Want to know what are the causes of gout?
Yes, you have chosen the right place. Let’s know what are the causes of gout.
Let’s start with genetics. Polymorphisms in several genes that are associated with gout can cause gout. The most important of which is SLC2A9. This regulates urate excretion by the kidney. Impaired renal excretion of urate also accounts for the occurrence of hyperuricaemia in chronic renal failure. Treatment with thiazide diuretics also cause gout.
Other risk factors for gout include metabolic syndrome,
high alcohol intake (predominantly beer,which contains guanosine),
a diet relatively high in red meat or fructose or relatively low in vitamin C or coffee,
and lead poisoning (saturnine gout).
The association between osteoarthritis and gout is thought to be due to reduction in levels of proteoglycan and other inhibitors of crystal formation in osteoarthritic cartilage, predisposing to crystal formation.
Some patients develop gout because they over produce uric acid. The mechanisms are poorly under stood, except in the case of a few rare disorders, in which gout is inherited in a Mendelian manner as the result of mutations in genes responsible for purine synthesis. Lesch–Nyhan syndrome for example, is an Xlinked recessive form of gout that is also associated with mental retardation, selfmutilation and choreo athetosis. Such conditions should be suspected if other clinical features are present or there is an early age at onset with a positive family history. Severe hyperuricaemia can also occur in patients with leukaemia undergoing chemotherapy due to increased purine turnover.
Primary hyper uricemia: These cases appear to be innate, neither secondary to an acquired disorder nor the result of a subordinate manifestation of an inborn error that leads initially to a major disease unlike gout. Some cases of primary gout have a genetic basis where others do not.
Secondary hyper uricemia: These cases develop in the course of another disease or as a consequence of drug use.
Idiopathic: In these cases, a more precise classification cannot be assigned.
|Primary hyper uricemia|
|A. Increased production of purine|
|2.Specific enzyme defects (e.g. Lesch Nyhan syndrome, glycogen storage diseases, Kelley-Seegmiller syndrome)|
|B. Decreased renal clearance of uric acid (Unknown cause 90% of primary gout)|
|A. Increased catabolism and turnover of purine|
|1. Myeloproliferative disorders|
|2. Lymphoproliferative disorders|
|3. Carcinoma and sarcoma (disseminated)|
|4. Chronic hemolytic anemias|
|5. Cytotoxic drugs|
|7. High fructose intake, high intake of Red meat, Seafood, offal|
|B. Decreased renal clearance of uric acid|
|1. Intrinsic kidney disease|
|3. Drug-induced (eg, thiazides, low-dose aspirin, Ciclosporin, Pyrazinamide)|
|4. Hyperlacticacidemia (eg, lactic acidosis, alcoholism)|
|5. Hyperketoacidemia (eg, diabetic ketoacidosis, starvation)|
|6. Diabetes insipidus (vasopressin-resistant)|
|7. Bartter syndrome|