The prevalence of hyperuricemia and gout is increasing year by year in China, and it is soaring in coastal areas, including Guangdong. In addition to the physical pain that gout brings to patients, its disabling nature often makes patients suffer from social discrimination. In the latest guidelines, the goal of gout treatment is even “cure”. However, this “curable” disease has gradually evolved into a situation where it is difficult to achieve a “cure” and a high disability rate because most patients miss the best early treatment period, have poor compliance with medication, and have difficulty changing their dietary habits.
20-30 years old become the main force of hyperuricemia
Gout is a heterogeneous group of diseases caused by disorders of purine metabolism and/or decreased uric acid excretion resulting in increased blood uric acid, including hyperuricemia, recurrent acute monoarthritis, gouty stone deposition, chronic gouty stone arthritis, gouty nephropathy, and uric acid urinary tract stones. Gout is divided into two categories: primary and secondary. Primary gout is caused by congenital enzyme defects except for about 1%, and most of the causes are unknown, often accompanied by obesity, hyperlipidemia, diabetes, hypertension and cardiovascular disease. Secondary gout can be caused by kidney disease, hematological disease or the use of certain drugs, tumor radiotherapy and other causes.
Patients with gout often have a positive family history of the disease, which is a polygenic genetic defect. Obesity, diet and alcohol consumption are all high-risk factors for gout. Cold, exertion, alcohol consumption, high-protein, high-purine diet, trauma, surgery and infection are all common triggers for the development of gout, and patients with hyperuricemia should pay more attention to these factors.
An important cause of kidney failure
It is worth noting that hyperuricemia and gout are often associated with hypertension, diabetes, hyperlipidemia, obesity and various cardiovascular diseases, which aggravate the damage to the kidneys, cardiovascular and other important organs. In recent years, the relationship between hyperuricemia and chronic kidney disease has become a hot spot for research at home and abroad. Almost all patients with gout have kidney damage, and about 1/3 of them have kidney symptoms, such as uric acid nephropathy, uric acid urinary tract stones, and acute uric acid nephropathy.
Among the many patients with hyperuricemia and gout, there is a common misunderstanding or hidden uneasiness when they take medication, and when they visit the clinic, they often ask the question, “Will taking uric acid-lowering drugs hurt the kidneys?” This deep-rooted traditional awareness of “taking uric acid-lowering drugs will hurt the kidneys” makes many gout patients so afraid that they disregard the advice of doctors and give up the standard treatment of gout. In fact, the kidney damage in patients with hyperuricemia and gout is not due to the action of drugs, but to the disease itself.
The reason why high uric acid causes serious damage to the kidney is because of the damaging effect of uric acid crystals on the tubular interstitium of the kidney on the one hand, and the continued elevation of uric acid will lead to vascular endothelial dysfunction through inflammation, resulting in hypertension, cardiovascular disease and kidney disease, which may eventually develop into end-stage renal failure if not treated in time.
Gout attack should be actively treated with uric acid reduction
Hyperuricemia is a high-risk factor for gout, and various guidelines at home and abroad point out that patients should undergo uric acid-lowering treatment after a gout attack, regardless of the uric acid level, and those who have started using it during the acute attack should continue to use it without stopping it.
Many of the patients contacted in the clinic have had the experience of being misdiagnosed as other rheumatic diseases by doctors after the initial arthritis attack when the blood uric acid was normal in the local hospital. He said that during an acute gout attack, about 1/3 of patients have “normal” blood uric acid levels, which does not negate the diagnosis of gout. When a gout attack occurs, the intense pain causes a stress response, and the endogenous hormones produced by the neuroendocrine response to stress promote the excretion of uric acid in the blood, causing the illusion of normal blood uric acid. Although the blood uric acid index shows normal at this time, the patient’s gout attack indicates that the blood uric acid concentration is supersaturated, so lowering uric acid is the key.
When treating gout, some doctors and patients are often eager to bring the elevated blood uric acid down to the normal range quickly, thinking that when the blood uric acid is normal, the gout will be relieved. This is not the case. A sudden reduction in uric acid levels not only does not help, but sometimes prolongs the duration of gout attacks. The sudden decrease in blood uric acid causes insoluble urate crystals deposited in the joints and surrounding tissues to fall off, leading to an acute gouty arthritis attack, also known as metastatic arthritis. Patients should not start uric acid-lowering drugs during the acute phase of gout (if they have been taking uric acid-lowering drugs, they should continue taking them without changing the dose). After the arthritis has resolved for 2 to 4 weeks, uric acid-lowering drugs should be started again under the guidance of a specialist.
A “cure” for a disease that is difficult to “cure”
In the latest guidelines, the goal of gout treatment is “cure”. Gout can be completely cured under the concept of drug-free clinical remission, but patients often miss the opportunity to treat gout due to their arbitrariness and poor compliance with medication.
In years of outpatient experience, we found that most gout patients do not care about their high blood uric acid, and when they have painful and swollen joints, most of them take the attitude of no treatment or random treatment until they have unbearable painful gout attacks and longer attacks, then they will rush to the rheumatology department for help. In this case, gout has often reached the middle stage, and patients miss the best early treatment time.
At the same time, most doctors and patients only pay attention to the acute treatment of gout, ignoring the prevention of uric acid reduction and complications during the intermittent period. When a gout attack is unbearable, patients will follow the doctor’s advice, take regular treatment, adhere to the medication, and abandon habits such as drinking alcohol, high-protein and high-purine diet. However, once the condition improves or the gout does not attack for a long time, most patients think that the gout has been cured and there is no need to continue using medication, and they resume smoking and drinking with impunity.
It is not difficult to control gout and achieve a drug-free clinical remission “cure”, but the difficulty of treating gout for a long time is often due to patients’ misunderstanding of the concept of “cure” for gout. Communication between doctors and patients and patient compliance are difficult to achieve.
During the intermittent and chronic periods, patients should adhere to uric acid-lowering therapy to keep blood uric acid within the standard range, and take appropriate uric acid-lowering medications along with prophylactic medications to prevent the rapid decrease of blood uric acid that can trigger acute arthritis.
What is the relationship between hyperuricemia and gout?
Hyperuricemia is the most important biochemical basis for the development of gout and the most direct cause. With the increase of hyperuricemia level, the prevalence of gout also increases gradually, but most of the hyperuricemia does not develop into gout, only the deposition of uric acid crystals in the body tissues causes damage to gout; in a small number of patients in the acute stage, the hyperuricemia level can also be in the normal range, therefore, hyperuricemia cannot be equated with gout.