Although gout is fundamentally caused by high levels of blood uric acid, the pain in the big toe during an acute flare-up is often excruciating. When an attack strikes, should your immediate priority be using medication to stop the pain, or should you start trying to lower your blood uric acid levels right away?
To answer this, we need to understand the true nature of gout. Gout isn’t simply joint pain; it is an inflammatory disease triggered when excess uric acid crystallizes and deposits in and around the joints. For most people, this is caused by the kidneys excreting too little uric acid, while a smaller percentage experience purine metabolism disorders that lead to uric acid overproduction.
According to the general consensus of international gout treatment guidelines, managing gout is divided into two distinct phases: the acute flare-up phase and the intercritical (remission) phase. The treatment goals and medications differ significantly depending on the stage you are in.
The Acute Gout Flare-Up Phase: Prioritize Pain Relief
Gout pain occurs when the blood uric acid concentration exceeds its solubility limit. This causes sodium urate crystals to precipitate in the joints, synovium, tendons, kidneys, and connective tissues, eventually forming gout stones (tophi). These crystals create local inflammatory stimulation, leading to the classic symptoms of redness, swelling, heat, and severe pain.
Crucially, you should not initiate uric acid-lowering medications during an acute gout attack. Why? Because taking these medications can cause your blood uric acid levels to drop too rapidly. This sudden drop causes the surface of existing tophi to dissolve, releasing insoluble crystals that actually worsen the inflammatory response and irritate local tissues, ultimately intensifying your pain.
During the agonizing acute phase, when joints are red, swollen, and hot, the primary and only goal of treatment is to safely and rapidly terminate the inflammation and relieve pain. At this moment, the joint cavity is filled with micro-crystals being actively attacked by your immune system. If you introduce drastic fluctuations in blood uric acid by starting lowering therapies now, you risk destabilizing the crystals and prolonging the inflammation—a phenomenon clinically known as a “mobilization flare.” Multiple clinical studies confirm that starting uric acid-lowering drugs during the acute phase can prolong or worsen pain in 20% to 30% of patients.
Therefore, global rheumatology guidelines—including the latest from the American College of Rheumatology (ACR) and the European Alliance of Associations for Rheumatology (EULAR)—explicitly recommend: First, use sufficient anti-inflammatory and analgesic medications. Wait until the joint pain and inflammation are completely resolved (usually 1 to 2 weeks) before starting or adjusting any uric acid-lowering treatment.
Several medications are used to manage gout pain:
- Colchicine: Inhibits granulocyte infiltration and leukocyte chemotaxis.
- NSAIDs and Analgesics: Such as ibuprofen, indomethacin, diclofenac, and acetaminophen.
- Short-acting Glucocorticoids: Such as prednisone (used for short courses).
An Alternative for Rapid Relief: BISPIT GOUT ATTACK 3310B
Some patients have reservations about traditional painkillers due to concerns over gastrointestinal irritation, liver and kidney burden, or allergic risks. To address this, BISPIT GOUT ATTACK 3310B offers an emergency relief option derived from an herbal formula.
Designed specifically for the early stages of an acute gout attack, this liquid formulation absorbs quickly and can be taken promptly when pain first appears, before it limits mobility. Its formula blends botanical extracts like D-glucosamine, tartary buckwheat, celery seed, and Christina loosestrife (Jin Qian Cao). It aims to use natural ingredients to soothe joint discomfort, alleviate redness and swelling, and potentially reduce local inflammatory responses—helping patients regain basic mobility faster. It is highly suitable for those looking to avoid traditional painkillers or who need to quickly address sudden discomfort on the go.
The Gout Intercritical Phase (Remission): Lower Uric Acid Levels
Once the redness, swelling, heat, and pain have completely disappeared, you enter the calm “intercritical phase.” Here, the logic of your treatment fundamentally shifts.
Even without intense pain signals, urate crystals still lurk in the joints and tissues, waiting to trigger the next attack. The core objective now transitions from “pain relief” to “long-term control of blood uric acid, dissolving crystals, and preventing recurrence.”
Extensive global research, such as the renowned Nottingham Gout Cohort Study, provides solid evidence: consistently maintaining blood uric acid below target levels (typically <360 μmol/L for those without tophi, and <300 μmol/L for those with tophi) reduces the frequency of acute attacks. It also promotes the dissolution of existing crystals and prevents severe complications like joint destruction, tophi formation, and kidney damage.
Common uric acid-lowering medications include:
- Uric Acid Synthesis Inhibitors: Such as Allopurinol and Febuxostat.
- Uricosuric Agents (Promote Excretion): Such as Benzbromarone.
The Most Common Gout Mistake
A dangerous mistake many patients make is only taking medication during a pain flare-up and stopping the moment the pain subsides. This behavior causes drastic fluctuations in blood uric acid levels, which paradoxically triggers more frequent acute attacks. It creates a vicious cycle of “flare-up -> medication -> relief -> stop medication -> flare-up again,” allowing the disease to silently worsen.
Gout management is a prolonged battle that requires patience. By relying on scientific management, treating the disease according to its specific phase, and proactively taking charge of your long-term health, you can ultimately achieve the goal of a life free from gout attacks.