Hyperuricemia

Introduction to hyperuricemia Hyperuricemia, also known as gout, is a group of diseases caused by dysbial metabolic disorders. Its clinical features are hyperuricemia and the resulting recurrent attacks of gouty acute arthritis and tophi deposits. Chalchopathic chronic arthritis and joint deformities often involve the formation of chronic interstitial nephritis and uric acid kidney stones in the kidney. basic knowledge The proportion of illness: 0.02% Susceptible people: no specific population Mode of infection: non-infectious Complications: gouty arthritis

Cause of hyperuricemia

Alcohol factor (65%):

Gout is associated with alcohol intake (especially beer) and excessive intake of meat (especially viscera and shellfish). Alcohol causes gout because the alcohol absorbs water in the liver tissue and increases the blood concentration. This makes the uric acid that is close to saturation accelerate into the soft tissue to form crystals, which causes the body's immune system to overreact (sensitive) and cause inflammation. .

High sugar factor (15%):

Recent studies have pointed out that high sugars (such as carbonated drinks and fructose) can cause gout, strenuous exercise, obesity and stress can also lead to an increase in uric acid concentration and induce gout.

Endocrine factors (10%):

Gout is mostly in the middle of the night because the body's anti-inflammatory substance promotes adrenocortical hormone secretion in the middle of the night at night. In addition, the pH value during sleep is acidic due to the accumulation of carbon dioxide in the body, while the temperature of the toe is lower. The liquid near the upper toe is absorbed by the body to increase the concentration of uric acid, so gout is most likely to appear in the midnight of the toe.

Hyperuricemia prevention

(1) Regular health checkups, and it is best to have a physical examination once a year if conditions permit.

(2) A balanced diet to reduce the consumption of sorghum food.

(3) Stop drinking and maintain a healthy weight.

(4) Those who have suffered from hyperuricemia or gout are restricted from eating food.

(5) Drink 8-10 cups of boiling water per day to help uric acid excretion.

Hyperuricemia complications Complications, gouty arthritis

Mainly gouty arthritis, gouty kidney disease, gouty kidney stones, gouty heart disease, gouty hypertension and other serious complications.

Symptoms of hyperuricemia Common symptoms Drinking fatigue, joints, local tingling, body discomfort, heat, nocturnal urinary tract, urinary urate, in the joints... Joint deformity gout nodules

1. Primary gout has been considered rare in China in the past, but in recent years, due to improved nutritional conditions, prolonged life expectancy, and attention to the disease, etc., more have been found, the prevalence increases with age, more Found in men, the ratio of male to female is about 20:1, women rarely ill, if most occur after the menopause, many cases reported a positive family history, mostly autosomal inheritance, a few are sexual inheritance, brain power Workers and economically well-nourished people have more morbidity, and the course of gout is quite long. Those who do not have kidneys have a good prognosis after effective prevention and treatment, generally do not affect life expectancy, and can work and live like normal people, but if improper prevention, not only acute attacks are very Great pain, and easily lead to joint deformities, kidney stones, kidney damage and other serious consequences, renal dysfunction, the prognosis is poor.

The natural course and clinical manifestations of gout patients can be roughly divided into the following four phases:

1 asymptomatic hyperuricemia period.

2 acute gouty arthritis episode.

3 gout interval (inter-critical gout).

4 chronic topheaucemic arthritis (chronic tophaceous).

(a) asymptomatic hyperuricemia

Serum urate concentration increased with age, and there were gender differences. There was no difference between males and females in childhood, with an average of 3.6 mg%. After sexual maturity, males were higher than females by about 1 mg%, and after female menopause, both tend to Close, so men can develop hyperuricemia after the developmental age, and women often occur after menopause, many people with hyperuricemia can continue to have symptoms for the rest of their lives, called asymptomatic hyperuricemia, only It is called gout when arthritis occurs. The higher the serum urate concentration, the longer the time, the more chances of gout and urinary calculi. The age of onset of gout reaches the highest peak around 40 years old.

(two) acute gouty arthritis

It is the most common first symptom of primary gout. It occurs in the lower extremity joints. The typical onset is very rapid. The patient can still be healthy when going to bed, but wakes up in the middle of the night due to foot pain. The symptoms develop to a peak within a few hours. The joints and surrounding soft tissues have obvious redness, heat and pain, and the pain is very severe. They can not even endure the cover of the bedding. When the large joints are involved, there may be joint exudate, and may be accompanied by headache, fever, increased white blood cells and other systemic symptoms. Most patients are onset. There are no prodromal symptoms before, but some patients have fatigue before the onset, body discomfort, and local tingling and other spurs. More than half of the patients are first on the toes, and about 90% of the patients are involved in the whole process. The toe, ankle, knee, finger, wrist, and elbow joints are also good sites, while the shoulders, hips, and spine joints are less common. The first onset often affects only a single joint, and repeated attacks increase the number of joints. Onset, but more in spring and autumn, mostly in the middle of the night, local joint damage such as sprained feet, wearing tight shoes and surgery, full of wine, excessive Labor, by the wet and the cold infections and so may be a predisposing factor.

Gout attacks last for several days to several weeks can be naturally relieved, joint activity can be completely restored, leaving only traces of skin color changes in the inflammatory area, and then there is an asymptomatic stage, the so-called gap period, which lasts for a natural month, several years or even more than ten years. Most patients relapse within a year. After that, they will be sent several times a year or several times. Occasionally, only one episode will occur once in a lifetime. A considerable number of patients have a tendency to become more and more frequent, and more and more joints are involved, causing chronic arthritis. Joint deformity, only a very small number of patients have no interstitial period since the initial attack, and directly continue to develop into chronic arthritis.

(3) tophi and chronic arthritis

In untreated patients, urate deposition in the joints increases, and the recurrent inflammation enters the chronic phase and cannot completely disappear, causing the joint bone erosion defect and surrounding tissue fibrosis, causing joint deformity and limited activity, in chronic diseases. On the basis of change, there may still be repeated episodes of acute inflammation, which makes the lesions more and more serious, and the deformity becomes more and more significant, which seriously affects the joint function. Individual patients have mild atypical symptoms in the acute phase, and are found after the occurrence of joint deformity, a few chronic Arthritis can affect the joints of the whole body including the shoulder and hip and the spine. In addition, urate crystals can be deposited in the tendons, tendon sheaths, and connective tissues of the skin near the joints, forming yellow-white, ridged creatures of different sizes, so-called gout. Nodules (or tophi), small as sesame seeds, as large as eggs or larger, often occur in the ear wheel, forearm extension, metatarsal toe, fingers, elbows, etc., but do not involve the liver, spleen, lungs and central nervous system The system is soft and soft at the beginning of the nodule. As the fibrous tissue proliferates, the texture becomes harder and harder, and the nodules at the vicinity of the joint are easily worn. It can be broken into a sputum tube, which can be discharged with white powdered urate crystals. However, due to the bacteriostatic effect of urate, secondary infection is rare, and the surrounding tissue of the fistula is chronic inflammatory granuloma, which is difficult to heal, gout nodules. The incidence is related to the severity of the disease and the increase of blood urate. The general literature reports that the blood urate is below 8mg/dl, 90% of the patients have no gout nodules, and those with a blood urate concentration of more than 9mg/dl, 50% have Gout nodules, the longer the course of the disease, the more chances of gout nodules, the short-lived soft nodules are limited in the diet, and the uric acid-lowering drugs can be gradually reduced or even disappeared, but the time is long, the quality Hard nodules, because fiber proliferation is not easy to disappear.

(4) Kidney disease

About one-third of gout patients who have been seen in clinical practice for a long time have kidney damage, which is manifested in three forms:

Gouty nephropathy

The deposition of urate crystals in renal tissue causes interstitial nephritis. In the early stage, only proteinuria and microscopic hematuria may occur, and there is a gap, so it is easy to be missed. As the disease progresses, proteinuria becomes persistent, and renal function is especially concentrated. Impaired function, increased nocturia, low urine weight, etc., the disease progresses further, and finally develops from chronic azotemia to uremia group. In the past, about 17% to 25% of gout patients died of renal failure due to Patients with gout are often accompanied by hypertension, arteriosclerosis, kidney stones, urinary tract infections, etc. The so-called gouty nephropathy may be the result of a combination of factors.

2. Acute renal failure

Because a large amount of uric acid crystals block the renal tubular lumen, leading to obstruction of urine flow and acute renal failure symptoms, such as giving active treatment such as drinking more water, alkaline drugs, lowering blood uric acid, etc., the condition can often be recovered.

3. Urinary tract stones

About 20% to 25% of patients with primary gout complicated with urinary acid urinary tract stones. Some patients have symptoms of kidney stones earlier than arthritis. Secondary uric acidemia has a higher incidence of urinary calculi. Sand-like stones can be asymptomatic with urine excretion. The larger ones often cause renal colic, hematuria and urinary tract infections. Pure uric acid stones can be transmitted through X-rays without development, but those with more mixed calcium salts can be used. Found on the urinary tract film.

Patients with gout are often associated with hypertension, hyperlipidemia, arteriosclerosis, coronary heart disease and diabetes (type II). Among the causes of death in older patients, cardiovascular factors far exceed the factors of renal insufficiency, regarding gout and the above diseases. The relationship between the two is generally considered to have no direct causal relationship, and may be related to obesity, diet, drinking and other common factors. Limiting diet and reducing body weight can often control hyperuricemia, diabetes, hypertension and hyperlipidemia.

Second, secondary gout

Most of them occur in myeloproliferative diseases such as acute and chronic leukemia, polycythemia, multiple myeloma, hemolytic anemia, lymphoma and various cancer chemotherapy, when the nucleic acid in the cell is decomposed and the uric acid is excessively produced; or in kidney disease High blood pressure, advanced arteriosclerosis, increased uric acid due to uric acid excretion due to renal failure, blood uric acid concentration in patients with secondary gout is often higher than the primary, and the incidence of urinary calculi is also high, but due to the course of the disease It can't be very long. The symptoms of the joints are not typical of the primary ones, and they are often covered by the primary diseases. They are difficult to be discovered. Because most of the patients are dying and have a short life span, the chronic phase performance is relatively rare. In addition, the drugs are rare. Primary hyperuricemia often occurs in the application of thiazide diuretics and diuretics, furosemide, acetazolamide, sodium salicylate in the large dose of uric acid, and in small doses inhibit renal tubular excretion of uric acid The blood uric acid is increased, and high uric acidemia and gout can occur due to kidney damage during chronic lead poisoning.

Adolescent and childhood gout are rare, occasionally seen in hepatic glycogenosis type I, due to lack of glucose-6 phosphatase, causing blood sugar lowering, causing increased glycogenolysis, excessive production of lactic acid, inhibition of renal tubular excretion of uric acid, and nuclear Glycoside consumption, sputum synthesis increased, resulting in hyperuricemia, patients with episodes of hypoglycemia as the main performance, followed by Lesch-Nyhan syndrome, due to the lack of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) Increased synthesis of uric acid, showing high uric acidemia, the disease is seen in male children within one year of onset, often cerebral palsy, mental decline, chorea-like hyperactivity and primary gout, light-type often to adolescents, No disability signs, when the symptoms of gout appear, attention is paid, the patient has a large amount of uric acid excretion in the urine, uric acid stones are often the first symptom, the nervous system performance is only seen in 20% of patients, only mild spinal-cylbellar motor disorders which performed.

Examination of hyperuricemia

Serum urate assay

The results of different detection methods are different. The normal value of uric acid in foreign males is 7mg/dl, and that of females is about 1mg/dl lower than that of males. Patients with gout are accompanied by an increase in blood urate, but due to the volatility of uric acid itself (such as increased secretion of adrenal cortex hormones during acute attacks, enhanced diuretic action), and effects of influent diuresis and drugs, sometimes blood urate is detected. It can be normal, and it must be checked repeatedly to avoid missed diagnosis.

Urine uric acid determination

It is of little help in diagnosing acute arthritis. Because more than half of patients with gout have normal uric acid excretion, they can understand uric acid excretion through urine examination. It is helpful to choose drugs and identify urinary calculi due to increased uric acid. The normal diet for 24 hours uric acid is discharged below 600mg.

Collateral fluid examination

In the acute phase, such as sputum, knee and other large joint swelling, the sac fluid can be extracted for optical microscopy, and the double-folded needle-shaped sodium urate crystal can be seen in the white blood cells, which has diagnostic significance. The positive rate of optical microscopy is only half of that of optical microscopy. Analysis of the synovial fluid is also helpful. The white blood cell count is generally between 1000 and 7000, up to 50,000, mainly the lobular granulocytes.

X-ray examination

In addition to soft tissue swelling, early acute arthritis develops normal joints, and bone changes occur after repeated episodes. First, the articular cartilage margin is destroyed, the articular surface is irregular, the joint space is narrow, and the lesion development is in the subchondral bone and bone marrow. It can be seen that the tophi deposits, the bone is pit-like defect, the size of the defect is small, the edges are sharp, the defect is semi-circular or continuous curved, and the bone edge can have proliferative reaction.

Tophi special inspection

The gout nodules can be biopsied, or identified by a special chemical test (Murexide), and can also be measured by ultraviolet spectrophotometer and uric acid enzyme decomposition.

Diagnosis and identification of hyperuricemia

diagnosis

1. The standard of hyperuricemia: under normal sputum diet, two fasting blood uric acid levels in the same day are male > 7 mg / dl or female > 6 mg / dl.

2. Classification of hyperuricemia: Classification diagnosis can help to find the cause of hyperuricemia and give targeted treatment. Patients with hyperuricemia were given a 24-hour urine test for uric acid levels after 5 days of low-grade diet.

(1) uric acid excretion type: uric acid excretion is less than 0.48mg / (kg.h), uric acid clearance rate is less than 6.2ml / min.

(2) Excessive uric acid production: uric acid excretion is greater than 0.51 mg / (kg.h), uric acid clearance rate is greater than or equal to 6.2 ml / min.

(3) Mixed type: uric acid excretion exceeds 0.51 mg/(kg.h), and uric acid clearance rate is less than 6.2 ml/min.

Considering the effect of renal function on uric acid excretion, corrected by creatinine clearance rate, according to the ratio of uric acid clearance rate/creatinine clearance rate, the classification of hyperuricemia is as follows: >10% is uric acid production excessive type; <5% is uric acid excretion Poor type; 5%~10% is mixed type.

Differential diagnosis

Due to the diversity of the disease, sometimes the symptoms are not typical, the following differential diagnosis must be considered:

(1) Rheumatoid arthritis: more common in young and middle-aged women, occurs in the joints of the fingers and wrists, knees, ankles, ankles, and spine. It is characterized by migratory symmetry and polyarthritis. Joint stiffness and deformity, repeated acute exacerbations on the basis of chronic lesions, easy to be confused with gout, but blood uric acid is not high, most rheumatoid factors are positive, X-ray shows joint surface roughness, joint space stenosis, even articular surface fusion, and gout bone The quality defect is significantly different.

(B) septic arthritis and traumatic arthritis: gout is often confused with septic arthritis or traumatic arthritis, but the latter two blood urate is not high, the sac fluid test without urate crystals, Traumatic arthritis often has a history of heavier injuries. The septic arthritis bursal fluid contains a large number of white blood cells, which can be used to identify pathogenic bacteria.

(3) Cellulitis: When the gout is acute, the soft tissue around the joint is often obviously red and swollen. If the symptoms of the joint itself are neglected, it is easily misdiagnosed as cellulitis, the latter is not high in blood urate, chills and fever, and increased white blood cells. Systemic symptoms are more prominent, and joint pain is often less obvious. It is not difficult to diagnose.

(4) pseudo-gout: caused by calcification of articular cartilage, mostly seen in the elderly, with the knee joint most often involved, the symptoms are similar to gout in acute attacks, but the blood urate is not high, the joint synovial fluid is checked for calcium pyrophosphate crystals. Or phosphorus gray, X-ray film shows cartilage calcium.

(5) Psoriasis (psoriasis) arthritis: often asymmetry involving the distal intercondylar joint, with joint damage and disability, joint space widening, toe (finger) end bone absorption, ankle joints are often involved, clinical The performance is similar to rheumatoid arthritis, accompanied by 20% of patients with elevated blood uric acid, which is not easy to distinguish from gout.

(6) Other arthritis: the acute phase must be differentiated from lupus erythematosus, recurrent arthritis and Reiter syndrome, and the chronic phase must be differentiated from the sequelae of hypertrophic joint disease, traumatic and septic arthritis. diagnosis.

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