Kliniczne aspekty chorób układu odpornościowego: część 1 i 2 | Clinical Aspects of Immune System Diseases: part 1 and 2

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Szacowany czas lekcji: 17 minut
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Allergic Diseases

Allergic diseases encompass a range of conditions resulting from an exaggerated immune response to typically harmless substances known as allergens. The immune system mistakenly identifies these substances as threats, leading to inflammation and various clinical manifestations. Common allergic diseases include allergic rhinitis, asthma, atopic dermatitis, and food allergies.

Allergic Rhinitis (Hay Fever)

Allergic rhinitis is an inflammation of the nasal mucosa caused by allergens such as pollen, dust mites, pet dander, or mold. It is characterized by:

  • Symptoms: Sneezing, nasal congestion, runny nose, and itchy, watery eyes. These symptoms can significantly impact quality of life and may be seasonal (occurring at certain times of the year) or perennial (year-round).
  • Pathophysiology: Upon exposure to allergens, the immune system produces immunoglobulin E (IgE), leading to the release of histamine and other inflammatory mediators. This results in vasodilation, increased vascular permeability, and stimulation of sensory nerves.

Asthma

Asthma is a chronic inflammatory disease of the airways that can be triggered by allergens, irritants, respiratory infections, or exercise. It is characterized by:

  • Symptoms: Wheezing, breathlessness, chest tightness, and coughing, particularly at night or early in the morning. Asthma symptoms can vary in frequency and severity.
  • Pathophysiology: In asthma, the airways become inflamed and hyperresponsive to various stimuli. Exposure to allergens triggers an inflammatory response, leading to bronchoconstriction, airway swelling, and mucus production, which obstruct airflow.

Atopic Dermatitis (Eczema)

Atopic dermatitis is a chronic skin condition characterized by dry, itchy, and inflamed skin. It often occurs in individuals with a family history of allergies or asthma and is associated with:

  • Symptoms: Red, inflamed patches of skin, intense itching, and potential secondary infections due to scratching. It commonly affects areas such as the face, elbows, and knees.
  • Pathophysiology: The condition is driven by an immune response to environmental allergens and irritants. Genetic factors can also contribute to a compromised skin barrier, leading to increased sensitivity and inflammation.

Food Allergies

Food allergies occur when the immune system reacts to specific proteins in certain foods, leading to a range of symptoms from mild to severe. Common food allergens include peanuts, tree nuts, shellfish, fish, milk, eggs, soy, and wheat.

  • Symptoms: Reactions can range from mild hives or gastrointestinal discomfort to severe anaphylaxis, which is life-threatening and requires immediate medical attention. Symptoms of anaphylaxis include difficulty breathing, swelling of the throat, rapid pulse, and loss of consciousness.
  • Pathophysiology: Food allergies involve the production of IgE antibodies against specific food proteins. Upon subsequent exposure, these antibodies trigger the release of histamine and other mediators, leading to allergic symptoms.

Autoimmune Disorders

Autoimmune disorders are a group of diseases in which the immune system mistakenly attacks the body’s own tissues, leading to inflammation and damage. This misdirected immune response can result from genetic predisposition, environmental triggers, and hormonal influences. Common autoimmune diseases include Systemic Lupus Erythematosus (SLE), which affects multiple organs, and Rheumatoid Arthritis, primarily impacting the joints.

Systemic Lupus Erythematosus (SLE)

Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease characterized by the production of autoantibodies that target various organs and tissues in the body. It primarily affects women of childbearing age but can occur in individuals of any age or sex. The unpredictable nature of SLE can lead to periods of exacerbation and remission, making management challenging.

Etiology and Risk Factors

  • Genetic Factors: A family history of lupus or other autoimmune diseases increases the risk, suggesting a genetic predisposition.
  • Environmental Triggers: Factors such as sunlight exposure, infections, and certain medications can provoke or exacerbate the disease in susceptible individuals.
  • Hormonal Influences: The prevalence of SLE in women suggests that hormones, particularly estrogen, may play a role in disease development.
  • Ethnicity: SLE is more common and often more severe in individuals of African, Asian, and Hispanic descent.

Pathophysiology

In SLE, the immune system produces autoantibodies against nuclear antigens, leading to the formation of immune complexes. These complexes can deposit in various tissues and organs, triggering inflammation and damage. The disease can affect multiple systems, including the skin, joints, kidneys, heart, lungs, and central nervous system. This multisystem involvement is a hallmark of SLE.

Clinical Manifestations

  • Constitutional Symptoms: Fatigue, fever, and weight loss are common initial symptoms.
  • Skin Involvement: The characteristic “butterfly” rash across the cheeks and nose, along with photosensitivity, is often seen. Other skin lesions, such as discoid lupus erythematosus, can occur.
  • Musculoskeletal Symptoms: Joint pain and swelling (arthritis) are common and may affect multiple joints.
  • Renal Involvement: Lupus nephritis is a serious complication characterized by inflammation of the kidneys, leading to proteinuria and potential kidney failure.
  • Hematologic Manifestations: Anemia, leukopenia, and thrombocytopenia may occur due to bone marrow involvement or immune-mediated destruction.
  • Neurological Symptoms: Headaches, seizures, and cognitive dysfunction may occur, reflecting central nervous system involvement.

Diagnostic Approach

  • Clinical Evaluation: A comprehensive history and physical examination focused on symptomatology and organ involvement.
  • Laboratory Tests:
    • Antinuclear Antibody (ANA) Test: A positive ANA test is common in SLE but not specific.
    • Specific Autoantibodies: Antibodies to double-stranded DNA (anti-dsDNA) and Smith antigen (anti-Sm) are more specific for SLE.
    • Complement Levels: Decreased complement levels (C3 and C4) may indicate disease activity.
  • Kidney Biopsy: In cases of suspected lupus nephritis, a biopsy may be performed to assess the extent of renal involvement.

Treatment

  • Pharmacotherapy:
    • Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Used for pain relief and inflammation.
    • Antimalarials: Hydroxychloroquine is commonly prescribed for skin and joint symptoms.
    • Corticosteroids: Used to control acute flares and manage severe manifestations of the disease.
    • Immunosuppressants: Medications such as azathioprine, mycophenolate mofetil, or cyclophosphamide may be used for severe disease or lupus nephritis.
  • Lifestyle Modifications: Patients are advised to avoid sun exposure, manage stress, and maintain a healthy lifestyle to help mitigate symptoms and prevent flares.

Complications

  • Organ Damage: Chronic inflammation and immune complex deposition can lead to permanent damage to organs, particularly the kidneys (lupus nephritis).
  • Cardiovascular Disease: Increased risk of atherosclerosis and cardiovascular events due to inflammation and traditional risk factors.
  • Infections: Immunosuppression from treatment increases susceptibility to infections.

Prognosis

  • Variable Outcomes: The prognosis for SLE varies widely among individuals, with many achieving good control of symptoms with appropriate treatment. Long-term survival rates have significantly improved, with current estimates indicating a 10-year survival rate of approximately 90%. However, ongoing monitoring and management are crucial to minimize complications and organ damage. Regular follow-up is essential to adjust treatment and monitor for disease activity.

Rheumatoid Arthritis (RA)

Rheumatoid Arthritis (RA) is a chronic inflammatory autoimmune disease primarily affecting the joints but can also have systemic effects. It is characterized by synovitis, leading to joint destruction, and is often associated with various extra-articular manifestations. RA can occur at any age but most commonly begins in middle adulthood and is more prevalent in women than men.

Etiology and Risk Factors

  • Genetic Factors: A family history of RA or other autoimmune diseases increases susceptibility, suggesting a genetic component. The presence of specific HLA-DRB1 alleles is associated with a higher risk of developing RA.
  • Environmental Triggers: Factors such as smoking, infections, and exposure to certain chemicals (e.g., silica) can trigger the onset of RA in genetically predisposed individuals.
  • Hormonal Influences: The higher incidence in women suggests that hormonal factors may play a role, with symptoms often fluctuating with hormonal changes.
  • Age: Although RA can occur at any age, its onset typically occurs between the ages of 30 and 60.

Pathophysiology

RA is characterized by an autoimmune response that leads to the activation of immune cells, including T cells, B cells, and macrophages, in the synovial membrane. This results in chronic inflammation, the formation of pannus (abnormal tissue), and the destruction of cartilage and bone. The inflammatory process also releases cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which perpetuate inflammation and contribute to systemic manifestations.

Clinical Manifestations

  • Joint Symptoms:
    • Symmetrical polyarthritis affecting small joints, such as the hands and feet, is typical.
    • Patients may experience morning stiffness lasting more than 30 minutes, swelling, tenderness, and decreased range of motion.
  • Systemic Symptoms:
    • Fatigue, low-grade fever, and malaise are common.
    • Extra-articular manifestations may include rheumatoid nodules, lung involvement (interstitial lung disease), and cardiovascular complications.

Diagnostic Approach

  • Clinical Evaluation: A thorough history and physical examination focusing on joint involvement and systemic symptoms.
  • Laboratory Tests:
    • Rheumatoid Factor (RF): Presence of RF antibodies is common in RA but not specific.
    • Anti-Citrullinated Protein Antibodies (ACPA): More specific for RA and may be present early in the disease.
    • Erythrocyte Sedimentation Rate (ESR) and C-Reactive Protein (CRP): Indicators of inflammation.
  • Imaging Studies:
    • X-rays can reveal joint erosions and deformities. MRI or ultrasound may be used for more detailed assessments of joint inflammation.

Treatment

  • Pharmacotherapy:
    • Disease-Modifying Antirheumatic Drugs (DMARDs): Methotrexate is the cornerstone of treatment for RA, helping to slow disease progression and reduce joint damage.
    • Biologic Agents: Targeted therapies such as TNF inhibitors (e.g., etanercept, infliximab) and other biologics (e.g., rituximab, tocilizumab) are used for moderate to severe cases.
    • NSAIDs: Nonsteroidal anti-inflammatory drugs provide symptomatic relief from pain and inflammation.
    • Corticosteroids: Used for rapid symptom control during flares or as a bridging therapy.
  • Lifestyle Modifications: Regular physical activity, weight management, and a balanced diet are essential for managing symptoms and maintaining joint function.

Complications

  • Joint Damage: Chronic inflammation can lead to irreversible joint damage, deformities, and loss of function.
  • Osteoporosis: Increased risk of osteoporosis and fractures due to inflammation and steroid use.
  • Cardiovascular Disease: Higher risk of cardiovascular events due to systemic inflammation.

Prognosis

  • Variable Outcomes: With early diagnosis and appropriate treatment, many individuals with RA can achieve significant symptom relief and maintain function. However, approximately 40% of patients may experience severe disease, leading to joint damage and disability. Long-term management is crucial, as individuals with RA have a reduced life expectancy of about 3-7 years due to increased cardiovascular risk and complications associated with chronic inflammation.