Lesions of the ENT organs in HIV infection

HIV infection (human immunodeficiency virus infection) is a slowly progressing anthroponotic infectious disease with a contact transmission mechanism, characterized by specific damage to the immune system with the development of severe acquired immunodeficiency (AIDS), which is manifested by opportunistic (secondary) infections, the occurrence of malignant neoplasms and autoimmune processes leading to human death.

ICD-10 code

B20 A disease caused by HIV that manifests itself in the form of infectious and parasitic diseases.

• B20.0 With manifestations of mycobacterial infection.
• B20.1 With manifestations of other bacterial infections.
• B20.2 With manifestations of cytomegalovirus disease.
• B20.3 With manifestations of other viral infections.
• B20.4 With manifestations of candidiasis.
• B20.5 With manifestations of other mycoses.
• B20.6 With manifestations of pneumonia caused by Pneumocystis carinii.
• B20.7 With manifestations of multiple infections.
• B20.8 With manifestations of other infectious and parasitic diseases.
• B20.9 With manifestations of unspecified infectious and parasitic diseases.

B21 A disease caused by HIV that manifests itself in the form of malignant neoplasms.

• B21.0 With manifestations of Kaposi's sarcoma.
• B.21.1 With manifestations of Burkitt's lymphoma.
• B21.2 With manifestations of other non-Hodgkin's lymphomas.
• B21.3 With manifestations of other malignant neoplasms of the lymphatic, hematopoietic and related tissues.
• B21.7 With manifestations of multiple malignant neoplasms.
• B21.8 With manifestations of other malignant neoplasms.
• B21.9 With manifestations of unspecified malignant neoplasms.

B22 Disease caused by HIV, manifested as other specified diseases.

• B22.0 With manifestations of encephalopathy.
• B22.1 With manifestations of lymphatic interstitial pneumonitis.
• B22.2 With manifestations of debilitating syndrome.
• B22.7 With manifestations of multiple diseases classified elsewhere,

823 Disease caused by HIV, manifesting as other conditions.

• B23.0 Acute HIV infection syndrome.
• B23.1 With manifestations of (persistent) generalized lymphadenopathy.
• B23.2 With manifestations of hematological and immunological disorders, not classified elsewhere.
• B23.8 With manifestations of other specified conditions.

B24 Disease caused by HIV, unspecified.

Z21 Asymptomatic infectious status caused by HIV.

Epidemiology

The routes of HIV transmission are contact, vertical and artificial (artificial). The dominant mechanism of transmission of the pathogen is contact, realized (sexually, which is due to the high concentration of the virus in seminal fluid and vaginal secretions).

In the early 1980s, the largest number of registered cases of HIV infection occurred in the United States and Central Africa south of the Sahara, and by the end of 2000, all continents were involved in the epidemic. In Russia, HIV infection has been registered since 1985, initially among foreigners, primarily people of African descent, and since 1987 among citizens of the former USSR.

Until the mid-1990s, the main route of HIV transmission in Russia was sexual, which determined the uniqueness of the epidemic process. Since the second half of the 1990s, the injection route has come to the fore - among drug addicts who practice parenteral administration of psychoactive substances. In recent years, the activation of the heterosexual mechanism of HIV transmission has been noted, as evidenced not only by the increase in the number of people whose main risk factor was heterosexual contacts, but also by the growth in the proportion of infected women. As a result, the risk of HIV transmission from mother to child also increases.

Causes HIV infections

HIV taxonomy: Kingdom Viridae. Family Retroviridaе. Subfamily Lentiviridae. Currently, 2 serotypes of the virus are described: HIV-1. HIV-2, differing in structural and antigenic characteristics. Of greater epidemiological significance is HIV-1, which dominates the current pandemic and is most widespread in Europe.

HIV was first isolated in 1983 by the French scientist L. Monganier at the Pasteur Institute from a removed lymph node and was named LAV (lymphadenopathy associated virus). At the same time, a group of American scientists led by R. Gallo at the National Cancer Institute (USA) isolated a retrovirus called HTLV-III (Human T-lymphotropic virus type III) from the blood of an AIDS patient. In 1986, the Committee on Taxonomy and Nomenclature of Viruses proposed to name the pathogen HIV (HIV - human immunodeficiency virus).

Transmission of HIV is limited by the localization of the pathogen in the human body, weak resistance in the environment and the absence of a carrier. HIV is found in the body of blood-sucking insects, but this phenomenon has no epidemiological significance and transmission of the virus with bites is not observed. Under natural conditions, HIV can survive in a dried state for several hours; in liquids containing a large number of viral particles, such as blood and ejaculate - for several days. In frozen blood serum, the activity of the virus persists for up to several years.

Heating to a temperature of 56 C for 30 minutes leads to a 100-fold decrease in the infectious titer of the virus; at 70-80 C the virus dies after 1 minute. After 1 minute, HIV is inactivated by solutions of 70% ethanol, 0.5% sodium hypochlorite, 6% hydrogen peroxide, as well as diethyl ether and acetone.

HIV is relatively insensitive to ultraviolet radiation and ionizing radiation.

Pathogenesis

When HIV enters the human body, it primarily affects cells carrying the CD4+ marker. In their cytoplasm, viral RNA is released, and with the help of the reverse transcriptase enzyme, its DNA copy is synthesized, which is integrated into the DNA of the host cell (provirus). With each new cell division, all of its offspring contain retroviral DNA. The affected cell begins to create structural elements of HIV, from which, with the help of the protease enzyme, new full-fledged viruses are assembled, which in turn affect target cells. Over time, most of them die. The number of cells carrying the CD4+ receptor decreases, which leads to a weakening of the cytotoxic activity of CD8+ lymphocytes, which normally destroy cells affected by the virus. As a result, control over pathogens of bacterial, viral, fungal, protozoan and other opportunistic infections penetrating the body, as well as over malignant cells, is lost.

At the same time, there is a disruption of the function of B-lymphocytes, the polyclonal activation of which leads, on the one hand, to hypergammaglobulinemia, and on the other hand, to a weakening of their ability to produce virus-neutralizing antibodies. The number of circulating immune complexes increases, antibodies to lymphocytes appear, which to a greater extent reduce the number of CD4+ lymphocytes. Autoimmune processes develop.

At the initial stages of the disease, the body produces virus-neutralizing antibodies that suppress freely circulating viruses, but do not affect those in cells (proviruses). Over time (usually after 5-7 years), the immune system's protective capabilities are depleted, and free viruses accumulate in the blood (the so-called viral load increases). The most important prognostic indicators of the occurrence of opportunistic infections are the number of CD4+ lymphocytes and the viral load.

Opportunistic infections, as a rule, have an endogenous source and arise due to the activation of a person’s own microflora due to a decrease in the immune system’s tension (endogenous activation of mycobacterium tuberculosis from Ghon foci, the appearance of Kaposi’s sarcoma and invasive cervical cancer as a result of the activation of herpes viruses of various types, the development of manifest forms of fungal and cytomegalovirus infections).

The cytopathic effect of HIV causes damage to blood cells, the nervous, cardiovascular, musculoskeletal, endocrine and other systems, which determines the development of multiple organ failure, characterized by a variety of clinical manifestations and the steady progression of the disease.

At all stages of HIV infection, except for the incubation period, manifestations of various AIDS-indicating diseases of the ENT organs are noted.

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Symptoms HIV infections

The diversity of clinical manifestations of HIV infection is due to the addition of opportunistic infections, among which the most significant are fungal, bacterial and viral infections. Lesions of the oral cavity and mucous membranes of the ENT organs in HIV-infected patients are considered one of the first clinical manifestations of the disease.

Mucosal and skin lesions usually begin with the development of candidiasis. Candidiasis of the nasopharynx and esophagus occurs in patients with manifestations of HIV infection in the head and neck area - more than a third of infected individuals at stages 3-4B of exacerbation of chronic sinusitis of fungal etiology. Candidiasis of the specified localization in young patients who do not have other reasons for immunosuppression is an indication for examination for HIV infection. Oropharyngeal and esophageal candidiasis is often combined with an increase in the cervical lymph nodes. Oral cavity lesions sometimes occur at the onset of the disease as a form of acute primary infection. In patients with AIDS, compared to the general population, cervicofacial actinomycosis, oral candidiasis combined with fungal tonsillopharyngitis, esophagitis and Kaposi's sarcoma - a marker of the transition of HIV infection to the AIDS stage (4B-B) are diagnosed more often. The diagnosis is confirmed by detecting blastospores and budding forms when sowing pathological material on "starvation" nutrient media. A biopsy with subsequent histological analysis can be performed as a diagnostic test.

Histoplasmosis is an infectious disease from the group of systemic mycoses caused by Histoplasma capsulatum, characterized by hyperplasia of the elements of the reticuloendothelial system, mainly in the lungs, as well as in the liver and spleen, without signs of purulent inflammation, with the development of cardiopulmonary, hepatosplenic-lymphatic or cutaneous-mucous-ulcer syndromes. This is a sapronosic non-contagious deep mycosis with an aspiration mechanism of pathogen transmission. A distinction is made between mycelial and yeast variants. Depending on the clinical course, primary pulmonary histoplasmosis and secondary disseminated are distinguished. In the latter case, ulcerative lesions of the mucous membranes (gums, palate, pharynx) and skin, often subcutaneous tissue and external genitalia are observed. The ulcer surface is bumpy, with granulation growths and infiltrations along their edges. The diagnosis is confirmed by microscopy of a smear from pathological material (sputum, bone marrow, spleen, liver puncture). Cases of cryptococcosis, coccidio-, strepto- and actinomycosis have also been described in AIDS patients. Systemic deep mycoses are characterized by a disseminated course with predominant damage to the respiratory tract, face, neck, jaws, and mucous membranes of the mouth and nose.

Over time, HIV-infected patients develop inflammatory processes of viral and bacterial origin on the skin and mucous membranes: repeated outbreaks of herpes simplex and herpes zoster, staphylococcal and streptoderma, elements of Kaposi's sarcoma.

The first manifestations of immunodeficiency may be bacterial lesions of the mucous membranes and skin. Under the guise of a banal infection of the ENT organs, it is not always possible to recognize the developing immunodeficiency. The following features of the clinical course of the disease should be alarming: frequent occurrence of otitis, sinusitis, tonsillitis, furuncles and carbuncles with an extended cycle of development; lack of a pronounced effect from the treatment, and in the case of chronicity - frequent exacerbations.

Bacterial infections in HIV-infected patients are caused by the formation of pathogen associations. Their manifestations may be: gingivitis, necrotic lesions of the gums or mucous membranes of the cheeks, palate, tonsils, posterior pharyngeal wall, nasal cavity (up to the formation of total perforation of the nasal septum): chronic periodontitis, stomatitis. Frequent development of acute purulent otitis media with complications, exacerbations of chronic ENT pathology are characteristic. Necrotic lesions of the gums, mucous membrane of the cheeks, palate, tonsils and nasal cavity in the form of deep crater-shaped ulcers are noted in patients with generalized lymphadenopathy in the transition stage to AIDS.

In recent years, lesions of the ENT organs in sexually transmitted diseases (chlamydial pharyngitis, urethritis, gonococcal pharyngitis, syphilis) and extrapulmonary tuberculosis (tuberculous otitis, tuberculosis of the pharynx and larynx) have become particularly relevant.

Among viral infections, clinical symptoms in HIV-infected individuals include lesions of the mucous membrane of the oral cavity and nose caused by the herpes simplex virus.

Herpes simplex. Caused by the herpes simplex virus (Herpes simplex) - a DNA-containing virus from the Herpesviridae family. Six types of the virus have been identified by antigen composition; the first is the most common.

The main clinical signs of acute herpes are the simultaneous appearance on the skin and mucous membranes of rashes in the form of grouped small blisters filled with transparent serous, gradually clouding contents. After 2-4 days, the blisters dry up with the formation of loose crusts, under which epithelialization gradually occurs. Sometimes the blisters merge into a multi-chamber flat blister, which, when opened, leaves erosions of irregular outlines. The rash is accompanied by a sensation of itching, tingling, and sometimes pain. Relapses often occur in the same place. Herpes is often localized on the lips, skin around the mouth, nose, less often on the skin of the cheeks, eyelids, and auricles. A special form of the disease is herpes fever (febris herpetica). It occurs suddenly, accompanied by chills and an increase in body temperature to 39-40 C, severe headache, meningeal signs with vomiting, sometimes clouding of consciousness and delirium. Muscle pain, reddening of the conjunctiva of the eyes, enlargement and soreness of the lymph nodes are common. On the 2-3 day, the temperature decreases, the patient's health improves: at this time, one or more foci appear, most often localized around the mouth and nose. Cases of herpetic meningoencephalitis and acute stomatitis have also been described. Primary herpetic gingivostomatitis is characterized by local and general manifestations. Children, adolescents, or adults under 25 years of age usually get sick. The disease is accompanied by fever and malaise, enlargement and soreness of regional lymph nodes. After 1-2 days, rashes may appear on the gums, hard palate and other areas of the oral mucosa and the red border of the lips.

Herpes zoster (shingles). This is a disease caused by the chickenpox virus (DNA-containing Varicella-Zoster virus from the Herpesvmdae family), clinically manifested by symptoms of damage to the central and peripheral nervous system, as well as a characteristic vesicular rash along individual sensory nerves. The rash of grouped vesicles on an erythematous base occurs acutely, usually on one side of the body. The disease is preceded by prodromal phenomena - a feeling of tingling, itching and, especially often, neuralgic pain along the rash. The disease may be accompanied by hyperalgesia, paresthesia, a tingling sensation; often fever, an increase in body temperature in some cases up to 38-39 C. Herpes zoster, developing in the area of the branching of the trigeminal nerve, is characterized by a severe course and pronounced pain syndrome. In HIV infection, the manifestations of herpes zoster can be of any localization, including on the face and oral mucosa: in such a situation, blisters and erosions occur along the upper and lower jaw branches of the trigeminal nerve on one side, accompanied by severe pain.

Recurrent herpes is characterized by the regular appearance of rashes in the same area, associated with some exogenous or endogenous factor (season, phase of the menstrual cycle, etc.); it is considered an AIDS-indicating disease.

Among the ENT pathologies in HIV-infected patients, the so-called Hunt syndrome (described by R. Hunt in 1907) is often encountered - a form of herpes zoster with damage to the geniculate ganglion: it manifests itself as rashes in the area of the external auditory canal and auricle, severe pain in the ear radiating to the face, back of the head and neck, often with phenomena of neuritis of the facial nerve. Other cranial nerves can be affected - most often the facial and auditory, less often the trigeminal, glossopharyngeal and vagus - which causes the polymorphism of the clinical picture (12 varieties of H. zoster oticus have been described). In patients with AIDS, simple herpes and herpes zoster occur with greater severity of skin manifestations, often accompanied by the layering of a secondary pyogenic infection.

People with immunosuppression have a higher incidence of lesions caused by the human papillomavirus, called intraoral papillomas (warts), condylomas, and epithelial hyperplasia. As a rule, these are nodular lesions covered with multiple papillary protrusions. The typical localization of such formations in the oral cavity is the gums of both jaws and the hard palate. Epithelial hyperplasia is most often located on the mucous membrane of the cheeks.

Hairy leukoplakia (oral viral, villous or hairy leukoplakia, flat condyloma) - protruding white folds above the surface of the mucous membrane, resembling hair in shape. A characteristic feature is a tight connection of the lesion with the mucous membrane: its surface can be smooth or wrinkled. The most common localization is the marginal border of the tongue; it is possible to spread to its ventral surface, damage to the mucous membrane of the lips, cheeks, floor of the mouth and palate, but not the commissure area. Such dense, white areas of the mucous membrane are comparable to classic leukoplakic lesions observed in elderly people. The disease is similar to candidiasis of the oral mucosa, hyperkeratotic form of lichen planus, carcinomatosis. Refers to unfavorable prognostic signs. Hairy leukoplakia of the tongue is probably caused by the Ebstein-Barr virus or human papillomavirus.

A viral wart is a benign skin neoplasm based on the proliferation of epidermal cells and the papillary layer of the dermis caused by the human papillomavirus (DNA-containing) from the Papillomavirus family and transmitted by contact. The disease partially affects HIV-infected individuals. About 50 types of the virus are known, of which 6 and 11 are associated with the formation of warts on the mucous membrane of the oropharynx. Particular attention should be paid to local kidney-shaped elements with a villous surface, sometimes on a stalk. The appearance of such formations on the lips of an adult against the background of lymphadenopathy, thrombocytopenia and other symptoms of opportunistic infections indicates a possible immunodeficiency. Multiple condylomas of the alveolar processes of the lower and upper jaws, and the palate have been described in HIV-infected individuals. Their appearance preceded the transition of the disease to the AIDS stage.

Cytomegalovirus infection. The causative agent is the DNA-containing virus Cytomegalovirus homini, belongs to the Herpesviridae family of the genus Cytomegalovirus. The mechanism of transmission of the pathogen is aspiration; the route is sexual and contact-household, since the virus is excreted with saliva. The possibility of transplacental transmission, as well as during kidney or heart transplantation, through breast milk has been proven. The probability of transmission of the virus during blood transfusion of an infected donor cannot be ruled out. The disease is characterized by a predominantly latent course in adults, as well as a generalized form with damage to the nervous system and internal organs during intrauterine infection of the fetus.

Cytomegalovirus infection may manifest itself as pneumonia, encephalitis, myelitis, retinitis, enterocolitis, esophagitis, myocardiopathy, polyneuropathy, polyradiculopathy. Cases of sensorineural hearing loss have been described.

Pneumocystis carinii. While pneumonia of this etiology is a common opportunistic infection in AIDS patients, pneumocystis otitis in HIV-infected patients rarely develops. S. Breda observed two AIDS patients in whom Pneumocystis carinii was detected during microscopic examination of ear polyp sections.

Molluscum contagiosum is a dermatosis of children caused by the virus of the same name and transmitted by contact: it is characterized by rashes in the form of small painless nodules with a central umbilical melting and a small opening from which a crumbly mass is released when pressed. The size of the nodules is from a pinhead to a pea; and the contents consist of keratinized epithelial cells and a large number of peculiar ovoid (so-called molluscum) bodies typical of this disease. The rash is often localized in the face and neck area. The nodules can be single or in groups and do not cause any sensations.

Kaposi's sarcoma is a disease of unclear etiology with predominant skin lesions, characterized by generalized neoplasm of blood vessels and dilation of capillaries, forming numerous cavities of various shapes and sizes, lined with swollen endothelium. It ranks first among blastomatous lesions in HIV-infected patients, affects young patients. As an initial symptom with lesions of the oral cavity, it occurs in 50-90% of cases.

The distinctive features of Kaposi's sarcoma caused by HIV infection are young age and multiple asymmetric foci located in the internal organs, mucous membranes and skin. Often the disease begins with lesions of the skin of the face, mucous membranes of the oral cavity and has the appearance of cherry-violet, purple spots or nodules on the gums, tongue, palate. Aggressive course of Kaposi's sarcoma with lesions of a large surface area in a short period is considered characteristic. Histological examination often reveals plasma cells in the infiltrate. One of the features of the disease is resistance to therapy. It should be noted that in HIV-infected patients, secondary infection with the formation of extensive ulcerative lesions on the skin often joins the manifestations of Kaposi's sarcoma. In AIDS, the disease is usually accompanied by candidiasis (hyperplastic form) and cytomegalovirus infection. Recently, descriptions of non-pigmented Kaposi's sarcoma of the oral cavity have appeared. Head (oral cavity) lesions in people under 60 years of age are considered a sign of immunodeficiency.

In the oral cavity, flat bluish, blackish or reddish spots appear in the initial stages of sarcoma, which subsequently darken, increase in size, often divide into lobes and ulcerate. The latter occurs on the oral mucosa more often than on the skin. Lesions in the mouth are painful until the ulceration stage.

Kaposi's sarcoma occurs in approximately 20% of AIDS patients with severe immunodeficiency. Red or brown spots on the scalp that develop into papules and plaques that tend to merge into infiltrates are most often located in the area of the auricles and postauricular folds. When localized on the hard palate, the formations quickly increase in size and ulcerate. Often, the rash is localized on the mucous membrane of the soft palate, cheeks, tonsils and larynx. They are spots, nodules or plaques of a red or cyanotic hue, which, when merged, form infiltrates with irregular outlines measuring 0.5-2 cm. Kaposi's sarcoma localized in the pharynx and larynx is accompanied by dysphagia and hoarseness; esophagus - dysphagia, bleeding from disintegrating infiltrates. Cervical lymph nodes are affected in 3% of cases. Kaposi's sarcoma is associated with opportunistic infections in 11%.

Non-Hodgkin's lymphoma was described in 1982. Manifestations are reddish dense elastic growths under intact epithelium in the retromolar area on the gum, developing in HIV-seropositive individuals. Histological examination reveals non-pigmented cellular lymphoblasts not associated with Hodgkin's disease (lymphogranulomatosis). Extranodal non-Hodgkin's lymphoma is characterized by enlarged lymph nodes, in more than half of cases - cervical. The tumor can spread to the mouth, nasopharynx and paranasal sinuses, and disgeminate liver and spleen lesions are also possible.

Stages

According to the classification by V.I. Pokrovsky (2001), the following stages are distinguished:

• I. Incubation.
• II. Primary manifestations, according to the course, are:
  • A. Asymptomatic;
  • B. Acute HIV infection without secondary diseases;
  • B. Acute HIV infection with secondary diseases.
• III. Latent (subclinical).
• IV. Secondary diseases.

A. Weight loss less than 10%; fungal, viral, bacterial lesions of the skin and mucous membranes, recurrent pharyngitis, sinusitis; shingles.

Phases:

• progression:
  • in the absence of antiretroviral therapy;
  • against the background of antiretroviral therapy.
• remission:
  • spontaneous;
  • after previously administered antiretroviral therapy;
  • against the background of antiretroviral therapy,

B. Weight loss of more than 10%; unexplained diarrhea or fever for more than 1 month; hairy leukoplakia; pulmonary tuberculosis; recurrent persistent viral, bacterial, fungal, protozoal lesions of internal organs; localized Kaposi's sarcoma; recurrent or disseminated herpes zoster.

Phases:

• progression:
  • in the absence of antiretroviral therapy;
  • against the background of antiretroviral therapy.
• remission:
  • spontaneous;
  • after previously administered antiretroviral therapy;
  • against the background of antiretroviral therapy.

B. Cachexia; generalized viral, bacterial, mycobacterial, fungal, protozoal, parasitic diseases, including candidiasis of the esophagus, bronchi, trachea, lungs; Pneumocystis pneumonia; extra-esophageal tuberculosis; disseminated Kaposi's sarcoma; atypical mycobacterioses; malignant tumors; CNS lesions of various etiologies.

Phases:

• progression:
  • in the absence of antiretroviral therapy;
  • against the background of antiretroviral therapy.
• remission:
  • spontaneous;
  • after previously administered antiretroviral therapy;
  • against the background of antiretroviral therapy.

V. Terminal.

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Diagnostics HIV infections

Diagnosis of HIV infection is always laboratory, not clinical. Secondary or concomitant diseases, detected clinically, allow determining the severity of the condition and indications for hospitalization, and developing treatment tactics.

A retrospective assessment of the patient's complaints, indicating the nature of the disease's development, is important, since some periods of the disease are asymptomatic.

Physical examination

It is necessary to identify signs of acute infection, enlarged lymph nodes, episodes of unexplained fever, cough or diarrhea and a history of skin and mucous membrane lesions, weight loss. It is important to assess the severity of the disease, the order of appearance of various symptoms over the past 2-10 years. It is necessary to collect an epidemiological history, clarify the duration and nature of parenteral manipulations, and identify a possible risk of infection.

Laboratory research

To confirm the diagnosis of HIV infection, virological, molecular genetic (PCR), serological (enzyme-linked immunosorbent assay (ELISA), immune blotting) methods are used. The standard and most accessible procedure is the detection of antibodies to HIV in ELISA with subsequent confirmation of their specificity in the immune blotting reaction.

Antibodies to HIV appear in a period of 2 weeks to 3 months from the moment of infection. In some cases, this period is extended to 6 months or more. When the first positive result is detected in the ELISA, the analysis is repeated, and if a positive response is obtained, the blood serum is sent for testing in the immune blotting reaction. The results of the latter are assessed as positive, doubtful or negative. Samples are considered positive if they detect antibodies to 2 or 3 glycoproteins of the HIV envelope (gp41, gp1 20 and gp160). Samples are considered negative if they do not detect antibodies to any of the HIV antigens. Samples that contain antibodies to one glycoprotein and/or any proteins of the virus are considered doubtful and require repeated testing.

Recently, the PCR method has been used. Setting up a quantitative variant allows us to estimate the replicative activity of HIV, i.e. the "viral load". At the stage of primary manifestations, it usually amounts to several thousand copies in 1 μl. At the stage of secondary diseases, the level of replicating viruses reaches hundreds of thousands of copies and millions in 1 μl in AIDS.

A persistently high concentration of HIV in the early stages of the disease is a poor prognostic sign, indicating the aggressiveness of the virus.

Primary diagnostics of HIV infection is an extremely important procedure, requiring a thorough analysis of the data from the doctor, since an incorrect diagnosis can have serious consequences for the patient (depressive reaction, suicide attempt, AIDS phobia). Laboratory confirmation of the diagnosis is mandatory. In case of doubtful results, dispensary observation is carried out.

Indications for consultation with other specialists

All HIV-infected patients are recommended to consult a therapist, neurologist, ophthalmologist before starting highly active antiretroviral treatment to identify contraindications to the prescription of certain medications. Patients who use psychoactive substances (or have used them previously) are referred to a narcologist. In the presence of pulmonary pathology, especially if antibacterial therapy is ineffective, an examination by a phthisiopulmonologist is necessary. Consultations with other specialists are carried out according to indications, depending on the identified pathology (secondary and/or concomitant diseases) to determine the scope of additional examinations and/or decide on the transfer of the patient to a highly specialized department.

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Differential diagnosis

Differential diagnostics of HIV infection is quite complicated and depends on the stage of the process. In primary manifestations, in the phase of acute infection 2B in the presence of mononucleosis-like syndrome, the disease must be differentiated from infectious mononucleosis, rubella, adenovirus infection, yersiniosis, acute leukemia, secondary syphilis, hyperkeratosis of the mucous membrane.

In the phase of generalized persistent lymphadenopathy, it is necessary to differentiate HIV infection from diseases that occur with enlargement of the lymph nodes: lymphogranulomatosis, chronic lymphocytic leukemia, toxoplasmosis, secondary syphilis, sarcoidosis. Unlike them, the indicated symptom in HIV infection in this phase is not accompanied by a deterioration in the patient's well-being.

At the stage of secondary diseases (4A-B), it is necessary to conduct differential diagnostics with immunodeficiencies not associated with retroviral infection, which may be a consequence of long-term treatment with high doses of glucocorticoids, cytostatics, radiation therapy. The immunosuppressive effect can be expressed in lymphogranulomatosis, lymphoid leukemia, myeloma disease and other oncological diseases. In case of manifestations of HIV infection in the oral cavity, it is necessary to differentiate them from various pathologies of the mucous membranes. Thus, in case of candidiasis, leukoplakia of the tongue, lichen planus, secondary syphilis, hyperkeratosis should be excluded. Candidiasis of the corners of the mouth is similar to streptococcal angular cheilitis. Histoplasmosis is similar in clinical manifestations to cancer of the oral mucosa. Acute herpetic stomatitis and ulcerative necrotic gingivostomatitis should be differentiated from foot-and-mouth disease, acute leukemia, agranulocytosis, erythema multiforme exudative, herpes zoster, disintegrating malignant tumor, severe form of candidiasis of the oral mucosa, secondary syphilis, allergic (drug-induced) stomatitis. Hairy leukoplakia is similar to candidiasis of the oral mucosa, hyperkeratotic form of lichen planus, carcinomatosis. Disintegrating Kaposi's sarcoma in the oral cavity is differentiated from cancerous, tuberculous, trophic ulcer and hard chancre. The causes of immunodeficiency in such patients are identified by studying the anamnesis, conducting an objective examination and laboratory tests. If signs of immunodeficiency are detected, the patient should be specifically examined for HIV carriage.

Treatment HIV infections

The goals of HIV treatment are suppression of viral replication using highly active antiretroviral therapy, prevention and treatment of opportunistic infections and associated syndromes.

Indications for hospitalization

Hospitalization of HIV-infected people is carried out based on the severity of the condition, depending on the identified secondary or concomitant disease: the degree of intoxication, failure of organs and body systems is assessed.

Non-drug treatment of HIV infection

Depending on the identified concomitant pathology, a regimen and diet are prescribed.

Drug treatment of HIV infection

The modern arsenal of medicines allows suppressing the replication of viruses in most patients for a certain, sometimes quite long period, and making the disease chronic. Therapy allows prolonging the patient's life, but is unable to completely stop the infectious process.

In Ukraine, according to the list in the standard, the following medicines are used:

• Nucleoside reverse transcriptase inhibitors:
  • abacavir;
  • zidovudine;
  • lamivudine;
  • didanosine;
  • stavudine;
  • phosphazide.
• Non-nucleoside reverse transcriptase inhibitors:
  • nevirapine.
• Protease inhibitors;
  • atazanavir;
  • indinavir;
  • lopinavir/ritonavir;
  • amprenavir;
  • saquinavir;
  • ritonavir;
  • darunavir.
• Fusion inhibitors:
  • eifuvirtide.

When deciding whether to start treatment with antiretroviral drugs, the following should be taken into account:

• degree of immunodeficiency (assessed by the number of CD4+ lymphocytes);
• risk of disease progression (based on viral load measurement);
• patient's readiness to begin treatment;
• patient awareness of the impact of therapy on quality of life, possible side effects:
• the importance of choosing the most simplified initial therapy regimen capable of producing a sustained virological response, in order to preserve the maximum choice of combinations for subsequent use;
• the feasibility of choosing one or another regimen of highly active antiretroviral therapy from a pharmacoeconomic point of view.

The principle of treatment for HIV-infected people is lifelong use of antiretroviral drugs.

In the treatment of such patients in otolaryngological practice, therapy of secondary and concomitant diseases plays an important role. In most cases, it has priority over the initiation of highly active antiretroviral therapy, since the severity of the patient's condition is determined by the presence of a particular nosology. The most common secondary diseases and their treatment regimens are listed below.

Cytomegalovirus infection

Treatment of the manifest form:

• ganciclovir 5 mg/kg intravenously (at least 1 hour) 2 times a day for 21 days or valganciclovir 900 mg 2 times a day orally for 21 days (less preferred).

Treatment of active form, secondary prevention:

• ganciclovir 1 g 3 times a day or valganciclovir 900 mg/day for 30 days orally or ganciclovir 5 mg/(kg x day) intravenously by drip (at least 1 hour) for 30 days (less preferred).

Varicella-zoster virus infection

• acyclovir 800 mg orally 5 times a day or 750-1000 mg intravenously 3 times a day or valacyclovir 1 g orally 3 times a day or famciclovir 500 mg orally 3 times a day for 7-10 days.

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Pneumocystis cystis infection

Selection scheme:

• co-trimoxazole (sulfamethoxazole/trimethoprim) 120 mg/kg 4 times daily for 21 days.

Alternative schemes:

• clindamycin 600-900 mg intravenously every 6-8 hours or 300-450 mg orally every 6 hours in combination with primaquine 15-30 mg/kg orally:

Primary and secondary prevention (with CD4+ lymphocyte concentration less than 200/μl):

• co-trimoxazole (sulfamethoxazole/trimethoprim) 480 mg 2 times a day (every other day).

Toxoplasmosis (the cerebral form is more common)

At the slightest suspicion of toxoplasmosis, treatment begins without waiting for the results of the examination. Selection scheme:

• sulfadoxine/pyrimethamine 2 tablets 2 times a day in combination with calcium folinate 25 mg intramuscularly every other day for 6 weeks.

Alternative schemes;

• co-trimoxazole (sulfamethoxazole / trimethoprim) 60 mg/kg 2 times a day;
• fluorouracil 1.5 mg/(kg x day) orally in combination with clindamycin 1.8-2.4 g orally or intravenously 2 times a day;
• doxycycline 300-400 mg/day orally or intravenously in combination with rithromycin 500 mg orally 2 times a day or sulfadiazine 1000-1500 mg orally every 6 hours.

Kaposi's sarcoma

Highly active antiretroviral therapy is certainly indicated to prevent disease progression and achieve clinical improvement. It is considered the main one, and in severe cases with damage to internal organs, prospidia chloride is prescribed at a dose of 100 mg intramuscularly for 30 days.

Candida infection

Candidal stomatitis. Selection scheme:

• clotrimazole 10 mg 5 times a day until symptoms disappear.

Alternative schemes

• fluconazole - 100 mg/day:
• nystatin 200,000 U 4-5 times a day;
• itraconazole - 100 mg/day

All drugs are taken in suspension form until symptoms disappear.

[ 17 ], [ 18 ], [ 19 ]

Candidal esophagitis

Selection scheme:

• fluconazole 200 mg/day orally (up to 800 mg/day) for 2-3 weeks.

Alternative schemes:

• itraconazole capsules 200 mg per day;
• amphotericin B 0.6 mg/(kg x day) intravenously for 10-14 days (rarely when it is impossible to use another regimen).

[ 20 ], [ 21 ], [ 22 ]

Cryptococcal meningitis

Selection scheme:

• Amphotericin B 0.7 mg/(kg x day) intravenously in combination with flucytosine 100 mg/(kg x day) orally for 2 weeks, then fluconazole 400 mg/day for 8 weeks or until cerebrospinal fluid is sanitized, followed by maintenance therapy with fluconazole 200 mg/day.

Alternative schemes:

• amphotericin B 0.7-1.0 mg/(kg x day) intravenously for 2 weeks, then fluconazole 400 mg/day for 8-10 weeks:
• fluconazole 400-800 mg/day orally in combination with flucytosine 100 mg/(kg x day) orally for 6-10 weeks;
• amphotericin B liposomal 4 mg/(kg x day) intravenously for 2 weeks, then fluconazole 400 mg/day for 8-10 weeks.

[ 23 ], [ 24 ], [ 25 ], [ 26 ]

Mycobacterial infection

Treatment is carried out using similar drugs and regimens used in patients without HIV infection. The therapy has a number of features - if the concentration of CD4+ lymphocytes is less than 100/μl, rifampicin or rifabutin should be prescribed at least 3 times a week, since less frequent use leads to the formation of resistance of the pathogen.

If the CD4+ lymphocyte level is less than 100/μl, anti-tuberculosis therapy is carried out with at least four drugs for 8 weeks, then two for 18 weeks. If the sputum culture results remain positive after 2 months of treatment, therapy is continued for another 7 months.

Treatment of extrapulmonary forms of tuberculosis is similar to that of pulmonary forms. The exceptions are miliary tuberculosis, tuberculosis of bones and joints, and tuberculous meningitis, the therapy of which is carried out for 9-12 months.

Treatment of tuberculosis and HIV infection should not be started simultaneously due to the cumulative side effects of the drugs used, adverse drug interactions, strict requirements for compliance with the regimen, and the likelihood of paradoxical reactions associated with the restoration of the immune system. Simultaneous highly active antiretroviral and anti-tuberculosis therapy can be started at a CD4+ lymphocyte level of less than 50/μl, if well tolerated.

Anti-tuberculosis therapy should not be combined with non-nucleoside reverse transcriptase inhibitors and protease inhibitors, with the exception of ritonavir and the combination of ritonavir and saquinavir.

The use of immunoglobulins in HIV-infected patients can be considered as pathogenetic therapy. Indications for the use of these drugs are varied:

• immunodeficiency (for replacement purposes);
• idiopathic thrombocytopenia with an autoimmune mechanism of development (20 g of protein per day);
• severe bacterial and viral secondary and concomitant diseases.

The doses of drugs and the duration of the course depend on the degree of immunodeficiency, the severity of the patient's condition, and the type of drug. A single dose of normal human immunoglobulin is 25-50 ml intravenously by drip; 3-10 transfusions are performed, repeated administration is possible after 24-72 hours.

Further management

Issues of temporary disability are resolved strictly individually, depending on the severity of the disease and the duration of certain clinical manifestations.

[ 27 ], [ 28 ], [ 29 ], [ 30 ]

Prevention

There is only non-specific prevention:

• prevention of sexual and perinatal transmission of HIV;
• control of transfused blood components and its preparations;
• prevention of HIV transmission during medical procedures;
• providing medical care and social support to HIV-infected people, their families and others.

Attempts to create a vaccine have not yet been successful.

AIDS prevention and control centers carry out epidemiological surveillance of HIV infection, which includes:

• identification of HIV-infected and AIDS patients;
• conducting an epidemiological investigation of all identified cases of AIDS and HIV infection;
• verification of laboratory tests for HIV conducted in medical institutions.

Forecast

The prognosis is absolutely unfavorable, there are no drugs that completely cure HIV infection. The introduction of highly active antiretroviral therapy has made it possible to significantly increase the duration and quality of life of HIV-infected people.