hyperuricaemia

see also:

• uric acid
• gout
• uricosuric agents
• oncology

• whilst low serum urate levels are associated with lower muscle mass, chronic illness and thus is associated with higher morbidity¹⁾, high uric acid (urate) levels (hyperuricaemia) is associated with gout and may also be caused by oncologic conditions

• the major cause of the rising prevalence in Western societies is perhaps the increasing intake of fructose
• in general hyperuricaemia is caused by either or combined:
  • decreased renal excretion
  • increased uric acid production
    • increased fructose intake - this generates uric acid and may reduce renal excretion
    • acute tumour lysis syndrome
    • etc
  • high purine intake
    • some people should avoid high intakes of purine containing proteins (eg. red meat, seafood) due to increased production of uric acid and risk of hyperuricaemia²⁾ * GIT microbiota affects on GIT uric acid and purine metabolism as well as uric acid absorption ===oncologic settings:=== *acute tumour lysis syndrome: post chemo of acute leukaemias and lymphomas *multiple myeloma *disseminated metastatic carcinoma *hydroxyurea ===associated non-malignant conditions=== *gout *hyperparathyroidism *psoriasis *sarcoidosis  *renal failure of any cause + diuretics * elevated serum uric acid levels are associated with the onset of chronic kidney disease [OR = 2.35 (1.59–3.46)] ³⁾ * associations but causal link as yet unproven: *atrial fibrillation *hypertension * for every 1 mg/dl increase in serum UA, the relative risk of HTN increased 1.13 times ⁴⁾ * diabetes mellitus * asymptomatic hyperuricemia is an independent risk factor for T2DM and insulin resistance [HR = 1.87 (1.33–2.62) and 1.36 (1.23–1.51) ⁵⁾ * acute myocardial infarction (AMI/STEMI/NSTEMI) * patients with acute myocardial infarction showed that patients with hyperuricemia are more likely to have major adverse cardiac events [RR = 3.44 (2.33–5.08)] and in-hospital mortality [RR = 2.10 (1.03–4.26)] ⁶⁾ * PFOS exposure ====summary:==== *serious and if recognised early, results in significant reduction in morbidity *pathogenesis: increased production, decreased excretion *major source is cell breakdown *major excretory PW is renal *with increased uric acid in kidneys ⇒ crystals in distal tubules ⇒ intrarenal obstruction ⇒ ARF *chronically elevated levels: renal colic, obstructive uropathy, CRF =====May cause 3 types of renal disease:===== *acute hyperuricaemic nephropathy *uric acid nephrolithiasis *gouty nephropathy =====symptoms & signs in the oncologic patient:===== *+/- asymptomatic *underlying malignancy *with symptoms of tumour lysis syndrome *acute oliguria following chemotherapy *renal colic ====investigations:==== *serum uric acid *U + E =====management in the oncologic patient:===== *pretreat hyperuricaemia- prior to chemo or XRT *hydration *consider Na Bicarbonate (alkalinise urine), diuretics *mannitol *peritoneal dialysis/haemodialysis =====management in the patient with gout===== *see gout**