Gout Treatment, Diet, Cause, Symptoms, Definition & Medication

Content

• Pathophysiology Of Gout
• Medicine Choices
• Inflammatory Findings

Taking vitamin C and eating a diet high in low-fat dairy products may be preventive. When gout causes severe joint pain, it is called a gout attack, a gout flare-up, or acute gout. Pain is typically accompanied by extreme joint tenderness, swelling, warmth, and skin redness. As the gout attacks continue, tophi will develop in the joints, tendons, bursae, subchondral bone, cartilage, ligaments, subcutaneous tissue, and synovium. Tophi are hard nodules of sodium urate deposits that may vary in number and location.

The most common cause of gout (about 90% of cases) is the inability to excrete enough uric acid in the urine. The most common is a genetic defect in substances referred to as organic anion transporters in the kidney, which leads to an excessive reabsorption of uric acid from the kidney – and thus too much uric acid in the blood. However, a defect in excretion of uric acid can also occur due to medications, such as diuretics, low dose aspirin, or alcohol.

Pathophysiology Of Gout

This is especially important if you also have other chronic conditions, like diabetes or heart disease. Intracellular monosodium urate crystal from synovial fluid, observed with polarized light microscopy. The folklore surrounding gout has also involved the eye, and before the 20th century, a myriad of common and unusual ocular symptoms were falsely ascribed to gout. Medical science has since documented eye involvement as a rare but definite aspect of gout.

Your blood uric acid level may be watched by your doctor until it is lowered to normal levels. During acute attacks, someone may be treated with nonsteroidal anti-inflammatory drugs such as ibuprofen or naproxen to relieve pain and inflammation and, if necessary, with corticosteroids like prednisone. If those do not help to control symptoms, colchicine may be useful within the first 12 hours of an attack. NSAIDs or oral colchicine may be prescribed in small daily doses to prevent future attacks as well. In some patients, anti-interleukin-1 therapy (anti-IL-1) has shown to be very effective in treating acute gout flare-ups. Gout is a chronic autoinflammatory disease with regular acute flares, which cause very painful joint inflammation .

Medicine Choices

Gout may occur after taking medicines that interfere with the removal of uric acid from the body. People who take certain medicines, such as hydrochlorothiazide and other water pills, may have a higher level of uric acid in the blood. In view of the effectiveness of our treatments, it is important for a correct diagnosis to be made as early as possible, and therapy begun quickly, when appropriate.

However, in September 2020, The Lancet published the FAST trial, which is a European trial very similar to the CARES trial, found a different result. Here, there was no difference in death rates in patients on febuxostat compared to those on allopurinol. This trial actually had many fewer dropouts in the study and overall reviewers have felt that the FAST trial is a more solid base than the CARES trial on which to base decisions about the use of febuxostat. Some have called for the FDA to reconsider its recommendations, but no changes made to date. The FAST trial gives considerable comfort to those patients presently on febuxostat.

Inflammatory Findings

Gout can be tricky to diagnose because many illnesses can cause joint pain and inflammation. Your doctor may suspect gout if you’ve had a sudden attack of joint pain followed by a period with no symptoms. because excess uric acid can builds up in the urinary tract and crystallize there. Kidney stones are more of a complication of gout than a symptom, but if you develop this equally painful issue your doctor should check your uric acid levels to see if gout might be a possibility. In some people, hyperuricemia leads to the formation of uric acid crystals that collect in joint tissue, leading to painful symptoms.

Urate

Normally, blood moves uric acid to the kidneys, and the uric acid exits the body in urine. A urinalysis is used to check uric acid levels in your urine and assess your risk of kidney stones. ​A urinalysis may be used to check uric acid levels in your urine and assess your risk of kidney stones. computed tomography for evaluating changes in feet of patients with chronic gouty arthritis.

Elevated serum urate levels may support diagnosis but are not sensitive or specific. Levels should be measured on several different occasions and it is possible for levels to be normal during and actute attack. You may not be able to prevent gout, but you may be able to avoid things that trigger symptoms. Taking medicines to lower uric acid can prevent progression of gout.

Talk to your doctor about the impact gout has on your emotional health, and ask for suggestions about ways to cope with it. Corticosteroids—given either orally or intra-articularly—are an appropriate treatment for patients who can’t tolerate an NSAID. As long as a septic joint has been excluded, an intra-articular injection of 40–80 mg triamcinolone acetonide or 40 mg of methylprednisolone acetate will result in major improvement within 24 hours for most patients. Another option is a seven- to 10-day course of oral prednisone, starting with 40 mg on day one and reducing the dosage by 5 mg/day. Elderly patients taking oral prednisone should also receive adequate calcium, vitamin D, and a proton pump inhibitor for gastrointestinal protection, as well as close monitoring of blood pressure, glucose, and mental status. The role of these techniques for gout classification in patients with early disease and any additional benefit over microscopic or clinical criteria requires careful consideration.

Is gout a clinical diagnosis?

Gout is typically diagnosed using clinical criteria from the American College of Rheumatology. Diagnosis may be confirmed by identification of monosodium urate crystals in synovial fluid of the affected joint. Acute gout may be treated with nonsteroidal anti-inflammatory drugs, corticosteroids, or colchicine.

Some people may have kidney stones before having their first attack of gout. Gout must be distinguished from conditions that can cause similar symptoms, such as calcium pyrophosphate deposition , a condition caused by the deposit of calcium pyrophosphate crystals, septic arthritis , and rheumatoid arthritis . The treatment of these conditions is different than those used in the management of gout. Attacks of gout may occur sporadically and last for several days. During these attacks, uric acid deposits may build up in cartilage, tendons, and soft tissues. Crystals that accumulate in the kidneys can lead to kidney stones and kidney damage.

Primary Care Physician

Gout may be secondary to sleep apnea via the release of purines from oxygen-starved cells. Studies in the early 2000s found that other dietary factors are not relevant. Specifically, a diet with moderate purine-rich vegetables (e.g., beans, peas, lentils, and spinach) is not associated with gout. Alcohol consumption is strongly associated with increased risk, with wine presenting somewhat less of a risk than beer or spirits. Eating skim milk powder enriched with glycomacropeptide and G600 milk fat extract may reduce pain but may result in diarrhea and nausea. Gout attacks usually get better on their own within about 3 to 10 days, even without treatment.

All of them had a baseline serum urate greater than 6 mg/dL. Other parameters evaluated in 1 study included erythrocyte sedimentation rate , C-reactive protein , number of tender joints , number of swollen joints, and pain score . All of them decreased with uricemia reduction, but only TRN and SP were statistically significant.

Specialty Care

A complete blood count, serum creatinine, and liver function test are useful for evaluating other comorbid diseases, monitoring drug toxicity after initiating therapy, and assessing contraindications to a specific drug. For example, if tests show evidence of bone marrow suppression, advanced renal failure, or rhabdomyolysis, colchicine is not indicated. If tests show renal insufficiency, therapy with uricosuric medications would not be effective because these medications require functional renal system to excrete excess urate. An additional proposed mechanism involves the role of an inflammasome and interleukin 1 (IL-1) in the pathogenesis of inflammation induced by MSU and CPPD . Cryopyrin inflammasome detects MSU and CPPD crystals and activates IL-1, resulting in an inflammatory cascade. These IL-1–mediated inflammatory effects of MSU crystals could be blocked by IL-1 inhibitors.