What Is Tophaceous Gout?

Gout is a common and complex type of arthritis, which can occur at all ages, with a higher incidence in men than in women. Gout patients often experience sudden joint pain at night, with acute onset, severe pain, edema, redness, and inflammation in the joints. The pain gradually decreases until it disappears, which lasts for several days or weeks. When the pain occurs, the patient wakes up in the middle of the night, and some patients describe that the pain is similar to the burning of a big toe. The most commonly affected joint is the big toe (medical term: the first metatarsal bone), but the affected joint is not limited to this, but it is also common in the joints of the hands, knees, elbows, etc. (see atlas). The affected joints will eventually become red and swollen and inflamed. After edema, the tissues will become soft, and the movement will be limited, which will eventually affect daily life. These symptoms will appear repeatedly, so once the joint has intense and sudden pain, it is necessary to see a doctor in time to manage and prevent symptoms.

Basic Information

English name: Gout
Visiting department: Rheumatology, Internal Medicine
Multiple groups: male
Common locations: First metatarsal bone (big toe), finger joint, knee joint, elbow joint
Common causes: High blood uric acid levels, causing urate deposition
Common symptoms: Joint pain, edema, inflammation, joint deformation, kidney stones, kidney failure

Contagious: no
Whether medical insurance: Yes
Can it be cured: no
Whether to relapse: Yes
Whether inherited: Yes
Common treatments: Medication, surgery if necessary
Whether it is life threatening: Yes

Gout is a crystal-associated arthropathy caused by the deposition of monosodium urate (MSU), which is directly related to hyperuricemia caused by purine metabolism disorders and / or decreased uric acid excretion, and belongs to the category of metabolic rheumatism. Gout can be complicated by kidney disease. In severe cases, joint damage and renal function damage can occur, often accompanied by hyperlipidemia, hypertension, diabetes, arteriosclerosis and coronary heart disease. ^[1]

As a chronic crystal arthritis-gout, hyperuricemia is the basis of gout. ^[2] Genetic factors affect the entire process of the occurrence and development of gout and hyperuricemia. Single-gene genetic diseases may affect key enzymes in the uric acid metabolism pathway. SNP can cause differences in uric acid transporters and the degree of inflammatory response. ^[2] Hyperuricemia and excessive saturation of uric acid in the urine cause urate to deposit in the lumen or interstitium of the renal tubules, leading to an acute inflammatory response.

Gout can be accompanied by a variety of metabolic diseases such as obesity, hypertension, diabetes, and lipid metabolism disorders. Obesity is one of the main risk factors for gout. Gout patients with different body mass index (BMI) have different clinical characteristics. ^[3] Individualized treatment needs to be given to different patients.

Gout stones often appear in patients with gout. It can be seen subcutaneously around the patient's ears, around the joints, tendons, and soft tissues. Gout stones are pale yellow or white ridges or vegetations of various sizes, with a hard texture similar to stones. ^[2] Goutstones formed in various parts of the body, especially the extremities, not only seriously affect the shape of the limbs, but also lead to joint deformities, dysfunction, nerve compression, skin rupture, and permanent sinus tract, which requires surgical treatment. ^[4]

The medicines for treating gout are mainly non-steroidal anti-inflammatory drugs and glucocorticoids, but the current drug treatment methods are less used; diet therapy is a more common and healthy treatment method mainly including the following aspects: reducing consumption of high purine foods, high fat Foods such as meat, game, seafood, yeast-containing foods and beverages; eat foods with lower purine content, such as rice, wheat, starch, sorghum, eggs, pig blood, duck blood, etc. as much as possible. ^[5]

Imaging manifestations of gout (2 photos)

Gout History

As early as the 5th century BC, Hippocrates had recorded clinical manifestations of gout. The word gout comes from the Latin Guta (a drop), which means that a drop of harmful fluid causes joint damage. The pain is like a gust of wind. It comes fast and goes fast. Ancient gout was more common in the emperor's generals, but with the improvement of living standards, the prevalence of gout / hyperuricemia (HUA) increased year by year. Increased uric acid production and / or decreased excretion can lead to the occurrence of HUA. ^[6]

/ Definition of gout / hyperuricemia

The international definition of HUA is: under normal purine diet, the fasting blood uric acid level twice on the same day: male uric acid> 420 mol / L, female uric acid> 360 mol / L. When the blood uric acid level exceeds the monosodium urate saturation of the joint and precipitates in the peripheral joints and surrounding tissues, it is called gout. HUA without gout is called asymptomatic HUA, because it has no obvious clinical symptoms and has not yet attracted enough attention. ^[6]

Risk factors for gout

I. Obesity

Obesity is a risk factor for gout. Obesity not only increases the risk of gout, but obese patients have an earlier onset of gout. With the increase of BMI, the incidence of gout increased significantly, and visceral fat was closely related to the occurrence of gout. ^[3]

Hypertriglyceridemia and obesity are both risk factors for gout. Obesity can lead to insulin resistance, which ultimately leads to reduced renal uric acid excretion through a variety of pathways. Obesity causes an increase in free fatty acids and increases the synthesis of uric acid by affecting the activity of xanthine oxidase and the like. ^[3]

Drinking

Excessive alcohol intake is an independent risk factor for gout attacks. Beer contains a large amount of purine, so the risk of gout is greatest. ^[6]

Possible reasons for drinking to promote elevated blood uric acid levels ^[6] :

(1) Ethanol stimulates the body to synthesize lactic acid, which competitively inhibits renal tubular uric acid excretion.

(2) Ethanol can promote uric acid production by increasing ATP degradation to adenosine monophosphate.

(3) Certain alcohols, especially fermented drinks such as beer, produce a large amount of purines during the fermentation process. Drinking large amounts for a long time can promote the occurrence of HUA and even gout.

(4) Drinking alcohol is often accompanied by intake of high purine foods, which increases the risk of HUA and gout.

(5) Chronic alcohol-related liver disease caused by long-term heavy drinking is associated with elevated insulin levels, which can inhibit the insulin signaling pathway, increase the risk of insulin resistance, increase the reabsorption of uric acid, and increase blood uric acid levels.

Third, hypertension

Hypertension is an independent risk factor for gout attacks. A 9-year follow-up of US residents found that participants with high blood pressure were significantly more likely to develop gout than non-hypertensive people. The possible reasons are: Hypoxia caused by high blood pressure leading to microvascular disease, followed by an increase in blood lactic acid levels, which inhibits urate secretion in the renal tubules, eventually causing uric acid retention and HUA; ^[6] In addition, many patients with hypertension have long The use of diuretics, tincture diuretics and thiazide diuretics can promote the increase of blood uric acid levels ^[6] .

Fourth, hyperglycemia

Hyperglycemia Hyperglycemia is a risk factor for HUA. Diabetic patients have increased purine catabolism, increased uric acid production, and elevated blood uric acid levels. HUA can aggravate kidney damage, reduce renal uric acid excretion, and further increase the incidence of HUA. But blood glucose is not related to changes in blood uric acid levels. ^[6]

Five, purine-rich foods

Purine-rich foods (eg, meat, seafood) can increase the risk of HUA / gout. ^[6] Fructose is a carbohydrate that can increase blood uric acid level, can promote uric acid synthesis and inhibit uric acid excretion, so a large amount of people who take fructose drinks can increase blood uric acid level.

Six, some drugs

The relative risks of gout for diuretics and thiazide diuretics were 2.64 and 1.70, respectively. Low-dose aspirin (75-150 mg / d), cyclosporine, tacrolimus, and pyrazinamide can increase blood uric acid and increase the risk of gout. ^[6]

Gout epidemiology

China lacks national gout epidemiological survey data, but according to gout prevalence reported at different times and in different regions, the prevalence of gout in China is currently 1% to 3%, and it is increasing year by year. ^[1]

According to the phase registration data of the National Rheumatism Data Center (CRDC) network registration and follow-up study, as of February 2016, based on 6,814 cases of gout patients found in 100 hospitals in 27 provinces, municipalities, and autonomous regions nationwide The average age of gout patients in China is 48.28 years (male 47.95 years, female 53.14 years), and they are gradually becoming younger, male: female 15: 1. More than 50% of patients with gout are overweight or obese. ^[1]

Globally, the prevalence of HUA / gout is higher in developed countries than in developing countries. Gout is more common in North America and Western European countries, with a prevalence of 1% to 4%, while the prevalence of gout is low in the former Soviet Union, Iran, Malaysia and other regions. ^[6]

Epidemiological studies have shown that hyperuricemia is associated with the progression of CKD to end-stage renal disease. ^[7]

Gout Causes

According to the 2016 Chinese Gout Diagnosis and Treatment Guide, the main reason for gout patients to visit is joint pain (41.2% for men and 29.8% for women), followed by fatigue and fever. There is a large difference in the causes of men and women. Male patients are mainly induced by drinking (25.5%), followed by high-purine diet (22.9%) and strenuous exercise (6.2%); female patients are mainly high-purine. Diet-induced (17.0%), followed by sudden cold (11.2%) and strenuous exercise (9.6%). ^[1]

At the doctor's appointment, the doctor will assess the patient's clinical manifestations and, if necessary, confirm the diagnosis with the help of X-ray examinations and laboratory tests (ie, biochemical examinations). ^[8]

Clinical manifestations of gout (6 photos)

Gout treatment

The drugs for treating gout are mainly non-steroidal anti-inflammatory drugs and glucocorticoids, but the current drug treatment methods are less used; diet therapy is a more common and healthy treatment method. Diet therapy mainly includes the following aspects: reduce consumption of high purine foods, high fat foods, such as meat, game, seafood, yeast-containing foods and beverages; eat foods with lower purine content, such as rice, wheat, starch, sorghum, as much as possible , Eggs, pig blood, duck blood, etc. Drinking more water can excrete uric acid through the urine; exercise more, strengthen exercise, and discharge excess body fat. ^[5]

Preventive gout treatment: one is to prevent the excessive production of uric acid, and the other is to promote the excretion of uric acid by the kidneys to prevent gout; gout will cause microcirculation disorders of the organs because of the deposition of uric acid in various organs, and we must actively prevent the heart and brain Vascular and renal complications. ^[9]

At present gout treatment mainly includes two aspects-treatment of pain and inflammatory response when gout attacks. Prevent gout attacks and reduce blood uric acid <6 mg / dl (357 mol / L). Patients with gout need life-long uric acid lowering or not with CKD, unless intolerance or adverse reactions occur. ^[7]

For obese gout patients, while paying attention to blood uric acid, pay attention to guide patients to exercise regularly, monitor blood pressure, blood glucose, blood lipids, liver transaminase and other indicators, give comprehensive treatment, maintain blood uric acid to meet standards, and reduce the number of affected joints as much as possible. ^[3]

Low purine diet, maintain a reasonable weight, quit drinking, drink more tea, drink more than 2000ml of water daily. Avoid overeating, alcoholism, cold and wetness, excessive fatigue and mental stress, wear comfortable shoes, prevent joint damage, and use drugs that affect uric acid excretion, such as certain diuretics and low-dose aspirin. Prevention and treatment of associated diseases such as hypertension, diabetes and coronary heart disease. ^[10]

Colchicine Colchicine is used early in the onset of gout to relieve symptoms quickly. The 2012 American Rheumatism Association (ACR) guidelines state that colchicine is taken within 36 hours of an acute gout attack, and prodromal application can prevent the onset of gout. Renal insufficiency is still a first-line drug, but it should be reduced because renal insufficiency will significantly reduce its clearance and increase drug toxicity. As much as 20% of oral medications are excreted through the kidneys, and in patients with severe renal failure, the half-life of colchicine is two to three times that of patients with normal renal function. At the same time, colchicine cannot be removed by dialysis, so its toxicity is exacerbated in CKD patients ^[7] .

The surgical indications for gout stones mainly involve the following aspects ^[4] :

(1) Goutstones cause limb deformities and cause dysfunctions that affect daily life;

(2) oppression of the skin, skin rupture has formed or is about to appear;

(3) sinus formation, chalk-like substance exudation or infection with different degrees;

(4) Joint movement disorders, nerve compression symptoms of compression.

Gout stones are <1 cm in diameter, and active conservative treatment is recommended. Some scholars believe that once gout stones are formed, it is generally difficult to reabsorb them. Those with a diameter of more than 1.5 cm strive for early surgery. ^[4]

Most patients with gout can control the development of the disease through drugs, and a few patients have poor or even ineffective results after medical treatment. Uric acid crystals are deposited on joints and tendons, and gout stones are gradually formed ^[11] . Gout stones are present in 12% -15% of patients with gout. Eventually the superficial skin ulcerates, forming ulcers or sinuses. Studies have shown that the incidence of non-healing of gout wounds is as high as 23%, and the dressing change time can reach 6 to 8 weeks. The average healing time is up to 4 months, which has a huge impact on patients' daily life, psychological and physical functions. ^[11]

If the uric acid control is not satisfactory in patients with gout, acute gout will recur, which is not conducive to wound healing. Due to poor blood flow and weak cell regeneration, gout wounds are often unhealed. ^{[11] In} this group of patients, the wound conditions were poor when they were admitted to hospital, and there were often different degrees of infection, and local inflammation such as redness, swelling, heat, and pain was obvious. The wounds are changed daily before surgery. According to the results of the drug sensitivity test, sensitive antibiotics are used to wet the wound. At the same time, a red light therapy instrument is used for physical therapy. If necessary, a simple negative pressure drainage device with lower medical cost is used to improve the wound healing effect Significantly. ^[11]

Gout prevention

Although the effect of dietary factors on the onset of gout has been confirmed by a large number of studies, the survey found that the knowledge rate of gout patients and doctors about gout diet knowledge was only 22% and 37.2%, respectively. ^{[12] The} following are specific diet-related recommendations:

1. Encourage the intake of soy products ^[12] .

Soy foods are rich in protein, soy isoflavones and polyunsaturated fatty acids. Six epidemiological surveys show that intake of soy foods has nothing to do with blood uric acid levels, hyperuricemia, and gout; five intervention trials found that legume protein, although increasing blood uric acid levels, was higher than that of Asians. The clinical impact of the amount of blood and the increase in blood uric acid level can be ignored. A recent domestic study found that patients with hyperuricemia were given a high-protein diet of beans for 3 months, and their blood uric acid levels were significantly reduced.

Encourage low-fat milk and yogurt ^[12]

Both short-term and long-term intake of dairy products, especially skimmed milk and low-calorie yogurt, reduce uric acid levels. In addition, glycomacropeptide and G600 in milk have anti-inflammatory effects, which may reduce the acute attack of gout by reducing the inflammatory response of monosodium urate in the joints.

Encourage the consumption of vegetables and fruits ^[12]

Consumption of purine-rich vegetables and fruits did not increase blood uric acid levels. A vegetable-based diet can reduce uric acid levels, and the same effect was observed even with spinach. The anthocyanins contained in cherries can reduce uric acid, anti-inflammatory and anti-oxidant effects, and can prevent the onset of gout.

Limit total protein intake ^[12]

V. Limiting Sugary Drinks

Emphasize on gout patients not to drink or drink sugary beverages, or to eat packaged foods such as pastries, desserts, cold drinks, etc. When cooking, pay attention to adding as little sugar as possible to reduce the intake of fructose-rich fruits; Vigorously promote the health risks of excessive intake of sugar products. ^[13]