Gout is a group of diseases caused by impaired purine metabolism and/or reduced 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 can even be described as “misunderstood”. In the following, I will try to summarize the details that need to be paid attention to in the clinical diagnosis and treatment of gout in the hope of helping primary care physicians.
Details 1. 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 greater the risk of 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 1: Gout is not unique to middle-aged men
Gout is commonly thought to be seen in middle-aged men over 40 years of age. Nowadays, with the improvement of living standard and the higher purine content in the diet, 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 teenagers with secondary gout.
For women after menopause, the incidence of gout is not low due to the greatly reduced levels of female estrogen.
Details three gout in the acute phase of the medication have 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 low-dose therapy (0.5 mg 3 times a day) due to the high side effects. Colchicine is now being withdrawn from clinical preference due to its side effects. Clinical discontinuation indicators: significant relief of inflammation and pain or severe GI reactions (nausea, vomiting, diarrhea, etc.).
2. Non-steroidal anti-inflammatory drugs (NSAIDs): At present, NSAIDs have replaced colchicine as the first-line drugs for controlling acute attacks of gout. 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 and the more adequate the dose (doubling the dose in the first two days), the more effective they are.
3. glucocorticoids: usually used in those for whom colchicine and NSAIDs are ineffective or intolerable. Prednisone is given orally at 20-30 mg per day and is tapered off after 3-4 days. The newer ones available in China are betamethasone sodium phosphate injection.
In conclusion, NSAIDs are recommended first for acute gouty arthritis, followed by steroid hormones orally or by local joint cavity injection, and colchicine is used as the third choice because its effective dose and toxic dose are too close.
Detail 4 Antibiotics cannot be used to control an acute attack of gout
In an acute attack of gout, the affected joints (mostly 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 therapy 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 penicillin and uric acid are excreted by the kidneys, and the former interferes with the excretion of the latter, causing the blood uric acid to rise, thus aggravating the condition.
The first thing you need to do is to take a look at the actual product.
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 use 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.
Detail 6: Do not take long-term “anti-inflammatory and analgesic drugs” to prevent gout attacks
The main culprit of gout is hyperuricemia. The key to preventing gout attacks is to control the blood uric acid, in addition to a low purine diet, and if necessary, to take uric acid-lowering treatment.
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.