Hyperuricemia is classified into :
Primary(Genetic)
I- Metabolic over production
• Idiopathic, 10-20% of patients with primary gout.
• Enzymatic defects. e.g:
(Hypoxanthine - guanine - phosphoribosyl -transferase) which is essential for reconversion of guanine, hypoxanthine into their mother substance so this enzymatic defect ===> accumulation of uric acid.
- Uric acid +++
- Choreoathetosis
- Mental retardation and self mutilation
• Glucose 6 phosphatase deficiency.
II-Renal
• Idiopathic under excretion (Isolated tubular defect), more than two thirds of individuals with primary gout.
Secondary
I- Metabolic over production.
• ++ nucleic acid. turnover e.g.
- Haemolysis.
- Myelo or Iympho proliferative diseases.
• Alcohol (diminished clearance)
II-Renal
• Acute or chronic renal failure.
• Altered tubular handling by drugs. e.g thiazides, low dose aspirin and cyclosporine ===> decrease renal excretion of uric acid.
• Lactic acidosis, alcohol.
• Lead nephropath has long been associated with out (saturnine gout).
One third of the body uric acid is derived from dietary sources and 2/3 from endogenous purine metabolism.
• One third of uric acid produced / day excreted through GIT.
• Two thirds of uric acid produced / day excreted through kidney.
• Over production of uric acid detected by excretion of> 1100 mg 1 day.
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Primary(Genetic)
I- Metabolic over production
• Idiopathic, 10-20% of patients with primary gout.
• Enzymatic defects. e.g:
(Hypoxanthine - guanine - phosphoribosyl -transferase) which is essential for reconversion of guanine, hypoxanthine into their mother substance so this enzymatic defect ===> accumulation of uric acid.
Lesh-Nyhan syndrome
- X linked recessive.- Uric acid +++
- Choreoathetosis
- Mental retardation and self mutilation
• Glucose 6 phosphatase deficiency.
II-Renal
• Idiopathic under excretion (Isolated tubular defect), more than two thirds of individuals with primary gout.
Secondary
I- Metabolic over production.
• ++ nucleic acid. turnover e.g.
- Haemolysis.
- Myelo or Iympho proliferative diseases.
• Alcohol (diminished clearance)
II-Renal
• Acute or chronic renal failure.
• Altered tubular handling by drugs. e.g thiazides, low dose aspirin and cyclosporine ===> decrease renal excretion of uric acid.
• Lactic acidosis, alcohol.
• Lead nephropath has long been associated with out (saturnine gout).
One third of the body uric acid is derived from dietary sources and 2/3 from endogenous purine metabolism.
• One third of uric acid produced / day excreted through GIT.
• Two thirds of uric acid produced / day excreted through kidney.
• Over production of uric acid detected by excretion of> 1100 mg 1 day.
Read Also :