Gout is a clinical manifestation of inflammatory arthritis that produces pain and swelling in different joints in the body. The symptoms occur in flares that last a week or two before disappearing.
- Several joints (Big toe, ankle, knee, lesser toe joints)
- Sacs that act as a cushion and connect soft tissues and bones (Bursae)
- Membranes surrounding tendons offer protection (Tendon sheaths)
- Kidneys (High uric acid can induce stone formation damaging the kidney)
- High uric acid (Some with high uric acid may remain asymptomatic)
- Family history of gout, consuming foods (mostly animal proteins) rich in purines (purine breaks down to urate) and fructose, sweetened drinks, alcohol, etc.
Signs Or Symptoms
Gout symptoms frequently start in the big toe (metatarsophalangeal joint) or a lower part of the leg. Gout develops when serum uric acid levels are high causing needle-shaped crystals to grow in and around the joints. As a result, the joint becomes inflamed and arthritic.
Symptoms of the affected joints are as follows
- Intense pain
These symptoms alternate between sudden flare and remission. Generally, symptoms of the joints are unilateral, which usually affects one joint.
Possible Gout Treatment
Gout is managed both by medication and lifestyle modification.
- Medication: Flares can be managed by nonsteroidal anti-inflammatory drugs (NSAIDs) (eg., ibuprofen), anti-inflammatory drugs (eg., colchicine), steroids, and uric acid lowering drugs (febuxostat, allopurinol, and pegloticase).
- Lifestyle changes: Weight loss, dietary modification, less alcohol consumption, avoiding purine-rich food (e.g., red meat), and stopping medications associated with hyperuricemia (like diuretics).
- Prevention: Follow-up with a physician to prevent the formation of tophi (uric acid crystals under the skin) and kidney stones.
- Age: People at an older age are at increased risk. Younger people rarely have gout, but they have a severe form.
- Gender: Gout is three to four times as prevalent among males than females.
- Family history
- Lifestyle: Alcohol consumption, eating a high-purine, high-fructose diet increase risk of gout.
- Heavy metal exposure: Research showed an association between chronic lead exposure and the risk of gout.
- Medications: Certain medications, such as diuretics, salicylate-containing drugs, cyclosporine, niacin in excess, and a low dose of aspirin, elevate the uric acid level.
- Obesity: Being overweight and having high levels of body fat may increase the risk of gout.
- Other comorbidities: Some common health conditions increase the risk of gout, which are as follows
- Renal impairment/kidney stone
- Abnormal cell proliferating conditions, such as hemolytic anemia, psoriasis, and certain types of cancers
- Kelley-Seegmiller syndrome or Lesch-Nyhan syndrome (Deficient in enzyme regulating urate level)
The progression of gout is separated into four phases:
- Asymptomatic hyperuricemia: High uric acid without gouty arthritis.
- Acute gouty arthritis: Onset and flares of pain, restricted range of motion, swelling, erythema, and swelling of the involved joint.
- Intercritical gout: A period between remission and recurrence when the secondary causes of hyperuricemia and prevention must be addressed.
- Chronic tophaceous gout: Deposition of sodium urate crystals (tophi) under the skin.
- Physical examination: Examining the affected joints for swelling, erythema, edema, etc.
- Laboratory test: Checking the serum uric acid level
- Ultrasound: Evaluating crystal deposition and other underlying causes
- Microscopy: Aspired liquid from joints can be examined under the microscope to find urate crystals.
Gout can be prevented by following some management protocols:
- Limiting alcohol intake
- Avoiding purine-rich food (red meat, organ meat, codfish, shellfish, etc.)
- Consuming a non-dairy, low-fat diet
- Maintaining permissible BMI
- Stop smoking
- Daily workout
- Staying hydrated
After remission from arthritic pain, uric acid lowering drugs should be taken and secondary causes of hyperuricemia must be addressed.
- Pseudogout (calcium pyrophosphate deposition)
- Rheumatoid Arthritis
- Psoriatic Arthritis
- Palindromic Rheumatism
- Reactive Arthritis
- One to two percent of men in the western world is affected by gout.
- The prevalence of gout is 0.12% in India.
- Gout develops at a higher rate in men and rarely occurs in premenopausal women.
An acute gout episode normally disappears in five to seven days without any clinical attention. However, 60% of patients experience a recurrence within a year. Gout patients are more likely to develop other metabolic diseases, such as hypertension and diabetes. Along with metabolic syndromes, renal disease and cardiovascular disease increases mortality.
If not treated and allowed to progress naturally, gout can lead to erosion and destruction of the affected joint. It may cause the formation of urate crystal deposits under the skin.
Uric acid accumulates and crystalizes in an aberrant purine metabolism causing gout. The crystal in monosodium urate form precipitates creating deposits (tophi) in joints, tendons, and surrounding tissues. Crystal protected by proteinaceous sheath prevents contact with cells and thereby prevents inflammation. Minor joint trauma, medical or surgical stress, or sudden fluctuations in uric acid levels might cause naked crystals to burst out of protein-protected tophi. They cause a local immune-mediated inflammatory response causing major symptoms of gout, such as pain, erythema, and swelling.
Without treatment, gout can lead to several complications as follows
- Chronic gout
- Obliteration of the joint surface, joint deformity
- Painless tophi (in the helix of the ear, over the large, thick, protruding part of the ulna, or on the heel cord)
- Kidney stones and other kidney dysfunctions
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