Hyperuricemia is a blood disorder defined by too much uric acid in the circulation. It is triggered either by an overproduction of uric acid or by a decrease in renal elimination. Over time, hyperuricemia can precipitate uric acid to urate crystals – uric acid salts. About 10% of hyperuricaemia cases are associated with gout. Heredity and overeating have predominant roles in hyperuricemia.

Definition of hyperuricemia

Hyperuricemia is a blood disorder defined by too much uric acid in the circulation.

Uric acid is normally found in the blood at a level of less than 70 milligrams per liter (mg / L). It comes from the permanent physiological destruction of proteins from food – food purines which change under the effect of the action of enzymes – or from the physiological destruction of cells and their DNA. Uric acid is constantly regulated by the kidney.

Hyperuricemia is triggered either by an overproduction of uric acid or by a decrease in renal elimination. Over time, hyperuricemia can precipitate uric acid to urate crystals (salts of uric acid).

Types d’hyperuricémies

There are three types of hyperuricemia:

• Primary, hereditary hyperuricemia;
• Secondary hyperuricemia, linked to a pathology;
• Idiopathic hyperuricemia, the cause of which is not necessarily characterized.

Causes of hyperuricemia

Hyperuricaemia often has multiple causes which combine increased production of uric acid and reduced elimination from the kidneys.

The causes of increased uric acid production are as follows:

• An enzymatic deficit with accelerated synthesis of purines;
• Excessive food intake of purines;
• An increase in the metabolism of purines: myelo / lymphoproliferative syndromes, psoriasis…;
• Enzymatic deficiency with acceleration of purine synthesis: Lesh Nyhan syndrome (hereditary disease of purine metabolism) or hypoxanthine-guanine phosphoribosyltransferase deficiency (HGPRT: enzyme involved in the purine rescue pathway);
• An acceleration of the degradation of Adenosine-TriphosPhate (ATP), a key molecule of cellular energy;
• Chemotherapy.

The causes of the decreased excretion of uric acid are as follows:

• Familial hyperuricaemic nephropathy: rare inherited kidney disease;
• Chronic kidney disease;
• An inhibition of tubular urate secretion: lactic acidosis, ketoacidosis (a complication in people with type 1 diabetes consisting of a build-up of toxic substances called ketones that make the blood too acidic), preeclampsia (high blood pressure without protein in urine), low dose salicylates, thiazides (diuretic drugs), ciclosporin (immunosuppressive agent);
• An increase in tubular reabsorption of urates: dehydration, diuretics, insulin resistance.

Diagnosis of hyperuricemia

Hyperuricemia is effective when the uric acid level exceeds 70 mg / L in the blood: it is measured using a blood test.

People affected by hyperuricemia

A hereditary predisposition to hyperuricaemia is found in 30% of patients. About 10% of hyperuricaemia cases are associated with gout.

Factors favoring hyperuricemia

Other factors can promote the occurrence of hyperuricaemia:

• Obesity;
• Acute alcoholism;
• A diet too rich in purines;
• The pregnancy ;
• Exposure to lead;
• Exposure to beryllium;
• Hyperparathyroidism (excessive secretion of thyroid hormones);
• Taking certain medications

No symptoms

In the majority of cases, hyperuricaemia is asymptomatic.

Renal colic

Renal colic is due to tension in the kidney, itself linked to the formation of urate stones in the urinary tract (urolithiasis).

Gout attack

Gout is one of the consequences of hyperuricemia: in the presence of sufficient local acidity in the medium, the microcrystals of uric acid precipitate in the joints leading to joint pain of the inflammatory type. Gout preferentially affects the big toes or the front of the foot and associates pain, redness and swelling.

Gouty Tophus

Tophi, subcutaneous deposits of uric acid crystals surrounded by inflammatory cells, are associated with gout: they are mainly deposited in the pinna of the ear, fingers and feet and release, when they s’ evacuate a whitish paste somewhat reminiscent of sebum.

Other symptoms

• Lower back pain;
• Presence of blood in the urine.

The treatment of asymptomatic hyperuricemia is based on a diet low in purines associated with good hydration: reduction of proteins of animal origin, alcoholic and sweet drinks, certain vegetables and legumes.

When symptoms exist, this diet should be combined with medical treatment which will be assessed on a case-by-case basis by the attending physician:

• Reduction in nucleic acid synthesis: drugs in which the active principle is allopurinol combined with colchicine to prevent gout attacks often triggered by the initiation of this treatment;
• Inhibition of renal uric acid reabsorption: drugs in which the active substance is benzbromarone;
• Enzymatic treatment is essentially used during acute uric acid outbreaks, especially in oncology.

In order to prevent hyperuricemia and / or limit symptoms, it is important to:

• Reduce proteins of animal origin: meat, poultry, fish, liver, kidneys, hearts, gizzards, sweetbreads, meat extracts, yeast extracts, game;
• Reduce alcoholic beverages: white spirits (strong spirits, white wines / champagnes) and beers and derivatives;
• Reduce sugary drinks (such as soda, lemonades, etc.);
• Reduce certain vegetables and legumes: peas, beans, spinach, lentils;
• Consume water rich in bicarbonates (carbonated);
• Stay hydrated.