Gout in the elderly
Introduction
Introduction to gout in the elderly Gout is a group of heterogeneous diseases caused by hereditary and/or acquired uric acid production and/or decreased excretion. Its clinical features are: hyperuricemia and urate crystallization, acute deposition Arthritis, tophi, chronic gout arthritis, gouty nephropathy. The above expressions may exist individually or in combination. basic knowledge Sickness ratio: 5% Susceptible people: the elderly Mode of infection: non-infectious Complications: diabetes, hyperlipidemia, hypertension
Cause
Gout of the elderly
(1) Causes of the disease
The occurrence of gout is multi-cause and can be divided into two major categories: primary and secondary.
Primary
(1) Molecular defects (unique) of unknown cause:
1 uric acid excretion is reduced (reduced renal clearance), accounting for 80% to 90% of the primary.
2 excessive production of uric acid, accounting for 10% to 20% of the primary.
Both of the above are polygenic genetic diseases.
(2) Enzyme and metabolic defects, accounting for 1% of the primary.
1 phosphoribosyl pyrophosphate (PRPP) synthetase hyperthyroidism.
Two times the jaundice-guanine phosphoribosyltransferase (HGPRT) was partially deficient.
3 adenine phosphoribosyltransferase (APRT) deficiency.
All three are X-linked sex chromosome hereditary diseases.
2. Secondary
(1) Excessive production of uric acid:
1 enzyme and metabolic defects: myogenic hyperuricemia; glycogen accumulation disease type I / von Gierke disease; HGPRT complete deficiency / Lesch-Nyhan syndrome.
2 excessive cell destruction: hemolysis, burns, trauma, chemotherapy, radiotherapy, excessive exercise.
3 cell proliferation: leukemia, lymphatic disease, myeloma, polycythemia.
4 external factors: sorghum diet, excessive drinking.
(2) Reduced uric acid excretion:
1 renal clearance reduction: kidney failure, drugs, ketoacidosis, lactic acidosis, toxins.
2 decreased extracellular fluid: dehydration, diabetes insipidus.
It is worth mentioning that HGPRT is partially deficient, clinically only gout, called primary gout, and HGPRT is completely devoid of symptoms, in addition to gout, and neurological damage, and belongs to secondary gout, Both of them are X-linked sex chromosome genetic diseases.
(two) pathogenesis
There is currently no evidence that dissolved uric acid is toxic, and the occurrence of gout depends on the concentration of blood uric acid and its solubility in body fluids.
1. Mechanism of hyperuricemia
In normal people, the synthesis and catabolic rate of sputum are in a dynamic equilibrium state, thus maintaining the stability of blood uric acid.
(1) Excessive absorption: 20% of uric acid in the body is derived from foods rich in sputum. Excessive intake can induce gout attacks, but it is not the cause of hyperuricemia.
(2) Excessive production: 80% of uric acid in the body is derived from sputum biosynthesis, and there are mainly three kinds of purine nucleotides involved in uric acid metabolism, namely hypoxanthine nucleotide, adenine nucleotide, and guanine nucleotide. Nucleotide production has two pathways: mainly from amino acids, phosphoribosyls and other small molecules of non-thiol precursors, synthesized through a series of steps, and the other pathway is from nucleic acids in cells (mainly including DNA and RNA) is decomposed. In the process of purine metabolism, there is still negative feedback regulation of mutual transformation and restriction. Enzymes are involved in the regulation of each link. Once the regulation of the enzyme is abnormal, the increase or decrease of blood uric acid can occur. The increase in production was mainly due to increased activity of PRPP synthase, partial deficiency of HGPRT, and lack of APPT. These patients accounted for only a minority of the primary gout population, generally less than 20%.
(3) Reduction of excretion: uric acid is the end product of sputum metabolism. About 1/3 of uric acid in normal people is in the intestine, and it is excreted by bacteria in the form of ammonia and carbon dioxide. About 2/3 is excreted by the kidney, human Lack of urate oxidase, so the mechanism of uric acid degradation as hyperuricemia has been ruled out, the process of uric acid excretion in the kidney can be divided into three stages:
1 glomerular filtration;
2 renal tubular reabsorption;
3 renal tubular secretion, in which the secretion of renal tubules plays a decisive role in the excretion of uric acid, accounting for 4/5 of total uric acid output, glomerular filtration only accounted for 1/5, most of the primary gout high uric acid The disease is related to abnormal uric acid excretion in the kidney, and is mainly caused by the secretion of renal tubules, accounting for 80% to 90% of the pathogenesis of primary gout. The decrease in renal clearance may be a molecular defect of unknown cause. Hyperglycemia of gout is also caused by renal excretion disorders. In fact, the reduction of uric acid excretion is often accompanied by increased production.
2. The mechanism of gout
The amount of uric acid produced by normal people is relatively constant every day. The amount of uric acid produced by catabolism in healthy adults is 600-700 mg per day, and the amount of uric acid produced by gout patients can be as high as 2000-3000 mg per day, if combined with the decomposition of sputum in exogenous foods. Uric acid, the total amount can exceed 3000mg, far exceeding the excretion capacity of the kidney, and the blood uric acid is increased, the uric acid production is not increased, and there is a renal excretion disorder, which can also cause uric acid accumulation, only hyperuricemia, even if combined Urinary acid stones can not be called gout, hyperuricemia only 10% to 20% of gout, gout means urate crystallisation, deposition of reactive arthritis or (and) tophi disease, when uric acid is in Superfluid in body fluids, generally exceeding 416.2mol/L (17mg/L), it is easy to deposit in tissues and organs, especially joints and surrounding subcutaneous tissues, auricles and kidneys, leading to gouty arthritis episodes, gout Stone formation and gouty nephropathy, in addition to concentration, there are some factors affecting the solubility of uric acid, such as decreased estrogen, lower temperature, increased H+ concentration, etc. can promote uric acid Freed dissolved state, the tissue is deposited.
Prevention
Gout prevention in the elderly
Third-level prevention
Usually the prevention of gout is divided into 3 levels. Primary prevention is to control hyperuricemia and avoid gout. Secondary prevention is early detection and effective treatment of gout. Third-level prevention is to prevent acute attacks and prevent the development of gout. Long-term stability, improve life and quality of life.
2. Risk factors and interventions
The main risk factors are as follows:
Adult males over the age of 140 and postmenopausal women;
2 family history of gout and hyperuricemia;
3 obese or overweight, hyperlipidemia, hypertension and atherosclerosis;
4 Long-term sorghum eating habits and alcoholics.
Interventions:
1 Correct bad eating habits, reasonable diet, quit smoking and drinking, eat less salt;
2 control weight, exercise regularly, prevent obesity;
3 high-risk population with hyperuricemia, succinate synthesis inhibitor or excretion may be used as appropriate.
3. Community intervention
With the development of economic development and urbanization, lifestyle changes, gout has become one of the important diseases that endanger people's health. Therefore, under the leadership of governments at all levels and the health department, social forces should be organized, with the community as the unit. Participate in the prevention and treatment of gout, strengthen health care, and actively carry out blood uric acid screening work through the community. The focus of the census is high-risk groups with risk factors for gout, and timely treatment measures can greatly reduce the incidence of gout.
Complication
Gout complications in the elderly Complications, diabetes, hyperlipidemia
Gout can be associated with diabetes, high blood lipids, high blood pressure, arthritis, uric acid, and urinary calculi leading to kidney failure.
Symptom
Gout symptoms in the elderly Common symptoms Back pain, severe pain, heat, fatigue, high blood pressure, chills, finger gout, isotonic, urine, diuretic, secondary infection
More common in obese middle-aged and post-menopausal women, males account for 95%, 5% to 25% may have a family history, often have a long period of hyperuricemia before onset, this period can be several years to dozens In the year, the main performances are:
Acute gout arthritis
Often the first symptom of gout, almost in all patients, this is caused by urate crystal deposition in the joint caused by inflammation, there are two sources of crystallization:
1 Supersaturated uric acid is released into the joint fluid. Under normal conditions, the pH is 7.4. The solubility of sodium urate at 380 °C is 380 mol/L (6.4 mg/dl). In the case of hyperuricemia, urate cannot. It completely combines with plasma albumin 1,2 globulin to form a soluble complex, and the local pH value of the joint decreases, and the temperature decreases to cause urate crystal precipitation.
2 gouts on the synovial membrane of the joints collapsed (crystal detachment), and the precipitated crystals activated HAGEMAN factor, serotonin, angiotensin, bradykinin, arachidonic acid and complement system; and chemotactic leukocytes, It releases leukotriene B4 (LTB4) and glycoprotein chemoattractant; monocytes can also release arthritis-1 (IL-1) after stimulation to trigger arthritis.
The typical onset is a sudden onset, more than midnight due to severe pain. The most susceptible part is the hallux sacral joint. Others are sputum, heel, wrist, finger, elbow and other joints, rarely occurring in the trunk joints such as the hip, pelvis. , shoulder, spine, etc., the first 392 cases of primary gout in the first toe joints in the first to be affected by the average of 63.7%, the highest reached 93.2%, the first episode, the single joint involvement is more common, accounting for about 90%, but with The number of recurrences increases, and 2 or 3 joints can be affected at the same time or in succession. Within a few hours, the joints can be red, swollen and hot, and the activity is limited. Those with severe pain can be cut, unbearable, and painful. Reddish and normal activities, when the larger joints are violated, there may be joint fluid accumulation, the attack often presents self-limiting, several hours, several days, several weeks of natural relief, joint redness and heat pain completely subsided, local can Detachment and itching are common to the disease, joint activity returns to normal, the period of remission is uncertain, several months, years and even life. The shortest period of remission in 392 cases of primary gout in China is only a few days, the longest is 16 years. The second joint appears Seizures, most recurrent episodes, a small number of patients without chronic remission into chronic arthritis, about 20% of patients may be associated with systemic symptoms, including chills, fever, fatigue, headache, nausea, body aches, leukocytosis and other systemic symptoms, The body temperature of a small number of patients can be as high as 39 ° C or above. The severity of systemic symptoms is directly proportional to the severity of joint disease. The disease is more frequent in spring and autumn. Drinking alcohol, sorghum diet, and sprained foot are important causes. Wear tight shoes and walk more. Subject to cold, fatigue, infection, surgery, and diuretics.
2. Chronic gouty arthritis
Mostly developed from the recurrence of acute arthritis, every patient who has not achieved treatment or treatment and has not achieved the purpose of treatment, manifested as multiple joint involvement, frequent attacks, shortened intermittent period, increased pain, and even pain after the attack. Incomplete remission, in severe cases, can also affect shoulder, hip, spine, ankle, chest lock, mandible and other joints and costal cartilage, showing shoulder and back pain, chest pain, intercostal neuralgia and sciatica, chest pain sometimes resembles angina Uric acid deposits in cartilage, synovium, tendon and soft tissue, causing tissue breakage and fibrosis and cartilage, bone destruction, degeneration of cartilage, thickening of synovial membrane, formation of vasospasm, defect of bone erosion and even Fractures, combined with increased tophi, incurs joint stiffness, ulceration, deformity, severely affect joint activities, and even life can not take care of themselves. If chronic arthritis is not actively treated, acute episodes can still occur repeatedly, making joint damage worse. .
3. Tophi
Tophi is a characteristic damage of gout. It is a chronic foreign body-like reaction caused by fine needle-like crystal deposition of monosodium urate. It is surrounded by monocytes, epithelial cells and giant cells, forming foreign body nodules, causing mildness. Chronic inflammatory reaction, in addition to the central nervous system, tophi can involve any part, most commonly in the joint and nearby and auricles, yellow and white bulging, small as sesame, as big as eggs, soft at first, As the fiber hyperplasia becomes hard as a stone, the number and size are related to the condition. If the condition continues to develop, the number of tophi can gradually increase and increase. The number of tophis in China is as high as 500, and the largest is 17cm×12cm×6cm. It is rare, the vicinity of the joint is easy to wear, and the outer surface of the nodular bulge is thin, easy to break into a fistula, with a white paste, and the tissue surrounding the fistula is chronic granuloma, which is difficult to heal. The reasons are:
1 The blood supply and nutrition of the ruptured nodules are poor, and the tissue regeneration ability is low;
2 uric acid is crystallized constantly overflowing from the rupture, stimulating local tissue and hindering wound healing;
3 ruptured skin and secondary infections form chronic suppuration, even affecting bone, causing chronic osteomyelitis is difficult to heal.
The incidence of tophi is an average of 37%, which is related to blood uric acid concentration and disease course. When blood uric acid is lower than 480mol/L (8mg/dl), it is rare. If the medical history is more than 5 years, about 30% of gout can occur. Stone; more than 10 years, the incidence can reach 50%, most tophis appear after arthritis, a few can be used as the first symptoms of gout, and no history of arthritis, Wemiek has reported 32 cases, its characteristics are: More common in women, occurs in the finger joints; the incidence of impaired renal function is high.
4. Gout nephropathy
Autopsy confirmed that 90% to 100% of patients with gout had kidney damage. Clinically, about one-third of gout patients had renal damage. The characteristic pathological change was urate crystals in the renal medulla or nipple. Cell and giant cell reaction is chronic interstitial inflammation, leading to tubular deformation, epithelial cell necrosis, atrophy, fibrosis, cirrhosis, luminal occlusion, and then involving the glomerular vascular bed, chronically, clinically may have proteinuria, Hematuria, isotonic urine, and then renal hypertension, nitrogen and blood stasis, although 17% to 25% of gout patients die of uremia, but rarely caused by gout alone, often with hypertension, arteriosclerosis , a combination of factors such as kidney stones or infection.
Acute obstructive nephropathy, also known as hyperuricemia nephropathy, is mainly seen in the rapid increase of blood uric acid caused by radiotherapy, chemotherapy, etc., resulting in a large number of renal tubules, extensive uric acid crystal acute infarction, acute renal failure.
5. Urine acidic urinary tract stones
The average incidence rate is about 20% to 25%, accounting for 5% to 10% of all urinary stones, and is related to blood uric acid concentration, urinary uric acid excretion, urine pH, and blood uric acid concentration greater than 780 mol/L (13 mg/dl). Or when the 24h uric acid excretion is more than 6000mol/L (100mg/dl), the incidence of stones can be as high as 50%. The uric acid is difficult to dissolve in the acidic solution. The test shows that the solubility of uric acid in the solution at pH 6.0 is at pH 5.0. When the pH is increased by 3.66 times, the urine pH is lower, and uric acid is easy to precipitate in the kidney. When the urine pH is 5.75, only 50% of the uric acid is dissolved; when the urine pH is 6.6, almost all of the uric acid is dissolved. In the state, the urine pH of gout patients is mostly below 6, so there are more chances of kidney stones.
About 80% of cases are simple uric acid stones, characterized by X-rays not being developed, and the rest are mixed stones containing calcium or oxalate. X-rays can be developed. Stones can be single or multiple, involving both kidneys. It is not uncommon for stones to occur mainly in the renal pelvis, kidney nipple and renal pelvis, and there is very little in the renal cortex. Stones can also occur in the ureter and bladder, but they are rarer than kidney stones. The main clinical manifestations of kidney stones are renal colic and hematuria, renal pelvis and Ureteral calculi can cause hydronephrosis and obstructive nephropathy due to obstruction. It is prone to urinary tract infection. In severe cases, it can impair renal function. It is very rare for gout patients to have clinical manifestations of kidney stones. Only 7 of 392 cases in China , accounting for 0.07%.
6. Other clinical manifestations
Insulin resistance syndrome (metabolic syndrome) characterized by obesity, essential hypertension, hyperlipidemia, type 2 diabetes, hypercoagulability, and hyperinsulinemia, the incidence is increasing, in the middle The elderly play an important role, often accompanied by gout. Currently, hyperuricemia and gout have been included in the metabolic syndrome. According to domestic statistics, there are 40% to 50% of primary gout and Hyperuricemia, accompanied by hypertension and hyperlipidemia, 3% to 35% with diabetes; atherosclerosis and coronary heart disease can reach 27%, the reasons are: 1 gout is more common in middle-aged, often Obesity, do not like sports, drinking, high-fat diet and other risk factors, it is conducive to the occurrence of atherosclerosis, 2 uric acid can be directly deposited in the arterial wall, damage the arterial intima, stimulate the proliferation of vascular endothelial cells, resulting in Blood lipids are easy to deposit in the wall of the tube, so hyperuricemia has been regarded as one of the risk factors for arteriosclerosis and coronary heart disease. Uric acid may be deposited on islet B cells, leading to disorder of glucose metabolism, and 3 genetic defects can cause Fat metabolism disorder, sugar Metabolic disorders and the occurrence of hypertension, primary gout with rheumatoid arthritis have been reported, 9 out of 392 cases in China, there are reports of systemic lupus erythematosus.
In general, middle-aged and elderly men often have family history and metabolic syndrome. On the basis of incentives, sudden joint pain or uric acid stone attack, gout can be thought of, blood uric acid is increased, and pain and redness are found. Inflammation or tophi can be diagnosed.
Determination of blood uric acid is one of the important basis for diagnosis. It is especially significant in the acute attack period. When testing blood uric acid, it should be performed on an empty stomach, and avoid the disturbance factors such as sorghum diet, drugs, and vigorous activity before blood draw. If the uric acid is normal, it should be repeated several times to avoid missed diagnosis. Some drugs that affect the excretion of blood uric acid by the kidney include salicylic acid, antihypertensive drugs, diuretics (hydrochlorothiazide), Tilden, double bean , glycine, methicillin, acesulfame, vitamin B, C and various X-ray contrast agents.
Examine
Gout check in the elderly
White blood cell
During the onset of acute arthritis, it can be increased to (10 ~ 15) × 109 / L, such as combined with secondary infection, white blood cells are significantly elevated.
ESR
ESR increased in about 20% of cases during the episode.
3. Urine routine
In some patients, acicular urate crystals can be found in the urine. In patients with kidney damage, proteinuria, red blood cells and casts can be found. When there are a large number of pus cells, urinary tract infection is suggested.
4. Blood uric acid
Uric acid oxidase method, normal male value is 150 ~ 380mol / L (2.4 ~ 16.4mg / dl), female 100 ~ 300mol / L (1.6 ~ 3.2mg / dl), generally male > 420mol / L (7.0mg / dl) Female >350mol/L (6mg/dl) can be identified as hyperuricemia. In most patients with acute exacerbation, uric acid is higher than 540mol/L (9mg/dl) and up to 1200mol/L (20g/dl). It must be pointed out that blood uric acid determination can be normal in some cases during the interval. About 10% to 15% of cases have no increase in blood uric acid during acute attack, and blood uric acid has fluctuations, so it needs repeated monitoring, blood. The degree of uric acid increase is not necessarily parallel to the severity of clinical symptoms.
5.24h uric acid determination
Normal people's free uric acid excretion in 24h urine is 24004800mol/L (400800mg). The uric acid excretion of gout patients is related to the cause and renal organic disease. The primary gout uric acid excretion can be increased, normal. After reducing and limiting the sputum diet for 5 days, the daily uric acid excretion still exceeds 357 mol (600 mg), which is considered to increase uric acid production.
6. Renal function test
Urine concentrated dilution or PSP test, endogenous creatinine clearance, urea nitrogen and creatinine examination, renal function impairment, some items may be abnormal.
7. Enzymatic examination
Red blood cell PRPP synthetase, HGRRT and xanthine oxidase activity can be determined to determine the presence of enzyme defects.
8. Other laboratory inspections
It can be seen that blood total cholesterol, -lipoprotein and triglyceride are elevated, HDL cholesterol is low, LDL cholesterol is increased, lipoprotein electrophoresis is abnormal, and glucose tolerance is abnormal.
9. Gout nodule content inspection
Specimens are taken from the nodule self-crushing effluent. If there is no puncture or puncture or biopsy, there are two methods for judging:
1 purple uric acid amine reaction: take 1 drop of nitric acid, drop on the specimen, heat to evaporate the phosphoric acid, and then drop 1 drop of ammonia water after cooling. If the uric acid specimen is dark purple red, the specificity is high, and the oxygen sputum is negative.
2 optical microscopy: the content of the nodule is clay-like, and the double-folded needle-like crystal is visible under the microscope.
10. Joint cavity puncture synovial fluid to check the acute arthritis episode. If there is joint cavity effusion, the synovial fluid can be taken for examination. Under the optical microscope, see the needle-shaped urate crystal with double refraction in the white blood cell. It was found that white blood cells, especially the lobular nucleus, increased.
11. X-ray examination of bones and joints
X-ray films of acute arthritis in addition to soft tissue swelling, no other special manifestations, chronic or recurrent episodes, visible cartilage destruction, irregular articular surface, cartilage surface, intraosseous, canal can be seen in the cavity Non-specific manifestations such as hyperplasia at the edge of the bone. Typically, urate erodes the bone to form a round or irregular necrotic cystic translucent defect, which is the X-ray characteristic of gout. The wire shows decalcification of the bone, narrowing of the joint cavity, deformation or dislocation.
12. Arthroscopy
In the onset of gout, tiny nodules are often seen on the synovial membrane. When the joint cavity is flushed, part of the crystals are seen to fall into the joint cavity.
13. X-ray dual energy bone density examination
When there is no change in the X-ray examination, the bone density of the damaged joint can be found early.
14. Urinary system stone examination
Ordinary radiography, can not show urate stones, because the X-ray can pass urate, must be intravenous pyelography can show stones and with or without hydronephrosis, can also be used for CT or B-mode ultrasound, radioactive Kidney chart examination also has a certain value.
15. Other items that can be selected may be selected according to the presence of the associated symptoms, such as electrocardiogram, echocardiography, cerebral blood flow map, fundus examination, cardiac function measurement, and the like.
Diagnosis
Diagnosis and diagnosis of gout in the elderly
Diagnostic criteria
If the patient is highly suspected of gout, but can not be diagnosed immediately, try colchicine treatment, if it can quickly control the symptoms, it is a powerful basis for diagnosis.
The American College of Rheumatology established a standard for the diagnosis of gout in 1997, a total of nine:
1 Acute arthritis episodes more than once, reaching the peak of attack within 1 day;
2 acute arthritis is limited to individual joints;
3 the entire joint is dark red;
4 first toe joint swelling and pain;
5 unilateral ankle arthritis acute attack;
6 have tophi;
7 hyperuricemia;
8 asymmetrical joint swelling and pain;
9 seizures can be terminated by themselves. Anyone with more than 3 criteria can be diagnosed if they have secondary gout.
Domestic, the diagnosis of primary gout has not yet been unified. According to the comprehensive clinical data of 392 cases in China, the following points are proposed as the basis for diagnosis:
1 recurrent episodes of asymmetry, non-walking toes, especially toe joints, ankle joints or other joints of the limbs are red, swollen, hot, painful, can be terminated by themselves, have special effects on colchicine treatment;
2 hyperuricemia, and can exclude secondary hyperuricemia caused by other factors, male > 390 mol (6.5 g / dl), female > 310 mol / L (5.2 mg / dl);
3 urate crystals were confirmed in gout nodules or joint effusions, and any two of the above three items could be diagnosed.
Differential diagnosis
Acute arthritis
Need to be identified with the following diseases:
1 acute rheumatoid arthritis: more common in adolescent women, with a history of streptococcal infection such as sore throat, mainly with large joint migratory pain, often accompanied by carditis and joint deformity, ring erythema and so on.
2 acute rheumatoid arthritis: more common in young and middle-aged women, the affected joints are more common with finger joints, joint swelling is fusiform, with symmetry and multiple features, with obvious morning stiffness, blood uric acid is not high, Rheumatoid factor and other immunological tests can be positive, colchicine treatment has no obvious effect, in the differential diagnosis should pay attention to the possibility of coexistence of primary gout and rheumatoid arthritis.
3 Traumatic arthritis: Because gout often occurs after trauma, it is easy to be misdiagnosed. It is important that there is no sudden night pain and nodules.
4 septic arthritis: more common in large joints such as knees, hips, ankles and elbows, small joints of the hands and feet are rare, mostly single joint involvement, accompanied by heavier symptoms of systemic poisoning, often can find the primary infection, slippery The membrane fluid is purulent and has no urate crystals.
5 pseudo-Gouty arthritis: occurs in elderly patients, but it is common to invade the hip, knee and intervertebral and pubis, and there are pyrophosphate crystals in the nodules and joint synovial fluid. The patient's blood uric acid is normal, the colchicine treatment is ineffective, and the cartilage calcification is seen on the X-ray.
2. Chronic gouty arthritis
(1) rheumatoid arthritis: the joints are chronic and rigid deformity, more common in young and middle-aged women, blood uric acid is not high, only the soft tissue swelling and osteoporosis in the early stage of the affected joint X-ray film, the articular surface can be narrow and uneven, and bone erosion occurs. In the late stage, there is bony tonic embolism, but the perforation-like bone defect at the edge of the joint is smaller than gout.
(2) psoriatic arthritis: seen in the onset of young and middle-aged, although 10% to 20% of patients have hyperuricemia, the finger involvement is the distal interphalangeal joint, and more nail changes, the lesion is The important condition for identification is that the toe (finger) of the X-ray is in the shape of a pen.
(3) Bone tumor: multiple fractures caused by fractures, deformed and misdiagnosed as bone tumors, but no history of acute arthritis and hyperuricemia, biopsy of patients with difficulty.
3. Urinary tract stones
X-ray can also be developed with other ingredients such as calcium oxalate, calcium phosphate and calcium carbonate stones. Mixed uric acid stones with hyperuricemia and corresponding gout are characteristic, and cystine stones are not developed, but blood Uric acid is not high.
4. Tophi
It should be differentiated from rheumatoid nodules, xanthomas nodules and rheumatic subcutaneous nodules. Nodule biopsy is the most reliable means of identification.
5. Identification of secondary gout and primary gout
Secondary gout has the cause of increased blood uric acid. Combined with the history of primary gout, clinical manifestations and laboratory tests, it is generally not difficult to distinguish.
