drugs from the group of bisphosphonates for preventive purposes.
In the pulmonary form of sarcoidosis, inhalation ( local) the use of corticosteroids does not provide a better therapeutic effect. They can be prescribed for concomitant reactive inflammatory processes.
Drugs of other pharmacological groups ( other than corticosteroids) are prescribed either in combination with the latter, or if the patient is individually intolerant to corticosteroids.

Standard regimens for systemic treatment of patients with sarcoidosis

Drugs	Dosage	Therapeutic effect
*Monotherapy ( course with one drug)*
*Glucocorticosteroids (GCS)*	0.5 mg/kg body weight per day ( the dose is indicated for prednisolone, which is the main GCS drug used in the treatment). Orally, daily. The dose is reduced gradually as the condition improves. The course of treatment lasts at least six months.	GCS have a strong anti-inflammatory effect. They suppress cellular biochemical reactions that are necessary for the formation of granulomas.
*Glucocorticosteroids*	0.5 mg/kg/day, orally, every other day. The dose is reduced according to the general scheme - once every 6–8 weeks the total daily dose is reduced by 5 mg. The course of treatment lasts 36–40 weeks.
*Methotrexate*	25 mg once a week, orally. Every other day, 5 mg of folic acid is prescribed to reduce side effects. The course of treatment is 32 – 40 weeks.	Inhibits cell growth, suppressing the formation of granulomas and reducing inflammation. In small doses it can be used for a long time, unlike corticosteroids. It is prescribed more often for chronic sarcoidosis.
*Pentoxifylline*	600 – 1200 mg/day in three doses, orally. The course of treatment is 24 – 40 weeks.	The drug is used to replace and gradually reduce the dose of corticosteroid drugs. In addition, it improves the supply of oxygen to tissues, which is used in pulmonary forms of the disease.
*Alpha tocopherol*	0.3 – 0.5 mg/kg/day, orally, for 32 – 40 weeks.	Improves cellular respiration, reduces the likelihood of developing atherosclerosis. In sarcoidosis it is rarely used alone ( often in combination with other drugs).
Combined treatment regimens
*Glucocorticosteroids and chloroquine*	GCS – 0.1 mg/kg/day, orally, without dose reduction. Chloroquine – 0.5 – 0.75 mg/kg/day, orally. The course of treatment is 32 – 36 weeks.	Chloroquine suppresses the immune system, affecting the intensity of the inflammatory process. In addition, the level of calcium in the blood gradually decreases. Often used for cutaneous forms of the disease and neurosarcoidosis.
*Pentoxifylline and alpha-tocopherol*	Dosages and regimen do not differ from those for monotherapy. Duration of treatment – 24 – 40 weeks.	Combined therapeutic effect of these drugs.

In addition to these standard regimens, non-steroidal anti-inflammatory drugs have been used in the treatment of sarcoidosis ( diclofenac, meloxicam, etc.). Their effectiveness turned out to be significantly lower than that of GCS. However, in the early stages of the disease and when GCS doses are reduced, non-steroidal anti-inflammatory drugs are recommended in a number of countries.

Local drug treatment

Local drug treatment is used mainly for cutaneous and ocular forms of sarcoidosis. In this case, special attention is paid to eye damage, since it differs from the general treatment strategy and poses a serious threat of complete and irreversible blindness.

To begin treatment for uveitis in sarcoidosis, accurate confirmation of the diagnosis is required. It is obtained by biopsy of nodules in the eye and detection of sarcoid granulomas in other organs. While the diagnosis is confirmed, it is recommended that the patient be admitted to the hospital. Inpatient treatment is also indicated for patients with severe inflammation, who may develop serious complications that threaten vision loss.

The selection of a specific treatment regimen for uveitis in sarcoidosis is made by an ophthalmologist. It depends on the localization of the inflammatory process ( anterior, posterior or generalized uveitis) and its intensity.

The following drugs are used in the treatment of uveitis in sarcoidosis:

With anterior uveitis - cyclopentolate, dexamethasone, phenylephrine ( in combination with dexamethasone for severe inflammation). The drugs are prescribed in the form of eye drops.
For posterior uveitis - dexamethasone, methylprednisolone as an intravenous dropper, as well as retrobulbar dexamethasone ( injection under the eye with an extended needle to deliver the drug to the posterior pole of the eye).
For generalized uveitis - a combination of the above drugs in a higher dose.

This scheme is called pulse therapy because it is aimed at quickly eliminating severe inflammation with high doses of drugs. After the end of pulse therapy, which lasts 10–15 days, the same drugs are prescribed in the form of drops. They are used for 2 to 3 months to maintain normal condition. The main criterion for the effectiveness of treatment is the disappearance of symptoms of inflammation. After diagnosis of sarcoidosis, patients with signs of eye damage should regularly visit an ophthalmologist for the rest of their lives for preventive check-ups.

Treatment of the cutaneous form of sarcoidosis is, in fact, not very different from systemic treatment. The same drugs can be used in parallel in the form of ointments or creams, which will enhance the local therapeutic effect. Given the side effects of treatment, some doctors do not recommend intensive treatment of cutaneous manifestations of sarcoidosis unless they are located on the face or neck. The fact is that the patients' problems in these cases are a cosmetic defect and do not pose a serious danger to their life or health.

Surgery

Surgical treatment for sarcoidosis is extremely rare. Removing enlarged lymph nodes in the chest is impractical, as it involves a large-scale operation, while sarcoid granulomas will form again. Surgical intervention is possible only in extreme cases to save the patient’s life in the terminal stages of the pathological process. Also, the need for surgical intervention may arise if pulmonary and extrapulmonary complications of sarcoidosis occur.

Patients with sarcoidosis may undergo the following types of surgical interventions:

Elimination of defect in case of lung collapse. Due to damage to the lung tissue, a pathological communication may occur between the air ducts and the pleural cavity. Due to the difference in pressure, this will lead to collapse of the lung and acute respiratory failure.
Lung transplant. This operation is performed extremely rarely due to the high cost and complexity of the procedure. The indication for it is widespread fibrosis of the lung tissue. Due to the overgrowth of bronchioles, the vital capacity of the lungs is critically reduced and respiratory failure occurs. After a lung transplant, more than half of patients live at least 5 years. However, there is a risk that the disease will develop again in the transplanted organ.
Stopping bleeding in the gastrointestinal tract. Usually the operation is performed laparoscopically ( without wide tissue dissection). A special camera and manipulators are inserted into the abdominal cavity to stop bleeding without serious risk to the patient’s health.
Splenectomy. It is practiced with a significant increase in it, if it has been proven that it contains sarcoid granulomas.

Irradiation

According to a number of studies conducted in the United States, sarcoidosis that is resistant to treatment with corticosteroids can be treated with radiation. In this case, only the affected area of the body is irradiated ( for example, only the chest). The best results were observed in patients with neurosarcoidosis. After 3–5 procedures, a stable remission was established with the disappearance of most acute symptoms.

Diet

There is no specific diet for patients with sarcoidosis. According to some studies, therapeutic fasting has proven to work best. In almost 75% of cases, it inhibits the development of the pathological process and leads to a pronounced improvement in the condition. However, it is not advisable to practice regular fasting on your own. This treatment method is used mainly in a hospital setting under the supervision of a physician. Ordinary fasting at home, which some patients voluntarily try to practice, not only does not provide a therapeutic effect, but can also sharply worsen the course of the disease.

Prevention of disease complications

Prevention of complications of the disease involves limiting contact with factors that could cause sarcoidosis. First of all, we are talking about environmental factors that can enter the body with inhaled air. Patients are advised to regularly ventilate the apartment and do wet cleaning to avoid air dust and mold formation. In addition, it is recommended to avoid prolonged sunbathing and stress, as they lead to disruption of metabolic processes in the body and intensification of the growth of granulomas.

Preventive measures also include avoiding hypothermia, as this can contribute to the addition of a bacterial infection. This is due to deterioration of lung ventilation and weakened immunity in general. If there is already a chronic infection in the body, then after sarcoidosis is confirmed, it is necessary to visit a doctor to find out how to control the infection most effectively.

In general, the prognosis for sarcoidosis is conditionally favorable. Death from complications or irreversible changes in organs is recorded only in 3–5% of patients ( with neurosarcoidosis in approximately 10–12%). In most cases ( 60 – 70% ) it is possible to achieve stable remission of the disease during treatment or spontaneously.

The following conditions are considered indicators of an unfavorable prognosis with severe consequences:

the patient's African-American origin;
unfavorable environmental conditions;
long period of temperature rise ( more than a month) at the beginning of the disease;
damage to several organs and systems simultaneously ( generalized form);
relapse ( return of acute symptoms) after completing the course of treatment with GCS.

Regardless of the presence or absence of these signs, people who have been diagnosed with sarcoidosis at least once in their lives should visit their doctor at least once a year.

Complications and consequences of sarcoidosis

As stated above, sarcoidosis itself rarely causes death or serious health problems. The main danger with this disease lies in the possibility of developing serious complications of the disease. They are divided into pulmonary, which is the most common, and extrapulmonary, which is usually more serious than pulmonary.

The most common complications and consequences of sarcoidosis are:

lung collapse;
bleeding;
frequent pneumonia;
stones in the kidneys;
heart rhythm disturbances;
pulmonary fibrosis;
blindness and irreversible vision loss;
psychological problems.

Lung collapse

Lung collapse occurs due to the collapse of lung tissue. Most often this happens if an acute inflammatory process or the growth of granulomas has led to rupture of the pleura. Then the pressure in the pleural cavity begins to equalize with atmospheric pressure. The lung, due to its structure, has its own elasticity. With equal pressure inside and outside, it quickly begins to compress. When compressed, not only does gas exchange not occur, but the blood vessels are also compressed, which leads to disruption of the functions of the heart. Without immediate medical attention, a patient with collapsed lungs may quickly die due to acute respiratory failure. Treatment involves surgically closing the lung defect and removing excess air from the pleural cavity to restore normal pressure. With timely intervention, serious consequences after a collapsed lung are not observed.

Bleeding

Bleeding in sarcoidosis occurs due to direct damage to blood vessels by inflammatory changes. In the pulmonary form, this complication rarely develops. Vascular damage is more common when granulomas are localized at various levels in the digestive system. Repeated nosebleeds are also often observed with sarcoidosis of the ENT organs.

Usually bleeding stops spontaneously and does not require serious measures to stop it. The situation is somewhat more severe in patients with liver sarcoidosis. The fact is that the liver produces a large number of coagulation factors ( substances necessary to stop bleeding). With severe impairment of liver function, the amount of coagulation factors in the blood decreases, which makes any bleeding longer and more abundant.

Frequent pneumonia

Frequent recurrent pneumonia is a common complication in patients at stages 2–3 of sarcoidosis. Due to poor ventilation and local disturbances, any infection can cause pneumonia. This happens especially often after starting a course of treatment with corticosteroids ( prednisolone, methylprednisolone, dexamethasone, etc.). This category of drugs weakens the immune system, increasing the risk of developing a bacterial infection.

Stones in the kidneys

As noted above, kidney stones or sand are found in a significant proportion of patients with sarcoidosis. This complication of the disease develops due to increased levels of calcium in the blood. Calcium enters the kidneys with the blood during filtration. In the renal pelvis it binds with other trace elements, forming insoluble salts. Patients may, in the middle of treatment for sarcoidosis, begin to complain of sharp, excruciating pain in the lower back in the kidney area. This forces us to interrupt the course of treatment for sarcoidosis and pay attention to the treatment of renal colic and removal of stones.

Heart rhythm disturbances

Heart rhythm disturbances, as mentioned above, can be a consequence of both cardiac and pulmonary forms of sarcoidosis. At first they are a symptom of the disease, but in severe cases they can be regarded as a complication. The fact is that a persistent rhythm disturbance leads to a deterioration in the supply of oxygen to the brain. In addition to repeated fainting, this is fraught with irreversible damage due to the death of nerve fibers. Resuscitation may often be necessary to restore normal heart rhythm.

Pulmonary fibrosis

Pulmonary fibrosis is the final stage of the pulmonary form of sarcoidosis. This process begins at stages 2–3 of the disease, when symptoms are just beginning to appear. Gradually, due to prolonged inflammation and compression of tissue by enlarged lymph nodes, normal lung tissue is replaced by connective tissue cells. These cells are unable to exchange gases, making it increasingly difficult for the patient to breathe. There is practically no effective treatment for pulmonary fibrosis. The only solution is an organ transplant.

Blindness and irreversible vision loss

Blindness and irreversible vision loss can occur with delayed treatment of the ocular form of sarcoidosis. The inflammatory process in the eye membranes leads to the launch of a number of pathological mechanisms ( direct tissue damage, increased intraocular pressure, papilledema). Many changes at eye level are irreversible. This is fraught with loss or sharp deterioration of vision, which practically guarantees disability. That is why patients with sarcoidosis, at the slightest sign of eye damage, urgently need to seek specialized help from an ophthalmologist. Timely help will most likely stop the inflammatory process and preserve vision.

Psychological problems

Psychological problems in patients with sarcoidosis are perhaps the least life-threatening but most common consequence of the disease. First of all, this applies to patients in the first stages who did not receive a specific course of treatment due to the possibility of spontaneous remission of the disease. Such patients are characterized by fear of death, depression, deep depression, and insomnia. These symptoms persisted even in many of those patients whose sarcoidosis did not progress.

Such problems are purely psychological in nature. Not the least role is played by the unclear origin of the disease and the lack of specific highly effective treatment. To combat such problems, doctors must be very careful in formulating a diagnosis and prognosis regarding the course of the disease. Patients are advised to consult a psychologist for specialized help.

Liver flukes belong to the class of trematodes, flatworms. They are less common than nematodes, but the diseases they cause can have a serious prognosis and lead to serious consequences.

The name “liver fluke” is applied to several species of trematodes localized in the liver and bile ducts of warm-blooded animals.

The term “fluke” used means that the helminth has two suckers - oral and abdominal, with the help of which it is fixed to tissues. Flukes that infect the hepatobiliary system include the following flukes.

Fasciola(Fasciola hepatica). Causes fascioliasis. The invasive form is the Adolescaria larva, which, after emerging from the intermediate host (mollusk), attaches itself to the film of water, aquatic plants, and garden greens.
Giant fasciola(Fasciola gigantica). It is also the causative agent of fascioliasis. The invasive form is adolescaria.
Feline or Siberian(Opisthorchis felineus). The causative agent of opisthorchiasis. The invasive form is a metacercariae larva that colonizes freshwater fish of the carp family.
Eastern or Chinese(Clonorchis sinensis). The disease is caused by clonorchiasis. The invasive form is a metacercariae found in fish and crayfish.
Lanceolate(dicrocoelium lanceatum). Causes dicroceliosis. The invasive form is a metacercariae that has invaded the second intermediate mediator, the ant.

This is interesting. Once in the ant's body, one lanceolate fluke larva penetrates the insect's brain, as a result of which its behavior changes. Throughout the day, the infested ant behaves as usual. But in the evening, when the temperature drops, it climbs to the top of the grass and hangs on it until the morning, clinging to the leaves or stems with its jaws. This increases the chance of the metacercaria being ingested by the definitive host.

The number of trematodes known today reaches 3000. They have a similar shape in the form of a plant leaf. The body is covered with a muscular skin sac. Dimensions vary between: length – 10…100 mm, width – 2…13 mm.

Liver flukes are biohelminths. That is, their development presupposes the presence of one or more intermediate intermediaries. The final hosts, in whose body they develop to adulthood, are some animals, including humans.

Having passed the required stage of development in intermediate hosts, the eggs turn into invasive larvae, which are located in the body of fish, crayfish, insects, and aquatic plants. They are subsequently ingested by their definitive hosts, and continue to develop into adults within their body.

Infection occurs when a person swallows helminth larvae. Depending on the type of the latter, this can happen in different ways.

When eating greens, vegetables or fruits with adolescaria found on them - when infected with Fasciola vulgaris or gianta (fascioliasis).
When eating fish infected with cat fluke (opisthorchiasis).
When eating crayfish or fish with Chinese fluke larvae (clonorchiasis).
In the case of the lanceolate fluke, dicroceliosis is contracted by ingesting invasive ants with metacercariae found on berries, vegetables, and edible herbs.

Reference. The human organs affected by the liver fluke are not limited to the hepatobiliary system - the liver, bile ducts and bladder. Other systems and tissues can also be colonized - skin, lungs, mammary glands, kidneys, spleen, pancreas. With prolonged invasion, diseases of the central nervous system, heart, blood vessels, and gastrointestinal tract develop. The development of oncological processes is possible.

Routes of infection

A person becomes infected with worms only orally, by ingesting their infective larvae. The route of infection depends on the type of fluke and its life cycle.

People at increased risk for trematode infections caused by flukes include:

peoples who use traditional raw fish dishes;
fishermen, hunters and outdoor enthusiasts who are in close contact with land and water;
children playing in nature;
sellers of fish products.

Important. A person infected with liver fluke is not dangerous to others as a source of infection. To become invasive, the helminth eggs it secretes must undergo development in intermediate hosts. Only after turning into adolescaria or metacercariae do they become dangerous to their final hosts.

Diagnosis

Attention. Liver fluke eggs can also be found in healthy people if they have eaten the liver of an infested animal. Such eggs are called transit eggs. They cannot cause infections because they need to undergo development in intermediate hosts. But they can cause misdiagnosis. Therefore, it is advisable not to eat the liver of any animals before the examination.

All possible preventive measures arise from the ways in which infection occurs:

You should not swim in polluted waters.
Drink untreated, unboiled water.
Eat vegetables and fruits that have not been washed with running tap water.
Eat raw or half-raw fish and crayfish.
You need to wash your hands often when you are in a place where flukes are possible.
The contents of latrines and toilets must be properly disposed of. Do not allow feces, which may contain fluke eggs, to get into the soil or water bodies.

State sanitary services monitor fish products sold in markets and stores and conduct sanitary education activities among the population.

Conclusion

Liver flukes are considered dangerous helminths, since their main damaging effect is aimed at a very important human organ - the liver. With intensive invasion and untimely treatment, the development of severe pathologies is possible - abscesses and cirrhosis of the liver, which are life-threatening.

Preventive measures, monitoring your health and timely consultation with a doctor - only this can reliably protect against flukes.