Secondary hyperuricemia, or gout that is a minor clinical manifestations, secondary to any genetic or acquired pathological process. Clinical mainly divided into two categories: A. generate excessive uric acid 1) excessive amount of high-purine food intake, 2) bone marrow proliferative diseases: multiple myeloma, 3) lymphoproliferative disease: infectious mononucleosis Cell Histiocytosis, 4) hemolytic anemia, 5) tumors, 6) psoriasis, 7) the cumulative lying liver disease: found I, III, V, VI, 8) fructose intake, 9) is not hereditary fructose Tolerance, 10) hypoxemia and organizations hypoperfusion, 11) intense muscle movement, 12) acute and chronic alcohol poisoning, B. reduce uric acid excretion 1) renal insufficiency, 2) ketoacidosis, 3) lactic acid Acidosis, 4) tubular absorb increased uric acid salts, 5) dehydrating agent and diuretic, 6) hyperparathyroidism, 7) parathyroid mechanism may be, 8) hypothyroidism, 9) hypertension, 10) Drugs: ethambutol, pyrazinamide, nicotinic acid, acetyl acid water Yang, 11) lead poisoning. 12) patients with cancer chemotherapy and radiotherapy, 13) adrenal mechanism may be, 14) renal diabetes insipidus, 15) hunger.
