In recent years, the prevalence of hyperuricemia and gout has increased significantly in China, and the trend is younger.
1.Acute gouty arthritis
The pain peaks in 24-48 hours and resolves itself to normal within a few days or weeks, and may recur later. About 90% of patients have a first episode involving a single joint, especially the first metatarsophalangeal joint. Based on the clinical features of recurrent acute monoarthritis with asymptomatic intervals, hyperuricemia, and an effective response to colchicine therapy, the diagnosis of typical cases should not be difficult. For a few atypical patients, the clinical diagnosis can be made by using the 12 items listed in the 1977 American College of Rheumatology criteria (clinical, laboratory, and x-ray manifestations), and meeting six or more of them. It should also be differentiated from dengue, cellulitis, septic arthritis, traumatic arthritis, and pseudogout.
It is worth emphasizing that the “gold standard” for the diagnosis of gout is to confirm the presence of uric acid crystals in the synovial fluid or stone tissue. The common method is to use polarized light microscopy to observe the phenomenon of needle-like negative double refraction, or to find needle-like or rod-like crystals under ordinary light microscopy, and can also see the phenomenon of leukocyte phagocytosis crystals, in the acute arthritis period has a 90% positive rate, so this test should be actively carried out.
2. Intermittent gout
This is the remission state between repeated acute attacks, usually without any discomfort or with only mild joint symptoms, therefore, the diagnosis in this period must rely on the past history of acute gouty arthritis attacks and hyperuricemia.
3.Chronic stage of gout
This stage is a consequence of the disease course extending for many years and the persistent high concentration of blood uric acid not being satisfactorily controlled, and the formation of gout stones or persistent non-remission of joint symptoms are the clinical characteristics of this stage. It is not difficult to diagnose in combination with X-ray or nodal biopsy to find uric acid salt, and this stage should be differentiated from rheumatoid arthritis, psoriatic arthritis and bone tumor.
4.Nephritic lesions
Patients with urate nephropathy initially show an increase in nocturia, followed by a decrease in urine specific gravity, hematuria, mild or moderate proteinuria, and even renal insufficiency. At this time, it should be distinguished from secondary gout caused by kidney disease. In the case of uric acid urinary tract stones, renal colic and hematuria are the main clinical manifestations, and most of them do not show up on X-ray plain film, while ultrasound examination may reveal them. Acute uric acid nephropathy should be considered in patients with widespread tumor dissemination or receiving radiotherapy for sudden onset of acute renal failure, which is characterized by a sudden and marked increase in blood uric acid and a large number of uric acid crystals and red blood cells in the urine.
Prevention and treatment of hyperuricemia and gout
1.Prevention
Patients with gout should adopt a low-calorie diet and maintain an ideal body weight, while avoiding high-purine foods (animal offal, seafood such as sardines, clams, oysters and thick meat soup, etc.), strictly abstaining from drinking various kinds of alcohol, and drinking more than 2000ml of water daily to ensure sufficient urine output. At the same time, avoid causative factors, such as overeating and alcoholism, cold and damp, excessive fatigue, mental tension, wearing comfortable shoes, preventing joint damage, and cautious use of drugs that affect uric acid excretion.
However, genetic factors are the root cause of hyperuricemia and gout, and some patients have family tendency to develop the disease clinically. Therefore, patients should not be led to believe that simply controlling their diet can “cure” gout. On the contrary, in addition to abstaining from alcohol, reducing purine intake and emphasizing regularity of life, patients should not be overly restricted in diet, and drug intervention is the main means of treating gout.
2.Medication treatment
The drug treatment of gout should be carried out in phases, with the acute phase focusing on the relief and elimination of symptoms.
(A) Anti-inflammatory and pain relief
1.The choice of three types of drugs
(1) Colchicine, non-steroidal anti-inflammatory drugs (NSAIDs) and steroid hormones can be chosen. Colchicine can inhibit neutrophil activity and inhibit tyrosine phosphorylation of protein, thus reducing uric acid crystals deposition, so the pain relief effect is fast and the diagnosis is confirmed according to the efficacy. The first dose of 1mg is given orally, followed by 0.5mg/2h until the severe pain is relieved, or until the drug is discontinued due to gastrointestinal symptoms. The extreme dose is 3mg/day.
The disadvantage of this drug is that it has more side effects and is more toxic.
①People with poor kidney function are prone to toxicity. Symptoms include severe diarrhea, myasthenia gravis, renal failure, bone marrow suppression, etc.
(2) Combined use with statin lipid-lowering drugs causes acute myopathy.
(2) If no therapeutic trial is required then NSAIDs are preferred. Commonly used drugs are anti-inflammatory pain, other anti-inflammatory analgesics are available. The author prefers to use Fotarine, Intazing, and Provera. If the patient’s original gastric disease can be added with gastric analgesics, such as ranitidine 150mg, 2 times / d.
(3) There are suggestions of local injection of glucocorticoids, which are effective in pain relief but prone to local osteoporosis. Unless both of the above methods cannot be used squarely, take this method (for example, it cannot be taken orally). Glucocorticoid or ACTH injections are also optional. Such hormones should not be applied for a long time.
(ii) Inhibition of uric acid production
Allopurinol, 0.1 t.i.d., is commonly used to inhibit xanthine oxidase and thus reduce the production of uric acid. The effect is seen 24 hours after taking the drug and reaches its peak in 2 weeks. If the serum uric acid is less than 300 μmo/L, the dose can be reduced, and the dose should be adjusted by blood test. In some patients, 0.1 t.i.d. must be taken for 1-2 months with no seizures before the dose is gradually reduced. Since this drug inhibits xanthine oxidase, and 6-mercaptopurine and azathioprine also rely on xanthine oxidase for inactivation, allopurinol increases the efficacy and toxicity of these two drugs, and also enhances the toxicity of cyclophosphamide, so care should be taken when using this drug.
(iii) Increase uric acid excretion
Drinking more water, more than 2000ml of water daily is an easy and effective method. The most important factor of uric acid crystallization when excreting from kidney is urine pH <5.5, i.e. acidic, which is more important than the increase of uric acid excretion, which is also the cause of uric acid stones and uric acid nephropathy. Therefore, we should drink more water and take alkaline medicine to make urine pH 6.2-6.8. Alkaline medicine can be 10% potassium citrate or sodium bicarbonate, but the former is better because citrate can reduce the formation of calcium oxalate stones. Propofol 0.5 b.i.d., benzbromarone 40-80 mg/d, thioxazone 0.2 b.i.d. Choose one of them and use it for one week.
The above anti-inflammatory and analgesic drugs, inhibiting uric acid production and increasing uric acid excretion can be used in combination. The onset of action of anti-inflammatory and analgesic drugs depends on how early or late they are administered. If the redness, swelling, pain and fever start to occur immediately, the pain often subsides quickly. If the redness, swelling, pain, and fever have been for several days before starting treatment, the effect will come very slowly. If the treatment is late, the effect should be maintained even if the treatment is slow. Treatment principles are the same as above.