Rheumatoid Arthritis

Rheumatoid Arthritis

1. Definition

Rheumatoid arthritis is a chronic systemic autoimmune disease in which the body’s immune system attacks the synovial membrane of joints, producing persistent inflammation, pain, swelling and progressive joint destruction. It is not limited to the joints; extra‑articular organs may also be involved.

2. Synonyms (if any)

• Chronic polyarthritis – emphasizes involvement of many joints.
• Autoimmune arthritis – highlights the immune‑mediated nature.

3. Causes / Etiology

1. Genetic predisposition – certain HLA‑DR alleles (especially HLA‑DR4) increase susceptibility; families with a history of RA have a higher risk.
2. Environmental triggers – smoking is the most important modifiable factor; it promotes citrullination of proteins and breaks tolerance.
3. Infections – bacterial or viral agents may act as a trigger by molecular mimicry, although a direct causative link is not proven.
4. Hormonal influences – the disease is more common in women; estrogen may modulate immune response.
5. Occupational exposures – silica dust and certain organic solvents have been associated with higher incidence.

Each of these factors contributes to loss of self‑tolerance and the production of auto‑antibodies that target joint tissue.

4. Types / Classification

5. Pathophysiology / Pathology – step by step

1. Auto‑antibody formation – loss of tolerance leads to production of rheumatoid factor (IgM against IgG) and anti‑citrullinated protein antibodies.
2. Synovial membrane activation – immune complexes deposit in the synovium, activating complement and attracting inflammatory cells (macrophages, T‑cells, B‑cells).
3. Cytokine cascade – release of TNF‑α, IL‑1, IL‑6, and other mediators sustains inflammation and stimulates fibroblast‑like synoviocytes.
4. Pannus formation – proliferating synoviocytes and inflammatory cells form a thick, vascularised pannus that invades cartilage and bone.
5. Enzymatic degradation – matrix metalloproteinases and osteoclast‑activating factors break down cartilage and bone, causing erosions.
6. Systemic effects – cytokines enter circulation, producing fatigue, anemia of chronic disease, and increased cardiovascular risk.

Each stage amplifies the next, creating a self‑perpetuating cycle of joint damage.

6. Clinical Features

• General (systemic) features – persistent fatigue, low‑grade fever, loss of appetite, weight loss, anemia, and occasional rheumatoid nodules on extensor surfaces.
• Joint‑specific features – symmetric swelling of small joints of hands and feet, morning stiffness lasting > 1 hour, warmth and tenderness over affected joints, reduced range of motion.
• Acute presentation – sudden increase in pain, swelling and warmth, often triggered by infection or stress; may mimic septic arthritis.
• Chronic presentation – gradual progression to joint deformities such as ulnar deviation, swan‑neck and boutonnière deformities, boutonnière contracture, and loss of function.
• Extra‑articular manifestations – rheumatoid nodules, pleuritis, pericarditis, interstitial lung disease, vasculitis, and ocular dryness.

The presence of systemic signs helps to differentiate RA from purely mechanical joint disorders.

7. Complications

• Acute complications – joint infection (septic arthritis) due to immunosuppression, acute inflammatory flares causing severe functional loss, and steroid‑induced hyperglycaemia.
• Chronic complications – joint deformities and subluxations, osteoporosis secondary to chronic inflammation and glucocorticoid use, cardiovascular disease (accelerated atherosclerosis), pulmonary fibrosis, and secondary amyloidosis.

Early control of inflammation reduces the risk of these long‑term problems.

8. Investigations / Diagnosis

1. Complete blood count – often shows normocytic anemia; leukocytosis may be present during flares.
2. Erythrocyte sedimentation rate (ESR) and C‑reactive protein (CRP) – elevated, reflecting active inflammation.
3. Rheumatoid factor (RF) – IgM antibody against Fc portion of IgG; positive in about 70 % of patients, helps confirm diagnosis.
4. Anti‑CCP (anti‑citrullinated protein antibody) – highly specific for RA; predicts more aggressive disease.
5. X‑ray of hands and feet – early stage may show soft‑tissue swelling; later stages reveal joint space narrowing, marginal erosions and osteopenia.
6. Ultrasound / MRI – detect early synovitis, pannus formation and erosions before they appear on plain radiographs.
7. Joint aspiration (if needed) – to exclude septic arthritis; synovial fluid is usually inflammatory (high WBC, neutrophil predominance).

Each test adds a piece of information that together confirms the clinical picture.

9. Differential Diagnosis

• Osteoarthritis – degenerative wear and tear, pain worsens with use, minimal morning stiffness, asymmetric joint involvement; radiographs show osteophytes rather than erosions.
• Psoriatic arthritis – associated with skin psoriasis, may involve distal interphalangeal joints, nail pitting, and sausage‑digit swelling; X‑ray may show pencil‑in‑cup deformity.
• Systemic lupus erythematosus (SLE) – often presents with non‑erosive arthritis, photosensitivity, renal involvement, and positive ANA; joint pain is usually migratory and not destructive.
• Gout – acute mono‑articular attacks, presence of monosodium urate crystals in synovial fluid, and tophi in chronic disease; serum uric acid is elevated.

Key distinguishing points are pattern of joint involvement, presence of erosions, serology and associated systemic features.

10. Management / Treatment

General management –

• Encourage regular low‑impact exercise (e.g., swimming, walking) to maintain joint mobility and muscle strength.
• Provide joint protection strategies such as splints and ergonomic modifications.
• Educate the patient about the chronic nature of the disease and the importance of adherence to therapy.

Modern medicine treatment –

1. Non‑steroidal anti‑inflammatory drugs (NSAIDs) – relieve pain and reduce inflammation; used for symptomatic control.
2. Glucocorticoids – short‑term low‑dose oral or intra‑articular steroids to control severe flares; taper as soon as possible to avoid long‑term side effects.
3. Disease‑Modifying Antirheumatic Drugs (DMARDs) –
   • Methotrexate – first‑line oral or subcutaneous DMARD; inhibits folate metabolism, reduces cytokine production.
   • Sulfasalazine, Leflunomide, Hydroxychloroquine – used as monotherapy or in combination when methotrexate alone is insufficient.
4. Biologic agents – target specific cytokines or cells:
   • TNF‑α inhibitors (e.g., etanercept, infliximab) – block a key inflammatory mediator.
   • IL‑6 receptor antagonist (tocilizumab) – reduces systemic inflammation.
   • B‑cell depleting agent (rituximab) – useful in seropositive disease resistant to other therapies.
5. JAK inhibitors – oral small‑molecule drugs that interfere with intracellular signalling pathways of multiple cytokines.

Diet and lifestyle advice –

• Adopt a balanced diet rich in omega‑3 fatty acids (fish, flaxseed) to exert anti‑inflammatory effects.
• Maintain a healthy body weight to reduce mechanical stress on joints and improve response to DMARDs.
• Avoid smoking; cessation lowers disease activity and improves treatment efficacy.
• Limit intake of processed foods, excess sugar and saturated fats as they may aggravate systemic inflammation.

11. Homeopathic Therapeutics (7 remedies, each with 7‑8 points)

1. Rhus Tox

• Causation: Joint pain after prolonged rest or after exposure to cold, damp weather.
• Characteristic symptoms: Stiffness and aching that improve with gentle motion; swelling that feels hot.
• Modalities: Worse in the morning and when cold; better with warmth and continued movement.
• Mental state: Irritable, impatient, wants to be active despite pain.
• Thirst and appetite: Thirst for warm drinks; appetite may be reduced during acute flare.
• Discharges/secretions: May have serous joint effusion that is thin and watery.
• Physical generals: Tendency to develop skin eruptions and rheumatic nodules.
• Constitution: Young to middle‑aged individuals who are active but forced to rest; benefit from warm compresses.
• How it helps: Addresses the underlying “rest‑worsens, motion‑helps” pattern typical of early RA flares.

2. Bryonia

• Causation: Joint pain following a single traumatic injury or over‑exertion.
• Characteristic symptoms: Sharp, stitching pain that is aggravated by any movement; joints feel bruised.
• Modalities: Worse on motion, better when the limb is completely at rest; prefers lying still.
• Mental state: Wants to be left alone, becomes irritable when forced to move.
• Thirst and appetite: Strong thirst for large amounts of cold water; appetite may be poor.
• Discharges/secretions: Thick, sticky synovial fluid may be present.
• Physical generals: Dry skin, constipation, tendency to develop dry cough.
• Constitution: Persons who are stoic, endure pain silently, but become very restless when forced to move.
• How it helps: Relieves the “pain‑worse‑movement, relief‑by‑rest” pattern seen in acute exacerbations.

3. Ruta Gravis

• Causation: Repetitive strain or over‑use of joints, especially in people who perform manual work.
• Characteristic symptoms: Burning, tearing pain in joints; stiffness that improves slowly with gradual motion.
• Modalities: Worse in damp, cold weather; better in warm, dry environment.
• Mental state: Restless, eager to work despite pain, often neglects self‑care.
• Thirst and appetite: Thirst for cold water; appetite may be normal.
• Discharges/secretions: May have thin, watery joint effusion.
• Physical generals: Tend to develop tendon sprains and bruises easily.
• Constitution: Laborers, students, or athletes who push themselves beyond limits.
• How it helps: Targets the chronic over‑use component that fuels pannus formation.

4. Causticum

• Causation: Joint pain after exposure to cold wind or after a fall; often follows a period of emotional suppression.
• Characteristic symptoms: Burning, tearing pain that spreads to surrounding tissues; joints feel weak.
• Modalities: Worse in cold, damp, or windy conditions; better with warmth and gentle motion.
• Mental state: Suppressed emotions, feels “stuck” and unable to express feelings.
• Thirst and appetite: Thirst for warm drinks; appetite may be reduced.
• Discharges/secretions: May have mucous discharge from eyes or nose.
• Physical generals: Skin may become dry and cracked; prone to ulcerations.
• Constitution: Individuals who are emotionally restrained, often introverted.
• How it helps: Relieves the cold‑induced aggravation and emotional component of chronic RA.

5. Kali Mur

• Causation: Joint pain after prolonged standing or after a minor injury; often in people with a family history of rheumatism.
• Characteristic symptoms: Stiffness and aching that improve with warm applications; swelling is soft and puffy.
• Modalities: Worse in damp, cold weather; better with heat and gentle exercise.
• Mental state: Anxious, fearful of worsening disease, often worries about future.
• Thirst and appetite: Thirst for warm water; appetite may be moderate.
• Discharges/secretions: May have thin, watery discharge from joints.
• Physical generals: Tendency to develop varicose veins and hemorrhoids.
• Constitution: Persons who are nervous, often over‑think, and have a hereditary predisposition.
• How it helps: Addresses the constitutional weakness and cold‑sensitive nature of the disease.

6. Natrum Muriaticum

• Causation: Joint pain following emotional grief or suppressed sorrow; often after a period of prolonged crying.
• Characteristic symptoms: Burning, throbbing pain in joints, especially wrists and elbows; swelling is firm.
• Modalities: Worse in warm, dry weather; better in cool, moist environment.
• Mental state: Reserved, feels lonely, holds back emotions, may be prone to depression.
• Thirst and appetite: Thirst for salty water; appetite may be reduced.
• Discharges/secretions: May have dry mucous membranes, scanty tears.
• Physical generals: Tendency to develop headaches and digestive disturbances.
• Constitution: Individuals who are introverted, keep feelings inside, and have a family tendency to rheumatism.
• How it helps: Treats the emotional‑linked aggravation that can trigger flares.

7. Lycopodium

• Causation: Joint pain after over‑eating or after a heavy meal; often in people with a history of digestive upset.
• Characteristic symptoms: Cramping, burning pain in joints that worsens in the evening; swelling is moderate.
• Modalities: Worse in the evening and when standing; better in the morning after a light walk.
• Mental state: Over‑confident, eager to please, fears failure, often feels insecure.
• Thirst and appetite: Thirst for warm drinks; appetite is strong but may cause indigestion.
• Discharges/secretions: May have flatulent abdominal distension.
• Physical generals: Tendency to develop skin eruptions on the abdomen.
• Constitution: Persons who are ambitious, work hard, and neglect rest.
• How it helps: Balances the digestive‑related aggravation and evening worsening typical of some RA patients.

8. Pulsatilla

• Causation: Joint pain after exposure to cold wind or after a viral infection; often in young women.
• Characteristic symptoms: Swelling that is soft, movable, and improves with warmth; pain is shifting from joint to joint.
• Modalities: Worse in warm, stuffy rooms; better in fresh air and cool environment.
• Mental state: Changeable mood, weepy, seeks comfort and reassurance.
• Thirst and appetite: Thirst for cold water; appetite may be variable.
• Discharges/secretions: May have thin, watery nasal discharge.
• Physical generals: Tendency to develop mild anemia and menstrual irregularities.
• Constitution: Young, emotional, often with a history of recurrent infections.
• How it helps: Fits the changeable, wind‑related pattern of joint pain seen in early disease.

12. Prognosis

The overall outlook depends on disease severity at presentation, speed of diagnosis, and adequacy of treatment. Early initiation of DMARDs and tight disease control usually lead to remission or low disease activity, preserving joint function. Poor prognostic factors include high anti‑CCP titres, early erosions on X‑ray, seropositivity, and presence of extra‑articular disease. With optimal therapy, many patients maintain a productive life, although some may develop permanent deformities.

13. Prevention

• Smoking cessation – the most effective modifiable preventive measure; reduces risk of onset and severity.
• Weight control – maintaining a normal body mass index lessens mechanical stress on joints and improves response to medication.
• Early screening in individuals with a family history or presence of auto‑antibodies (RF, anti‑CCP) allows prompt treatment before irreversible damage occurs.

These steps lower the likelihood of disease development and mitigate progression.

14. Diet

• Recommended foods – oily fish (rich in omega‑3), flaxseed, walnuts, fresh fruits and vegetables, whole grains, and low‑fat dairy; they provide anti‑inflammatory nutrients and antioxidants.
• Foods to avoid – processed meats, refined sugars, trans‑fat laden snacks, excessive alcohol, and high‑salt items; they promote systemic inflammation and may interfere with medication metabolism.

A balanced anti‑inflammatory diet supports the pharmacologic control of disease and improves overall health.