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Crystals deposit disease

  1. Gout is a disorder of purine metabolism, and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating in joints, on tendons, and in the surrounding tissues.
  2. These crystals then trigger a local immune-mediated inflammatory reaction with one of the key proteins in the inflammatory cascade being interleukin 1β.
Gout (Ref. Hari. 18th ed., Pg-2837)
  1. Gout is a metabolic disease most often affecting middle-aged to elderly men and postmenopausal women, due to an increased body pool of urate with hyperuricemia.
  2. It is characterized by episodic acute and chronic arthritis, due to deposition of Monosodium urate crystals (AIPG 2012) in joints and connective tissue tophi.
  3. The risk for deposition in kidney interstitium or uric acid nephrolithiasis.
  4. The metatarsophalangeal joint of the first toe is most commonly involved, (Small joints) but tarsal joints, ankles, and knees are also affected.
  5. During acute attack the joint is very painful, red hot and swollen there is grade IV tenderness.
  6. Chronic gout patient may present with uric acid stone or tophi in skin or tubulo interstitial disease.
  7. Abrupt decrease in serum urate levels is more common a cause for acute gout than an abrupt increase in urate levels. Initiation of hypo uricemic therapy can precipitate acute attacks.
  8. Patient may be asymptomatic with high serum uric acid for years
  9. Development of arthritis correlates with level of serum uric acid
  1. Best and the most specific test is analysis of synovial fluid - Uric acid crystals are best seen as needle shaped crystals by polarizing light microscope.
  2. Serum uric acid levels are usually high but it can be normal or low at the time of the acute attack.
  3. Over 90% of individuals with sustained hyperuricemia occur due to decreased uric acid excretion.

Extra Edge (Ref. Hari. 18th ed., Pg- 2838):


Excretion of >800 mg of uric acid per 24 h on a regular diet suggests that causes of overproduction of purine should be considered.

Table: Classification of Hyperuricemia by Pathophysiology
  1. Urate Overproduction
    1. Primary idiopathic
    2. HPRT deficiency
    3. PRPP synthetase overactivity
    4. Hemolytic processes
    5. Lympho and myeloproliferative diseases
    6. Alcohol
    7. Psoriasis
    8. Obesity
  2. Decreased Uric Acid Excretion
    1. Primary idiopathic
    2. Renal insufficiency
    3. Hypothyroidism
    4. Hypertension
    5. Acidosis
    6. Hyperparathyroidism
    7. Drug ingestion (PGI June 08)
      1. Salicylates,
      2. Diuretics
      3. Alcohol
      4. Cyclosporine
      5. Ethambutol
      6. Pyrazinamide
  3. Combined Mechanism
    1. Glucose-6-phosphatase deficiency
    2. Fructose-1-phosphate aldolase deficiency
    3. Alcohol
Radiographic Features
  1. Cystic changes, well-defined erosions with sclerotic margins (often with overhanging bony edges), and soft tissue masses are characteristic radiographic features of advanced chronic tophaceous gout.
  2. Tophi appear as characteristic punched out cysts or deep erosions with over hanging bony edges (Martel’s or G’ sign).
Treatment (Ref. Hari. 18th ed., Pg-2838)
  1. Acute attack
    1. NSAID usually indomethacin. But aspirin is contraindicated because it raises the uric acid level.
    2. Colchicine: it inhibits granulocyte migration but can cause diarrhea
  2. Prophylaxis
    Allopurinol: It is a xanthine oxidase inhibitor

    Extra Edge Allopurinol is not used in a acute attack (LQ 2012)


  3. Uricosuric drugs: Probenecid, sulphinpyrazone.

    Recent Advances Losartan, fenofibrate, and amlodipine have some mild uricosuric effects.

Recent Advances New Drugs (Ref. Hari. 18th ed., Pg-2838)
  1. Febuxostat = Xanthine oxidase inhibitor drug (LQ 2012)
  2. Benzbromarone It is new uricosuric drug
  3. Rasburicase: It converts purine to allantois which is a water soluble compound. (LQ 2012)
Basic Biochemistry: Purine pathway. Allopurinol blocks the conversion of xanthine to uric acid. The urate oxidase rasburicase catalyses the oxidation of uric acid to allantoin, a highly water-soluble metabolite readily excreted by the kidney.


Extra Edge
All the diuretics are contraindicated in Gout because they cause hyperuricemia.
The only diuretic which has uricosuric effects so can be given in Gout is TIENELIC ACID!!!
Extra Edge: Pharmacotherapy
  1. Modulation of purine metabolism has pharmacotherapeutic value.
  2. Purine synthesis inhibitors inhibit the proliferation of cells, especially leukocytes.
  3. The inhibitors are
    1. Azathioprine, an immunosuppressant used in organ transplantation, autoimmune disease such as rheumatoid arthritis or inflammatory bowel disease.
    2. Mycophenolate mofetil is an immunosuppressant drug used to prevent rejection in organ transplantation; it inhibits purine synthesis by blocking inositol monophsophate dehydrogenase.
    3. Methotrexate indirectly inhibits purine synthesis by blocking the metabolism of folic acid (it is an inhibitor of the Dihydrofolate reductase).
    4. Allopurinol is a drug that inhibits the enzyme xanthine oxidase and, thus, lowers the level of uric acid in the body. So it is useful in the treatment of gout.
Pseudogout CPPD Deposition disease (AIIMS Nov 12) (Ref. Hari. 18th ed., Pg-2839)
The deposition of CPPD (Calcium Pyrophosphate Dihydrate ) crystals in articular tissues is most common in the elderly.
Conditions Associated with Calcium Pyrophosphate Dihydrate Disease (Ref. Hari. 18th ed., Table-332.2)
  1. Aging
  2. Disease-associated (4H)
    1. Primary Hyperparathyroidism
    2. Hemochromatosis (AIPG 2010)
    3. Hypophosphatasia
    4. Hypomagnesemia
    5. Chronic gout
  3. Post meniscectomy
  4. Hereditary

Extra Edge: The knee is the joint most frequently affected in CPPD arthropathy (Large joints).


  1. Calcium pyrophosphate dihydrate crystals, as seen in a fresh preparation of synovial fluid, illustrate rectangular, rod-shaped, and rhomboid weakly positive birefringent crystals
  2. Meniscal calcification is a important diagnostic feature of CPPD.
  1. NSAIDs
  2. By intraarticular glucocorticoid injection
Calcium Apatite Deposition Disease (Ref. Hari. 18th ed., Pg-2839)
  1. Apatite is the primary mineral of normal bone and teeth. 
  2. Abnormal accumulation can occur in areas of tissue damage (dystrophic calcification), in hypercalcemic or hyperparathyroid states (metastatic calcification), and in certain conditions of unknown cause
  3. Apatite aggregates are commonly present in synovial fluid in an extremely destructive chronic arthropathy of the elderly that occurs most often in shoulders (Milwaukee shoulder) and in a similar process in hips, knees, and erosive osteoarthritis of fingers.
  4. Diagnosis
    Definitive diagnosis of apatite arthropathy depends on identification of crystals from synovial fluid or tissue
  5. Treatment: NSAIDs or oral colchicine

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