Of hyperuricemia (HU; synonyms: Uric acid metabolism disorder; ICD-10-GM E79.0 Hyperuricemia without signs of inflammatory arthritis or tophic gout: asymptomatic hyperuricemia) is when there is an elevated concentration of uric acid in the blood above normal values. Gout (synonyms: Gout diathesis; Gout; Omagra; Podagra; Uratnephropathy; Uricopathy; ICD-10-GM M10.9-: Gout, unspecified) is used when arthritis urica (uric acid-related bone inflammation) or topical gout (gouty tophi/urate deposition in soft tissue or cartilage) is present. Gout is one of the rheumatic diseases.According to the S2e guideline, gout is associated with hyperuricemia, which is defined as an elevation of serum uric acid of ≥ 6.8 mg/dl (408 µmol/l). Below, hyperuricemia and gout are described in a joint chapter. In pre-menopausal (menopausal) women, hyperuricemia is said to occur when the uric acid level exceeds 5.7 mg/dl; in men, it occurs only when the concentration exceeds 7 mg/dl. In the international literature, hyperuricemia is spoken of independently of gender when the uric acid concentration is more than 6.5 mg/dl (> 390 μmol/dl).Hyperuricemia whose cause is not detectable by clinical methods is referred to as primary. Secondary gout occurs as a result of other diseases or disorders associated with increased purine synthesis or decreased purine degradation in the presence of high cellular turnover, resulting in an increase in the amount of uric acid. Disorders of kidney function or kidney diseases in which the excretory capacity is reduced can also be the cause of secondary hyperuricemia/gout. Based on the cause, the following forms of hyperuricemia are distinguished:
- Primary familial hyperuricemia (idiopathic or familial hyperuricemia):
- Disorder of renal uric acid excretion – 99% of cases; appears to be polygenically inherited and is quite common (disease of affluence)
- Increased synthesis of uric acids in the presence of a defined enzyme defect (e.g., a deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase; HGPRTase for short) <1%.
- Secondary hyperuricemia – acquired as a result:
- Decreased renal excretion of uric acid: e.g. chronic renal failure (process leading to a slowly progressive reduction in renal function).
- Increased uric acid formation: e.g. hemoblastoses (collective term for malignant diseases of the hematopoietic system, e.g. leukemias) or too high purine intake through food (meat, beans).
Symptomatic hyperuricemia with deposition of urate crystals in joints, tissues or organs is called gout.Gouty arthritis is the most common form of arthritis in Germany. Sex ratio: males to females is 4: 1 to 9: 1. Premenopausal females are protected by the uricosuric (promoting uric acid excretion) estrogens. Peak incidence: the maximum incidence of gout is in the 40th year of life in men and around the 50th to 60th years of life in women.The average age for the first attack of gout is between the 30th and 45th years of life in men and between the 50th and 60th years of life in women. The prevalence (disease incidence) for hyperuricemia is 20% and for gout in men is 1-2% (in Western countries). The prevalence for gout depends on age and gender and shows an increase worldwide. In the over-65 age group, the prevalence for symptomatic gout is 7%. In contrast, the prevalence of gout in women increases only after the age of 85 years (2.8%). In affluent countries, approximately 20% of men have hyperuricemia. Course and prognosis: Hyperuricemia that has been present for many years may be asymptomatic or may lead to gout and associated complications such as arthritis urica (gouty arthritis; inflammation of the joints caused by uric acid; occurs as monarthritis/inflammation of one joint) due to the secretion of salts of uric acid in various parts of the body. In one study, only 22% of those with uric acid levels ≥ 9 mg/dl (535 µmol/l) developed an attack of gout (within 5 years). The earlier the disease is diagnosed, the better the prognosis. If the disease has already taken a chronic course and changes in the joints are detectable, movement restrictions are to be expected.Men with gouty arthritis even have an increased cardiovascular risk (risk of cardiovascular disease). If the kidneys are damaged (gouty kidney; nephrolithiasis (kidney stones); urate nephropathy (gouty nephropathy)), dialysis may even be required. Patients who do not receive uric acid-lowering treatment after an initial gout attack experience a recurrence within the 1st year in 62% of cases, 78% within 2 years, and 89% within 5 years. Comorbidities (concomitant diseases): gout is associated (linked) with an increased risk of type 2 diabetes mellitus. Other relevant comorbidities include: cardiovascular disease (coronary artery disease (CAD), heart failure/heart failure, atrial fibrillation), nephrologic disease (renal failure/kidney failure, nephrolithiasis/kidney stones), dyslipidemia (hypercholesterolemia, hypertriglyceridemia), and osteoporosis/osteopenia (reduction in bone density; precursor to osteoporosis) (due toGlucocorticoids); furthermore, bronchial asthma, chronic obstructive pulmonary disease (COPD), and chronic atrial fibrillation (AF).
