Crystalline Arthritis

Crystalline Arthritis is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

Definition

Crystalline arthritis is caused by deposition of microcrystals in joints and periarticular tissues. Common types of crystalline arthritis are gout, pseudogout, and apatite disease.

Classification

  • Clinical phases of gout can be divided into asymptomatic hyperuricemia, acute gouty arthritis with intercritical asymptomatic periods, and chronic arthritis.
  • Asymptomatic hyperuricemia is defined as serum uric acid levels >7 mg/dL without arthritis or evidence of urate nephropathy.
  • Men are much more commonly affected by gouty arthritis than women. Most premenopausal women with gout have a family history of the disease.

Etiology

  • Gout is characterized by hyperuricemia that can be because of underexcretion or overproduction of uric acid. Urate crystals may be deposited in the joints, subcutaneous tissues (tophi), and kidneys. Intrinsic renal disease impairs excretion of uric acid. Several genetic polymorphisms are also associated with changes in uric acid excretion. Medications such as loop diuretics, low-dose aspirin, cyclosporine, and ethanol all interfere with renal excretion of uric acid.

Starvation, lactic acidosis, dehydration, preeclampsia, and diabetic ketoacidosis also can induce hyperuricemia. Overproduction of uric acid occurs in myeloproliferative and lymphoproliferative disorders, hemolytic anemia, and polycythemia. Overproduction may also occur because of intake of purine rich diet.

  • Pseudogout results when calcium pyrophosphate dihydrate crystals deposited in bone and cartilage are released into synovial fluid and induce acute inflammation. Risk factors include older age, advanced OA, neuropathic joint, gout, hyperparathyroidism, hemochromatosis, diabetes mellitus, hypothyroidism, and hypomagnesemia.

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General Principles

Definition

Crystalline arthritis is caused by deposition of microcrystals in joints and periarticular tissues. Common types of crystalline arthritis are gout, pseudogout, and apatite disease.

Classification

  • Clinical phases of gout can be divided into asymptomatic hyperuricemia, acute gouty arthritis with intercritical asymptomatic periods, and chronic arthritis.
  • Asymptomatic hyperuricemia is defined as serum uric acid levels >7 mg/dL without arthritis or evidence of urate nephropathy.
  • Men are much more commonly affected by gouty arthritis than women. Most premenopausal women with gout have a family history of the disease.

Etiology

  • Gout is characterized by hyperuricemia that can be because of underexcretion or overproduction of uric acid. Urate crystals may be deposited in the joints, subcutaneous tissues (tophi), and kidneys. Intrinsic renal disease impairs excretion of uric acid. Several genetic polymorphisms are also associated with changes in uric acid excretion. Medications such as loop diuretics, low-dose aspirin, cyclosporine, and ethanol all interfere with renal excretion of uric acid.

Starvation, lactic acidosis, dehydration, preeclampsia, and diabetic ketoacidosis also can induce hyperuricemia. Overproduction of uric acid occurs in myeloproliferative and lymphoproliferative disorders, hemolytic anemia, and polycythemia. Overproduction may also occur because of intake of purine rich diet.

  • Pseudogout results when calcium pyrophosphate dihydrate crystals deposited in bone and cartilage are released into synovial fluid and induce acute inflammation. Risk factors include older age, advanced OA, neuropathic joint, gout, hyperparathyroidism, hemochromatosis, diabetes mellitus, hypothyroidism, and hypomagnesemia.

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