Gout and pseudogout are the 2 most common crystal-induced arthropathies. They are debilitating illnesses in which recurrent episodes of pain and joint inflammation are caused by the formation of crystals within the joint space and deposition of crystals in soft tissue.[1, 2, 3] If untreated, these disorders can lead to joint destruction and renal damage. Rarely, gout can produce significant ocular findings.[4] The incidence of age-related macular degeneration (ARMD) is higher in patients with gout.[5]
Gout is inflammation caused by monosodium urate monohydrate (MSU) crystals. Pseudogout is inflammation caused by calcium pyrophosphate (CPP) crystals and is sometimes referred to as calcium pyrophosphate disease (CPPD).
Gout-related images are provided below.
Gout. Acute podagra due to gout in an elderly man. 
Gout. Radiograph of erosions with overhanging edges. 
Gout. Needles of urate on polarizing microscopy. Although gout is associated with hyperuricemia, the level of uric acid does not itself precipitate gout; rather, acute changes in the level of uric acid cause gout. Most individuals with hyperuricemia do not have gout, but if high uric acid levels go untreated, 90% of patients develop gout within 30 years. Hyperuricemia is found in 90% of individuals with gout, but it is also found in patients taking diuretics and even in those taking low doses of aspirin.
Primary gout is related to underexcretion or overproduction of uric acid. Secondary gout is related to myeloproliferative diseases or their treatment, therapeutic regimens producing hyperuricemia, renal failure, renal tubular disorders, lead poisoning, hyperproliferative skin disorders, enzymatic defects (eg, deficient hypoxanthine-guanine phosphoribosyl transferase, and glycogen storage diseases).[6]
Gout is definitively diagnosed based on the demonstration of urate crystals in aspirated synovial fluid. Classic radiographic findings may also be diagnostic. (See Workup).
Improvements in early diagnosis and the availability of definitive treatment have significantly improved the prognosis of gout, as evidenced by the declining incidence of disabling chronic tophaceous gout. However, tophaceous gout may still develop because of misdiagnosis, poor management, medication intolerances, and/or poor patient compliance.
Treatment of gout is important to relieve pain, prevent disease progression, and prevent tissue deposition of uric acid (eg, in the kidneys) that may produce kidney stones or urate nephropathy.[7] (See Treatment.)
Treatment of the acute phase of pseudogout is identical to that of gout. Unlike gout, however, no specific therapeutic regimen exists to treat the underlying cause of pseudogout, but colchicine and hydroxychloroquine are effective for prophylaxis.
Lowenhook described symptoms of gout in the 1600s. In 1848, Sir Alfred Garrod linked gout with hyperuricemia, but the pathophysiology of acute gouty arthritis was not described fully until 1962.
Since then, gout has been associated with a large number of different autoimmune and metabolic disorders. Specific therapies and prophylactic measures have been developed to address the underlying problem.
Pseudogout, which may be clinically indistinguishable from gout, was recognized as a distinct disease entity in 1962.
Gout is inflammation caused by monosodium urate monohydrate (MSU) crystals. Pseudogout is inflammation caused by calcium pyrophosphate (CPP) crystals and is sometimes referred to as calcium pyrophosphate disease (CPPD).
Gout-related images are provided below.
Gout. Acute podagra due to gout in an elderly man. Gout. Radiograph of erosions with overhanging edges. Gout. Needles of urate on polarizing microscopy. Although gout is associated with hyperuricemia, the level of uric acid does not itself precipitate gout; rather, acute changes in the level of uric acid cause gout. Most individuals with hyperuricemia do not have gout, but if high uric acid levels go untreated, 90% of patients develop gout within 30 years. Hyperuricemia is found in 90% of individuals with gout, but it is also found in patients taking diuretics and even in those taking low doses of aspirin. Primary gout is related to underexcretion or overproduction of uric acid. Secondary gout is related to myeloproliferative diseases or their treatment, therapeutic regimens producing hyperuricemia, renal failure, renal tubular disorders, lead poisoning, hyperproliferative skin disorders, enzymatic defects (eg, deficient hypoxanthine-guanine phosphoribosyl transferase, and glycogen storage diseases).[6]
Gout is definitively diagnosed based on the demonstration of urate crystals in aspirated synovial fluid. Classic radiographic findings may also be diagnostic. (See Workup).
Improvements in early diagnosis and the availability of definitive treatment have significantly improved the prognosis of gout, as evidenced by the declining incidence of disabling chronic tophaceous gout. However, tophaceous gout may still develop because of misdiagnosis, poor management, medication intolerances, and/or poor patient compliance.
Treatment of gout is important to relieve pain, prevent disease progression, and prevent tissue deposition of uric acid (eg, in the kidneys) that may produce kidney stones or urate nephropathy.[7] (See Treatment.)
Treatment of the acute phase of pseudogout is identical to that of gout. Unlike gout, however, no specific therapeutic regimen exists to treat the underlying cause of pseudogout, but colchicine and hydroxychloroquine are effective for prophylaxis.
Historical background
Gout is one of the oldest diseases in the medical literature.[8, 9] Since the time of the Greeks, many authors have written about gout as the result of personal excess; its association with a diet rich in meat and alcohol gained it the sobriquet, “the king of diseases and the disease of kings”. However, among the abstinent was John Milton, who lived a life of rigorous self-discipline and yet, to his anger and despair, suffered from what commonly was regarded as just punishment of the dissolute.Lowenhook described symptoms of gout in the 1600s. In 1848, Sir Alfred Garrod linked gout with hyperuricemia, but the pathophysiology of acute gouty arthritis was not described fully until 1962.
Since then, gout has been associated with a large number of different autoimmune and metabolic disorders. Specific therapies and prophylactic measures have been developed to address the underlying problem.
Pseudogout, which may be clinically indistinguishable from gout, was recognized as a distinct disease entity in 1962.
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