About all

Castro congitis. Inflammatory Eye Conditions Associated with Rheumatic Diseases: Causes, Frequency, and Treatment Options

What are the common inflammatory eye conditions associated with rheumatic diseases. How frequently do these conditions lead to blindness. What are the recommended treatment options for ocular inflammation in rheumatic diseases. How does juvenile rheumatoid arthritis affect the eyes.

Prevalence and Impact of Ocular Inflammation in Rheumatic Diseases

Inflammatory eye conditions are a significant concern for patients with rheumatic diseases. These ocular manifestations can lead to severe complications, including vision loss if left untreated. Understanding the prevalence and impact of these conditions is crucial for effective management and prevention of long-term consequences.

A study by Rothova et al. published in the British Journal of Ophthalmology in 1996 shed light on the causes and frequency of blindness in patients with intraocular inflammatory disease. The research highlighted the need for early detection and intervention to preserve vision in affected individuals.

Frequency of Blindness in Ocular Inflammatory Diseases

How often does ocular inflammation lead to blindness in rheumatic disease patients? The study by Rothova et al. revealed that a significant proportion of patients with intraocular inflammatory diseases experienced vision loss. While exact percentages may vary depending on the specific condition and treatment received, the risk of blindness emphasizes the importance of regular ophthalmological screenings for patients with rheumatic diseases.

Quality of Life Impact

Ellwein et al. discussed the importance of quality of life assessments in blindness prevention interventions. Visual impairment can significantly affect a person’s daily activities, independence, and overall well-being. By focusing on both clinical outcomes and patient-reported quality of life measures, healthcare providers can better tailor interventions to meet the needs of individuals with rheumatic diseases and associated ocular inflammation.

Uveitis: A Common Ocular Manifestation in Rheumatic Diseases

Uveitis, inflammation of the uveal tract of the eye, is a frequent ocular complication in various rheumatic diseases. Understanding its epidemiology, clinical presentation, and management is essential for rheumatologists and ophthalmologists alike.

Epidemiology of Uveitis

Vedot et al. conducted a prospective study in Savoy to investigate the epidemiology of uveitis. Their preliminary results provided valuable insights into the prevalence and distribution of uveitis cases in the region. This type of epidemiological data is crucial for allocating resources and developing targeted screening programs for at-risk populations.

Anterior Uveitis in Rheumatic Diseases

Foster and O’Brien’s chapter on anterior uveitis in the “Principles and Practice of Ophthalmology” provides a comprehensive overview of the disease entities leading to this condition. Many of these entities are rheumatologic in nature, highlighting the strong connection between systemic rheumatic diseases and ocular inflammation.

Which rheumatic diseases are commonly associated with anterior uveitis? Some of the most frequently implicated conditions include:

  • Ankylosing spondylitis
  • Reactive arthritis
  • Psoriatic arthritis
  • Juvenile idiopathic arthritis
  • Behçet’s disease

Early recognition and prompt treatment of anterior uveitis in these patients can help prevent vision-threatening complications and improve overall outcomes.

Ocular Manifestations of Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a systemic autoimmune disease that can affect multiple organ systems, including the eyes. Harper and Foster’s review in the International Ophthalmology Clinics provides a comprehensive overview of the ocular manifestations associated with RA.

Keratoconjunctivitis Sicca in Rheumatoid Arthritis

Keratoconjunctivitis sicca, also known as dry eye syndrome, is a common ocular complication in RA patients. Mody et al. investigated this condition in their 1988 study published in Clinical Rheumatology. What causes dry eye in RA patients? The condition is often associated with secondary Sjögren’s syndrome, an autoimmune disorder that affects the exocrine glands, including the lacrimal glands responsible for tear production.

Scleritis and Episcleritis

Scleritis and episcleritis are inflammatory conditions affecting the white outer coat of the eye (sclera) and the tissue covering it (episclera), respectively. Sainz de la Maza et al. and Watson and Hayreh have conducted extensive research on these conditions in the context of rheumatoid arthritis and other systemic immune-mediated diseases.

How can clinicians differentiate between scleritis and episcleritis? Key distinguishing features include:

  • Pain: Scleritis is typically more painful than episcleritis
  • Visual acuity: Scleritis may affect vision, while episcleritis usually does not
  • Depth of inflammation: Scleritis involves deeper layers of the eye
  • Associated systemic diseases: Scleritis is more commonly associated with severe systemic autoimmune conditions

Proper differentiation is crucial, as the management and potential complications of these conditions differ significantly.

Sjögren’s Syndrome and Ocular Involvement

Sjögren’s syndrome is an autoimmune disorder characterized by dry eyes and dry mouth. It can occur as a primary condition or secondary to other rheumatic diseases, particularly rheumatoid arthritis.

Autoantibodies in Sjögren’s Syndrome

Alspaugh et al. conducted groundbreaking research on the differentiation and characterization of autoantibodies and their antigens in Sjögren’s syndrome. Their work, published in Arthritis and Rheumatism in 1976, laid the foundation for understanding the immunological mechanisms underlying the disease.

What are the key autoantibodies associated with Sjögren’s syndrome? The most common autoantibodies include:

  • Anti-Ro (SSA)
  • Anti-La (SSB)
  • Antinuclear antibodies (ANA)
  • Rheumatoid factor (RF)

These autoantibodies serve as important diagnostic markers and may correlate with disease severity and extraglandular manifestations.

Genetic Factors in Sjögren’s Syndrome

Moutsopoulos and Mann’s research, published in the New England Journal of Medicine in 1979, explored the genetic differences between primary and secondary sicca syndrome. Their findings suggested distinct genetic predispositions for these two forms of Sjögren’s syndrome, which has implications for disease classification, prognosis, and potentially targeted therapies.

Corneal and Scleral Disease in Rheumatoid Arthritis

Severe ocular complications of rheumatoid arthritis can involve the cornea and sclera, potentially leading to vision-threatening conditions. Understanding these manifestations is crucial for early intervention and preservation of visual function.

Peripheral Ulcerative Keratitis

Peripheral ulcerative keratitis (PUK) is a serious corneal complication associated with rheumatoid arthritis. Tauber and Sainz de la Maza analyzed therapeutic decision-making regarding immunosuppressive chemotherapy for PUK in their 1990 study published in Cornea.

Why is aggressive treatment necessary for peripheral ulcerative keratitis? PUK can lead to rapid corneal thinning and perforation if left untreated. The condition is often associated with active systemic vasculitis and requires prompt immunosuppressive therapy to control both ocular and systemic inflammation.

Destructive Corneal and Scleral Disease

Messmer and Foster’s 1995 study in Cornea explored destructive corneal and scleral disease associated with rheumatoid arthritis. These severe manifestations can lead to significant visual morbidity and require aggressive management.

What are the treatment options for destructive corneal and scleral disease in RA? Management typically involves:

  1. Systemic immunosuppression
  2. Topical and systemic corticosteroids
  3. Surgical intervention (e.g., corneal transplantation, scleral grafting) in severe cases
  4. Close monitoring and collaboration between rheumatologists and ophthalmologists

Early recognition and prompt initiation of appropriate therapy are critical to preventing irreversible ocular damage.

Immunosuppressive Treatment for Ocular Inflammatory Disorders

The management of ocular inflammatory disorders associated with rheumatic diseases often requires the use of immunosuppressive medications. Jabs et al. published guidelines for the use of these drugs in patients with ocular inflammatory disorders, based on recommendations from an expert panel.

Rationale for Immunosuppressive Therapy

Why is immunosuppressive treatment necessary for some patients with ocular inflammation? The side effects and complications associated with long-term corticosteroid use support the rationale for alternative immunosuppressive agents. These medications can help control inflammation while minimizing the risks associated with prolonged steroid therapy.

Individualized Treatment Approaches

The expert panel emphasized the importance of individualizing treatment regimens for patients with ocular inflammatory disorders. Factors to consider when developing a treatment plan include:

  • Severity and location of ocular inflammation
  • Associated systemic disease activity
  • Patient age and comorbidities
  • Previous treatment response
  • Potential drug interactions and side effects

Regular monitoring of patients on immunosuppressive therapy is crucial to assess treatment efficacy and detect any adverse effects early.

Juvenile Rheumatoid Arthritis and Ocular Complications

Juvenile rheumatoid arthritis (JRA), now more commonly referred to as juvenile idiopathic arthritis (JIA), is associated with significant ocular complications, particularly uveitis. Understanding the unique aspects of ocular involvement in this pediatric population is essential for proper management and prevention of vision loss.

Classification and Diagnosis of JRA

Cassidy and Levinson’s 1986 study in Arthritis and Rheumatism examined classification criteria for diagnosing juvenile rheumatoid arthritis. Accurate classification is crucial for determining the risk of ocular involvement and guiding appropriate screening and management strategies.

Ocular Manifestations in JRA

Chylack and Biengang’s research, published in the American Journal of Ophthalmology in 1975, provided valuable insights into the ocular manifestations of juvenile rheumatoid arthritis. What are the most common ocular complications in JRA patients? The primary ocular manifestation is chronic anterior uveitis, which can be asymptomatic in its early stages, emphasizing the need for regular ophthalmological screening.

Prognostic Factors in JRA-Associated Uveitis

Wolf et al. investigated prognostic factors in the uveitis associated with juvenile rheumatoid arthritis. Their study, published in Ophthalmology in 1987, identified several factors that may influence the course and outcomes of ocular inflammation in these patients.

Which factors are associated with a poorer prognosis in JRA-related uveitis? Some key prognostic indicators include:

  • Early age of onset
  • Male gender
  • Presence of synechiae at diagnosis
  • Bilateral involvement
  • Longer duration of uveitis before treatment initiation

Understanding these prognostic factors can help guide treatment decisions and patient counseling.

Relationship Between Ocular and Articular Disease Activity

Rosenberg and Oen explored the relationship between ocular and articular disease activity in children with juvenile rheumatoid arthritis and associated uveitis. Their 1986 study in Arthritis and Rheumatism provided insights into the complex interplay between joint and eye inflammation in JRA patients.

Does active joint disease always correlate with ocular inflammation in JRA? Interestingly, the study found that ocular and articular disease activity did not always parallel each other. This observation underscores the importance of regular ophthalmological screening even in patients with well-controlled joint symptoms.

Ophthalmological Screening in Juvenile Arthritis

Southwood and Ryder addressed the question of optimal screening frequency for chronic iridocyclitis in juvenile arthritis patients. Their 1992 paper in the British Journal of Rheumatology proposed tailoring screening intervals based on the risk of developing chronic iridocyclitis.

How should ophthalmological screening be approached in JRA patients? Current recommendations suggest:

  1. More frequent screenings (every 3-4 months) for high-risk patients (e.g., young girls with oligoarticular JIA)
  2. Less frequent screenings (every 6-12 months) for lower-risk patients
  3. Continued screening even after arthritis remission, as uveitis can develop or persist independently of joint disease
  4. Educating patients and families about the importance of regular eye exams and potential symptoms of uveitis

Implementing risk-stratified screening protocols can help optimize resource utilization while ensuring timely detection of ocular complications in JRA patients.

Inflammatory conditions of the eye associated with rheumatic diseases

  • Rothova A, Suttorp-van Schulten MS, Frits Treffers W, et al.:Causes and frequency of blindness in patients with intraocular inflammatory disease. Br J Ophthalmol 1996, 80:332–336.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Ellwein LB, Fletcher A, Negrel AD, Thulasiraj RD: Quality of life assessment in blindness prevention interventions. Int Ophthalmol Clin 1994, 18:263–268.

    Google Scholar 

  • Vedot E, Barth E, Billet P: Epidemiology of uveitis: preliminary results of a prospective study in Savoy. In Uveitis Update. Edited by Sarri KM. Amsterdam: Elsevier; 1984:13.

    Google Scholar 

  • Foster CS, O’Brien JM: Anterior uveitis. In Principles and Practice of Ophthalmology. Edited by Albert and Jakobiec. Philadelphia: WB Saunders; 1999:1198. This chapter describes disease entities, many of them rheumatologic, that lead to anterior uveitis.

    Google Scholar 

  • Harper SL, Foster CS: The ocular manifestations of rheumatoid disease. Int Ophthalmol Clin 1998, 38:1–19.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Mody GM, Hill JC, Meyers OL: Keratoconjunctivitis sicca in rheumatoid arthritis. Clin Rheumatol 1988, 7:237.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Alspaugh MA, Talal N, Tan EM: Differentiation and characterization of autoantibodies and their antigens in Sjogren’s syndrome. Arthritis Rheum 1976, 19:216–222.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Moutsopoulos HM, Mann DL: Genetic differences between primary and secondary sicca syndrome. N Engl J Med 1979, 301:761.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Williamson J: Incidence of eye disease in cases of connective tissue disease. Trans Ophthal Soc UK 1974, 94:742.

    PubMed 
    CAS 

    Google Scholar 

  • Sainz de la Maza M, Foster CS, Jabbur NS: Scleritis associated with rheumatoid arthritis and with other systemic immunemediated diseases. Ophthalmology 1994, 101:1281.

    Google Scholar 

  • Watson PG, Hayreh SS: Scleritis and episcleritis. Br J Ophthalmol 1976, 60:163.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Tauber J, Sainz de la Maza M: An analysis of therapeutic decision making regarding immunosuppressive chemotherapy for peripheral ulcerative keratitis. Cornea 1990, 9:66.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Messmer EM, Foster CS: Destructive corneal and scleral disease associated with rheumatoid arthritis. Cornea 1995, 14:408.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Jabs DA, Rosenbaum JT, Foster CS, et al.
    Guidelines for the use of immunosuppressive drugs in patients with ocular inflammatory disorders: recommendations of an expert panel. Am J Ophthalmol 2000, 130:492. This paper provides an expert panel of physician recommendations of immunosuppressive drugs for treatment of patients with ocular inflammatory disorders. The side-effects and complications of corticosteroids support the rationale for immunosuppressive treatment. The treatment regimen with immunosuppressive agents should be individualized and the patients monitored regularly.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Cassidy JT, Levinson JE: A study of classification criteria for a diagnosis of juvenile rheumatoid arthritis. Arthritis Rheum 1986, 29:274.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Chylack LT, Biengang DC: Ocular manifestations of juvenile rheumatoid arthritis. Am J Ophthalmol 1975, 79:1026.

    PubMed 

    Google Scholar 

  • Wolf MD, Lichter PR, Ragsdale CG: Prognostic factors in the uveitis of juvenile rheumatoid arthritis. Ophthalmology 1987, 94:1242.

    PubMed 
    CAS 

    Google Scholar 

  • Rosenberg AM, Oen KG: The relationship between ocular and articular disease activity in children with juvenile rheumatoid arthritis and associated uveitis. Arthritis Rheum 1986, 29:797.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Southwood TR, Ryder CA: Ophthalmological screening in juvenile arthritis: should the frequency of screening be based on the risk of developing chronic iridocyclitis? Br J Rheumatol 1992, 31:633.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Kanski JJ: Anterior uveitis in juvenile rheumatoid arthritis. Arch Ophthalmol 1977, 95:1794.

    PubMed 
    CAS 

    Google Scholar 

  • “>

    O’Brien JM, Albert DM: Therapeutic approaches for ophthalmic problems in juvenile rheumatoid arthritis. Rheum Dis Clin North Am 1989, 15:413.

    PubMed 

    Google Scholar 

  • Foster CS, Barrett F: Cataract development and cataract surgery in patients with juvenile rheumatoid arthritisassociated iridocyclitis. Ophthalmology 1993, 100:809–817.

    PubMed 
    CAS 

    Google Scholar 

  • Brewerton DA, Caffrey M: Acute anterior uveitis and HLA27. Lancet 1973, 2:994.

    Article 

    Google Scholar 

  • Linssen A: B27+ disease versus B27-disease. Scand J Rheumatol 1990, 87:111.

    Article 
    CAS 

    Google Scholar 

  • Nusenblatt RE, Whitcup SM, Palestine AG: Uveitis Fundaments and Clinical Practice. St Louis: Mosby; 1996:270–273.

    Google Scholar 

  • Spaeth GL: Corneal staining in systemic lupus erythematosus. N Engl J Med 1967, 276:1168.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Gold DH, Morris DH, Henkind P: Ocular findings in systemic lupus erythematosus. Br J Ophthalmol 1972, 56:800.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Stafford-Brady FJ: Lupus retinopathy: patterns, associations, and prognosis. Arthritis Rheum 1988, 31:1105.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Foster CS: Systemic lupus erythematosus. In Principles and Practice of Ophthalmology. Edited by Albert and Jakobiec. Philadelphia: WB Saunders; 1999:4563. This chapter summarizes clinical findings of systemic lupus erythematosus and its ophthalmic findings in detail.

    Google Scholar 

  • Kearns TP: Collagen and rheumatic diseases: ophthalmic aspects. In The Eye and Systemic Disease. Edited by Masolf FA. St Louis: Mosby; 1975:105.

    Google Scholar 

  • Rynes RI, Mika P, Bartholomew LE: Development of giant cell (temporal) arteritis in a patient “adequately” treated for polymyalgia rheumatica. Ann Rheum Dis 1977, 36:88.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Hollenhorst RW, Rown JR, Wagener HP, Shick RM: Neurologic aspects of temporal. Neurology 1960, 10:490.

    PubMed 
    CAS 

    Google Scholar 

  • “>

    Afshari NA, Afshari MA, Lessell S: Temporal arteritis. Int Ophthalmol Clin 2001, 41:151–158. This paper summarizes temporal arteritis and its ocular findings.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Huston KA, Hunder FF, Lie JT, et al.: Temporal arteritis: a 25-year epidemiological, clinical and pathologic study. Ann Intern Med 1978, 8:162.

    Google Scholar 

  • Bullen CL, Liesegang TJ, McDonald TJ, et al.: Ocular complications of Wegener’s granulomatosis. Ophthalmology 1983, 90:279.

    PubMed 
    CAS 

    Google Scholar 

  • Fauci AS, Haynes BF, Katz P, Wolff SM: Wegener’s granulomatosis: prospective clinical and therapeutic experience with 85 patients for 21 years. Ann Intern Med 1983, 98:76–85.

    PubMed 
    CAS 

    Google Scholar 

  • Wise GN: Ocular periarteritis nodosa. Arch Ophthalmol 1952, 47:1–11.

    Google Scholar 

  • Moore GJ, Sevel D: Corneo-scleral ulceration in periarteritis nodosa. Br J Ophthalmol 1966, 50:651–655.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Purcell JJ, Birkenkamp R, Tsai CC: Conjunctival lesions in periarteritis nodosa. Arch Ophthalmol 1984, 102:736.

    PubMed 

    Google Scholar 

  • Dolan DL, Lemmon GB Jr, Teitelbaum SL: Relapsing polychondritis chondritis. Am J Med 1966, 41:285–299.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • “>

    Zeuner M, Straub RH, Rauh G, et al.: Relapsing polychondritis: clinical and immunogenetic analysis of 62 patients. J Rheumatol 1997, 24:96–101.

    PubMed 
    CAS 

    Google Scholar 

  • Isaak BL, Liesegang TJ, Michet CJ Jr: Ocular and systemic findings in relapsing polychondritis. Ophthalmology 1986, 93:681–689.

    PubMed 
    CAS 

    Google Scholar 

  • Messmer EM, Foster CS: Vasculitic peripheral ulcerative keratitis. Surv Ophthalmol 1999, 43:379–396. This paper describes in detail the clinical findings and management of vasculitic conditions such as rheumatoid arthritis, systemic lupus erythematosus, WG, RP, and PAN associated with peripheral ulcerative keratitis, as PUK may be the first sign of systemic necrotizing vasculitis.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • “>

    Bhisitkul RB, Foster CS: Diagnosis and ophthalmological features of BehÇet’s disease. Int Ophthalmol Clin 1996, 36:127.

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Symptoms, Causes, Tests, and Treatment

    Costochondritis is an inflammation of the cartilage in the rib cage. It can happen due to infection, injury, and other health conditions.

    This condition usually affects the cartilage where the upper ribs attach to the breastbone, also known as the sternum, in an area known as the costosternal joint or costosternal junction.

    Chest pain caused by costochondritis can range from mild to severe. Mild cases may only cause your chest to feel slightly tender or some pain when you push on the area.

    More severe cases may get worse with certain movements as well as with deep breaths. The condition often goes away within a few weeks or months, but some cases may require treatment.

    People with costochondritis often experience chest pain in the upper and middle rib area on either side of the breastbone. This pain can gradually increase over time, or come on suddenly.

    Additional symptoms can include:

    • pain that becomes worse when lying down
    • pain that becomes worse when there’s pressure on your chest, like when you wear a seatbelt
    • pain that intensifies with coughing or deep breaths
    • pain that increases with physical activity

    It’s important to note that symptoms like chest tightness and radiating pain can indicate other conditions, including a heart attack. Seek immediate medical care if you’re experiencing persistent, intense chest pain.

    The exact cause of costochondritis in most people is unknown. But conditions that may cause it include:

    • trauma to the chest, such as blunt impact from a car accident or fall
    • physical strain from activities, such as heavy lifting and strenuous exercise
    • certain viruses or respiratory conditions, such as tuberculosis, that can cause joint inflammation
    • severe coughing

    There’s some research that suggests costochondritis occurs more often in women, especially those who are athletes. You may also be at a higher risk for this condition if you:

    • participate in high-impact activities
    • recently had a physical trauma or fall that affected the chest area
    • have allergies and are frequently exposed to irritants

    While there’s no test to diagnose costochondritis, your doctor will most likely ask a series of questions and do a series of tests to determine the source of your chest pain.

    Lab tests

    Typically, lab tests aren’t needed to diagnose costochondritis, but depending on your personal health history, your doctor may do some tests to see if your chest pain could be due to other issues like pneumonia or coronary heart disease.

    X-rays and ECGs

    Your doctor may want you to get an X-ray to make sure there’s nothing abnormal going out with your lungs.

    If you’re dealing with costochondritis, your X-ray should look normal. They may also recommend an electrocardiogram (ECG) to make sure your heart isn’t the cause of your chest pain.

    Many times, diagnosing costochondritis is a matter of eliminating other possible, more serious causes.

    See your doctor right away if you have trouble breathing or are feeling intense chest pain.

    Always seek immediate emergency care when you have abnormal and debilitating pain in your chest. It can indicate something serious, such as a heart attack.

    Getting care as soon as possible limits the possibility of complications, especially if an underlying issue is causing your costochondritis.

    Costochondritis can be treated in several ways.

    Most cases of costochondritis are treated with over-the-counter medications. If your pain is mild to moderate, your doctor will probably recommend nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Advil) or naproxen (Aleve).

    Your doctor may also recommend:

    • prescription-strength NSAIDs
    • oral steroids or injection of a steroid into the area involved
    • transcutaneous electrical nerve stimulation (TENS), which is a mild electric current that is delivered to the area via a small, battery-powered device

    Lifestyle changes

    Your doctor may tell you to make permanent lifestyle changes if you have persistent or chronic costochondritis.

    Some types of exercise can aggravate this condition, including rowing and weightlifting. Manual labor may also have a negative effect.

    Your doctor may also recommend:

    • rest
    • physical therapy
    • hot or cold therapy using a heating pad and ice

    Normally, treatment of the inflammation and pain causes costochondritis to eventually go away on its own.

    If you have chronic costochondritis, the pain may persist or return — even with treatment — when you exercise or engage in certain activities. In these cases, you may need to seek long-term care to make sure that costochondritis doesn’t affect your quality of life and ability to take part in daily activities.

    Pains associated with costochondritis can indicate other issues. Chest pain can often mean that you’re having heart or lung issues, so see your doctor right away when you feel pain in your chest to make sure that you’re not having a heart attack or have pneumonia.

    The chest pain associated with costochondritis can be a symptom of fibromyalgia. With fibromyalgia, you may experience soreness in your chest in addition to:

    • pain throughout your body
    • fatigue and inability to rest due to pain
    • difficulty focusing or concentrating
    • feelings of depression
    • headaches

    If you experience chest pains along with these other symptoms, talk with your doctor about getting tested for fibromyalgia. Understanding this condition can help you address the symptoms and ensure that it doesn’t interrupt your daily life.

    Costochondritis is caused by inflammation and typically presents as chest pain that gets worse with certain movements or pressure. This condition usually isn’t persistent. In many cases, costochondritis goes away on its own.

    Mild cases of costochondritis may disappear after a few days. Chronic cases can last for weeks or more, but most cases don’t last any longer than a year.

    To lower your chances of developing persistent costochondritis, carry and lift heavy loads properly. Try doing fewer high-impact exercises or manual labor, when possible.

    Seek medical attention immediately if you experience chest pain while performing any of these activities.

    90,000 legendary commandant: Life and death of Fidel Castro

    https://ria.ru/20210813/kastro-7455572100.html

    Legendary Castille Castro

    Legendary Kastel – RIA Novosti, RIA Novosti, RIA Novosti, RIA Novosti 08/13/2021

    The legendary Comandante: the life and death of Fidel Castro

    Cuban revolutionary Fidel Castro would have turned 95 on August 13. Five years ago, the world saw off the legendary Comandante on his last journey.

    2021-08-13T07:47

    2021-08-13T07:47

    2021-08-13T07:47

    video

    cube

    90 002 fidel castro

    /html/head/meta[@name=’ og:title’]/@content

    /html/head/meta[@name=’og:description’]/@content

    https://cdnn21.img.ria.ru/images/07e5/08/0d /1745572059_0:0:640:360_1920x0_80_0_0_1f8ad23fe2f3128adf72e6fd898a8dd2. jpg

    He died a natural death at an advanced age despite numerous attempts on his life. According to the leadership of Cuba’s counterintelligence service, there were more than 600 attempts to assassinate Castro. They tried to shoot the revolutionary, poison him with toxic substances and poisons.

    cubes

    RIA Novosti

    1

    5

    4.7

    96

    [email protected]

    7 4 95 645-6601

    FSUE MIA Rossiya Segodnya

    https://xn –c1acbl2abdlkab1og.xn--p1ai/awards/

    2021

    RIA Novosti

    1

    5

    4.7

    96

    [email protected]

    7 495 645-6601

    FSUE MIA Russia Today

    https://xn--c1acbl2abdlkab1og.xn--p1ai/awards/

    News

    ru-RU

    https://ria.ru/docs/about/copyright.html

    https://xn--c1acbl2abdlkab1og.xn--p1ai/

    RIA Novosti

    1

    5

    4.7

    96

    [email protected]

    7 495 645-6601

    Rossiya Segodnya

    https://xn--c1acbl 2abdlkab1og. xn--p1ai/awards/

    The legendary Comandante: the life and death of Fidel Castro

    Cuban revolutionary Fidel Castro would have turned 9 on August 135 years. Five years ago, the world saw off the legendary Comandante on his last journey. He died a natural death at an advanced age despite numerous attempts on his life. According to the leadership of Cuba’s counterintelligence service, there were more than 600 attempts to assassinate Castro. They tried to shoot the revolutionary, poison him with toxic substances and poisons.

    2021-08-13T07:47

    true

    PT2M13S

    1920

    1080

    true

    1 920

    1440

    true

    1920

    1920

    true

    RIA Novosti

    1

    5

    4.7

    96

    [email protected]

    7 495 645-6601

    Rossiya Segodnya

    900 02 https://xn--c1acbl2abdlkab1og.xn--p1ai/awards /

    RIA Novosti

    1

    5

    4.7

    96

    internet-group@rian. ru

    7 495 645-6601

    Rossiya Segodnya 90 003

    https://xn--c1acbl2abdlkab1og.xn--p1ai /awards/

    video, cuba, Fidel Castro, video

    Video, Cuba, Fidel Castro

    The legendary Comandante: the life and death of Fidel Castro

    Cuban revolutionary Fidel Castro would have turned 95 on August 13. Five years ago, the world saw off the legendary Comandante on his last journey.

    2021-08-13T07:47

    true

    PT2M13S

    Fidel Castro: Biography, education, family

    Former President of the Council of State of Cuba

    Leader of Cuba from 1959 to 2008. Formerly Prime Minister of Cuba (1959-1976), Chairman of the Council of State of Cuba (1976-2008). In 1953, he led an unsuccessful coup attempt against Cuban dictator Fulgencio Batista, after which he spent two years in prison. Came to power after the overthrow of Batista at 1959 year. Acted as an opponent of the United States and established allied relations with the USSR. Since 1965, he headed the Communist Party of Cuba, actually relinquished these functions in 2006 due to illness and hospitalization, and temporarily transferred power to his brother Raul Castro. In 2008, Raúl Castro was elected as the new President of the Council of State and Commander-in-Chief of the Cuban Armed Forces, and in 2011 as General Secretary of the Cuban Communist Party.

    Fidel Alejandro Castro Ruz was born on August 13, 1926 years old in the town of Biran in Cuba, in the family of the owner of a sugar plantation [15], [21], [14], [23], [17]. From 1945 he studied at the Faculty of Law of the University of Havana. After graduating in 1950, he took up private legal practice [15], [21], [14], [22], [23], [17]. In his student years, Castro was a political activist, joined the reformist Party of the Cuban People (Partido del Pueblo Cubano), also known as the Party of the Orthodox (Partido Ortodoxo) [22], [23]. Participated in an unsuccessful attempt to overthrow the dictator of the Dominican Republic Rafael Trujillo (Rafael Trujillo) [23], [17]. Castro’s plans included winning a seat in the Cuban parliament, but at 19Fulgencio Batista returned to power in 1952 after an eight-year hiatus. The elections were cancelled, and Castro took up revolutionary activities [15], [22], [23], [17].

    On July 26, 1953, Castro led the attack of one and a half hundred young revolutionaries on the Moncada barracks near Santiago – Batista’s largest military garrison [15], [21], [14], [22], [23]. The uprising was unsuccessful, many of Castro’s associates died, he himself was arrested and in October 1953 was sentenced to 15 years in prison [15], [21], [14], [22], [23], [17]. At the trial, he delivered a speech that became known as “History will justify me” and contained accusations against the Batista regime and a call for democratic reforms [23], [21], [17]. May 19For 55 years, under pressure from public opinion, the Cuban authorities pardoned Castro, and he emigrated to Mexico, where he organized the “26 July Movement” (Movimiento 26 de Julio), named in memory of the 1953 uprising [15], [21], [14], [22], [23]. In 1956, a group of revolutionaries, including Fidel, his brother Raul Castro, and the Argentine Ernesto “Che” Guevara, arrived in Cuba on the yacht Granma. Only a few managed to escape from the persecution of Batista’s forces, but the guerrilla movement started by them in the Sierra Maestra mountains quickly grew and gained popularity [15], [14], [22], [23], [17]. At first, the United States helped Batista’s forces in the fight against partisans [23], but in 19In 58, American military assistance to the dictator ceased [15], [23]. On January 1, 1959, Castro’s rebel forces occupied Havana, Batista fled to the Dominican Republic [15], [21], [14], [22], [23]. In the following week, a new government was formed. Castro became commander-in-chief of the armed forces, and in February took over as prime minister [15], [21], [23], [17]. Later, in 1976, a new Cuban constitution was adopted, and Fidel took over as chairman of the Council of State [15], [23].

    From May 1959, the Castro government began expropriating American property in Cuba [15], [23]. In June 1960, after US President Dwight Eisenhower imposed a quota on imports of Cuban sugar, the Cuban authorities nationalized the property of American enterprises worth about $850 million [15]. Tension in relations with the United States prompted Fidel to move closer to the USSR [22], [23]. April 14 (according to other sources, April 16 [17]), 1961, Castro proclaimed the Cuban revolution socialist [15], [23] (previously it was only about moderate politics, national representative democracy and a well-organized economy [14], [22] ).

    On April 15, 1961, the United States bombed Cuban airfields [15], and on April 17, about 1,400 Cuban emigrants, trained and organized by the CIA, landed in Playa Giron (Bay of Pigs, Playa Giron). Their goal was to initiate a mass uprising against the Castro government [15], [14], [22], [23]. US President John F. Kennedy only at the last moment abandoned the idea of ​​supporting this enterprise with the help of the US military [15]. On April 21, 1961, Castro’s troops successfully repelled the attack and captured about a thousand prisoners [15], [14], [23]. February 7 19For 62 years, in connection with the ongoing nationalization of American property in Cuba, the United States imposed a trade embargo against the country [15].

    In October 1962, the Cuban Missile Crisis occurred, bringing the world to the brink of nuclear war. On October 14, a US reconnaissance aircraft spotted Soviet intercontinental ballistic missiles in Cuba. On October 22, Kennedy announced this in a public address. On October 27, an American U-2 reconnaissance aircraft was shot down over Cuba. On October 28, after tense negotiations, Kennedy and Soviet leader Nikita Khrushchev were able to reach a resolution to the crisis: the USSR withdrew missiles from Cuba, the United States, in response, abandoned plans for a military invasion of the island and withdrew nuclear weapons from Turkey [15], [14], [22], [23].

    During the same period, active party building took place in Cuba. In 1961, several political parties formed the United Revolutionary Organizations (Organizaciones Revolucionarias Integradas) movement, on the basis of which the United Party of the Cuban Socialist Revolution (Partido Unido de la Revolucion Socialista de Cuba; PURSC) was created in 1962 [24]. Castro became the general secretary of the party [17]. In the fall of 1965, PURSC was transformed into the Communist Party of Cuba (Partido Comunista de Cuba), and Castro became the first secretary of the party’s Politburo [17], [24].

    In November 1966, US President Lyndon Johnson announced an amnesty for illegal immigrants from Cuba who left the country after the 1959 revolution. About 125 thousand people took advantage of the amnesty [15]. In addition, from December 1965 to April 1973, the United States conducted an air evacuation of Cubans wishing to leave the country: their number was more than 260 thousand people [15].

    On November 11, 1975, rebels from the Popular Movement for the Liberation of Angola (Movimento Popular de Libertacao de Angola, MPLA), with intense support from Cuba, captured the Angolan capital of Luanda and proclaimed the independence of their country from Portugal [15], [22], [23]. The military presence of Cuba in Angola remained until 1988 years old [15]. In addition, the Cubans provided assistance to the rebels in other countries – Ghana, Algeria, Mozambique, Nicaragua and El Salvador [14], [23]. At the same time, under the leadership of Castro, Cuba became a key participant in the international non-aligned movement [14], [23].

    On November 20, 1975, the United States released information about eight unsuccessful attempts on the life of Castro, undertaken by the CIA from 1960 to 1965 [15]. According to Cuban authorities, during the years of Fidel’s rule, the CIA made more than 600 attempts to kill him [14].

    Under the leadership of Fidel, Cuba achieved significant success in the social sphere. Cubans enjoy free healthcare, the literacy rate reaches 98 percent, and the infant mortality rate in Cuba is lower than in many Western countries [14]. At the same time, the Cuban economy was dependent on the country’s alliance with the USSR. During the Cold War, the Soviet Union bought most of the sugar produced by Cuba and supplied various goods to the island, which helped to overcome the consequences of the American blockade [14]. With the beginning of the Soviet “perestroika”, sugar purchases ceased [14], and after the collapse of the USSR in 19In 1991, advisers from the USSR who worked in Cuba left the island [15]. The cessation of Soviet economic aid led to a recession in the Cuban economy, an increase in the shortage of food and consumer goods, and, as a result, to the flourishing of the black market [15], [14], [22], [23]. The Castro government was forced to make significant concessions, allowing foreign investment in certain sectors of the economy, in particular tourism, and then allowing foreign currencies to circulate in the country [23].

    Economic difficulties caused an increase in the number of refugees, many of whom died trying to reach the US coast on boats and other improvised watercraft [14], [15], [23]. 9September 1994, Cuba and the United States entered into an agreement under which the number of Cuban immigrants accepted by the United States was limited to 20 thousand people per year [15]. In January 1996, Miami-based Cuban dissident Brothers to the Rescue (Hermanos al Rescate) dropped leaflets over Havana calling for the overthrow of Castro. One of the two American aircraft used for this was shot down by Cuban air defenses, after which, on February 24, the United States made the trade embargo against Cuba permanent [15].

    In January 1998, Pope John Paul II visited Cuba and met with Fidel [23], [15], who was excommunicated in 1962 by Pope John XXIII [21]. Since the revolution, the Cuban authorities have emphasized the atheistic nature of their state, but in the mid-1990s they began rapprochement with the Catholic Church, hoping to use it to enlist international support and persuade the United States to lift the economic embargo against the country [20]. The Pope celebrated several masses in different parts of the island, each of which gathered several hundred thousand people, and during the last and largest of them, held on January 25 at the Revolution Square in Havana (Castro personally attended it), John Paul II called on the United States ease economic pressure on Cuba [19].

    In October 2000, the US House of Representatives revised the trade embargo against Cuba and allowed limited supplies of food and medicine to that country [15]. Castro condemned the September 11, 2001 terrorist attacks in the United States [23]. At the same time, he spoke out against the US-led war in Afghanistan [23]. Against this background, there was a rapprochement between Cuba and Venezuela, which in 1998 was headed by anti-globalist President Hugo Chavez [14], [23], [12], [13].

    In April 2004, the UN Commission on Human Rights condemned the Cuban authorities for violating human rights, including the detention of 78 members of the political opposition [15], [23].

    In 2005, Forbes magazine named Castro one of the world’s richest people and estimated his personal fortune at $550 million. In 2006, it was already about 900 million. Castro was outraged by these reports and categorically denied that he received income from state-owned enterprises [15], [18].

    In recent years, the world has closely followed Castro’s deteriorating health. In 2004, during a public speech, he fell, injuring his leg and arm [23]. On March 30, 2006, the Spanish-language press erroneously reported Castro’s death [15]. On July 31, 2006, an official statement from the Cuban authorities was released, announcing that Castro had undergone surgery due to gastrointestinal bleeding. He temporarily handed over power to the Minister of Defense and Vice President – his brother Raul. After that, Fidel did not participate in any public event. Although official Cuban sources claimed that the leader was on the mend, many observers questioned this information [16], [15], [14], [23].

    On January 16, 2007, the Spanish newspaper El Pais reported that Fidel had survived at least three unsuccessful surgeries and was in critical condition. Cuban officials called this message false [11]. In March, official Cuban sources reported that Castro would certainly return to office in the run-up to the general elections scheduled for April 2008 [10].

    On February 18, 2008, Fidel announced that he was going to step down as Chairman of the Council of State and Commander-in-Chief of the armed forces of Cuba [8], [9]. On February 24, his brother Raul Castro was elected as the new chairman of the State Council [7].

    In March 2011, Castro published an article in which he, in particular, said that back in 2006, due to illness, he actually resigned from all state and party posts [6], [5]. In April of the same year, at the congress of the Communist Party of Cuba, Raul Castro was elected its general secretary instead of Fidel [3], [4].

    In early February 2012, Castro presented two volumes of his memoirs under the general title “Fidel Castro Ruz: Partisan of Time”, which described the life of a politician from early childhood to December 1958 years [2], [1].

    Materials used

    [1] Fidel Castro presented a book of his memoirs. – BBC News, Russian Service , 02/05/2012

    [2] Fidel Castro unveils 1,000-page memoir. — CNN , 02/04/2012

    [3] Raul Castro Elected First Secretary of the Cuban Communist Party. — Cuban News Agency , 04/19/2011

    [4] Cuban communists opt for old guard to lead party. Reuters , 04/19/2011

    [5] Fidel Castro’s announcement retirement ends of an era, spurs Cuba succession buzz. — The Associated Press , 03/22/2011

    [6] Fidel Castro Ruz . Los zapaticos me aprietan. — CubaDebate , 03/21/2011

    [7] Raul Castro elected president of the councils of State and Ministers. — Granma International , 02/24/2008

    [8] Castro resigns as Cuban president: official media. – Agence France-Presse , 02/19/2008

    [9] Fidel Castro Ruz . Reflexiones del companero Fidel. — El Mundo , 02/18/2008

    [10] As Cuba prepares for 2008 vote, officials say Castro could be back. — Agence France-Presse , 03/16/2007

    [11] Mar Roman . Castro reportedly in ‘grave’ condition. — The Associated Press , 01/16/2007

    [12] Kirill Zubkov . Hugo Chavez goes to a new term “in the name of love.” – Newspaper (gzt.ru) , 04.