Why is there a lack of effective diagnosis and treatment for gout in medical clinical practice?
Release time:
2025-09-22
Gout is characterized by swelling, pain, joint involvement, recurrent attacks, and the accumulation of urate crystals, forming tophi. The earliest Chinese Traditional Medicine (TCM) understanding of gout (formerly known as "bi syndrome") can be found in the "Questions on Bi Syndrome" in the Huangdi Neijing. It attributes gout to the combined effects of wind, dampness, and cold, forming "bi" (bi). It further categorizes gout into three types: wandering bi, painful bi, and fixed bi. The pain associated with bi syndrome is described as roaming through the joints, resembling a tiger's bite. During the Eastern Han Dynasty, the medical sage Zhang Zhongjing further elaborated on the pathogenesis of gout. In the "Golden Chamber Essentials: Pulse Symptoms and Treatments for Stroke and Lijie Diseases," Zhang Zhongjing wrote that pain in the joints (i.e., gout) and inability to bend or stretch are caused by drinking alcohol and sweating in the face of wind. This coincided with the discovery of a link between alcohol consumption and gout by the renowned Greek physician Galen, who was also a contemporary. This fact demonstrates that ancient Chinese Traditional Medicine (TCM) and Western medicine, originating in Europe, explored the causes of gout simultaneously, and their understanding of the causal conditions was essentially the same.
Gout is characterized by swelling, pain, joint involvement, recurrent attacks, and the accumulation of urate crystals, forming tophi.
The earliest Chinese Traditional Medicine (TCM) understanding of gout (formerly known as "bi syndrome") can be found in the "Questions on Bi Syndrome" in the Huangdi Neijing. It attributes gout to the combined effects of wind, dampness, and cold, forming "bi" (bi). It further categorizes gout into three types: wandering bi, painful bi, and fixed bi. The pain associated with bi syndrome is described as roaming through the joints, resembling a tiger's bite. During the Eastern Han Dynasty, the medical sage Zhang Zhongjing further elaborated on the pathogenesis of gout. In the "Golden Chamber Essentials: Pulse Symptoms and Treatments for Stroke and Lijie Diseases," Zhang Zhongjing wrote that pain in the joints (i.e., gout) and inability to bend or stretch are caused by drinking alcohol and sweating in the face of wind. This coincided with the discovery of a link between alcohol consumption and gout by the renowned Greek physician Galen, who was also a contemporary. This fact demonstrates that ancient Chinese Traditional Medicine (TCM) and Western medicine, originating in Europe, explored the causes of gout simultaneously, and their understanding of the causal conditions was essentially the same.
Thereafter, throughout the Sui, Tang, Song, Yuan, Ming, and Qing dynasties, TCM's understanding of gout was divided into five categories based on syndrome differentiation, stratifying treatment from the exterior to the interior: (1) Damp-heat Bi-blockage Type, with the principle of clearing heat and dampness, unblocking the meridians and relieving pain; (2) Wind-cold-dampness Bi-blockage Type, with the principle of dispelling wind and cold, removing dampness and unblocking the meridians; (3) Phlegm and Blood Stasis Type, with the principle of resolving phlegm and dispersing nodules, activating blood circulation and unblocking the meridians; (4) Spleen and Kidney Yang Deficiency Type, with the principle of strengthening the spleen and kidneys, warming yang and dispelling cold; and (5) Liver and Kidney Yin Deficiency Type, with the principle of tonifying the liver and kidneys, and removing wind and dampness.
Since then, TCM's treatment of gout has been based on the principles of "removing dampness and promoting urination, dispelling wind and activating blood circulation, reducing inflammation and relieving pain, and nourishing the liver and kidneys." It should be said that, based on modern physiology and pathology's research on the theories of uric acid production and excretion, as well as the author's exploration of the underlying causes of gout, TCM's understanding of gout is truly profound. It penetrates beyond superficial symptoms to reveal the essence of renal uric acid excretion as a "deficiency syndrome," far surpassing the fundamental theories of Western medicine. Its definition of gout as a "kidney function disease" is quite accurate.
However, TCM's inherent historical limitations have limited its practitioners' ability to incorporate scientific data to aid diagnosis. Furthermore, TCM's siloed practice significantly hinders the exchange of medical information. In individual gout treatment, the lack of biochemical testing and verification of uric acid clearance makes it easy to confuse gouty arthritis with rheumatic arthritis, making it difficult to correctly categorize and treat gout. The "activating blood circulation and unblocking meridians, removing dampness and promoting urination" approach, in reality, carries the blind, traditional treatment cues and cannot avoid the risk of drug-induced renal failure. The timing of "resolving phlegm and dispersing nodules, and tonifying the liver and kidneys" is indeed difficult to grasp. Incorrectly tonifying deficiency syndromes can be counterproductive. This is a flaw in Traditional Chinese Medicine (TCM) itself and a regret left over from history.
Since the fifth century AD, the treatment of gout abroad has followed a symptomatic approach of "anti-inflammatory and analgesic." For example, ancient Egyptian herbal prescriptions included colchicine from the safflower family, a modern-day anti-arthritis agent. However, nearly all clinicians are well aware that "anti-inflammatory and analgesic" treatments merely relieve symptoms and are not beneficial for treating gout. In recent years, several "uric acid-lowering" drugs developed abroad have entered the Chinese market. However, in clinical practice, physicians have discovered that using only chemical drugs to lower uric acid carries significant clinical risks and is often unpredictable. The same drug may be effective in some patients but not others, or may initially be effective but then lose effectiveness. As for the reasons behind this, the response is generally "the mechanism remains unclear."
The current state of Western medicine uric acid-lowering treatment in China is independently implemented by rheumatology, endocrinology, and orthopedics departments in scattered tertiary hospitals. The theoretical level varies widely, and the choice of dosage form and dosage is entirely determined by physicians' clinical experience. There is a lack of unified implementation standards. When uric acid levels rebound after discontinuation of medication, patients are often educated with a simple, conservative approach of "lifelong medication." Over time, despite some successful cases, gout has not yet shown the expected clinical cure results, indicating that Western medicine's uric acid-lowering treatment is still exploratory. Furthermore, the American College of Rheumatology (ACR) frequently updates its gout prevention and treatment guidelines with medication risk warnings. This millennium-old disease of gout has become increasingly shrouded in mystery.
It seems everything is waiting for a new perspective.
Professor Wu Husheng, Deputy Director of the Department of Rheumatology and Immunology at Peking University Health Science Center and Director of the Department of Rheumatology and Immunology at Beijing Jishuitan Hospital, published the monograph "Wu Husheng's 2016 Perspectives on Hyperuricemia and Gout," and Professor Gu Jieruo, Director of the Department of Rheumatology and Immunology at the Third Affiliated Hospital of Sun Yat-sen University in Guangzhou, doctoral supervisor, and expert receiving the State Council Special Contribution Allowance, published the monograph "Gu Jieruo's 2019 Perspectives on Hyperuricemia and Gout." Both monographs describe the latest status of clinical research and exploration of gout in both China and abroad. Currently, research has entered the field of basic disciplines such as genetics and genomics, and over 20 gene fragments, including SLC2A9 and ABCG2, have been discovered to be associated with gout. These findings are hoped to provide a breakthrough in identifying the source of gout. However, experts have concluded that despite progress in gout immunogenetics and discoveries in polymorphisms of gout susceptibility genes, there is insufficient direct evidence to definitively establish that hyperuricemia causes gout.
When the authors of this book (a team of engineers) were building a mathematical model to analyze the probability of gout, they found that even important viewpoints on which consensus has been reached in clinical medicine have many problems that cannot stand scrutiny and are questionable.
For example, the theory that hyperuricemia is the most important biochemical basis for gout. Clinically, epidemiological studies show that only approximately 10% of patients with hyperuricemia develop gout, which fails to explain why approximately 90% of patients with hyperuricemia are naturally immune. For example, the theory that hyperuricemia is caused by both excessive uric acid production and/or decreased uric acid excretion, with excessive uric acid production accounting for 10% and decreased uric acid excretion accounting for 90%. In gout prevention and control, why do physicians focus on the 10% factor and prioritize restricting a high-purine diet as the primary factor for controlling uric acid levels, while failing to address the known 90% of factors and providing corresponding clinical countermeasures for the primary cause of decreased uric acid excretion?
For example, the theory that hyperuricemia and gout exhibit significant genetic heterogeneity. At the grassroots level, gout has clear shared lifestyle habits and similar external factors. Logical analysis cannot confirm a familial, recessive, or dominant, genetic relationship between current gout patients and those of the ancient aristocracy. If medical clinicians generalize the concept of heredity and genes, it becomes clinically meaningless. In reality, gout must have a consistent, yet as-yet-unidentified underlying underlying cause that applies to all forms of hyperuricemia. Until this underlying cause is truly discovered and confirmed, effective diagnosis and treatment of hyperuricemia and gout cannot be expected in clinical practice.
To be continued...
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