Просмотров: 9 778
Gout
Irina Alexandrovna Zborovskaya – doctor of medical sciences, professor,cathedral professor of hospital therapy with the course of clinical rheumatology of the doctors improvement faculty of Volgograd state medical university, director of the Federal Budgetary State Institution (FBSI) “Research and development institute of clinical and experimental rheumatology” of the RAMS, head of the regional Osteoporosis Center, presidium member of the Association of rheumatologists of Russia, member of the editorial boards of the magazines “Scientific and practical rheumatology” and “Modern rheumatology”
Definition. Gout is a common disorder of purine metabolism that can lead to elevated levels of serum uric acid. Gout is caused by excess stores of uric acid that accumulate mainly in tissues of the musculoskeletal system and organs. Gout typically causes inflammation in joints and other structures and can lead to their destruction and sclerosis.
Epidemiology. Gout is present in approximately 0, 3% of the general population in Europe and the USA. In Russia it is present in 0,1% of the general population. Gout makes up 5% of all rheumatic diseases in Europe and 7 – 8% of all rheumatic diseases in Russia. The incidence of gout is rising in the world. The prevalence for men is 95 – 98%. Gout is likely to present in men over 30 years. However, the prevalence for women has increased considerably over the past years. Early onset of the disease, development of complications, renal and cardiovascular involvement are the most common clinical manifestations of gout nowadays.
Aetiology and pathogenesis. Uric acid is a byproduct of purine metabolism. In plasma, extracellular and synovial fluid it is found mainly in salts (i.e.urates). When the pH is 7, 4, mono-sodium salt makes up 98% of uric acid. Mono-sodium salt is removed easily from plasma with the help of hemofiltration or dialysis. Uric acid does not bind with plasma proteins.
Purine synthesis and breakdown typically occur in all tissues, however, uric acid usually forms in the areas where xanthine oxidase is present, it is mainly in the liver and small intestine. The amount of uric acid in the body is determined by the ratio of the rates of uric acid synthesis to its excretion. The rate of uric acid synthesis depends on the amount of purines in the diet of a person and the rate of synthesis, regeneration and catabolism of purines. Normally 66 – 75% of uric acid is excreted with urine, and the rest – with faeces. Approximately 98 – 100% of uric acid from glomerular filtrate is reabsorbed in proximal tubules, half of which is secreted back in these tubules, and about 40% is reabsorbed again. As a result, only 8 – 12% of filtrated uric acid is excreted with urine.
The concentration of serum uric acid depends on age and sex. In adults it depends on height and body weight, blood pressure, renal function and alcohol consumption. Normal concentration of serum uric acid in women of childbearing age and in adult men is 360 and 416 mcmol/l (6 and 7 mg%), respectively. In postmenopausal women the concentration of serum uric acid increases and equals the concentration, which is typical of men.
More common causes of gout include hereditary predisposition and alimentary factors. The incidence of hyperuricemy is 2 – 13,2%. The higher the concentration of serum uric acid, the more likely gout is to develop. As a rule, the first attack of gout develops after 20 – 40 years following the onset of hyperuricemy. However, the mere presence of hyperuricemy is not sufficient to cause the onset of gout as only 10% of patients with hyperuricemy develop gout.
The factors which contribute to deposition of urates and inflammation of joints in people with hyperuricemy remain unknown (with the exception of family cases). Hyperuricemy typically develops due to a variety of factors. They are the following:
1. Factors contributing to increased synthesis of uric acid
- Specific enzyme defects, enhanced nucleoprotein metabolism
- Excessive intake of food which is rich in purines; excessive alcohol, fructose consumption
- Myeloproliferative and lymphoproliferative syndromes, polycythemia
- Cytotoxic drugs, vitamin B12
- Disorder of renal function and reduction of extracellular fluid volume
- Drugs which slow down excretion of uric acid
- Fasting and accumulation of ketone compounds
- Arterial hypertension
- Endocrine diseases: hypothyroidism, hyperparathyroidism, ketoacidosis.
Classification
1. According to aetiology and pathogenesis, the following types of gout are singled out:- Primary (idiopathic) gout
- Secondary gout (associated with some other disease or drug-induced)