Abstract |
In most cases (98-99â%) primary hyperuricemia is caused by impaired renal excretion of uric acid. Overproduction of uric acid is rare. Secondary hyperuricemia has to be differentiated from primary forms. Clinical manifestations of hyperuricemia are acute inflammatory arthritis, tenosynovitis, bursitis, chronic arthropathy and accumulation of urate crystals in the form of tophaceous deposits. In addition renal complications can occur. Pathophysiology and diagnosis of gout were described. Treatment of gout has two goals: Treatment of the acute gout attack, to terminate pain and disability and treatment of hyperuricemia by lifestyle modification and with urate lowering drugs. A serum uric acid value below 6â
mg/dl (360â
µmol/L) should be achieved.
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Authors | Wolfgang Gröbner |
Journal | Deutsche medizinische Wochenschrift (1946)
(Dtsch Med Wochenschr)
Vol. 140
Issue 21
Pg. 1615-26
(Oct 2015)
ISSN: 1439-4413 [Electronic] Germany |
Vernacular Title | Hyperurikämie und Gicht. |
PMID | 26488103
(Publication Type: Case Reports, English Abstract, Journal Article)
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Copyright | © Georg Thieme Verlag KG Stuttgart · New York. |
Chemical References |
- Allopurinol
- Furosemide
- Colchicine
|
Topics |
- Allopurinol
(therapeutic use)
- Arthritis, Gouty
(diagnosis, drug therapy, etiology)
- Colchicine
(therapeutic use)
- Diagnosis, Differential
- Drug Therapy, Combination
- Furosemide
(therapeutic use)
- Gout
(diagnosis, drug therapy, etiology)
- Humans
- Hyperuricemia
(diagnosis, drug therapy, etiology)
- Life Style
- Male
- Middle Aged
|