Myth 1: Hyperuricemia is gout
Many people believe that high uric acid in the blood is gout and must be treated. In fact, although hyperuricemia is the most important biochemical basis of gout, it is not a synonym for gout. Gout is a disease caused by abnormal purine metabolism and/or decreased uric acid excretion. The clinical characteristics are hyperuricemia, recurrent acute monoarthritis, gout stone deposition caused by sodium urate, and chronic gout stone arthritis. Without formal treatment, they often develop into gouty nephropathy.
Myth 2: Restricting a high-purine diet is sufficient
Studies have pointed out that even if the use of foods with extremely low purine content is strictly restricted, the decrease in blood uric acid concentration is limited; On the contrary, if there is no moderation in diet, it can rapidly increase the blood uric acid concentration to a state where it may attack at any time. On the other hand, gout patients are often accompanied by hyperlipidemia, hypertension or diabetes. These diseases need food control, so diet control is necessary.
Gout diet principle is to avoid high purine foods, such as animal viscera, sardine, clams, crabs, etc. Containing moderate amounts of purines include fish and shrimp, meat, peas, spinach, and so on. As for fruits, vegetables, milk, eggs, etc., the content of purine is relatively low.
Myth 3: Suffering from gout results from improper diet
There are two main categories of people with high incidence of gout: men aged 40 to 60, and those who consume a high fat diet and alcohol. Women are mostly postmenopausal, especially those who have high blood pressure and take diuretics.
2. Obesity with hyperuricemia, hypertriglyceridemia, hyperglycemia, and hypertension.
Take drugs that affect uric acid excretion, such as diuretics and low-dose aspirin.
4. Have a family history of gout, or trace a history of urinary tract stones among family relatives.
Myth 4: The location of gout attacks is limited to joints
In 70% of gout patients, the first site of onset is in the first big toe (first metatarsophalangeal joint). Pain can also occur in the dorsum of the foot, Achilles tendon, heel, ankle, and knee joints. In addition, upper limb joints such as fingers and elbows may also occur. More than 90% of patients have their first onset at the lower limb joints.
Why are lower limb joints, especially the first big toe, prone to seizures? The reason is not yet clear. However, gout attacks occur after uric acid becomes sodium urate crystals, and inflammation occurs. Therefore, gout can occur in places prone to crystallization. Crystallization is prone to occur sequentially in areas with strong acidity, frequent movement, load-bearing areas, and low temperatures. Therefore, the areas where crystallization is prone to occur are joints, auricles, kidneys, urinary tracts, etc. These sites are consistent with many conditions that are prone to crystallization, and joints, especially the first big toe, meet all conditions.
Myth 5: Treatment can be stopped after uric acid is stabilized and pain is relieved
The treatment of gout must adhere to lifelong medication and dietary therapy. Some patients abandoned medication after their uric acid stabilized. However, with such a casual withdrawal, uric acid soon rose again. The correct treatment is to allow the doctor to slowly reduce the dosage after the uric acid drops to the target value (blood uric acid 300-360 umol/l). Before that, it is necessary to adhere to regular medication.
Generally, gout treatment is divided into three stages, as follows:
Stage 1 is treatment for gout attacks. This is a treatment for pain relief, mainly with anti-inflammatory and analgesic drugs.
The second stage is the initial treatment of controlling uric acid after the gout attack disappears. The duration of medication, combined with dietary therapy and daily care, is 3-6 months. The types of drugs used vary depending on the type of hyperuricemia. In principle, patients with low excretion should use uric acid excretion promoting drugs, while patients with excessive production should use drugs that inhibit uric acid synthesis.
Stage 3 is followed by initial treatment for uric acid control, with lifelong uric acid control treatment, as well as medication and dietary treatment to prevent complications or recurrence.
