Increased Uric Acid, Hyperuricemia – Causes, Symptoms
Hyperuricemia: a syndrome characterized by increased blood levels of monosodium urate (uric acid salt) due to increased production or reduced excretion.
Gout is a clinical form of persistent increased uric acid. Gout is a disease resulting from tissue deposits of monosodium urate crystals.
Normal values of uric acid
– 3-7 mg% in men;
– 3-6 mg% in women – pre-menopausal, after menopause the values are the same for both sexes.
Sources of uric acid
The main sources of uric acid are: de novo synthesis – the primary source, and diet (meat products contain large amounts of uric acid). A third of uric acid is eliminated through the intestines and two-thirds through the kidney. Thus, you can meet high levels of uric acid in either an increased intake or in an increased synthesis of the body or a decreased elimination (example: chronic renal failure).
Causes of increased uric acid
Hyperuricemia may be primary, due to inherited defects in the synthesis of purines or secondary to diseases or conditions.
Primary Hyperuricemia: idiopathic (possibly genetic), consists of an increased de novo production and/or decreased elimination.
Secondary hyperuricemia (due to another disease) may be:
1. high uric acid (hyperuricemia) through an increase in production like in chronic hemolysis (destruction of blood elements), chronic myolysis (destruction of muscle fibers), treatment with chemotherapy (which quickly destroys a large number of cancer cells that release many uric acid).
2. increased uric acid ( hyperuricemia ) by a decrease in elimination like in chronic renal failure or acidosis states.
Symptoms of increased uric acid
1. Asymptomatic hyperuricemia (persistent high uric acid without symptoms).
2. Acute attacks of gout, which consists of uric acid salt deposits in the joints, very painful.
Acute gouty arthritis (raised uric acid – manifest hyperuricemia) is more common in men and has an acute onset, brutal (minutes, hours) usually at night with strong joint pain and inflammation (redness, swelling, warmth ) and/or pyrexia.
Usually affects one joint. The most commonly affected joint is usually metatarsophalangeal joint of the finger I and tarsus joints, ankles, knees.
This form of hyperuricemia lasts from a few days (mild) to several weeks (severe).
Episodes of exacerbation are repeated and can be triggered by food excess, trauma, surgery, alcohol, myocardial infarction, stroke.
3. Chronic gout is the stage of hyperuricemia represented by gouty tofi. Tofi are localized in the articular cartilage and in underlying bone, in the synovium, tendons and other periarticular structures, in the epiphysis, subcutaneous tissue and renal interstitium.
Gouty tofi is currently present in 25-50 % cases of hyperuricemia. Tofi usually occur after a long period of evolution of hyperuricemia with repeated exacerbation of acute gouty arthritis. A gouty tofi looks like a little superficial growth, painless , yellowish-white on the fingers, palm, sole, which increases in volume and may ulcerate. At this stage of hyperuricemia there can occur chronic gouty arthropathy (with joint deformities).
A persistent high uric acid may have consequences on the kidney: kidney stones (20 % of patients with hyperuricemia), uric or urate nephropathy (may cause irreversible chronic renal failure).