Arthritis - General Information
NATIONAL JOURNAL OF HOMOEOPATHY 1999 Mar / Apr VOL VIII NO 2.
Dr C H Asrani

Arthritis is the inflammation of a joint, which is characterized by pain, swelling and limitation of joint movement. Arthritis can be classified in several ways:

• Involvement of joints
• Cause of Arthritis
• Seropositive/ Seronegative

1. Involvement Of Joints -
   Monoarthritis & Polyarthritis.
   1. Monoarthritis:
      • Pyogenic arthritis
      • Tubercular arthritis
      • Haemophilic arthritis
      • Secondary osteoarthritis
      • Gout - sometimes
   2. Polyarthritis:
      • Rheumatoid arthritis
      • Primary osteoarthritis
      • Juvenile chronic polyarthritis
      • Sero-negative spondyloarthropathies
2. Causes-
   • Degenerative (Osteoarthritis)
   • Metabolic (Gout)
   • Auto-immune (Rheumatoid arthritis)
   • Infective (Pyogenic or Tubercular)
   • Secondary (to Psoriasis)
3. Seropositive - commonest being Rheumatoid arthritis, Still's disease Seronegative spondyloarthropathies.

Aetio-Pathology: This is an articular disease of the old age, associated with degenerative changes, the result of aging of the tissues. Clinical manifestation usually appears at 40 yrs, but in many cases, disease may remain asymptomatic for long periods. The weight bearing joints of the lower extremity ie knee & hip are more susceptible. Osteoarthritis may even afflict the younger age group, as a result of :

• repeated trauma/ fractures either in or around the joints.
• Overweight.
• Poor posture.
• Congenital deformity of a joint.

Clinical Features: The disease has an insidious onset, is slowly progressive and joint changes are irreversible. The earliest manifestation is stiffness, which is later accompanied by pain. The symptoms are aggravated by physical exertion (friction) and relieved by rest. Swelling is much more common with knee than the hip joint. It is due to a combination of osteophyte formation with increase in the amount of synovial fluid in the joint.
Examination of the affected joint may reveal tenderness and crepitus. The muscles surrounding the joint may be wasted, making it appear larger by contrast.
Symptoms of the disease are purely local with no systemic involvement.

Diagnosis: There are serological tests that can diagnose OA. History, clinical examination and Plain X-ray of the affected joint are enough to confirm the diagnosis.

Treatment: Pathological changes being irreversible, treatment is aimed at: relief of symptoms of pain and stiffness:

• Loss of weight for those over weight,
• Physiotherapy with Quadriceps strengthening exercises is helpful.
• Local heat, SWD, massage etc are advised for temporary relief.
• Correction of faulty posture and avoidance of factors likely to inflict stress on the affected joint for a part of management.

An acute attack is sudden in onset, frequently nocturnal and either without precipitating cause or following rapid fluctuation in the serum urate levels from food, alcohol, surgery, infection or uricosuric drugs.
During an acute attack theres swelling, part extremely tender, with all the signs of inflammation and severe pain in a joint - often the 1st meta-tarsophalangeal joint of the big toe (podagra).

There are asymptomatic periods between acute attacks
The causes aren't fully understood, but gout is claimed to be a disorder of purine metabolism. Purines are nitrogenous substances found in high-protein foods, and the end product of their digestion is uric acid. Normally uric acid is expelled in urine. In gout, the acid crystals are retained in the blood and then deposited in joints and cartilage, where they form lumps called tophi. Uric acid deposits can also build up as stones in the kidneys and lead to permanent scarring. Joints affected by gout degenerate in the same way as those affected by rheumatoid arthritis, and can eventually lose their ability to move.

Laboratory Findings:

• Elevated S. uric acid levels. (>7.5 mg/dL).
• ESR and WBCs are often raised, during an attack

Treatment: Acute attack Bed rest is important in the acute attack. Management between attacks - Diet - it is important to avoid obesity, fasting, excessive alcohol and dehydration. Specific foods that precipitate attacks are to be avoided. A high liquid intake and more importantly, a urine output of 2 liters or more will aid urate excretion.

Allopurinol - Xanthine oxidase inhibitor promptly lowers plasma uric acid concentration. Ideal dose is 100 mg TDS To begin with a 100 mg OD or BD as maintenance dose, depending upon the levels. The problem being hereditary, Allopurinol is to be continued life long with 6 monthly checks of S uric acid.

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