Gout

Gout is an inflammatory arthritis caused by monosodium urate crystals forming in and around joints. It commonly causes sudden attacks of severe pain, heat and swelling, often at the base of the big toe. Effective treatment addresses both the immediate inflammation and the long term urate crystal deposits that cause attacks to recur.

What gout is Gout is a form of inflammatory arthritis caused by monosodium urate crystals forming within joints and surrounding tissues. These crystals can trigger sudden episodes of intense inflammation called gout flares or gout attacks. The affected joint can become extremely painful, hot, swollen and difficult to move within a few hours. Gout is more than a series of isolated painful attacks. Urate crystals can remain in tissues between flares and gradually accumulate when the underlying urate level remains high. Long term treatment can dissolve these crystal deposits, prevent future flares, shrink tophi and reduce permanent joint damage. Uric acid and urate Uric acid is produced when your body breaks down substances called purines. Purines occur naturally within your cells and are also present in some foods and drinks. At the usual acidity of blood, most uric acid exists in a chemical form called urate. The terms uric acid and urate are often used interchangeably in everyday healthcare. Urate travels in the blood to the kidneys. Most is removed through urine, while a smaller amount leaves through the bowel. Your serum urate level rises when production exceeds removal. In most people with gout, reduced kidney excretion contributes more than unusually high production. This does not necessarily mean that the kidneys are failing. Inherited kidney handling, medicines, dehydration and chronic kidney disease can each affect urate removal. How crystals form When urate remains above its saturation point, monosodium urate crystals can begin to form. Crystallisation is influenced by urate concentration, temperature, acidity and the local joint environment. The feet are commonly affected partly because peripheral joints are cooler than the centre of the body. Crystal formation usually develops over time. One large meal does not create an entire crystal burden overnight. An individual attack begins when deposited crystals provoke a strong immune response within or around a joint. Why a gout attack is so painful The immune system recognises exposed urate crystals as a danger signal. White blood cells enter the joint and release inflammatory chemicals. Blood vessels widen and become more permeable. Fluid and inflammatory cells collect within the tissues. This produces rapid swelling, heat, tenderness and severe pain. Even light contact from clothing or bedding may become intolerable. The intensity of pain does not necessarily mean that permanent damage has occurred during that one attack. Repeated untreated inflammation and persistent crystal deposition can, however, damage cartilage, bone and surrounding structures over time. Hyperuricaemia is not the same as gout Hyperuricaemia means that the urate concentration in your blood is higher than the laboratory reference range or crystal saturation threshold. It is an important requirement for most gout, but it is not the same diagnosis. Many people have raised serum urate without developing symptoms or clinically apparent crystal deposits. A high result alone does not prove that current joint pain is caused by gout. Conversely, serum urate can fall temporarily during an acute gout flare. A result within the laboratory range during an attack does not reliably exclude gout. Asymptomatic hyperuricaemia Asymptomatic hyperuricaemia means raised serum urate without gout attacks, tophi or urate related stones. Routine urate lowering medicine is not generally prescribed solely because one blood result is high. The overall clinical context matters. Very high levels, cancer treatment, kidney stones or unusual metabolic conditions may require a different assessment. Lifestyle and cardiovascular risk factors can still be reviewed when hyperuricaemia is found. The aim is to avoid turning a laboratory number into a disease label without evidence of crystal related illness. The typical acute gout attack A gout flare usually begins rapidly, often overnight. Pain commonly reaches severe intensity within hours. The joint becomes swollen, warm or hot and very tender. The skin may look red, purple or otherwise different from its usual colour. Redness can be harder to recognise on black or brown skin. Heat, swelling, tenderness and change from the person's usual skin appearance remain important. Movement becomes difficult, and weight bearing may be impossible when the foot, ankle or knee is affected. Early attacks often affect one joint. Several joints may become involved in longstanding or severe disease. Podagra and the big toe The first metatarsophalangeal joint lies at the base of the big toe. A gout attack at this site is called podagra. Podagra is the classic gout presentation. The joint can become so sensitive that the pressure of a bedsheet causes severe pain. The big toe pattern strongly suggests gout in the right clinical context, but it does not prove it. Infection, trauma, osteoarthritis, bunion related inflammation and other crystal disorders can also affect this region. A first severe attack should be assessed rather than diagnosed from the joint location alone. Other joints gout can affect Gout can affect the midfoot, ankles, knees, fingers, wrists and elbows. The olecranon bursa over the back of the elbow can become inflamed or contain tophi. Hip, shoulder and spinal involvement are less common and may be difficult to recognise. Later disease can involve several joints at once and may resemble rheumatoid or another inflammatory arthritis. Atypical location increases the importance of careful examination and confirmation when the diagnosis remains uncertain. How long an attack lasts Without treatment, a gout flare commonly lasts one to two weeks. Symptoms then usually settle as the inflammatory response resolves. The joint may remain tender, stiff or sensitive after the most severe pain has passed. Early effective treatment can shorten the attack and reduce suffering. Complete improvement between early attacks does not mean that the underlying crystal deposits have disappeared. Without urate control, attacks may become more frequent, last longer and involve more joints. The interval between attacks The symptom free period between attacks is called the intercritical period. A person may feel completely well during this time. Urate crystals can nevertheless remain within joints and tissues. This explains why long term treatment is taken every day rather than only when pain occurs. The absence of symptoms does not show that gout has cured itself. Follow up after a flare provides an opportunity to measure serum urate, review risk factors and discuss prevention. A trigger is not the whole cause People often identify an event shortly before a flare. Examples include alcohol, dehydration, illness, trauma or a large meal. These events may alter urate levels or disturb established deposits, helping to trigger inflammation. The trigger is not the same as the underlying cause. Gout develops because monosodium urate crystals have accumulated over time. Blaming one meal can obscure genetics, kidney handling and medicines that contribute more strongly. Avoiding one suspected trigger may reduce some attacks but usually does not dissolve existing crystals. Alcohol Excess alcohol can increase gout risk and provoke flares. Beer and spirits are commonly associated with increased risk. Alcohol can raise urate production, reduce kidney excretion and contribute to dehydration. A binge may be more likely to trigger an attack than the same amount spread over time. The effect varies between individuals. Not every person who drinks alcohol develops gout, and some people with gout do not drink. Alcohol advice should remain proportionate and non judgemental. Dependence requires medically supported reduction because sudden withdrawal can be dangerous. Purine rich foods Some foods contain substantial purines. Examples include organ meats, certain game meats, some red meat, shellfish and oily fish. These foods can increase serum urate modestly and may contribute to flares in susceptible people. Dietary purines are only one part of urate balance. Most purines arise from normal turnover within your own body. NICE found insufficient evidence that one specific gout diet reliably prevents attacks or lowers serum urate enough to control the disease. A balanced eating pattern is more useful than an extreme list of prohibited foods. Large meals and sugary drinks A very large meal can accompany other flare triggers, including alcohol use and dehydration. Drinks sweetened with fructose can increase urate production and add substantial energy intake. Regular high intake may contribute to gout and metabolic risk. An occasional drink does not explain gout by itself. Replacing sugar sweetened drinks with water or unsweetened alternatives can support overall health. Dietary change should complement rather than replace urate lowering treatment when medicine is indicated. Dehydration and acute illness Dehydration can reduce kidney urate excretion and temporarily concentrate urate in the blood. Vomiting, diarrhoea, fever, fasting and reduced fluid intake can therefore precipitate a flare. Acute illness can also alter inflammation, kidney function and medicine levels. Hospital admission and surgery are recognised times when attacks may occur. Fluid advice must account for heart failure, kidney disease or another condition requiring restriction. Drinking excessive water is not appropriate for everyone. Trauma, surgery and rapid urate change An injury to a joint can provoke inflammation around existing crystals. Surgery can produce wider changes in fluid balance and metabolism. A rapid rise or fall in serum urate can destabilise deposits and trigger a flare. This is why attacks can initially become more frequent after effective urate lowering therapy begins. An early treatment related flare does not mean that the long term medicine is failing. Preventive anti inflammatory treatment and gradual dose titration can reduce this problem. Sex and age Gout is more common in men, particularly from middle age onwards. Premenopausal women generally have lower serum urate because oestrogen promotes urate excretion. Risk rises in women after menopause. Earlier menopause can extend the period of increased susceptibility. Gout can occur in younger adults, but unusual early onset may suggest a strong inherited tendency, kidney disease, medicines or a rare metabolic cause. Sex and age alter probability but never confirm the diagnosis. Genetics and health problems in the family Genes strongly influence how the kidneys and bowel transport urate. Gout often runs in families because inherited differences affect serum urate and crystal formation. A health problems in the family does not mean that diet is irrelevant, but it explains why similar lifestyles can produce different outcomes. Some genetic variants also increase the risk of severe reactions to allopurinol in particular ancestral populations. Testing is considered according to clinical context and prescribing standards rather than offered routinely to everyone. Body weight and metabolic health Living with overweight or obesity increases gout risk and may increase flare frequency. Body size can influence urate production, insulin resistance, kidney excretion and inflammation. Hypertension, dyslipidaemia, type 2 diabetes and cardiovascular disease commonly coexist with gout. Weight is not a moral cause of disease. Genetics, medicines, pain, income, sleep and food access all influence body weight. Gradual sustainable weight loss can reduce serum urate and improve wider health when appropriate. Crash dieting or prolonged fasting can provoke attacks. Chronic kidney disease The kidneys remove most urate from the body, so chronic kidney disease can raise serum urate. Gout is common in people with reduced kidney function. Treatment choices also become more complex because some flare medicines can cause harm. The relationship works in more than one direction. Gout and hyperuricaemia are associated with kidney disease, hypertension and cardiovascular risk. This association does not prove that lowering urate will reverse established chronic kidney disease. Kidney function should be assessed because it affects diagnosis, medicine selection, dosing and long term risk. Diuretics and other medicines Thiazide and loop diuretics can raise serum urate by reducing kidney excretion. They are often prescribed for hypertension, heart failure or fluid retention and may be clinically important. A diuretic should not be stopped independently because the untreated condition may be dangerous. Clinicians can review whether an alternative is suitable or whether gout should be treated while the diuretic continues. Low dose aspirin, ciclosporin, tacrolimus and some cancer treatments can also affect urate or gout risk. A medicine association does not prove causation Many people taking diuretics never develop gout. Many people with gout are not taking a diuretic. A medicine may add to inherited, kidney and metabolic risks rather than act as the only cause. The indication for the medicine matters. Changing an effective cardiovascular treatment solely to lower urate may be inappropriate. A structured review weighs the benefit of the medicine against its contribution to gout. When the treatment must continue, urate lowering therapy can still control gout effectively. Gout and cardiovascular disease Gout frequently occurs alongside hypertension, diabetes, chronic kidney disease and cardiovascular disease. These conditions share risk factors, including age, excess body weight and kidney impairment. A gout review is an opportunity to check blood pressure, smoking, kidney function and wider cardiovascular risk. Gout should not be treated as proof that a heart attack or stroke will occur. Managing cardiovascular risk requires established interventions rather than assuming that urate lowering medicine replaces them. Diagnosing gout clinically A rapid overnight onset of severe pain, redness and swelling in the first big toe joint is strongly suggestive of gout. Tophi also provide an important clue when the appearance and location are typical. Gout should also be considered when a similar attack affects the ankle, midfoot, knee, hand, wrist or elbow. The clinician asks how quickly symptoms started, whether previous attacks resolved and which risk factors are present. A typical history can support a clinical diagnosis, but serious alternatives must still be considered. The physical examination The clinician observes joint swelling, skin change and whether the joint feels warm. They assess tenderness, range of movement, weight bearing and whether inflammation appears centred within the joint or surrounding skin. Other joints are examined for inflammation, deformity or tophi. The skin is checked for wounds, ulcers, bites or possible entry points for infection. Temperature and general observations matter, but normal observations do not completely exclude septic arthritis. Serum urate testing NICE recommends measuring serum urate when symptoms and signs suggest gout. A level of 360 micromoles per litre, equivalent to 6 milligrams per decilitre, or more supports the clinical diagnosis. The result should not be interpreted in isolation. Hyperuricaemia can occur without gout. Kidney function, medicines, alcohol, hydration and the timing of the test affect interpretation. A serum urate result does not distinguish gout safely from septic arthritis in an acutely hot joint. Serum urate can be normal during a flare Serum urate can fall during an acute attack because urate shifts into tissues and inflammatory processes alter handling. A result below 360 micromoles per litre during a flare does not rule out gout when the clinical suspicion remains strong. NICE advises repeating the serum urate at least two weeks after the flare has settled. The later result provides a more representative baseline for long term management. This limitation should be explained so that a single normal result does not create false reassurance. Joint aspiration Joint aspiration uses a sterile needle to remove synovial fluid from a swollen joint. The fluid can be examined under polarised light microscopy for monosodium urate crystals. Gout crystals are classically needle shaped and show strong negative birefringence under specialised microscopy. Aspiration is particularly useful when the diagnosis is uncertain, the pattern is atypical or infection needs exclusion. The procedure may also reduce pressure in a large effusion, but its main purpose in this setting is diagnostic safety. Crystals confirm gout but do not automatically exclude infection Finding monosodium urate crystals confirms that gout crystals are present in the sampled joint. Septic arthritis and gout can occasionally occur together. Fluid should therefore be sent for cell count, Gram stain and culture when infection is a concern. A person who remains systemically unwell or fails to improve needs reassessment even when crystals were identified. Clinical reasoning must not stop at the first positive finding. Imaging when uncertainty remains Imaging is not routinely required for a classic gout presentation. If aspiration cannot be performed or uncertainty persists, NICE advises considering X ray, ultrasound or dual energy CT. Ultrasound may show urate deposits on cartilage, including the double contour sign, or identify tophi and inflammation. Dual energy CT can distinguish urate deposits from surrounding tissues in selected cases. No imaging result should delay urgent management when septic arthritis is suspected. X rays in longstanding gout Early gout often produces no specific X ray abnormality. Longstanding disease can cause well defined erosions with overhanging bony edges and preserved joint space until later stages. Tophi may appear as soft tissue masses, sometimes with calcification. These findings indicate chronic crystal deposition rather than the severity of one current flare. X rays can also reveal osteoarthritis, fracture or another cause of pain. Septic arthritis is the critical differential diagnosis Septic arthritis is infection within a joint. It can destroy cartilage rapidly and lead to sepsis or death. Like gout, it can cause sudden severe pain, heat, swelling, skin colour change and restricted movement. Fever, shivering or feeling systemically unwell increases concern, but infection can occur without fever. Older adults, immunosuppressed people and those with prosthetic joints may show fewer typical signs. If septic arthritis is suspected, NICE advises immediate referral through the local urgent care pathway. Risk factors for septic arthritis Risk increases with a prosthetic joint, recent joint surgery or injection, immunosuppression and poorly controlled diabetes. Skin infection, ulcers, injecting drug use and infection elsewhere in the body can provide a route for bacteria. Previous joint disease can increase susceptibility. Known gout does not protect someone from infection. A first attack in an unusual joint or a flare that behaves differently deserves careful review. Antibiotics taken before aspiration may reduce culture yield, but treatment should not be dangerously delayed when sepsis is suspected. Cellulitis Cellulitis is infection of the skin and deeper soft tissue. It can cause pain, warmth, swelling and skin colour change near a joint. The inflammation may be more diffuse than gout and may extend beyond the joint margins. A wound, ulcer or skin break can provide an entry point. Fever and systemic illness may occur. Gout and cellulitis can be difficult to distinguish, and they can occasionally coexist. Spreading redness, lymphatic streaking, pus or rapidly worsening illness requires urgent assessment. Calcium pyrophosphate crystal arthritis Calcium pyrophosphate crystal arthritis is sometimes called pseudogout. It is caused by different crystals from gout. It commonly affects the knee, wrist, shoulder, ankle or elbow and becomes more common with age. The attack can be indistinguishable from gout or septic arthritis on appearance alone. Joint fluid microscopy can identify calcium pyrophosphate crystals. The long term urate lowering medicines used for gout do not treat calcium pyrophosphate deposition. Osteoarthritis and inflammatory arthritis An osteoarthritis flare can cause joint pain and some swelling, particularly in a previously damaged joint. Osteoarthritis usually produces a more gradual, activity related pattern rather than maximal pain within hours. Rheumatoid arthritis can cause persistent symmetrical swelling, prolonged morning stiffness and systemic symptoms. Psoriatic arthritis can affect individual fingers or toes and may be associated with psoriasis or nail changes. Gout can coexist with any of these disorders, so one previous diagnosis should not explain every new joint symptom automatically. Trauma and other causes A fracture, ligament injury, tendon problem or bleeding into a joint can produce sudden pain and swelling. Anticoagulant treatment can increase the likelihood of bleeding after minor trauma. A careful account of injury, bruising and function helps guide imaging and treatment. Bursitis can cause swelling over the kneecap or elbow without inflammation throughout the joint. The differential diagnosis becomes broader when pain is persistent, atypical or associated with neurological or systemic features. Treating an acute gout flare The immediate goal is to reduce inflammation and pain safely. NICE recommends an NSAID, colchicine or a short course of oral corticosteroid as first line treatment. The best option depends on kidney function, cardiovascular disease, gastrointestinal risk, diabetes, other medicines and individual preference. None of the three options is automatically best for every person. Treatment is most effective when started early after symptoms begin. Rest, elevation and cold therapy Resting the affected joint can reduce painful loading during the most intense phase. Elevating the limb may help swelling when the foot, ankle or knee is involved. A wrapped ice pack can be applied for up to about 20 minutes at a time. Ice should not touch bare skin directly. Cold therapy is an addition to prescribed anti inflammatory treatment rather than a replacement. Movement can be reintroduced gradually as pain settles to reduce stiffness and loss of function. NSAIDs for a gout flare Non steroidal anti inflammatory drugs reduce inflammatory prostaglandin production. Examples used in gout include naproxen and other suitable NSAIDs. Aspirin is not used as the anti inflammatory treatment for a gout flare. NSAIDs can provide effective pain relief when started promptly. A proton pump inhibitor may be added to reduce upper gastrointestinal injury. The medicine is normally used for a short course and reviewed if symptoms do not improve as expected. NSAID safety NSAIDs can cause stomach or intestinal bleeding, kidney injury, fluid retention and cardiovascular complications. Risk rises with older age, previous ulcer, chronic kidney disease, dehydration, heart failure and anticoagulant or antiplatelet treatment. Combining two NSAIDs increases harm and is not appropriate. Over the counter availability does not make ibuprofen or another NSAID safe for every person. Someone with vomiting, dehydration or acute kidney deterioration may need a different flare treatment. Colchicine Colchicine reduces the inflammatory response to urate crystals. It does not lower the serum urate level. Low dose regimens are preferred because higher doses increase toxicity without improving benefit sufficiently. Diarrhoea, nausea, vomiting and abdominal pain are common adverse effects. Colchicine has a narrow therapeutic range. Taking more than prescribed can cause severe or fatal poisoning. Tablets should be stored safely and never shared or used as repeated unsupervised rescue doses. Colchicine interactions and organ function Colchicine is cleared through the kidneys and liver and interacts with several medicines. Kidney or liver impairment can increase exposure and toxicity. Some macrolide antibiotics, antifungal medicines, antiviral medicines and cardiovascular drugs can cause dangerous interactions. Muscle pain, weakness, tingling, severe gastrointestinal symptoms or unusual bruising during treatment requires medical advice. A clinician or pharmacist should check the complete medicine list before colchicine is prescribed. Corticosteroids A short course of oral corticosteroid can treat a gout flare when NSAIDs or colchicine are unsuitable. Corticosteroids reduce inflammation quickly and can be effective in people with kidney impairment. They can raise blood glucose, affect mood and sleep, worsen infection and cause fluid related effects. Known or suspected septic arthritis must be considered before corticosteroid treatment suppresses the inflammatory response. People with diabetes may need temporary glucose monitoring advice during treatment. Corticosteroid injections An intra articular corticosteroid injection can treat inflammation within one accessible joint after infection has been reasonably excluded. An intramuscular injection is another option when NSAIDs and colchicine are contraindicated, ineffective or not tolerated. A joint should not be injected as routine gout treatment when septic arthritis remains possible. Temporary glucose elevation, local flare and rare injection related infection can occur. The decision depends on joint accessibility, diagnostic certainty and clinician expertise. Specialist treatments for difficult flares Interleukin 1 inhibitors can suppress a major inflammatory pathway involved in gout. NICE advises against routine use unless NSAIDs, colchicine and corticosteroids are contraindicated, ineffective or not tolerated. A rheumatology service should assess the person before this treatment is prescribed. This restriction reflects cost, infection risk and the need for specialist oversight. Most gout flares can be managed without biologic treatment. Existing urate lowering treatment should usually continue If you already take allopurinol, febuxostat or another urate lowering medicine, it should not normally be stopped during a gout flare. Stopping and restarting causes further urate fluctuation and may increase future flares. The flare is treated with an anti inflammatory medicine while the usual urate lowering treatment continues. A dose should not be increased or restarted after a prolonged interruption without appropriate advice. A suspected serious medicine reaction is different and requires urgent clinical assessment. Follow up after a flare A gout attack should lead to review after the acute inflammation has settled. The clinician measures serum urate or repeats it if the acute result was low. Kidney function, cardiovascular risk, medicines and possible triggers are reviewed. The person receives a plan for treating another flare promptly if one occurs. Long term urate lowering treatment is discussed rather than waiting passively for repeated attacks. Lifestyle change is supportive, not a punishment Gout is sometimes portrayed as a consequence of overindulgence. This stereotype is inaccurate and stigmatising. Inherited urate handling, kidney function and medicines often play a major role. Lifestyle measures can reduce triggers and improve wider health, but they may not lower urate enough to dissolve crystals. Advice should focus on practical opportunities rather than blame, shame or an unrealistic perfect diet. Effective medicine should not be withheld until someone achieves a weight or dietary target. Healthy weight management When appropriate, gradual sustained weight loss may reduce serum urate and flare frequency. It can also improve blood pressure, diabetes, cardiovascular risk and lower limb joint load. Rapid weight loss, fasting and ketogenic states can temporarily raise urate and trigger attacks. The plan should account for pain, mobility, culture, finances and previous weight management experiences. Exercise can improve health even before weight changes occur. A balanced diet rather than a rigid gout diet NICE advises that evidence is insufficient to recommend a specific diet as a reliable treatment for gout. A balanced pattern can emphasise vegetables, fruit, whole grains, suitable protein sources and unsweetened drinks. Reducing excessive portions of organ meat, red meat, shellfish and other high purine foods may help some people. Low fat dairy products can fit within a balanced diet and may be associated with lower gout risk. Dietary advice should remain nutritionally adequate and should not create unnecessary food fear. Alcohol moderation Reducing excessive alcohol can decrease flare triggers and improve wider health. The type, amount and pattern of drinking matter. Binge drinking can combine alcohol, dehydration and a large meal. A person may choose to identify whether one drink repeatedly precedes attacks, but this does not replace urate control. UK low risk drinking guidance provides a general framework, while individual advice may be stricter because of medicines or illness. Dependence requires specialist support rather than abrupt cessation without medical advice. Hydration Avoiding dehydration may reduce one common flare trigger and helps lower the risk of some kidney stones. Water is usually the most suitable drink, but no fixed large volume is safe for everyone. Heart failure, advanced kidney disease and some endocrine disorders may require fluid restriction. Hydration cannot overcome persistently high urate caused by genetics, kidney impairment or medicines. It supports a treatment plan rather than replacing it. When urate lowering therapy is offered NICE recommends offering treat to target urate lowering therapy to people with multiple or troublesome flares. It should also be offered with chronic kidney disease stages 3 to 5, diuretic treatment, tophi or chronic gouty arthritis. The option should be discussed after a first or later flare even when these specific features are absent. A previous stone caused by uric acid or a very high urate level can also influence the discussion. The decision is shared and considers benefits, monitoring, comorbidities and personal priorities. Urate lowering therapy is usually long term Urate lowering therapy works by maintaining serum urate below the level that supports crystal formation. Existing crystals then dissolve gradually. This process can take months or years when the crystal burden is large. Stopping treatment after attacks improve allows urate to rise and crystals to form again. NICE describes urate lowering treatment as typically lifelong. Long term treatment is different from the short anti inflammatory course used for an acute flare. When treatment is started NICE recommends usually starting urate lowering therapy two to four weeks after a flare has settled. This provides time to discuss long term treatment when severe pain is no longer dominating the consultation. For people with frequent flares and no clear symptom free interval, treatment can begin during a flare with appropriate flare management. This is more accurate than an absolute rule that allopurinol or febuxostat must never start during an attack. If treatment is already established, it normally continues throughout a flare. Treat to target management Treat to target means adjusting the urate lowering dose according to measured serum urate rather than leaving everyone on one standard dose. Treatment begins at a low dose. Serum urate is usually checked monthly while the dose is increased as tolerated. The dose that reaches target varies widely between people. Symptoms alone cannot show whether serum urate is adequately controlled, especially during the symptom free interval. Once target is stable, NICE advises considering annual serum urate monitoring. The usual serum urate target NICE recommends aiming for a serum urate below 360 micromoles per litre, equivalent to 6 milligrams per decilitre. This target lies below the level at which crystal formation is favoured under usual conditions. Maintaining the level below target allows deposits to dissolve gradually. The target is not simply a laboratory reference range. It is a treatment goal linked to crystal biology. One result below target is encouraging but does not mean that longstanding deposits have already disappeared. When a lower target is considered NICE advises considering a serum urate target below 300 micromoles per litre, or 5 milligrams per decilitre, in more severe gout. This includes people with tophi or chronic gouty arthritis. A lower target can also be considered when frequent attacks continue despite urate remaining below 360 micromoles per litre. The aim is faster dissolution of a larger crystal burden. Dose escalation still requires safety monitoring and shared decision making. Starting low and increasing gradually Rapid urate change can mobilise existing crystals and provoke attacks. A low starting dose followed by gradual titration reduces this problem and improves medicine safety. Kidney function and other medicines influence the initial dose and monitoring plan. The final effective dose may be higher than the starting dose or a traditional fixed dose. Failure to reach target on a low dose does not automatically mean that the medicine has failed. Preventing flares when urate falls Gout attacks can become temporarily more frequent when urate lowering therapy starts or the dose increases. This happens because existing deposits become unstable while crystals begin to dissolve. NICE recommends discussing preventive anti inflammatory treatment during titration. Colchicine is offered when suitable while the target is being reached. A low dose NSAID or low dose oral corticosteroid can be considered when colchicine is unsuitable. This temporary increase in flares should be explained before treatment so that the person does not abandon an effective long term plan. Allopurinol Allopurinol reduces urate production by inhibiting an enzyme called xanthine oxidase. It is widely used because it is effective, familiar and suitable for many people when introduced carefully. NICE recommends either allopurinol or febuxostat as a first line treat to target option, considering comorbidities and preference. Allopurinol is specifically preferred first line for people with major cardiovascular disease. It is taken regularly, including during symptom free periods. Allopurinol and kidney disease Allopurinol can be used in many people with chronic kidney disease, but the starting dose and titration require care. A low dose reduces the risk of adverse reactions. The dose is then adjusted according to urate response and tolerability. Kidney function alone should not lead to permanent undertreatment when cautious titration can reach the target safely. Monitoring may include kidney function, liver function and blood counts according to local practice and clinical circumstances. Specialist advice is useful when kidney disease is advanced or treatment options are limited. Allopurinol rash and hypersensitivity A skin rash after starting allopurinol requires prompt medical advice. The medicine is generally stopped while the reaction is assessed. Most reactions are not life threatening, but a rash can be the first sign of rare severe hypersensitivity. Urgent help is needed for blistering, peeling skin, mouth ulcers, facial swelling, fever, breathing difficulty or widespread illness. Risk is greatest during the early treatment period and with inappropriate starting doses. Allopurinol should not be stopped for several days and then restarted at the previous full dose without clinical guidance. Important allopurinol interactions Allopurinol has a major interaction with azathioprine and mercaptopurine because it can greatly increase their toxicity. These medicines are used for inflammatory disease, transplantation and some cancers. Combining them requires specialist dose adjustment and close monitoring or avoidance. The full prescription and over the counter medicine list should therefore be reviewed before treatment. This interaction is uncommon but potentially severe and should not be missed. Febuxostat Febuxostat also inhibits xanthine oxidase and lowers urate production. It is taken once daily and can be effective when allopurinol is unsuitable or fails to reach target. NICE permits either febuxostat or allopurinol as first line urate lowering therapy after considering comorbidities and preferences. Dose titration and serum urate monitoring remain necessary. Febuxostat is not simply prescribed and left unmonitored. Liver tests and potential interactions are considered according to prescribing guidance. Febuxostat and cardiovascular disease For people with major cardiovascular disease, NICE recommends allopurinol as first line treatment. Major cardiovascular disease includes previous myocardial infarction, stroke or unstable angina. MHRA advice states that febuxostat should be used cautiously in people with pre existing major cardiovascular disease. The evidence has evolved and is not accurately summarised as febuxostat being forbidden for every cardiovascular patient. The choice requires individual assessment, particularly when crystal and tophus burden is high or treatment is being initiated. Other urate lowering options Uricosuric medicines increase urate excretion through the kidneys. They are used less commonly and require suitable kidney function and stone risk assessment. Specialist services may use combination treatment when xanthine oxidase inhibition alone cannot achieve target. Pegloticase breaks down urate but is reserved for severe treatment resistant disease in specialist settings. The medicine choice depends on previous reactions, kidney function, cardiovascular history and access to monitoring. Most people can achieve control with carefully titrated allopurinol or febuxostat. Tophi A tophus is a collection of monosodium urate crystals surrounded by chronic inflammatory tissue. Tophi commonly form around fingers, toes, elbows, ears, tendons and bursae. They may feel firm and can appear yellow or white beneath thin skin. Tophi can restrict movement, compress nerves, damage joints or ulcerate through the skin. They indicate a substantial crystal burden and are a clear reason for long term treat to target therapy. Tophi can shrink Sustained serum urate below target allows crystals within tophi to dissolve. Smaller deposits may disappear, while large longstanding tophi can take years to shrink. A lower urate target below 300 micromoles per litre may be considered to speed dissolution. Improvement depends on maintaining treatment rather than using medicine only during pain. Surgery is occasionally needed for ulceration, infection, severe compression or major functional obstruction. Chronic gouty arthritis Repeated flares and persistent deposits can produce chronic inflammatory joint pain and swelling. The pattern can involve several joints and may resemble rheumatoid arthritis. Erosions and deformity can reduce grip, walking and other daily activities. Acute attacks can still occur on top of the chronic symptoms. Urate lowering treatment remains central because anti inflammatory medicines alone do not remove the underlying deposits. Permanent joint damage Tophi and repeated inflammation can erode bone and damage cartilage. The joint can become stiff, unstable or deformed. Tendons may also be affected. Damage may not reverse completely after urate is controlled, although pain and inflammation can improve. Early long term treatment prevents this outcome more effectively than waiting for visible tophi. Exercise, occupational therapy, footwear support and occasionally surgery may be needed when damage is established. Kidney stones Uric acid can crystallise within the urinary tract and form kidney stones. Stones may cause severe loin pain radiating towards the groin, nausea, vomiting or blood in the urine. Some people with gout develop calcium based stones rather than uric acid stones, so the stone type may need investigation. Hydration, urine chemistry and urate lowering treatment can form part of prevention. Fever, shivering or reduced urine with stone symptoms can indicate an obstructed infected kidney and requires urgent assessment. Gout and chronic kidney disease Chronic kidney disease raises gout risk by reducing urate excretion and limits some anti inflammatory options. Repeated NSAID use can further injure susceptible kidneys. Long term urate control can prevent gout flares and urate deposits in people with kidney disease. It should not be presented as a proven treatment that reverses chronic kidney disease itself. Kidney care includes blood pressure control, diabetes management, medicine review and avoidance of nephrotoxins where possible. Referral to rheumatology Specialist referral is considered when the diagnosis remains uncertain or aspiration and imaging require expert input. Referral is also appropriate when treatment is contraindicated, poorly tolerated or ineffective despite an adequate treat to target approach. Advanced kidney disease, organ transplantation, severe tophaceous disease and frequent attacks can complicate management. An IL 1 inhibitor or unusual urate lowering strategy requires specialist oversight. The purpose of referral is to improve diagnostic and treatment precision, not because every case of gout requires hospital care. Gout can be controlled Gout is one of the few inflammatory arthritides in which the underlying deposit can be removed through sustained biochemical treatment. Attacks may continue for several months while old crystals dissolve, especially when disease is longstanding. Reaching and maintaining the serum urate target is more important than expecting immediate permanent freedom from attacks. Regular monitoring, dose titration and adherence turn treatment from temporary pain control into disease modification. With effective long term management, many people become free from flares and tophi can shrink or disappear.

Gout occurs when monosodium urate crystals accumulate and trigger joint inflammation. A flare needs prompt anti inflammatory treatment, but lasting control requires sustained urate lowering to a measured target so that the underlying crystal deposits gradually dissolve.