A recent news hit Weibo's hot search: Mr. Liu, a 21-year-old IT practitioner, was busy with his work. He drank drinks when he was thirsty, and ate takeaway when he was hungry. After working overtime, he suddenly fell into a coma and was admitted to the emergency intensive care unit.
After examination, Mr. Liu's blood sugar level exceeded the normal value by more than 20 times. According to the analysis of the visiting doctor, the patient's sedentary and unhealthy diet for a long time were the main reasons for the accident.
But what we want to talk about today is not the well-known problem of beverages raising blood sugar, but the entanglement between beverages and gout.
Clinically, there are many patients who do not eat seafood or drink and still get gout. In fact, it is inseparable from the love of drinking beverages.
How sugar-sweetened beverages can trigger gout
High uric acid is considered to be the "fourth highest" after high blood sugar, high blood lipids, and high blood pressure. Long-term high uric acid will directly cause gout attacks, causing great pain to patients.
Modern medicine believes that in addition to seafood and drinking, there is another type of food that can increase uric acid in daily life that is easily overlooked, that is, beverages (excluding water).
It is the living habit of many young people to be inseparable from cola, milk tea and juice every day.
However, clinical data show that excessive intake of sugar-sweetened beverages can easily lead to gout.
The most important reason is that these drinks contain fructose, which can produce uric acid after being metabolized in the body. Long-term intake of fructose is equal to the increase of uric acid production, which can easily lead to hyperuricemia and then gout.
Fructose is a monosaccharide, widely present in fruits and honey, which directly produces uric acid during the decomposition process in the body, which is equivalent to increasing the source of endogenous uric acid.
At the same time, fructose will reduce the excretion of uric acid by the kidneys, which will further increase the uric acid in the body.
Therefore, if the prevention of gout only focuses on reducing the intake of purine (uric acid is the end product of purine metabolism) and ignores the intake of fructose, it may still lead to gout attacks, or even repeated attacks.
Some people say that fructose is not good, then drink "sugar-free drinks" and "zero-calorie drinks".
This view is wrong.
Sugar-free drinks just do not contain fructose or sucrose, but sweeteners are added to make people taste sweet. Excessive intake of sweeteners will still be converted into sugar in the human body, and the amount of purines will increase after metabolism.
This can understand why doctors in rheumatology do not recommend gout patients to drink "sugar-free drinks" and "zero-calorie drinks".
The following health reminders are recommended for everyone to keep in mind, which can better prevent gout or reduce the attack of gout.
First, eat a moderate amount of fruit every day, try not to juice the fruit, and never drink the juice as water; second, drink less sugary beverages, and never drink the beverages as water; third, mango, lychee, cantaloupe , Hawthorn and other fruits with high fructose content, do not eat too much at one time.
The disease is divided into 4 stages from mild to severe
The causes of gout are complex.
This is a crystal-related arthropathy caused by the deposition of monosodium urate (MSU), which is directly related to hyperuricemia caused by disturbance of purine metabolism and/or decreased uric acid excretion, and belongs to metabolic rheumatism.
Clinically, gout is generally divided into four stages: asymptomatic hyperuricemia, acute attack, intermittent attack and chronic tophi.
These four stages can be said to be the objective manifestations of the severity of the disease from mild to severe, and the development of the disease from front to back, and each stage has different clinical characteristics.
1. Asymptomatic hyperuricemia period
This is the early stage of the onset of gout. At this time, most people do not have any discomfort, but the blood uric acid level is found to be elevated during the physical examination.
This stage can last for years or even decades before progressing to the next stage of gout (acute attack), and some people may never enter the acute attack of gout for a lifetime.
For such people, it is recommended to adjust lifestyle, moderate low-purine diet, drink more water, and control weight, and uric acid-lowering therapy is not recommended.
2. Acute attack period
This is the first stage of hyperuricemia patients progressing to gout. It is mostly manifested as sudden redness, swelling, heat, pain and dysfunction of joints in the middle of the night or in the early morning. The pain is severe, and the pain peaks within 12 hours. Natural relief within 2 weeks.
The most commonly affected joint is the unilateral first metatarsophalangeal joint, but the dorsum of the foot, heel, ankle, and knee may also be involved.
Colchicine, NSAIDs, or glucocorticoids are commonly used to control symptoms during acute exacerbations.
It is recommended that the patient follow a strict low-purine diet, take active anti-inflammatory and analgesic treatment, apply local cold compress to the affected joint, and pay attention to rest.
3. Intermittent episodes
This refers to the intermittent attacks of gouty arthritis. As the disease progresses, the number and frequency of attacks gradually increase, and the affected joints gradually develop from the lower limbs to the upper limbs, from the distal small joints to the large joints, and the symptoms and signs of the attacks gradually tend to Not typical.
It is recommended that patients actively seek medical treatment, choose appropriate uric acid-lowering drug therapy, and a low-purine diet.
4. Chronic tophi stage
This is the result of the unsatisfactory control of long-term significant hyperuricemia and the deposition of a large number of urate crystals in the subcutaneous, joint synovium, bone and soft tissues around the joint.
Tophi typically occurs in the pinna of the ear, which is shaped like a "small stone" and is also commonly found around joints that have recurring attacks.
Clinically, it can manifest as persistent joint swelling, deformity or dysfunction, and sometimes acute attacks.
It is recommended that patients actively control serum uric acid and strictly follow a low-purine diet to prevent the occurrence of complications.
Gout is very harmful to the human body.
In the short term, it can lead to gouty arthritis, acute pain, and affect the quality of life; in the long run, it can lead to uric acid nephropathy such as chronic uric acid nephropathy, renal insufficiency, and even develop into renal failure and uremia.
Long-term high uric acid can also induce uric acid stones and further aggravate renal insufficiency.
In addition, hyperuricemia caused by gout can easily induce cardiovascular and cerebrovascular diseases such as hypertension, coronary heart disease and stroke.
In a word, gout, a metabolic disease, is easy to be related to other diseases, and they are often not isolated, and can also be bad, and we must pay attention to them.
Why does the onset begin to become "younger"
According to clinical observations, the prevalence of gout in my country has gradually increased in recent years, and the age of the affected group is gradually "younger".
The incidence of gout is related to congenital genetic factors and has a genetic predisposition. According to clinical medical statistics, the probability of a family history of gout in gout patients is about 10%-20%.
We believe that the "rejuvenation" of gout is mainly related to the changes in eating habits and lifestyles of contemporary young people.
Specifically, the change in dietary structure means that young people prefer a high-energy, high-purine diet, such as a high proportion of seafood and meat, while a low proportion of fresh vegetables, excessive intake of sugar-sweetened beverages, fruit juices and alcohol, while Drink less water; lifestyle changes refer to young people’s fast-paced life, high work pressure, often staying up late, eating irregularly, and prone to overeating. If physical activity becomes less and less, obesity occurs, which is even worse.
To prevent gout from becoming "younger", 8 things should be done.
1. Reduce the intake of high-purine foods; 2. Quit smoking and limit alcohol; 3. Strengthen exercise, but avoid strenuous exercise; 4. Reduce the intake of fructose-rich beverages; above); 6. Control weight; 7. Consciously increase the intake of fresh vegetables; 8. Regularly eat and rest as much as possible.
It can be seen that the "younger" high-risk groups of gout are also easy to identify - unhealthy diet, obesity, irregular work and rest, alcoholism, and drink love.
These groups of people with a family history of gout or hyperuricemia are at higher risk of developing gout.
Gout "cure" can not be stopped
Gout is easy to obtain and difficult to treat, and the current mainstream treatment method is uric acid-lowering therapy.
Since the pathophysiological basis of gout pathogenesis is hyperuricemia, control of serum uric acid level is the cornerstone of gout treatment.
Studies have shown that effective uric acid-lowering drug therapy can not only control serum uric acid below the target threshold, but also prevent monosodium urate crystal formation, reduce the number of gout attacks, relieve pain in patients, and make gout the only "curable" chronic disease. arthritis.
The commonly used uric acid-lowering drugs in China are divided into two categories: "inhibiting uric acid synthesis" and "promoting uric acid excretion", such as allopurinol, febuxostat and benzbromarone.
Allopurinol and febuxostat reduce uric acid synthesis by inhibiting xanthine oxidase activity; benzbromarone inhibits renal tubular uric acid reabsorption and promotes uric acid excretion by inhibiting renal tubular uric acid transporter-1.
Many gout patients are anxious and feel that the treatment process is long.
It should be emphasized that uric acid-lowering therapy is indeed a long-term systematic project that achieves the target. Even if the blood uric acid has dropped to a normal level, the drug cannot be stopped.
Once the drug is stopped, the blood uric acid will quickly return to the level before treatment, which will not only cause gout attacks again, but also bring the risk of kidney, cardiovascular and cerebrovascular involvement if the blood uric acid does not reach the control standard for a long time.
Under normal circumstances, the target of uric acid-lowering treatment for gout patients is blood uric acid <360 μmol/L, which should be maintained for a long time; if the patient has tophi, chronic gouty arthritis or frequent gouty arthritis attacks, the target of uric acid-lowering treatment should be blood Uric acid <300μmol/L, until the tophi is completely dissolved and the symptoms of frequent arthritis are improved, and then the treatment target is changed to blood uric acid <360μmol/L, and maintained for a long time.
Therefore, the general principle of uric acid-lowering treatment is to maintain the minimum dose of drugs to maintain the blood uric acid level continuously.
In addition, it is rare in clinical practice that the disease cannot be controlled with drugs, and most patients with poor control are due to poor compliance and irregular medication.
Gout patients need to take uric acid-lowering drugs for life. Clinical "cure" only refers to a state in which blood uric acid returns to the normal range and arthritis does not recur.
During the course of taking the medicine, the patient should regularly monitor the routine blood and urine, liver and kidney function.
Since the side effects caused by uric acid-lowering drugs are more common in the early stage of treatment, the frequency of monitoring related indicators is relatively high in the early stage of treatment, for example, blood and urine routine, liver and kidney function are reviewed every 2-4 weeks, and every 6-12 weeks after the blood uric acid reaches the standard Just recheck once.
In general, the long-term use of uric acid-lowering drugs brings small and controllable side effects to the human body.
Li Changhong (Author: Physician of Rheumatology and Immunology, Third Hospital of Peking University)