Gout is a group of diseases caused by impaired purine metabolism and/or decreased uric acid excretion, resulting in increased uric acid in the blood with damage to joints, kidneys and other organs. The disease is most common in young and middle-aged people aged 40-60 years old, with a ratio of about 20:1 between men and women, and most women develop it after menopause.
In recent years, with the improvement of living standard and change of diet structure, the incidence of hyperuricemia and gout in China has increased rapidly. Gout, which used to be a “disease of wealth” only for the rich and powerful, is now becoming more and more commonplace.
Although hyperuricemia and gout are relatively common in clinical practice, the diagnosis and treatment of this disease by primary care physicians is not standardized, and it can even be said to be “misunderstood”. Below, I will try to summarize the details of clinical diagnosis and treatment of gout, hoping to help primary care physicians.
The first detail is that gout should not be diagnosed/excluded based on blood uric acid.
Hyperuricemia is the main biochemical basis of gout. The higher the blood uric acid, the higher the risk of developing gout, but not all patients with hyperuricemia will progress to “gout”.
According to statistics, about 10% of patients with hyperuricemia will develop gout, while the rest will only be in a chronic hyperuricemic state without arthritic symptoms, which can only be called “hyperuricemia” and not diagnosed as gout.
Furthermore, although most gout patients have high blood uric acid, there are a few gout patients who do not have high blood uric acid when they have an acute attack.
Therefore, hyperuricemia and gout cannot be completely equated, and gout cannot be diagnosed or ruled out based on blood uric acid levels alone.
The clinical diagnosis of gout is generally based on the presence of increased blood uric acid, recurrent acute monoarthritis and asymptomatic intervals, and the effectiveness of colchicine in relieving symptoms. The “gold standard” for the diagnosis of gout is confirmation of the presence of uric acid crystals in synovial fluid or stone tissue.
Note: Normal range of blood uric acid: 150-417 μmol/L for men; 100-357 μmol/L for pre-menopausal women, and approximately the same range as men for post-menopausal women. A blood uric acid value >420 μmol/L is usually defined as hyperuricemia.
Detail 2: Gout is not only for middle-aged men
Gout is commonly thought to be seen in middle-aged men over the age of 40. Nowadays, with the improvement of living standards, the purine content in the diet is getting higher and higher, and the age of onset of gout is getting younger and younger, and it is not uncommon to see gout patients in their twenties, and there are even teenage patients with secondary gout.
For women after menopause, the incidence of gout is not low due to the greatly reduced levels of female estrogen.
The acute phase of gout, the medication has to be careful
In the acute phase of gout, the primary problem is to control joint inflammation as soon as possible and relieve the patient’s pain. The main drugs used are colchicine, non-steroidal anti-inflammatory drugs and glucocorticoids.
Colchicine: The traditional high-dose therapy has been gradually replaced by small-dose therapy (0.5 mg per time, 3 times a day) due to the large side effects. Colchicine has been gradually withdrawn from clinical preference due to its side effects. Clinical discontinuation indicators: significant relief of inflammation and pain or severe gastrointestinal reactions (nausea, vomiting, diarrhea, etc.).
2, non-steroidal anti-inflammatory drugs (NSAIDs): At present, non-steroidal anti-inflammatory drugs have replaced colchicine as the first-line drugs to control acute attacks of gout. Some studies have shown that: there is no difference between NSAIDs, and the key to successful treatment is not the choice of NSAIDs, but the timing and dose of NSAIDs, the earlier they are used, the more adequate the dose (double the dose in the first two days), the more obvious the efficacy.
3. Glucocorticoids: usually used for those who are ineffective or intolerant to colchicine and NSAIDs. Oral prednisone 20-30 mg daily, 3-4 days after the gradual reduction and discontinuation of the drug. The newer ones available in China are betamethasone sodium phosphate injection.
In conclusion, the first recommendation for acute gouty arthritis is the use of non-steroidal anti-inflammatory drugs, followed by steroid hormone oral or local joint cavity injection, and colchicine is used as the third choice because its effective dose and toxic dose are too close.
Details four, can not use antibiotics to control the acute attack of gout
During an acute attack of gout, the affected joints (mostly seen in the big toe and dorsum of the foot) rapidly develop redness, swelling, heat, pain and dysfunction, and in severe cases, fever and elevated white blood cells may also occur.
Without detailed history taking, physical examination and blood uric acid examination, it is easy to be misdiagnosed as local infectious inflammation (e.g., dengue, etc.) and given high doses of penicillin and other antibiotics, which is the most common misdiagnosis and mistreatment in gout treatment.
Since acute attacks of gout are self-limiting in nature, most patients can gradually resolve the disease on their own within 3-10 days without any treatment. This spontaneous remission is often mistakenly attributed to the use of antibiotics by doctors or patients, but this is not the case.
Gout is a sterile inflammation caused by the deposition of supersaturated urate crystals in the joints and surrounding soft tissues, and antibiotic treatment is not effective at all. On the contrary, the use of antibiotics such as penicillin during the acute phase of gout is not only ineffective in controlling attacks, but may also exacerbate gout by raising blood uric acid. This is because both penicillin and uric acid need to go through the kidney excretion, the former has an interference effect on the excretion of the latter, resulting in an increase in blood uric acid, thus aggravating the condition.
The acute attack period is not appropriate to add uric acid-lowering drugs
The problem that needs to be solved during the acute attack of gout is joint inflammation and pain, and symptomatic drugs with anti-inflammatory and analgesic effects (such as non-steroidal anti-inflammatory drugs, colchicine, etc.) should be chosen, while uric acid-lowering drugs (such as gout lixian, allopurinol, etc.) do not have anti-inflammatory and analgesic effects, and are ineffective in controlling the acute attack of arthritis and relieving joint pain.
On the contrary, because they can significantly lower the blood uric acid level, they can induce the dissolution of gout stones on the surface of joints and release insoluble urate crystals, which are phagocytosed by converging white blood cells and release inflammatory factors and hydrolases, thus aggravating joint inflammation or causing “metastatic gout”.
Therefore, it is not advisable to add uric acid-lowering drugs during an acute attack of gout, but rather to take uric acid-lowering drugs after the pain symptoms have completely subsided and the acute phase has passed; however, if the patient has previously started taking uric acid-lowering drugs, they should continue to take them without stopping them (note: it is a very common misconception to stop uric acid-lowering drugs during an acute attack).
The purpose of this is to try to maintain the relative stability of the patient’s blood uric acid concentration during the acute phase and to avoid aggravation of the disease due to significant fluctuations in blood uric acid concentration. Some patients do not standardize their medication, using uric acid-lowering drugs as anti-inflammatory and analgesic drugs, using them during acute attacks and stopping them after arthritis attacks, which is often counterproductive.
The six details, not long-term use of “anti-inflammatory and analgesic drugs” to prevent gout attacks
The main culprit of gout is hyperuricemia. To prevent gout attacks, the key is to control blood uric acid, in addition to a low purine diet, if necessary, to take uric acid reduction therapy.
Some doctors do not understand this, and in order to prevent gout attacks, let patients take long-term non-steroidal anti-inflammatory drugs (anti-inflammatory pain, etc.) or colchicine, which not only fails to prevent the effect, but may also lead to serious kidney damage.
Non-steroidal anti-inflammatory drugs, colchicine and glucocorticoids are all drugs that control acute attacks of gout and have a rapid anti-inflammatory and pain-relieving effect. However, these drugs neither affect uric acid metabolism nor increase uric acid excretion, so they are purely symptomatic treatment, not causal treatment, and treat the symptoms but not the root cause.
In addition, the side effects of these drugs are generally large, and can cause serious gastrointestinal reactions, but also can lead to kidney damage. Therefore, these drugs are only suitable for short-term application during the acute attack period, and should be reduced as soon as possible after the acute attack and discontinued within a short period of time.
The author once saw a gout patient who suffered from recurrent gout attacks and was told that anti-inflammatory pain could prevent gout flare-ups, so he took high doses daily. One year later, the kidney function test showed that the blood creatinine and urea nitrogen were abnormally high. The patient was then asked to stop taking the drug, and his kidney function soon recovered.