Gout Treatment​ in Hyderabad, India

PACE Hospitals is recognized for advanced care in gout disease treatment in Hyderabad, India. Our experienced gout specialists focus on accurate gout test, diagnosis, and effective management of both acute and chronic gout conditions.

At PACE Hospitals, we provide personalized gout treatment plans designed to reduce pain, prevent flare-ups, and protect joint health. With expertise in handling complex cases, our team ensures long-term relief and improved quality of life for patients.

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Gout Treatment

Why Choose PACE Hospitals for Gout Disease Treatment?

The diagnosis of gout involves a combination of clinical evaluation and laboratory testing. It includes examining the affected joints, assessing symptoms, and analyzing joint fluid or blood samples. The presence of uric acid crystals in the joint fluid, confirmed through microscopy, serves as a definitive diagnostic marker. Additionally, imaging studies and blood tests to measure uric acid levels can support the diagnosis and help rule out other conditions.

The rheumatologist considers the following before selecting the appropriate tests to diagnose gout: 

• Medical history and prior history of gout 
• Physical examination

Medical history and prior history of gout 

A thorough medical history is essential for identifying symptoms, risk factors, and potential triggers of gout. It aids in accurate diagnosis and helps distinguish gout from other joint disorders. History needs to begin with the following questions:

• When did you first experience joint pain or swelling?
• Do you experience redness, warmth, or stiffness in the joint?
• How would you describe the pain (e.g., sharp, throbbing)?
• How long do the flare-ups last?
• Which joints are typically affected?
• How often do the attacks occur?
• Have the attacks become more frequent or severe over time?
• Have you noticed any triggers like specific foods, alcohol, or stress?
• Do you have a history of kidney disease, hypertension, or diabetes?
• Is there a family history of gout or similar joint problems?
• Are you taking any medications, especially diuretics or antiplatelets 
• Does joint pain limit your daily activities or movement?

Physical examination 

Physical examination findings in gout generally correlate with the patient's clinical history. The affected joint is often red, swollen, warm, and tender to the touch. In cases of chronic gout, flare-ups may involve multiple joints and can trigger a systemic inflammatory response syndrome (SIRS), which may mimic the clinical presentation of sepsis. Additionally, tophi, subcutaneous deposits of monosodium urate crystals, may be present in patients with long-standing hyperuricemia. These nodular formations are commonly found in the joints, ears, finger pads, tendons, and bursae.

Diagnostic Evaluation

Based on the above information, a rheumatologist advises certain diagnostic tests to detect gout. The following are the tests that might be recommended to diagnose gout:

• Synovial (joint) fluid analysis 
• Laboratory tests
• Serum uric acid 
• Complete blood count (CBC)
• Urine test 
• Erythrocyte sedimentation rate (ESR)
• Serum creatinine 
• Imaging tests 
• X-rays
• Ultrasound 
• Dual-energy computed tomography (DECT)

Synovial (joint) fluid analysis

Gout is confirmed by the presence of monosodium urate (MSU) crystals in synovial fluid, which appear needle-shaped and negatively birefringent under polarized light microscopy. These crystals trigger joint inflammation, producing the classic symptoms of gout. During acute flares, synovial fluid is typically cloudy, with elevated white blood cell counts and a predominance of neutrophils. However, the presence of crystals does not exclude infection, as gout and septic arthritis can coexist, making arthrocentesis essential for accurate diagnosis and differentiation.

Laboratory tests 

• Serum uric acid: This test evaluates the amount of uric acid in the blood. Elevated uric acid levels can cause crystal formation in the joints, resulting in inflammation and pain. However, uric acid levels may be normal during an acute gout attack. Therefore, results must always be interpreted alongside symptoms and clinical findings, as they are not diagnostic on their own.
• Complete blood count (CBC): In gout, it may show elevated white blood cells during acute inflammation. Hemoglobin and platelets usually remain normal, but it is not a diagnostic test to rule out infection or other causes of joint pain.
• Urine test: This test is performed to check for the presence of uric acid crystals, blood, or signs of urinary tract infection in patients with gout. It helps assess kidney function and detect complications such as uric acid stones. While urinalysis alone cannot diagnose gout, it provides important information to support the diagnostic process.
• Erythrocyte sedimentation rate (ESR): This is a blood test that measures inflammation in the body. In gout, ESR levels are often elevated during acute attacks, reflecting active inflammation. However, ESR is a nonspecific marker and cannot confirm gout on its own, but it helps assess the severity of inflammation.
• Serum creatinine: This test evaluates serum creatinine levels to assess kidney function, which may be impaired in patients with gout. Reduced renal function can decrease uric acid excretion, increasing the risk of gout. Although not directly diagnostic, creatinine testing provides essential information about underlying renal issues that may result in the development or progression of gout.

Imaging tests 

• X-Rays: This test is used to visualize joint structures and is primarily helpful in ruling out other causes of joint pain, such as fractures or osteoarthritis. Joint damage due to gout may not be visible on X-rays until the disease has progressed over several years, making them less useful for early diagnosis.
• Ultrasound: This test uses sound waves to detect signs of gout in joints and soft tissues. It can identify features such as urate crystal deposits, joint effusion, and the double contour sign, which suggests crystal buildup on cartilage surfaces. Ultrasound is a non-invasive tool that can support the diagnosis of gout, particularly during acute flares or when joint aspiration is not feasible.
• Dual-energy computed tomography (DECT): This advanced imaging technique utilizes two distinct X-ray energy levels to identify and differentiate urate crystal deposits from surrounding tissues, specifically. DECT helps detect uric acid crystals in joints and soft tissues, even in early or atypical cases of gout. It is especially valuable when the diagnosis is uncertain or when joint fluid analysis is not possible.

Stages of Gout

Gout progresses through each stage with its own clinical features. With timely and appropriate treatment, progression to the final stage of chronic tophaceous gout can often be effectively prevented. The following are the 4 stages of gout:

• Asymptomatic hyperuricemia: At this stage, uric acid levels in the blood are high, but no symptoms are present. No joint damage occurs, and treatment is usually not required unless levels are very high or associated with other conditions.
• Acute gout attacks: In gout, the asymptomatic hyperuricemia stage often precedes the first acute gout attack; however, many individuals never progress to symptoms. Acute gout typically presents as sudden, severe monoarticular joint pain, most commonly in the big toe, with swelling, redness, and warmth. Attacks often occur at night and may be mistaken for an infection due to systemic signs, such as pyrexia (fever)and an elevated white blood cell count. Triggers include trauma, alcohol use, fasting, diuretics, and urate-lowering therapy. Over time, attacks may become polyarticular and less intense, with tophi developing in chronic cases.
• Intercritical gout: After the resolution of an acute gout attack, the patient enters the intercritical stage. During this phase, there are no symptoms such as joint pain or swelling, and the patient generally feels well. However, elevated uric acid levels persist, and urate crystal deposition may continue silently. Subclinical joint inflammation can also be present despite the absence of overt symptoms.
• Chronic tophaceous gout: It can develop over years in untreated or poorly managed cases, leading to joint destruction and deformity. Gouty tophi are chalky urate crystal deposits surrounded by inflammation, commonly seen in fingers, toes, knees, and bursae. Though typically appearing years after initial attacks, microtophi may occur earlier, specially in patients with hyperuricemia. Tophi can also appear in unusual locations like heart valves or the cornea, reflecting the systemic nature of the disease.

Gout Differential Diagnosis

The differential diagnosis of gout requires consideration of other conditions that can mimic its presentation, particularly acute monoarticular or polyarticular joint inflammation. Conditions to consider in the differential diagnosis of an acute gout flare include:

• Pseudogout (Calcium pyrophosphate crystal deposition disease): This condition may mimic gout clinically but results in the deposition of calcium pyrophosphate dihydrate (CPPD) crystals instead of monosodium urate. Under polarized light, CPPD crystals appear rhomboid-shaped and reflect light differently compared to the needle-shaped monosodium urate crystals seen in gout, aiding in their differentiation.
• Basic calcium phosphate (BCP) crystal disease: It is also known as apatite-related arthritis. This condition involves the deposition of basic calcium phosphate (BCP) crystals around joints, leading to inflammation and pain. These deposits can cause severe inflammation, mimic other arthritic disorders, and may result in joint damage over time.
• Septic arthritis: Septic arthritis must be ruled out, especially in patients with fever or worsening joint symptoms despite gout treatment. It presents with a hot, swollen, tender joint, and the diagnosis relies on synovial fluid analysis, Gram stain, and culture.
• Osteoarthritis: It may cause joint pain and swelling, but typically presents as a more chronic condition with less inflammation.
• Psoriatic arthritis: Joint inflammation related to psoriasis can sometimes mimic gout, particularly when it presents acutely and involves the lower extremities.
• Cellulitis: It is a prevalent bacterial skin illness that affects the underlying tissues and deep layers of the skin. It typically manifests as a heated, painful, swollen, red patch of skin that spreads quickly and is frequently accompanied by chills and fever.
• Trauma: It can cause acute joint pain and swelling due to injury.

The differential diagnosis for tophaceous gout includes:

• Dactylitis: It involves significant swelling of the fingers or toes, giving them a sausage-like appearance. It results from inflammation of the joints and surrounding soft tissues, commonly seen in psoriatic arthritis and other inflammatory conditions.
• Rheumatoid arthritis: This chronic inflammatory arthritis often presents with joint swelling and pain, sometimes with a sudden onset. It typically affects multiple joints symmetrically and may be accompanied by systemic symptoms.
• Osteomyelitis: It is a bone infection, usually caused by bacteria, that results in inflammation and swelling of the bone tissue.

Goals of Gout Treatment

Immediate pain relief and long-term disease control are the main goals of gout management. A proper course of treatment can lessen pain, avoid problems, and enhance quality of life. The important goals include: 

• To relieve acute pain and inflammation during flare-ups
• To minimise joint damage and preserve function
• To prevent recurrent flares
• To reduce and maintain serum uric acid levels 
• To address coexisting conditions or complications associated with gout, such as cardiovascular and kidney diseases.

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Depending on the symptoms and cause of gout, treatment plans may vary from one individual to another. Management typically includes medications to reduce pain and inflammation during acute attacks, along with long-term strategies to lower uric acid levels. The treatment of gout follows a systematic approach, which includes the following steps:

Nonpharmacological treatment 

Non-pharmacological management of gout focuses on lifestyle and dietary changes to decrease uric acid levels and prevent future flare-ups. These include:

• Dietary changes: Dietary changes include limiting the intake of purine-rich foods (e.g., red meat, organ meats, shellfish), avoiding high-fructose corn syrup and sugary beverages, reducing alcohol consumption, especially beer and spirits, and increasing intake of low-fat dairy products, vegetables, and whole grains.
• Hydration: Drinking plenty of water, ideally 2 to 3 liters daily, helps dilute uric acid levels in the blood. This promotes its excretion through the kidneys and reduces the risk of gout flare-ups and kidney stone formation.
• Weight management: Maintaining a healthy Body mass index (BMI) is crucial for reducing the risk and severity of gout attacks. Excess weight contributes to increased production and decreased elimination of uric acid, leading to crystal accumulation in the joints. Long-term management of gout can be significantly improved through gradual weight loss achieved by a balanced diet and regular physical activity.
• Physical activity: Regularly perform moderate physical activity, but when gout develops, stay away from activities that put excessive stress on the afflicted joints.
• Other lifestyle measures
• Smoking cessation is recommended for overall health and to reduce comorbidity risk.
• Applying Ice packs can help relieve joint inflammation and pain.
• Managing stress through relaxation techniques, meditation, or gentle activity can help during flare-ups.

Pharmacological treatment of gout 

It can be divided into two main categories, including medications for acute gout attacks and medications for long-term prevention of gout flares by lowering uric acid levels.

Acute gout flare 

Acute gout flare management aims to reduce inflammation and pain, ideally starting within 24 hours of onset. Nonpharmacological measures like rest and ice packs can be combined with first-line treatments such as NSAIDs, anti-mitotic agents, or systemic glucocorticoids. Treatment need to continue for 7–10 days to prevent rebound flares.

• NSAIDs: NSAIDs are most effective when initiated within 48 hours of the onset of gout symptoms. Treatment typically lasts for 5 to 7 days, with no specific NSAID significantly preferred over others. High-dose, fast-acting NSAIDs are generally recommended.
• Oral glucocorticoids: Glucocorticoids are recommended for gout patients who cannot use NSAIDs or anti-mitotic agents, especially those with renal impairment. They are effective for both monoarticular and polyarticular flares and need to be tapered after symptom improvement. Use need to be cautious in cases of infection, uncontrolled diabetes, or recent surgery due to potential adverse effects. Frequent or long-term use is discouraged to minimize complications.
• Parenteral glucocorticoids: Intravenous (IV) or intramuscular (IM) glucocorticoids are recommended for patients who cannot take oral medications or are not suitable candidates for intra-articular injections. Treatment typically starts with higher doses and is tapered as symptoms improve, often transitioning to oral therapy. Other hormonal options may be effective but are limited by cost and availability.
• Anti-mitotic agent: An anti-mitotic agent derived from a natural plant source has been used for over 3500 years and is effective when taken within 24 hours of a gout flare. Clinical trials have shown that it can decrease pain by more than 50% within 24 hours compared to a placebo. Its lipophilic properties enable efficient cellular uptake after oral administration, and it primarily acts by targeting tubulin, with metabolism occurring mainly in the liver.
• Interleukin-1 inhibition: IL-1 antagonists have shown effectiveness in managing refractory gout flares. These agents are typically given as short courses via subcutaneous injections, and may offer greater symptom relief than some traditional therapies. However, their use is limited due to uncertain risk-benefit profiles and higher costs.

Chronic gout (Preventing future attacks and complications)

Urate-lowering therapy (ULT), with a goal of maintaining serum urate levels(below 6 mg/dL), is essential to prevent recurrent gout flares and long-term complications. Achieving this target helps dissolve existing urate crystals, reduce the frequency of flares, and protect joint and kidney health. ULT can be classified into three main categories based on its mechanisms of action.

• Xanthine oxidase inhibitors (XOI): Xanthine oxidase inhibitors (XOIs) reduce uric acid production and are the first-line urate-lowering therapy in gout. Regular monitoring of liver, kidney function, and blood counts is necessary. While generally well-tolerated, these drugs may cause side effects ranging from mild skin rashes to rare but severe hypersensitivity reactions, particularly in patients with certain genetic risk factors.
• Uricosuric drugs: Uricosuric agents increase urate excretion by inhibiting renal reabsorption and are used in patients with normal kidney function and low urinary uric acid. They are contraindicated in those with kidney stones or severe renal impairment. Common side effects include gout flares, kidney stones, and gastrointestinal intolerance.
• Uricase pegloticase (Recombinant uricase): A pegylated recombinant uricase is used for refractory gout to rapidly lower serum urate by converting it to a more soluble compound. Administered every 2 weeks via IV, treatment requires monitoring for antibody development and infusion reactions and is contraindicated in patients with certain enzyme deficiencies. Another non-pegylated form is used to prevent uric acid nephropathy in tumor lysis syndrome but is not approved for gout treatment.

Surgical procedures

• Tophectomy: Tophectomy is a surgical procedure to remove tophi, uric acid crystal deposits in patients with chronic gout. It is considered when medical therapy is ineffective, or complications such as pain, joint damage, or infection occur.
  

Gout Prognosis

The prognosis of gout depends largely on individual factors, especially the presence of comorbidities such as cardiovascular disease, that is associated with an increased mortality. With proper medical treatment and adherence to lifestyle modifications, most patients can maintain a good quality of life and experience minimal long-term effects. However, individuals who develop symptoms at a younger age are more likely to have a more severe and progressive form of the disease. Without consistent treatment and lifestyle changes, recurrent flares and joint damage become more likely over time.

Frequently Asked Questions (FAQs) on Gout Treatment

What is gout?

It is a type of inflammatory arthritis resulting from increased uric acid levels in the blood, leading to the formation of needle-like crystals within the joints. This crystal deposition triggers episodes of sudden, intense pain, swelling, and redness, commonly affecting the big toe; however, other joints may also be involved.

What foods should I avoid for gout?

Managing gout involves reducing or avoiding high-purine foods such as red meat, organ meats, and certain shellfish. Alcohol, particularly beer and liquor, along with sugary drinks and high-fructose foods, should also be avoided. A diet rich in fruits, vegetables, whole grains, and low-fat dairy is recommended. Adequate water intake is essential to help eliminate excess uric acid from the body.

Can gout last over a month?

Yes, gout attacks can last for over a month, especially when left untreated or poorly managed. While typical flares resolve within 1 to 2 weeks, some people may experience long-term or recurrent episodes with ongoing pain, swelling, and joint stiffness. Factors including delayed treatment, frequent flares, high uric acid levels, or underlying health conditions can contribute to extended flare duration. Proper treatment and timely intervention are important in reducing the severity and length of gout attacks.

Is gout a fatal disease?

No, gout cannot result in death directly, but it can cause major side effects that eventually may threaten life. The illness is associated with a higher risk of metabolic syndrome, chronic renal disease, and cardiovascular disease, but it does not itself cause death. Untreated or inadequately managed, these related illnesses can have a substantial effect on general health and raise the chance of death. Preventing these long-term effects of gout requires early diagnosis and appropriate treatment.

Why gout is more common in males?

Gout is more common in men because they generally have higher uric acid levels, a key risk factor for the condition. This difference is partly due to the effect of estrogen in women, which helps lower uric acid levels. Men typically reach adult uric acid levels during puberty, while women's levels remain lower until after menopause. As a result, men are at greater risk of developing gout earlier in life.

Will gout go away on its own?

Although an acute gout attack may resolve on its own within a few weeks, relying solely on this is not advisable. Gout attacks can cause severe pain, and without treatment, they may progress to chronic gout and joint damage. While symptoms may temporarily improve, the underlying issue of elevated uric acid remains, increasing the risk of recurrent attacks and complications.

What is the main cause of gout?

Gout is primarily caused by high levels of uric acid in the body, which form sharp crystals in the joints and trigger pain and inflammation. This happens when the body either produces too much uric acid, or the kidneys are unable to remove it efficiently. Factors such as genetics, diet, obesity, certain medications, and kidney problems can contribute to elevated uric acid levels. If left untreated, gout attacks can become frequent and lead to permanent damage in the joints.

What is the meaning of gout?

The word "gout" comes from the Old French word "gote," meaning "a drop," which comes from the Latin word "gutta." It dates back to the 13th century. In medieval times, people believed gout was caused by drops of thick fluids leaking from the blood into the joints. This idea is similar to what we now know about uric acid crystals building up in the joints.

What kind of diet is best for gout?

A diet low in purines is typically advised to treat gout. This involves staying away from meals such as organ meats, red meat, and some seafood that can cause an increase in uric acid levels. To help lower the chance of gout attacks, instead, concentrate on eating a lot of fruits, vegetables, and low-fat dairy products. A balanced diet and lots of water consumption can also aid renal function and the removal of excess uric acid. These adjustments help lessen the probability of intense flare-ups and enhance general wellness.

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