Edema with HIV: how are they manifested and how to eliminate? What pains are pursued with hiv infection Pain in the joints with hiv when it starts.

For citation: Belov B.S., Belova O.L. HIV infection: rheumatological aspects // BC. 2008. No. 24. S. 1615

At the beginning of the 21st century, infection caused by the human immunodeficiency virus (HIV) remains one of the most important medical and social problems. According to WHO, in 2007 there were 33.2 million people living with HIV in the world. At the same time, HIV infection was the cause of 2.1 million deaths. Approximately 2.5 million new HIV infections are diagnosed each year, predominantly in Central and East Asia and Africa (especially in the Sahara Desert).

In Russia, as of December 31, 2007, the total number of officially registered cases of HIV infection was 403,100 (including 2,636 among children). Acquired immunodeficiency syndrome (AIDS) was diagnosed in 3639 patients. However, given that the AIDS stage does not begin until several years after the transmission of the virus, the reported number of HIV-positive people is only a fraction of the actual number of infected people both in Russia and around the world.
HIV is an RNA-containing virus, belongs to the family of retroviruses and contains a number of enzymes - reverse transcriptase (revertase), integrase and protease. HIV infects differentiated host cells that carry the CD4 receptor. When HIV enters the cell, the viral RNA is reversed into DNA, which, in turn, is integrated into the DNA of the host cell, remaining there for life (DNA-provirus). In the future, under the influence of a number of factors, activation of HIV infection occurs with progressive damage to the above cellular structures. As the disease progresses, autoimmune processes are triggered, resistance to secondary infections and tumors decreases. All this determines the multiorganism of the lesion and the variety of clinical symptoms.
The pronounced clinical polymorphism of HIV infection includes various rheumatological manifestations that occur in 30-70% of cases. The first reports of HIV-associated rheumatological syndromes appeared in the mid-1980s. and included descriptions of cases of polymyositis, vasculitis, reactive arthritis, and Sjögren's syndrome (the latter was later called diffuse infiltrative lymphocytic syndrome). To date, the range of described rheumatic syndromes associated both directly with HIV infection and with anti-retroviral therapy is very wide (Table 1) .
Joint damage
Arthralgia is the most common (25-45%) rheumatic manifestation of HIV infection. Pain, as a rule, is mild, intermittent, has an oligoarticular type of lesion, predominantly affects the knee, shoulder, ankle, elbow and metacarpophalangeal joints. In 5-10% of cases (more often in the late stages of the disease), there may be an intense pain syndrome that lasts for ≤ 24 hours, characterized by severe pain in the joints of the upper and lower extremities (often in the knee, elbow and shoulder), which often causes the need for narcotic analgesics.
HIV-associated arthritis (3.4-10%) is similar to that developing in other viral infections and is characterized by subacute oligoarthritis with a predominant lesion of the joints of the lower extremities in the absence of soft tissue pathology and association with HLA B27. In the synovial fluid, inflammatory changes are not determined. X-ray of the joints showed no pathological symptoms. As a rule, spontaneous relief of the articular syndrome is observed.
HIV-associated reactive arthritis (ReA) develops in 3-10% of cases. It can occur more than 2 years before the diagnosis of HIV infection or against the background of the onset of clinical manifestations of AIDS, but most often manifests itself in a period of already existing severe immunodeficiency. The typical symptomatology of seronegative peripheral arthritis is characteristic with a predominant lesion of the joints of the lower extremities, the development of severe enthesopathy, plantar fasciitis, Achilles bursitis, dactylitis (“sausage fingers”) and a pronounced limitation of the mobility of patients. There are bright extra-articular manifestations (keratoderma, annular balanitis, stomatitis, conjunctivitis), advanced symptoms of the HIV-associated complex (subfebrile condition, weight loss, diarrhea, lymphadenopathy), frequent association with HLA B27 (80-90%). The defeat of the musculoskeletal apparatus of the body is not typical. The process often acquires a chronic relapsing course.
The development of psoriasis (20%) is considered as an unfavorable prognostic sign in HIV-infected patients, since it is a predictor of recurrent, life-threatening infections (primarily pneumocystis pneumonia). In such patients, the whole range of skin changes characteristic of psoriasis (exudative, pemphigoid, eczematous, pustular, etc.) is detected. The distinctive features of HIV-associated psoriatic arthritis include the rapid progression of articular manifestations and the correlation between the severity of skin and joint lesions. It is emphasized that any patient with a severe attack of psoriasis or a form of the disease resistant to conventional therapy should be tested for HIV infection.
Undifferentiated spondyloarthropathy (3-10%) manifests itself in the form of oligoarthritis, spondylitis, enthesopathy, dactylitis, onycholysis, balanitis, urethritis. However, symptoms are not enough to make a diagnosis of ReA or psoriatic arthritis. Duration - up to several months, often ends with disability.
Muscle involvement in HIV infection occurs in 30% of cases and ranges from uncomplicated myopathy and fibromyalgia or asymptomatic elevation of creatine phosphokinase levels to severe, disabling forms of polymyositis. HIV-associated polymyositis develops quite early and may be one of the first manifestations of the disease in question. Its main manifestations are similar to those in idiopathic polymyositis: myalgia, weight loss, weakness of proximal muscle groups, increased serum CPK, myopathic type of changes on the electromyogram (myopathic action potentials of motor units with early activation and complete low-amplitude interference, fibrillation potentials, positive sharp teeth). Morphological examination of muscle biopsy specimens reveals signs of inflammatory myopathy: chronic inflammatory infiltration of the perivascular and interstitial area around myofibrils in combination with their necrosis and repair, as well as, compared with idiopathic polymyositis, a low content of CD4+ cells in endomysial infiltrates.
With nematode myopathy, a rather rare pathology in patients with HIV infection, muscle weakness and hypotension first appear in the pelvic girdle, then in the muscles of the shoulder girdle, and as the disease progresses, they become generalized. When examining biopsy specimens of muscle fibers in a light microscope, the main defect is revealed - nemaline bodies in the form of rod-shaped or filamentous inclusions located under the sarcolemma or in the thickness of the muscle fiber.
Myopathy may be seen in HIV-associated cachexia whose diagnostic criteria are weight loss greater than 10% of baseline, chronic diarrhea (>30 days), chronic fatigue, and documented fever (>30 days) in the absence of other causes .
More than 20% of HIV-infected people develop vasculitis affecting the arteries of small, medium and large calibers. The leading syndrome in HIV-associated vasculitis is most often sensory-motor neuropathy.
Diffuse infiltrative lymphocytic syndrome (DILS) occurs in 3-8% of HIV-infected patients - carriers of HLA DR6 / 7 (Caucasians) or - DR5 (Negroids). It is characterized by the development of xerophthalmia, xerostomia, painless enlargement of the parotid glands, persistent lymphocytosis due to CD8 T-lymphocytes, and diffuse lymphocytic infiltration of internal organs. The most serious complication is lymphocytic interstitial pneumonitis, which develops in 25-50% of patients with DILS. In about 30% of cases, paralysis of the VIII pair of cranial nerves is observed, due to mechanical compression of the inflamed tissue of the salivary gland. Other neurological manifestations include aseptic meningitis and symmetrical motor peripheral neuropathy. Within the framework of DILS, the development of lymphocytic hepatitis, polymyositis, interstitial nephritis, type IV tubular acidosis has been described. Unlike DILS, in Sjögren's syndrome: a) antibodies to Ro- and La-antigens are detected, b) cellular infiltration of the salivary glands is caused by CD4 T-lymphocytes, c) association with HLA B8 is much more common and DR3.
HIV-infected patients may develop a variety of clinical manifestations and laboratory phenomena that occur in systemic rheumatic diseases. Table 2 shows the so-called lupus-like manifestations of HIV infection. Along with the above, the rheumatoid factor in this pathology is detected in 17% of cases, IgG - antibodies to cardiolipin - in 20-30%, and in the late stages of HIV - in 95%, antineutrophil cytoplasmic antibodies by indirect immunofluorescence or ELISA - in 18 and 43% cases, respectively. The presence of cell-specific antibodies, cryoglobulins (more often with concomitant hepatitis C), an increase in the concentration of acid-labile interferon-a has been described.
In light of the above, it should be remembered that in patients with active SLE, false-positive HIV test results (by ELISA or Westernblot) are possible, which become negative with clinical improvement. At the same time, HIV infection leads to subsidence of immunopathological disorders in SLE and rheumatoid arthritis (RA) and aggravates the course of the disease in reactive urogenic arthritis and Lyme disease. These facts highlight the important role of CD4 T-lymphocytes in the pathogenesis of SLE and RA compared with reactive arthritis and Lyme disease.
Reports from the early 1990s the frequency of septic complications from the musculoskeletal system in the considered category of patients does not exceed 1%. However, in a recently published work by Spanish authors, the incidence of septic lesions of this localization was 41%.
Septic arthritis associated with HIV infection usually develops in intravenous drug addicts or in concomitant hemophilia. The main pathogens are Gram-positive cocci, Haemophilus influenzae, Salmonella. The disease is manifested by acute monoarthritis, predominantly of the hip or knee joint. In "intravenous" drug addicts, damage to the sacroiliac, sternocostal and sternoclavicular joints is possible. The leading etiological agent of osteomyelitis and pyomyositis is Staphylococcus aureus. In general, HIV infection does not significantly affect the course of septic lesions of the musculoskeletal system. The latter, as a rule, are successfully cured with adequate antibiotic therapy and timely surgical intervention.
Tuberculosis is one of the most common life-threatening HIV-associated opportunistic infections. At the same time, the share of lesions of the musculoskeletal apparatus accounts for 2% of cases. The most common localization of the tuberculous process in these patients is the spine, but there may be signs of osteomyelitis, mono- or polyarthritis. Unlike classical Pott's disease, tuberculous spondylitis in the context of HIV infection can occur with atypical clinical and radiological symptoms (mild pain, lack of involvement of intervertebral discs in the process, formation of foci of reactive bone sclerosis), which leads to delays in diagnosis and timely treatment. In this regard, many authors strongly recommend including computed tomography and magnetic resonance imaging in the examination plan for these patients.
Damage to the osteoarticular system by atypical mycobacteria develops, as a rule, in the late stages of HIV infection, when the level of CD4-lymphocytes does not exceed 100/mm3. Among the pathogens of this group, M. haemophilum and M. kansasii predominate (50 and 25% of cases, respectively). At the same time, several foci of infection are noted, and manifestations such as nodules, ulcers and fistulas are observed in 50% of patients.
The main causative agents of mycotic lesions of the joints in HIV-infected patients include Candida albicans and Sporotrichosis schenkii. In southern China and the countries of Southeast Asia, the dimorphic fungus Penicillium marneffei is considered the leading etiological agent. The defeat of this fungus occurs, as a rule, in the late stages of HIV infection and proceeds with fever, anemia, lymphadenopathy, hepatosplenomegaly, acute mono-, oligo- or polyarthritis, multiple subcutaneous abscesses, the formation of skin ulcers and fistulas, multifocal osteomyelitis.
The diagnosis of infection of the musculoskeletal system in HIV-infected patients can be difficult for the following reasons: 1) the absence of leukocytosis in peripheral blood and synovial fluid, especially in the late stages of HIV infection; 2) atypical localization of the lesion; 3) pathogens isolated from the joint and from the blood may be different in case of polymicrobial etiology of the lesion; 4) problems with the identification of the pathogen in the presence of previous antibiotic treatment; 5) blurring of symptoms in the late stages of HIV infection, when signs of damage to other organs and systems come to the fore in the clinical picture.
It is necessary to remember the possibility of developing rheumatological syndromes in association with antiretroviral therapy. In particular, 1 year after the introduction of zidovudine, a drug from the group of nucleoside inhibitors of HIV reverse transcriptase, into clinical practice, reports of “zidovudine” myopathy appeared in the literature. This syndrome is characterized by an acute onset with the development of myalgia, palpatory muscle soreness, and proximal muscle weakness after an average of 11 months. from the start of treatment. An increase in the concentration of muscle enzymes in the blood serum and a myopathic type of EMG are characteristic. When examining a biopsy of muscle tissue, a specific toxic mitochondrial myopathy is detected with the appearance of "torn red fibers" reflecting the presence of pathological mitochondrial crystalline inclusions. Termination of treatment leads to an improvement in the patient's condition. At the same time, creatine kinase levels normalize within 4 weeks, and muscle strength is restored after 8 weeks. from the moment of discontinuation of the drug.
The use of protease inhibitors can lead to rhabdomyolysis (especially in combination with statins), as well as lipomatosis of the salivary glands. Cases of the development of adhesive capsulitis, Dupuytren's contracture and dysfunction of the temporomandibular joint have been described in the treatment with indinavir.
Osteonecrosis, like other types of bone tissue damage (osteopenia, osteoporosis), is widespread among HIV-infected patients, which is due both to the disease itself and to ongoing antiretroviral therapy. The most common localization of aseptic necrosis is the head of the femur, the defeat of which (in the absence of complaints) was detected using magnetic resonance imaging in more than 4% of HIV-infected patients. Aseptic necrosis of the femoral head in 40-60% of cases is bilateral and can be combined with osteonecrotic lesions of other localizations (head of the humerus, femoral condyles, carpals and lunate bones, etc.). As the disease progresses, in more than 50% of cases, there is a need for surgical treatment - hip replacement.
To date, a combination of three or more antiretroviral drugs has been used very actively and with sufficient success to treat HIV infection. This approach is called highly active antiretroviral therapy (HAART). It should be noted that in 1997-1998. In the literature, there are descriptions of cases of the development of cytomegalovirus retinitis and abscessing infection caused by the M. avium intracellulare complex in HIV-infected patients who took HAART for several weeks. Despite the differences in the etiology, pathogenesis, and localization of the lesion, in all these cases there was a pronounced inflammatory component, accompanied by an increase in the number of CD4+ cells and the restoration of an active immune response to a focal infection that existed before the start of HAART. The terms "immune reconstitution inflammatory syndrome" or "immune reconstitution syndrome" have been proposed to refer to such reactions. Moreover, the development of systemic autoimmune diseases (SLE, RA, polymyositis) has been described within this syndrome. This phenomenon may be due to both the weakening of the immunosuppressive effect of HIV infection on an already existing autoimmune disease, and the development of the disease de novo.
For the treatment of rheumatic pathology that has developed as part of HIV infection, the same drugs are used as in HIV-negative patients. Among non-steroidal anti-inflammatory drugs, indomethacin is the drug of choice. In vitro studies have shown the ability of this drug to suppress HIV replication by 50%. Hydroxychloroquine is successfully used in HIV-associated arthropathies. It is noteworthy that this drug, administered at a dose of 800 mg/day, was comparable in antiretroviral activity to zidovudine. The appointment of methotrexate, previously considered absolutely contraindicated, can be justified in patients with psoriasis and psoriatic arthritis that developed as part of HIV infection, but this requires careful monitoring of viral load and CD4+ cell count. The development of severe forms of systemic vasculitis with damage to vital organs (lungs, kidneys, brain), as well as active SLE and polymyositis, is an indication for the appointment of glucocorticoids, possibly in combination with cytostatics with mandatory control over the severity of immunosuppression.
Currently, experience is accumulating in the use of biological agents (primarily TNF-a-blockers) for the treatment of rheumatic pathology in the context of HIV infection. There are reports indicating the efficacy and fairly good tolerability of etanercept, infliximab, and abatacept in RA, reactive and psoriatic arthritis, advanced psoriasis, and Crohn's disease in combination with HIV infection. However, in some cases, the drugs had to be canceled due to the development of an intercurrent infection. Most authors consider it necessary to continue research in this area in order to develop clearer indications for prescribing the above drugs and methods of monitoring treatment in this category of patients.
Thus, the high frequency of the disease, a wide range of symptoms, the changing clinical picture under the influence of HAART, the expanding possibilities for the use of antirheumatic drugs (including biological agents) - all this indicates the high importance of the problem of HIV infection in modern rheumatology. A rheumatologist must necessarily have up-to-date information on various aspects of HIV infection and constantly maintain a high index of alertness in relation to this formidable disease.

Literature
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2. Data on the website: www.stopspid.ru/society/situation_in_russia/id.38/
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6. Calabrese L.H. Rheumatic aspects of acquired immunodeficiency syndrome. Rheumatology. Eds. J.H. Kippel, D.A. Dieppe. Mosby Year Book Ltd. 1994; sect. 4: p. 7.1.-7.10.
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8. Belzunegui J., Santisteban M., Gorordo M., Barastay E, Rodriguez-Escalera C, Lopez-Dominguez L, Gonzalez C, Figueroa M. Osteoarticular mycobacterial infections in patients with the human immunodeficiency virus. Clin. Exp. Rheumatol. 2004; 22:343-345.
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25. Beltran B. Nos P., Bastida G., Iborra M., Hoyos M., Ponce J. Safe and effective application of anti-TNF-alpha in a patient infected with HIV and concomitant Crohn’s disease. gut. 2006; 55: 1670-1671.

People infected with the immunodeficiency virus often experience pain of various etiologies.

In order to understand why this or that part of the body hurts with HIV, you need to determine the cause of this symptom. According to statistics, in almost half of those infected with AIDS, discomfort is associated with the disease itself, while in the rest they are the result of treatment or in no way related to the infection. So, what pains in HIV most often bother the patient?

There are psychological (fear of death, the inability to enjoy life, a heightened sense of guilt) and physical pain. The latter include:

• head;
• localized in the abdomen and chest;
• in the upper gastrointestinal tract: oral cavity, pharynx and larynx;
• joint and muscle.

What muscles hurt with HIV?

If muscles hurt with HIV, this indicates tissue damage by the pathogen. This condition occurs in 30% of infections. The mildest form is simple myopathy. The most severe is disabling polymyositis. It develops quite early, so it is often considered as one of the first signs of the disease. However, even with myopathy, performance is greatly reduced. How do muscles hurt with HIV? Characteristic are aching discomfort, which does not become stronger or weaker. It should be noted that the pain of the back and neck is the most inconvenient for a person. With HIV, this is a normal phenomenon, which, however, greatly interferes with a full life. Muscle pain with HIV can be stopped, but it must be understood that damaged tissue can hardly be restored. For this, analgesics are successfully used. The most effective are intramuscular injections.

Joint Pain in HIV

Each infected at least once wondered if the joints hurt with HIV? The fact is that this kind of manifestation is usually attributed to other ailments. However, it is the most common symptom. It occurs in more than 60% of patients with AIDS. Such pains are really very well disguised as rheumatism, therefore anthropathy itself is often called a rheumatic syndrome.

Most often, large joints hurt with HIV, such as:

Such pains are not permanent and last no more than a day. They pass on their own, without additional interventions. It occurs due to the fact that blood circulation in the bone tissue is disturbed. Very often, discomfort is felt in the evening or at night, much less often during the day.

There are two main signs that will help to detect the connection between human immunodeficiency virus infection and joint pain:

• Damage to small joints, such as intervertebral discs. This condition is called undifferentiated spondyloarthropathy.
• The presence of several rheumatoid diseases in one patient at the same time is combined spondyloarthritis.

Both that, and another speaks about the direct relation of pains to an infection. Joint damage can occur as follows:

• Asymmetric damage to large joints (mainly the lower extremities), accompanied by severe pain, usually associated with bone necrosis.
• Symmetrical arthritis that develops rapidly and is very similar to rheumatism. Most often occurs in men and is accompanied by damage to various joints and their groups.

Thus, pain in HIV infection occurs quite often and their intensity is different. Unfortunately, you can only get rid of the symptom for a while, but it is impossible to eliminate the damage itself.

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Diseases of the musculoskeletal system in HIV

Hello!
Legs hurt, aching, tired, in the knees, muscles on the inside of the thighs, calves. Already in the morning they hurt as if they were on their feet all day. I don’t know the reason, I’m starting to think about a side effect of therapy, since for the first time such incomprehensible muscle pains were received at the beginning of therapy (edurant, tenafovir, abacavir), there was severe diarrhea, for several months, I began to lose weight, and my legs too, and before so far my legs have not returned to their previous state, although I have recovered, but there is no leg. My question is related to therapy, does it affect leg pain? What examinations to pass? I noticed that in the SC there are a lot of people with sticks, or they don’t walk well, is this also from therapy?

I don't know what you eat, but I didn't understand you at all. Or am I eating something wrong?
Ilya, I did not start therapy in suspended animation.
And yet, how would you comment on the scientific work on the link above?
And what to do with a painful muscle, which doctor to check and how?
Thanks a lot!

This is a metaphor, it is clear that not in suspended animation. However, the meaning is exactly this - immunity in HIV sometimes behaves inadequately, with and without therapy, just in different directions, and in any of them. For someone, autoimmune processes are activated as immunodeficiency increases and normalize on therapy, for someone they fade without therapy and are activated on therapy, and both have their own logic.
Try to dig at a rheumatologist, for example, in any case, exclude something specific.

Belov B.S. Belova O.L. HIV infection: rheumatological aspects, Regular issues of "BC" No. 24 dated 10/29/2008 p. 1615. To the topic.

Now everything is clear where the pain in the joints and bones comes from. It doesn't look like it's from tenofovir. The muscle on the back of the thigh is very disturbing. It really hurts and pulls my leg since April, that is, it began to hurt even before therapy. How to test this muscle? To what doctor to go? KFK handed over repeatedly - normal.
Thank you!

Although, nevertheless, pain in the joints and bones began after taking the therapy.

Although, nevertheless, pain in the joints and bones began after taking the therapy. After the start of therapy, the immunity wakes up, however, with a bunch of arrows in the head and a hole from a shotgun in the chest, and does not always behave adequately.

What pains are pursued with HIV infection

When a person learns that he is infected with the immunodeficiency virus, premature death is not the worst thing to think about. Pain is a painful consequence of the development of the disease. What hurts with HIV, and is it possible to fight the pain?

What kind of pain can be caused by HIV infection

1. Already in the early stages of the course of the infection, soreness in the muscles appears (aching muscle pain is characteristic). This is a consequence of damage to muscle tissue. It is observed in 1/3 of all infected people. Primary muscle damage is called myopathy. Movements become stiff and cause discomfort. The extreme degree of tissue damage is polymyositis. The person becomes disabled. He is practically immobilized, the slightest dynamic causes suffering.
2. With HIV infection, changes affect all components of the musculoskeletal system. Patients have pain in the spine, joints, aching bones. More than half of the carriers complain about such sensations. First of all, the virus affects large articular joints:

• hip;
• shoulder;
• elbow;
• knee.

Gradually, stiffness passes to small joints. Fingers begin to crackle. Soreness of movements is clearly manifested in the morning. Then the infected develops limbs, and during the day the pain subsides. Usually, with the transition of the disease to a latent stage, this phenomenon disappears. It is due to the fact that the delivery of nutrients and oxygen to the tissues of the motor system is disrupted.

Joint pain alone does not indicate HIV. But if a person has several arthritic processes at the same time, an additional study will not hurt. A blood test will help determine if there is a viral load.

A person with retroviral infection complains of pain in the neck. The cause is often bacterial infections, which are manifested by ulcerative lesions of the oral cavity. Local inflammatory processes that accompany the penetration of HIV into the body cause an increase in lymph nodes in the neck and jaws.

Various viral and bacterial infections attack a person with HIV. This happens due to a drop in the level of T-lymphocytes in the blood. Immunodeficiency viruses infect these cells first. The course of infections is accompanied

• weakness;
• body aches;
• rise in temperature;
• enlargement of the lymph nodes.

At the pre-AIDS stage, the disease is supplemented by opportunistic infections. As the disease progresses, it becomes more and more difficult to deal with them. AIDS is characterized by the irreversibility of concomitant diseases. At this stage, the patient's life is filled with pains of varying intensity and origin. Early diagnosis and timely therapy help to maintain health and avoid terrible consequences.

Sore throat

With HIV, the patient often has a sore throat. Shortly after infection, the cause of a sore throat may be:

• lesions of the oral mucosa,
• various throat infections.

If the cause of the sore throat is a viral infection, it cannot be cured with traditional methods. You need to take powerful drugs. This feature is characteristic of the presence of HIV in the body. When a patient cannot get rid of a common cold for a long time, his blood is sent for additional tests.

The negative impact of the human immunodeficiency virus on the ENT organs increases over time. At the stage of AIDS, the patient is given a lot of trouble by tonsillitis, which occurs in severe forms.

Headaches in HIV

Headaches in HIV at the initial stage accompany ordinary infections.

Causes that cause severe pain in a later period:

• damage to the central nervous system;
• oncological diseases;
• brain infections.

In order to save yourself from the suffering of AIDS or delay its approach, a person with a positive HIV status should be attentive to their state of health. It is recommended that you report any changes to your doctor.

Antiretroviral therapy online

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The site is intended for medical and pharmaceutical workers 18+

HIV, ART and joints

good afternoon, I have been taking stokrin and combivir therapy for 5 years, Immune 600, the load is not ODA, there were no side effects, but in the last six months, the joints began to crackle strongly, you raise your hand, the joint of the shoulder, knees, inguinal, wrist, crunches, there was back pain and gives into the left hand. I asked the doctor of the speed center if there was a connection with taking therapy, to which he waved it off and said that it was mine, although I don’t think that it can’t start to crackle so abruptly, I did an MRI of the thoracic cervical osteochondrosis, they said neither of them, did ecg is not theirs either.
And back pains with crunches remained as they were, this crunch is heard at a distance. From milgama, the pain goes away for a while, but only for a while, so I think what it is and how to deal with it. I noticed that the pain begins to intensify when I get a little cold, and the crunch is constant. I would be grateful for advice.

Hello, please help! VN is not determined, IP 650, on therapy. Arthritis since childhood, I have been taking NSAIDs, but despite this, my knee ached and swollen, and a rheumatologist (does not know about HIV) prescribed a physio ultrasound with hydrocortisone. Can hydrocortisone affect IS?

Depends on dose and exposure. On average, none or not significant.

I am immensely grateful to you

Ilya, thanks. Ambene was also prescribed for 5 days, they haven’t sold it in Russia for a couple of years, I ordered it, I need to start, I’m afraid because of the hormone, I’m worried, please tell me, will the IP not fall much? Thanks

Ekaterina, Ilya, good evening! I got a knee injury on two legs, crosses sprain of the 2nd degree and a linear rupture of the posterior medial horn of the meniscus on one, we are trying to treat it conservatively, due to the long wearing of artesis and bandages, muscle otrophy has begun, the doctors prescribed exercise therapy in the complex to pump up the muscles, and they offer injections platelet-rich plasma into the joint, please tell me, is there any risk with HIV, is it dangerous? She didn't tell the doctors about her illness. Thanks

Good day, tell me, I found out about the status in March, I was admitted to the hospital with cd4-5, at the moment the cells have risen to 102 Vn, it is not determined, but there are problems with the leg) at first I thought the sciatic nerve, MRI. X-ray, osteoscanning shows inflammation of the bone, a focus in the hip bone, an orthopedist, sent to a neurosurgeon, he sends to a traumatologist, in general they hear that HIV and no one wants to do anything already: I ​​don’t walk for a month, I move on a stick. Maybe someone knows what to do what antibiotics and in general what it could be? For art 6 months of kyvex + efavirens

Ideally, a biopsy and a good histologist, if possible, sow. Understand, decide.

Thanks Ilya. There are no other complaints, no pain, and I really hope that there won't be any. But it is better to check, at least in order to follow the dynamics.
And what does “how effective are the doses” mean (he doesn’t take d3 yet, it’s better to pass the tests first, I don’t want to treat it at random, it’s not clear what, it’s not clear what).

The thing is that sometimes the same 5000 IU per day can be excessive, which is not harmful, but only redundant. Therefore, you can tweak, say, up to 15-20 thousand IU per week, for example, taking Fri-Sat-Sun only.

Hello.
My martyr has been taking the tenovofir, lamivudine, efavirenz regimen for a year now, there are no complaints about side effects, VN but, IS 255, the dynamics are positive. And I don’t want to jump from scheme to scheme without real evidence. That's just I began to notice a crunch in the knees and ankles when he squats down. In general, I want to examine him on this issue. Where to begin? What tests do you need to pass, what indicators to pay attention to? As I understand it, definitely do densitometry, plus check calcium and d3? Is that all, or is there something else? I've been reading a lot about markers of inflammation, but I really didn't understand much. In general, what to do with the crunch? He will not go to the therapist and rheumatologist in the clinic, because he does not trust. Apparently we will go to private clinics for our hard-earned money, so we don’t want to take too much, so tell me which and in what sequence the tests really need to be passed.

As I understand it, definitely do densitometry, plus check calcium and d3? The first and third - it is desirable to have at least once every few years, as guidelines. The first - in order to compare later, in five years, 25 (OH) D3 - in order to understand how effective doses of D3 are, you can not look at the base one, there is no D3 yet. Just the crunch is not a reason to fuss if there are no other complaints

Good evening everyone)) I am new to your forum, I have known about the status since the end of April last year and since May 2016 I have already been on therapy (aluvia and tenofovir). Accidentally, I stumbled upon this particular discussion, the topic is directly mine, sore; since the autumn of last year, various uncomfortable sensations have been tormenting in the legs, from the knee to the foot, that is, the lower part: sometimes numbness, now like heaviness, sometimes pains stretching as if, sometimes it comes by itself, it also goes away; last year I took samples for rheumatism - everything was fine according to the tests, I checked the veins / blood vessels, my doctor from the SC did not talk about such side effects, although I complained to her about it more than once; they also assumed the option of a pinched nerve in the pelvic region due to the fact that I lift the child in my arms and forbade it, but now, for example, this issue has been bothering me for two weeks, although I don’t carry weight, I don’t drink, I have an adequate lifestyle, tell me what to do? Since it really brings a lot of discomfort, is 735 somewhere like that; thank you very much in advance for your reply!

With a high degree of probability, problems in the lumbar spine may be somewhere further along the nerves. A good vertebroneurologist will find and show where and what.

Doctor,
I just noticed that in your first answer I missed - “there were at least some suspicions towards the IP.”
it was a question? And what is IP?

Yes, I understand, not just everything ..
I realized that the process has begun with t / b joints, and now we need to prepare for their prosthetics.
Doctor, please, I have a question for you:
- does this mean that now the same thing will gradually happen to all my other joints?
— if so, is it possible to stop or slow down this process?
..or should I accept - what is it now?!
Thanks in advance for your reply!

No, it doesn't. And with these, too, you can butt.
Yes, it is possible, but these questions are not for me, but for a specialized specialist. Consider the situation outside the context of HIV.

only if the specialized specialist finds out about HIV and therapy, then he sends to the doctors in the SC, and the doctors in the SC say - we don’t know why you have to look for another specialized specialist. Vicious circle.

Thank you Doctor!
So I will fight!

Good evening! Please help me figure it out!
In the late 2000s, he received a residence permit in Malta.
In 2015, I found out about my HIV+ status and registered with the local SC.
Since February 2016, he began therapy - Kivexa + Isentress.
Now I have CD4 - 1136, Vir.L - undetectable.
Three months ago I had intermittent sharp pains in my back.
thighs of the left leg. I did not attach importance, because I thought it was related to the gym.
But gradually the pain became more and more
Once again I read the instructions for both drugs, which indicate that there is a possibility of Osteronecrosis.
Now I'm in Moscow for work. Had an MRI yesterday
“There is a lack of coverage of the femoral heads by 1/3.
In the region of the edges of the articular surfaces of the femoral heads and acetabulum,
bone growths. Chondromalacia of the articular cartilage of the femoral heads
and acetabular cavities of 2-3 degrees, articular gaps are narrowed. In the cavity of the joints is determined
physiological fluid. Soft tissues without features, increased l / y at the level of research were not detected.
Conclusion: bilateral dysplastic osteoarthritis of the hip joint 2 tbsp.”
I called my doctor. doctor and told everything.
He was sincerely surprised, said that this was the first such case for them.
He said that if I want, I can go there and ask to change therapy.
The SC is beautiful there, there are good people, but one problem is a small population
and apparently very little experience. I see that doctors are ready to help, but it seems that they themselves are facing this for the first time.
After reading a lot of different things, I no longer understand how I should be, completely confused.
I would like to ask you please advise
In Moscow, I still have to be a month at work. But if you can not waste so much time and you need something
urgently change, I can leave.
The main question is: should I change therapy or not? If you do not change, then what to do with the problem in the t/b joint that is progressing?!
And if you change therapy, then to what, what options can there be?
My condition is definitely getting worse, the pain is getting worse, and it is getting more and more difficult to move my leg.
Please, advise how to be?!

Joint Pain in HIV

Quite often it happens that the joints hurt with HIV. The reason for this phenomenon is the development of degenerative-dystrophic changes in the bone and cartilage tissue against the background of the aggressive spread of the virus and a decrease in the protective function of the body. Diseases of the musculoskeletal system in HIV infection are observed in more than 50% of patients.

Etiology and pathogenesis of joint pain

Under the influence of HIV infection, the protective functions of the body are activated and produce antibodies to the pathogen. Their detail lies in the defeat and utilization of diseased connective tissue cells. Due to severe disorders in the body, dysfunction of the immune system occurs. This leads to the fact that antibodies destroy not only disease-causing agents, but also healthy cells of their own body. Under the influence of a negative factor, all organs and systems, including the musculoskeletal system, suffer.

The following are prone to the development of rheumatic syndromes: HIV carriers, patients with a vivid clinical picture of infection, and people with a total defeat of the immune system (AIDS).

In general, immunodeficiency affects large joints. More often, the patient experiences pain at night, which is associated with impaired blood circulation in the bone and cartilage tissue. As a rule, the pain syndrome is short-lived and disappears after a few hours without the use of drugs. With significant degenerative disorders, the symptoms are lulled due to the development of rheumatic syndromes.

Symptoms and course of HIV-associated arthritis

At the initial stages, pain in the joints is perceived as a manifestation of neuropathy. Only after the appearance of more serious symptoms in the form of swelling and hyperemia of the periarticular skin, there is a suspicion of the development of arthritis. The disease is inflammatory in nature and provokes a violation of venous and arterial blood flow inside the joint.

HIV-associated arthritis

A severe form of the disease, which leads to complex internal disorders and obvious visual changes in the structure of the joint. Refers to rapidly progressive diseases, manifests itself acutely. It mainly affects the joints of the lower and upper extremities with deformity of the phalanges of the fingers. It draws the periarticular tendons into the pathological process. The main symptoms of this type of arthritis are pronounced pain with increasing intensity and swelling of the soft tissues. With the active development of the disease, failures in the hydration and nutrition of the skin are noted, which is manifested by their dryness and rejection of the upper layers of the epidermis. A severe form of the disease leads to complications in the form of inflammation of the mucous membranes of the internal organs.

HIV-associated reactive arthritis

The first signs of the disease appear in the first weeks of infection in the body. In this case, a person does not suspect that he is HIV-infected, but at the same time he experiences all the extensive symptoms of arthritis:

In reactive arthritis, the lymph nodes are enlarged.

• pain syndrome, which is more pronounced after waking up;
• swelling of the joints;
• hyperemia of periarticular tissues;
• inflammatory reaction in other structural units;
• swollen lymph nodes due to improper outflow of blood;
• thickening of the toes.

The article presents basic data on the epidemiology, distribution and pathogenesis of pneumocystosis, as well as its clinical manifestations, modern diagnostic methods and approaches to the treatment and prevention of this disease in HIV infection. Schemes for the treatment and prevention of pneumocystis pneumonia with the main (Biseptol, pentamidine) and reserve drugs, as well as the necessary components of pathogenetic therapy are given.

In recent years, pneumocystosis has attracted the attention of many researchers in connection with the HIV pandemic, although it has been studied before, first as a problem of childhood pathology, and then as a problem of nosocomial infections. Among opportunistic infections in AIDS, it occupies one of the leading places.

Since the discovery of the causative agent of pneumocystis pneumonia (PP) in 1909 until 1981, only a few dozen cases of the disease have been described worldwide, mainly in malnourished infants and adult patients with hematological and oncological diseases treated with immunosuppressants. The incidence of PP has increased dramatically since 1981. This disease became the main clinical manifestation of AIDS, on the basis of which its first cases were recognized in the United States: PP was detected at the first examination in 64% of patients, and at later stages was recorded in another 20% patients.

There is still debate about the taxonomic position of pneumocystis. A number of experts attribute them to fungi, since there is evidence of similarity between the nucleotide sequences of ribosomal RNA P. carini and similar structures Saccharomyces cervisae and Neurospora crassae .

Pneumocysts are widespread in all regions of the world and in almost all animals - wild, synanthropic and agricultural. Numerous studies have shown a wide carriage of pneumocystis among people in various geographical areas, both in the general population and in individual contingents of the population. We have found widespread R. carinii in the department of HIV infection in hospitalized patients (92.9%) and in staff (80%).

Manifest forms of the disease develop in weakened infants (mainly the first 4-6 months of life), and in older age groups they occur only with severe immunodeficiency, and there is a clear connection with the nature of the latter. Thus, the average incidence of PP in HIV infection is currently more than 50%, and in other immunodeficiency states it does not exceed 1%.

Factors predisposing to the development of the disease are disorders of cellular and humoral immunity. PP can occur with isolated B- or T-cell deficiency, as well as in people with mixed immunodeficiencies. The importance of humoral protection is evidenced by the fact that the disease often develops in children with congenital agammaglobulinemia or hypogammaglobulinemia. However, the main predisposing factors are diseases with a predominant violation of T-cell immunity. A decrease in the number of T-helpers (CD4 cells) and an increase in the content of cytotoxic cells (T-suppressors or CD8 cells) leads to the manifestation of the disease. Risk groups for the development of clinically significant PP are premature, debilitated newborns and young children with agammaglobulinemia and hypogammaglobulinemia, rickets, malnutrition; patients with leukemia, oncological diseases; organ recipients receiving immunosuppressants; elderly people from nursing homes; patients with tuberculosis and HIV infection.

The pathogenesis of PP is associated with mechanical damage to the walls of the interstitium of the lungs. The entire life cycle of pneumocysts takes place in the alveolus, to the wall of which they are very tightly attached. For the development of pneumocysts, an increased oxygen content is necessary. Gradually multiplying, they fill the entire alveolar space, capturing more and more areas of the lung tissue. With close contact of trophozoites with the walls of the alveoli, phospholipids are damaged, the stretching of the lungs is gradually disturbed, and the thickness of the alveolar walls increases (5-20 times). As a result, an alveolar-capillary block develops, leading to severe hypoxia. An aggravating moment is the formation of areas of atelectasis, which aggravates the violation of ventilation and gas exchange. Concomitant lung diseases in HIV infection, most often cytomegalovirus pneumonia, contribute to the severe course of the disease.

The most characteristic symptoms of PP in AIDS patients are: shortness of breath (90-100%), fever (60%), cough (50%), while in non-HIV patients these indicators are somewhat different (for example, cough is recorded much more often, in 80–95% of cases).

Shortness of breath is the earliest symptom of PP, observed in almost all patients. At first, it is expressed with moderate physical exertion, which is especially noticeable when climbing stairs. If functional tests (veloergometry) are carried out during this period, then after a 5-minute load, breathing becomes more frequent and superficial (and in healthy people - deeper), which indicates the inefficiency of external respiration. This period can be extended in time and sometimes reaches several weeks and even months. We observed a patient in whom the time from the onset of dyspnea on exertion to the full clinical picture with dyspnea at rest up to 50 per minute, fever and cough was 4 months. Gradually, shortness of breath increases and begins to disturb patients already at rest. An increase in body temperature may be accompanied by chills, excessive sweating. At the beginning of the disease, subfebrile temperature is usually observed; subsequently, it either increases (up to 38–39 ° C), or remains subfebrile. Higher numbers are recorded, as a rule, in young children. The temperature curve is characterized by a gradual increase, a constant, remitting or irregular character. The cough is dry, usually without discharge, although the appearance of sputum is possible in patients with concomitant bronchitis of another etiology or in smokers. At the beginning of the disease, an obsessive cough is characteristic due to a constant feeling of irritation behind the sternum or in the larynx. In the future, the cough is almost constant and acquires a pertussis-like character, it is especially disturbing at night. There are no seizures and reprises characteristic of whooping cough.

In adults, PP, as a rule, manifests itself more severely, there is a protracted and recurrent (up to 3-6 or more manifestations) course with high mortality.

Clinical examination of the lungs often fails to reveal any characteristic changes. Percussion can be determined by a short shade of pulmonary sound, auscultatory - hard breathing, increased in the anterior upper sections, sometimes scattered dry rales. In the study of other organs, an increase in the size of the liver is usually observed, and an increase in the spleen is often noted. In connection with the possible dissemination of pneumocysts in organs (which occurs more often) and the likelihood of developing extrapulmonary pneumocystosis, the examination of the patient should be very thorough. Pneumocysts can affect almost any organ, with the exception of the articular capsules and the prostate gland. Damage to the lymph nodes, spleen, liver, bone marrow, mucous membrane of the gastrointestinal tract, eyes, thyroid gland, heart, brain and spinal cord, thymus, peritoneum, etc. are described.

In the study of peripheral blood, specific changes in PP are not observed. Changes characteristic of the late stages of HIV infection are often recorded: anemia, leukocytopenia, thrombocytopenia, etc. ESR is always increased and can reach 40-60 mm/h. The most characteristic biochemical nonspecific indicator is a significant increase in the total activity of lactate dehydrogenase (LDH) as a reflection of respiratory failure. According to the observations of foreign researchers, unfavorable prognostic signs in PP are high LDH activity (more than 500 IU/l); prolonged course with the development of relapses; respiratory failure and / or concomitant cytomegalovirus pneumonia, as well as low levels of hemoglobin (below 100 g / l), albumin and Y-globulin.

In patients with HIV infection, the development of pneumocystosis is usually observed when the number of CD4-lymphocytes decreases below 0.2x10 9 /l.

If the patient does not receive treatment, shortness of breath (up to 70 per minute or more) and signs of pulmonary heart failure increase, pneumothorax and even pneumomediastinitis may develop, and later on - pulmonary edema. An untreated disease often leads to the death of the patient.

If PP is suspected in a patient with HIV infection, the diagnosis should be established on the basis of a combination of clinical and laboratory data. The main clinical signs of the disease include a combination of severe dyspnea and minimal physical changes. When analyzing laboratory parameters, attention should be paid to an increase in the total activity of LDH and a decrease in blood RO 2, which indicates respiratory failure. These signs, although not specific, are characteristic of PP. X-ray examination cannot be a valuable diagnostic method, because and other opportunistic infections cause similar symmetrical interstitial changes (like a "cotton" or "veiled" lung) on ​​the x-ray, and in 5-10% of cases the x-ray may remain normal.

Serological diagnostic methods are unreliable. To isolate the pathogen from sputum, methods of induced sputum production are used (stimulation of cough shocks with 2-3% saline); in the future, direct microscopy of stained smears is used. A bronchoalveolar lavage study is also used, which increases the possibility of obtaining a positive result from 60% to 90%. Recently, for more accurate diagnosis, PCR methods, immunofluorescent methods with mono- and polyclonal antibodies have been developed and are being used.

Despite the fact that an effective therapy has now been developed, the mortality rate from PN in HIV infection in patients receiving treatment exceeds 10%, and in its absence ranges from 25% to 80%.

Treatment of PP must necessarily be combined with the therapy of HIV infection (the appointment of combined antiretroviral therapy, if the patient has not received it before), as well as with pathogenetic and symptomatic therapy.

In the 70s. of the last century, the high efficiency of the combination of trimethoprim and sulfamethoxazole (co-trimoxazole, Biseptol) for the treatment and prevention of pneumocystosis was demonstrated. Even earlier, in the 60s. pentamidine has been successfully used. Currently, despite the synthesis of new drugs, Biseptol and pentamidine remain the main means of treating PP. In our country, pentamidine is not registered, so the main drug for the treatment and prevention of pneumocystosis is Biseptol.

Biseptol, containing 480 mg of active ingredients (80 mg of trimethoprim and 400 mg of sulfamethoxazole), is prescribed at the rate of 20 mg / kg of trimethoprim per day. This dose is divided into 4 parts to be taken every 6 hours. The tablet form is usually used, but in severe cases of the disease and in violation of absorption in the gastrointestinal tract, the drug is administered intravenously. To do this, a single dose (1 ampoule contains 20 mg of trimethoprim) is dissolved in 250 ml of 5% glucose solution. The course of treatment lasts 21 days. In the first 3-4 days of taking, not only the lack of effect is possible, but also a temporary deterioration - increased shortness of breath, increased body temperature. At the end of the course of treatment, maintenance therapy is carried out - adults take Biseptol 1 tablet (480 mg) 1 time per day.

On average, after PP, 75% of patients survive, and in some medical centers this figure reaches 90%. With relapses, about 60% of patients survive. One of the criteria for the effectiveness of treatment is the frequency of relapses, the probability of which in the first 6 months after the first episode of PP is about 35%, and in the next 6 months it reaches 60%.

Adverse reactions are usually observed from 6 to 14 days of taking co-trimoxazole. They can be manifested by fever, rash and itching, nausea, liver enlargement, diarrhea, leukocytopenia, thrombocytopenia, agranulocytosis, increased activity of serum transaminases, creatinine levels, etc. Skin rashes, liver damage, neutropenia and thrombocytopenia are more often observed in patients with significant disorders liver and kidney function (especially if creatinine clearance is below 15 ml / min), therefore co-trimoxazole cannot be prescribed to these categories of patients. Some reactions may disappear with continued treatment. After 2 weeks of taking the drug, it is necessary to conduct a control study of peripheral blood. In case of detection of severe violations, the appointment of folic acid preparations is indicated.

Abroad, with intolerance or insufficient effectiveness of co-trimoxazole, patients are prescribed pentamidine parenterally (the drug is not absorbed in the gastrointestinal tract). It is administered intravenously slowly at a dose of 4 mg/kg/day, diluted in 250 ml of 5% glucose solution, or in the form of an aerosol (an aqueous solution at a daily dose of 4 mg/kg). With pentamidine inhalation, toxic reactions are recorded less frequently and are less pronounced than with intravenous administration (the most severe toxic effects include hepato- and nephrotoxicity, hypoglycemia). However, the inhalation route of pentamidine administration in advanced disease has a number of limitations: the possibility of bronchospasm, irritation of the pharyngeal mucosa, uneven ventilation of different parts of the lungs, etc. Pentamidine inhalation is more often used for prophylactic purposes, although this method of prevention also has a number of disadvantages, the main of which is the likelihood development of extrapulmonary pneumocystosis and pneumothorax. The duration of the intravenous course of treatment is 21 days.

The third most commonly used drug in PN is dapsone (a reserve drug), commonly used to treat leprosy. Dapsone (100 mg once a day) is recommended to be combined with trimethoprim (15-20 mg/kg/day to 100 mg once a day every 8 hours). The duration of treatment is 21 days. This combination is well tolerated. Its main side effect is hemolysis in patients with glucose-6-phosphate dehydrogenase deficiency. It is also possible to develop methemoglobinuria.

Another backup regimen for moderate PP is the combination of clindamycin (1.2 g/day IV or po) and primaquine (0.03 g/day po) for 21 days. This regimen also cannot be prescribed to patients with glucose-6-phosphate dehydrogenase deficiency, and methemoglobin levels should be monitored at 2-3 weeks of treatment.

Pathogenetic therapy is aimed mainly at improving respiratory and cardiovascular activity. Particularly intensive pathogenetic therapy should be in the development of respiratory failure, pulmonary edema, acute pulmonary heart failure. There are reports of an improvement in the quality of life of patients with PP with the use of corticosteroids, especially when they are prescribed even before the development of acute respiratory failure. But even with an already developed severe course of pneumonia (pulmonary edema, distress syndrome), it is advisable to use prednisolone (usually 40 mg 2 times a day for 5 days, then 40 mg 1 time a day for 5 days, then 20 mg per day). day before the end of treatment).

In the absence of life-threatening complications, but in the presence of respiratory failure, the use of corticosteroids contributes to a more rapid decrease in hypoxia. For this purpose, prednisone is prescribed at 60 mg per day in 2-3 doses in the morning for 7 days, followed by gradual withdrawal.

A short course of corticosteroid therapy avoids the dissemination of pneumocysts from the lungs to other organs. The use of corticosteroids is inappropriate for mild disease and the absence of negative dynamics. If patients have other opportunistic diseases, corticosteroids should be prescribed with caution, since against the background of their use, progression of these diseases and even generalization of the process (herpetic infection, cytomegalovirus infection) is possible.

Artificial ventilation of the lungs is prescribed according to the indications, if there are conditions for its implementation; 20-30% of patients who receive it recover and continue to live for another 6-12 months.

In the absence of primary preventive treatment, PP develops in the late stages of HIV infection in 80% of patients, and the probability of relapse in the absence of secondary prevention is 70% (within 1 year). In patients receiving co-trimoxazole, the frequency of PP is 3.5% per year. In addition, co-trimoxazole acts on other microorganisms, due to which it has a preventive effect against a number of infections (toxoplasmosis, pneumococcal pneumonia, etc.).

In Russia, prophylactic treatment of PP is carried out in patients with CD4-lymphocyte levels less than 0.2x10 9 /l (primary prevention) and patients who have previously undergone PP (secondary prevention). With an unknown level of CD4 cells, prevention of pneumocystosis is carried out in patients with stage IIIB during the period of clinical activity in the presence of pulmonary pathology, as well as in all patients with stage IIIB (according to the clinical classification of HIV infection, 1989). Abroad, indications for chemoprophylaxis of pneumocystosis are episodes of PP in history, the level of CD4-lymphocytes is less than 0.2x10 9 /l, as well as fever of unknown origin for 2 weeks.

For prevention, co-trimoxazole is used (3 days a week for adults, 2 tablets of 480 mg, for children - in accordance with body weight). An alternative regimen is pentamidine 300 mg/mo aerosol or 4 mg/kg IV for 2-4 weeks, or dapsone 200 mg plus pyrimethamine 75 mg and folinic acid 25 mg weekly.

For secondary prevention within 4 weeks after the end of the course of treatment of an acute process, it is recommended to take 1 tablet (480 mg) of co-trimoxazole daily (maintenance therapy), and then, in the absence of negative clinical and radiological dynamics, transfer the patient to the primary prevention regimen. When signs of activation of the disease appear, they switch to a daily intake of the drug in accordance with the treatment regimen.

More than half of HIV-infected people have joint disease. Initially, symptoms resembling rheumatoid arthritis appear. The disease develops from 5 days to 2 months. At the same time, under the influence of a severe autoimmune disorder, the patient's condition worsens, which requires immediate medical intervention.

Types of arthritis in HIV

Under the influence of a strong immunodeficiency, rheumatic disorders are noted in the human joints, which provoke the development of many diseases. With HIV infection, aching pains appear, which are often perceived as a manifestation of neuropathy. Only after the large joints begin to swell, and the pain syndrome increases, there is a suspicion of the development of a disease such as arthritis. Under its action, degenerative damage to the inflamed areas occurs.

HIV-associated arthritis

The disease has a rather complex clinical picture. The disease affects the upper and lower extremities, which leads to swelling of the fingers. Achilles tendons are drawn into the pathological process. In this case, there is severe swelling and increasing pain. In the process of the development of the disease, dryness and peeling of the skin in the affected areas may appear. In more severe cases, inflammatory processes of the mucous membranes of some organs are noted. The genitourinary system is especially affected.

HIV-associated reactive arthritis

With this type of disease, it is impossible to determine the presence of a pathogenic infection in the joints, which complicates the process of making a diagnosis. The first signs appear already in the second week after infection. The phalanges of the fingers of the lower and upper extremities swell, the joints hurt. Tendons suffer, which is manifested by swelling and severe pain. With a complication, an inflammatory process develops on the mucous membranes of the organs. Treatment consists of special nonsteroidal drugs and basic therapy aimed at combating arthritis. With this disease, the following symptoms are noted, which are localized in the legs:

• soreness of the joints (in the morning when trying to move);
• swelling of the affected areas;
• inflammation of the lymph nodes due to a violation of the outflow of blood;
• redness of the skin;
• inflammation of the periarticular structures.

Reiter's syndrome

Pathology can develop several years before infection and manifest itself only under the influence of active antibodies to an autoimmune disease. Tendon and ligament attachment points are damaged. The disease leads to deformation of the nail plate and lesions of the skin. It has a chronic course with periodic remissions. The exacerbation takes place against the background of an illness of moderate severity. The development of erosive arthritis leads to disability. In order to achieve a good therapeutic effect, in addition to the standard drug treatment, physical rehabilitation means are used.

Reiter's syndrome leads to the development of concomitant diseases such as conjunctivitis and stomatitis.

HIV-associated psoriatic arthritis

Skin manifestations of the disease are observed in 15% of patients. Basically, they accompany the articular manifestations of the disease. Rarely occur during remission of the underlying disease. Signs are manifested in redness of some areas of the skin and rashes. With the active development of the disease, the formation of erosions is noted, which is typical for psoriasis. On palpation of the affected areas, there is a strong coarsening and thickening of the skin, not accompanied by pain. The condition indicates the development of a dangerous infection. Treatment is reduced to the use of special therapy, massage, therapeutic exercises and physiotherapy.

Acquired immunodeficiency syndrome (AIDS) quite often leads to inflammation of the joints. Osteoarticular lesions occur in more than 60% of patients with HIV symptoms. The virus disrupts the normal work of lymphocytes to protect, in particular, the joints. Bacteria easily penetrate defenseless joints and cause foci of inflammation, as well as secondary infectious arthritis. The likelihood of developing tumors increases.

It is also common for people with HIV symptoms to experience pain in large joints (elbows, shoulders, knees). The pain does not last long and is explained by impaired blood circulation in the bone tissue (especially at night).

We list some rheumatological manifestations in HIV symptoms:
- arthralgia of the knee, shoulder, ankle, elbow and metacarpophalangeal joints is the most common joint disease in HIV infection;
- HIV-associated arthritis is mild and similar to arthritis in other viral diseases of the joints;
- HIV-associated reactive arthritis may occur may occur long before the onset of the first symptoms of HIV infection. But even during the period of full development of AIDS, it also manifests itself quite often;
- Psoriatic arthritis, which occurs when the body is affected by the HIV virus, develops very quickly, and there is a strong correlation between damage to the skin and joints. Remember an important rule: any patient with a sudden onset of psoriasis or a form of the disease resistant to conventional therapy must be tested for symptoms of HIV infection;
- Polymyositis during HIV infection can be a sign of the presence of the virus in the blood and joints, since its manifestations can be traced early enough. There is weight loss (more than 10% weight loss), muscle weakness, muscle hypotension (first manifested in the pelvic girdle, then in the muscles of the shoulder girdle), fever for a long time, chronic diarrhea and constant chronic fatigue;
- septic arthritis in AIDS patients most often affects the group of "intravenous" drug addicts and is complicated in some cases by concomitant hemophilia. The most common infectious agents are salmonella, cocci and Haemophilus influenzae. The immunodeficiency virus, as a rule, does not significantly affect the course of septic lesions. The prognosis for appropriate and adequate antibiotic therapy is favorable;
- Tuberculosis, as the most common opportunistic infection when infected with HIV, can lead to tuberculous spondylitis, osteomyelitis and arthritis. Most often localized in the spine, proceeds atypically (without pain and involvement of the intervertebral discs in the process), which leads to delays in diagnosis;
- Mycotic lesions of the joints in HIV infection, as a rule, occurs in the later stages of the disease and is very difficult. Anemia, lymphadenopathy, acute polyarthritis and multiple subcutaneous abscesses, fistulas and ulcers are not uncommon ...
- the development of rheumatological syndromes in the treatment of AIDS is sometimes due to the individual perception of therapeutic agents used in antiretroviral therapy. For example, there is a syndrome of "zidovudine" myopathy. It proceeds quite sharply, and is expressed in soreness in the muscles, myalgia and muscle weakness. This complex of symptoms occurs approximately 11 months after the start of treatment. Termination of treatment leads to improvement in the patient's condition, for example, muscle strength is restored after 8 weeks of cessation of anti-AIDS treatment;
Osteoporosis and osteonecrosis are common in people with symptoms of HIV infection. Most often, aseptic necrosis of the femoral head (and humeral head) is diagnosed, which leads to the need for surgical treatment. In about 50% of cases, it is necessary to perform prosthetics of the hip joint.