[Pathophysiology and treatment of secondary hyperuricemia].
Hyperuricemia caused secondly from acquired disorders which affect production or excretion of uric acid is defined as secondary hyperuricemia. Many conditions are associated with this type of hyperuricemia and are classified into three types according to the underlying pathophysiology, including accelerated purine nucleotide degradation, ATP breakdown and purine de novo biosynthesis as overproductive type, use of drugs affecting renal urate handling and renal insufficiency as underexcretion type, or overintake of alcohol or fructose as mixed type. Determining uric acid clearance and urate excretion is important for pointing out original disorder; however, sometimes the result from correcting causal factor should be waited for to fix up a final diagnosis. Anti-hyperuricemia agents are used according to the pathophysiology.
Tsutani
Hiroshi
H
National Hospital Organization Awara Hospital.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000437:Alcoholism / Q000150:complications; D000493:Allopurinol / Q000627:therapeutic use; D004232:Diuretics / Q000009:adverse effects; D006074:Gout Suppressants / Q000627:therapeutic use; D006801:Humans; D033461:Hyperuricemia / Q000145:classification / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy*; D007041:Hypoxanthine Phosphoribosyltransferase / Q000502:physiology; D011685:Purine Nucleotides / Q000378:metabolism; D051437:Renal Insufficiency / Q000150:complications; D014527:Uric Acid / Q000378:metabolism
D004232:Diuretics; D006074:Gout Suppressants; D011685:Purine Nucleotides; D014527:Uric Acid; D000493:Allopurinol; D000255:Adenosine Triphosphate; D007041:Hypoxanthine Phosphoribosyltransferase