1. Definitions
Gout (gout) is a group of metabolic diseases caused by purine metabolism disorders and/or decreased uric acid excretion, accompanied by damage to joints, kidneys and other organs. The clinical characteristics of gout are hyperuricemia, recurrent acute arthritis, tophi formation, tophi chronic arthritis and joint deformity, and chronic interstitial nephritis and kidney stones are involved.
2. Epidemiology
In recent years, with the prosperity of the motherland, the continuous improvement of people's living standards and the change of dietary structure, the incidence of hyperuricemia and gout in mainland China has increased rapidly. With the improvement of material living standards, gout, a "disease of wealth" that only had high-ranking officials and nobles in ancient times, is now often encountered around us. The onset of gout has obvious age characteristics, primary gout is most common in middle-aged people, 40-50 years old is the peak of the disease, the ratio of male to female prevalence is about 20:1, female patients are mostly onset after menopause, more in coastal areas than in the interior, more in cities than in rural areas; at present, due to the higher and higher purine content in the diet, the age of onset of gout is getting younger and younger, gout patients in their twenties are not uncommon in clinical practice, and there are even juvenile patients with secondary gout.
3. Etiology
Gout can be divided into two main categories: primary and secondary. The etiology and pathogenesis of primary gout are not fully understood, but are related to the following factors:
(1) Purine metabolism disorders lead to increased uric acid production
Hypoyellow guanine phosphoribosyltransferase (HGPRT) deficiency and Lesh-Nyhan syndrome, increased phosphoribospyrope pyropurine (PRPP) synthase activity, hemolysis, myeloproliferative disorders, polycythemia, psoriasis, rhabdomyolysis, strenuous exercise, alcohol consumption, obesity, and purine-rich foods can all lead to hyperurate production.
(2) Decreased uric acid excretion
It is the main mechanism of the pathogenesis of the disease, and the patients caused by this factor account for about 90% of the total number of patients. Many diseases (renal insufficiency, polycystic kidney disease, diabetes insipidus, hypertension, acidosis, hypothyroidism, hypoparathyroidism, gestational hypertension, Batter syndrome, Down syndrome, etc.) and drugs (low-dose aspirin, diuretics, levodopa, ethambutol, pyrazinate, niacinamine, cyclosporine, etc.) can cause low urate excretion.
(3) Mixed factors
Glucose-6-phosphatase and fructose-1-phosphoalact deficiency, ethanol, shock and other factors can cause hyperurate production and reduce urate excretion.
(4) Environmental factors
The incidence of gout has obvious age characteristics, which are related to ethnicity, dietary structure, mental factors, high blood sugar, high insulin and high triglyceride glycerol.
(5) Genetic factors 10%-20% have a positive family history, and it is now considered that primary gout is inherited dominantly on sex chromosomes.
(6) Genetics Gout and hyperuricemia are complex polygenic genetic diseases. Gene-related factors play a role in the pathogenesis of gout. For example, genes related to increased uric acid synthesis include HPRT gene and PRS gene, and genes related to decreased uric acid excretion include human urate transporter gene.
Fourth, clinical manifestations
There are four main stages in the development of gout:
(1) Asymptomatic hyperuricemia
The normal range of serum uric acid is 150 to 417 micromol/L for men and 100 to 357 micromol/L for premenopausal women, and the range for postmenopausal women is about the same as that for men. Hyperuricemia is usually defined as a serum uric acid value > 420 micromol/L. Hyperuricemia is the main biochemical basis of gout. The higher the serum uric acid, the greater the risk of developing gout, but not all patients with hyperuricemia will progress to gout. Many patients have hyperuricemia that has been present for many years before the first gout attack, and may even be asymptomatic for life, becoming asymptomatic hyperuricemia, which is called gout only when arthritis occurs.
(2) Acute attack of gout
The first attack of gout is usually in a single joint, but severe polyarticular gout can also be the first manifestation of the disease. About half of the patients, the first metatarsophalangeal joint is the most common joint for gout attacks, and most of them occur suddenly at night, especially at 1-2 a.m., showing symptoms of acute arthritis, with local redness, swelling, heat, pain, limited movement, and systemic symptoms such as fever, leukocytosis and increased erythrocyte sedimentation rate.
(3) Inter-attack period of gout
After the first attack of gout subsides, it begins to enter the interstitial period of gout attacks. During this period, the joints can return to normal.
(4) Chronic tophi gout
Tophi forms in the interval of severe hyperuricemia. Tophi tends to occur in specific districts, such as olecranon, distal interphalangeal joints, wrist joints, etc., and the longer the course of the disease, the more opportunities for tophi to form. The appearance of tophi is a raised yellow-white vegetation of different sizes, and the tophi located in the thin part of the skin is easy to break down and form a fistula, which can be discharged with white powdery uric acid crystals, and the tissues around the fistula are chronic granulomas that are not easy to heal. Urate deposition in the joints can cause the destruction of bone and cartilage in the joints, causing pain, swelling, deformity and impaired joint function, forming tophi chronic arthritis.
(5) Renal lesions
About 40% of long-term patients develop renal impairment, which mainly manifests in:
Gouty nephropathy Urate crystals can be deposited in kidney tissue to form interstitial nephritis, which can be clinically manifested as renal pain, proteinuria, microscopic hematuria, and finally uremia.
Acute obstructive nephropathy Sudden and significant increase in blood and urinary urate, which can form urate crystals, which are deposited in renal tubules, collecting ducts, renal pelvis, and urinary catheters, causing urinary tract obstruction, manifested as oliguria, anuria, and acute renal failure.
Urate uric tract stones are formed due to the deposition of urate concentration, which can cause renal colic, hematuria, pyelonephritis, hydronephrosis, etc.
(6) Skin lesions
Dermatological features of gout include nodular tophi, excretory tophi, chronic ulcers, and panniculitis.
5. Treatment
The principles of treatment of gout are: control hyperuricemia, prevent urate deposition, quickly stop the onset of acute arthritis, prevent the formation of uric acid stones and renal damage.
(1) General handling
Stay away from foods high in alcohol and purines: sardines, heart, liver, kidneys, scallops, shrimp, chicken, meat, beef, mushrooms, peanuts, spinach, rice, green beans, drink fruit juice drinks containing fructose carefully, drink plenty of water appropriately, exercise regularly (strenuous exercise should be avoided, because strenuous exercise may induce gout arthritis attacks), maintain an appropriate weight, and proper weight loss for obese people can help reduce uric acid levels.
(2) Treatment of acute exacerbations
1. Control the patient's symptoms, reduce inflammation and reduce pain:
a. Colchicine mainly controls the occurrence and development of inflammation by inhibiting the chemotaxis of inflammatory cells, but the side effects of high-dose colchicine are greater, and it has been gradually replaced by low-dose therapy. At present, due to the side effects of colchicine, it has gradually withdrawn from the clinical first choice. Clinical discontinuation indicators: inflammation and pain are significantly relieved or the patient has severe gastrointestinal reactions (nausea, vomiting, diarrhea, etc.).
b. Non-steroidal anti-inflammatory drugs (NSAIDs) have replaced colchicine as the first-line drug for controlling acute gout attacks with significant relief of pain symptoms within 24 hours. However, the adverse reactions of non-steroidal anti-inflammatory drugs in the digestive tract are more common, and patients with peptic ulcers are contraindicated.
c. Glucocorticoids and adrenocorticotropic hormone are mainly used for patients with acute attacks of gout and colchicine and non-steroidal anti-inflammatory drugs that are ineffective or intolerant.
2. Alkalinization of urine: assist urate excretion, and the target of urine PH value is 6.2-6.9, such as sodium bicarbonate tablets or potassium citrate.
3. Topical medications: such as flurbiprool patch, piroxicam patch, voltarin ointment.
In summary, nonsteroidal anti-inflammatory drugs (NSAIDs) are recommended for acute gouty arthritis first, followed by oral or local intra-articular steroid injections, and colchicine is considered a third choice because of the proximity of the effective dose to the toxic dose.
(3) Drugs for the treatment of hyperuricemia
Urate-lowering drugs mainly include uric acid-stimulating excretion drugs and xanthine oxidase inhibitors, oral urate-lowering drugs to promote uric acid excretion, such as benzbromarone, note that urinary stones should not be used. Inhibits uric acid production, such as febuxostat, allopurinol.
(4) Physical therapy
Physiotherapy is an adjunctive treatment that should generally be used in the chronic phase and should be temporarily discontinued in patients who are experiencing an acute attack of fever or joint inflammation, such as electrotherapy, thermotherapy, ultrasound, etc
(5) Surgical treatment
Joint deformities caused by tophi can be corrected with surgery.
Department of Anesthesiology, Affiliated Hospital of Chengde Medical College, Ji Guoyu
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