The 4 Stages Of Gout

Content

• How Can An Attack Of Gout Be Treated?
• Treatments For Hyperuricemia
• Is Gout Hereditary?
• What Is The Best Diet For Gout?
• Uricase Medications

The primary risk factor is hyperuricemia, although only a small proportion of patients with hyperuricemia develop gout, often taking 20 to 30 years to develop. The two mechanisms by which hyperuricemia can develop are either undersecretion of uric acid by the kidneys or overproduction of uric acid (only 10% of cases). If the disease is refractory to monotherapy with either of XOI option, then a uricosuric agent can be added to an XOI as a second-line approach.15 Uricosuric drugs block renal tubular urate reabsorption. These drugs can be used in patients with under excretion of urate, but are generally not recommended in patients with advanced kidney disease. Podagra treatment may consist only of short-term treatment to shorten and lessen the symptoms of a podagra attack.

How Can An Attack Of Gout Be Treated?

The elbow joint was irrigated through a small arthrotomy and a bulb suction drain was placed. The volar forearm had bulging muscles that contracted with electrocautery stimulation, and there was no evidence of necrosis, pus, or odor (Figure 1). Gouty tophi were not grossly observed in the fascia or muscle, but small tophi (∼0.25–0.5 mm) were seen sporadically in the synovial sheaths of the flexor tendons, which can occur after many years in patients with poorly controlled gout . The wounds were covered with sterile sponges attached to a conventional wound vacuum (V.A.C.Ulta™ Negative Pressure Wound Therapy System, KCI Medical, USA).

What is the best treatment for acute gout?

Drugs used to treat gout flares and prevent future attacks include:Nonsteroidal anti-inflammatory drugs (NSAIDs).
Colchicine.
Corticosteroids.

A typical gout attack is characterized by the sudden onset of severe pain, swelling, warmth, and redness of a joint. The clinical presentation of acute gouty arthritis is not subtle with very few mimics other than a bacterial infection. Acutely, gout can be managed with non-steroidal anti-inflammatory drugs (e.g. naproxen), colchicine, prednisolone, or newer cytokine blocking agents (e.g. IL-1 blockers such as anakinra or canakinumab) if refractory disease 12. In the long-term, xanthine oxidase inhibitors (e.g. allopurinol or feboxustat), uricosuric drugs (e.g. probenecid), or uricase agents (e.g. pegloticase) may be used to reduce urate levels and prevent further acute flares 12.

Treatments For Hyperuricemia

This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent. Gout is a disorder of purine metabolism, and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating and forming deposits in joints, on tendons, and in the surrounding tissues. Microscopic tophi may be walled off by a ring of proteins, which blocks interaction of the crystals with cells and therefore avoids inflammation. Naked crystals may break out of walled-off tophi due to minor physical damage to the joint, medical or surgical stress, or rapid changes in uric acid levels.

If you’re overweight, you are likely to have higher-than-normal uric acid levels, a primary risk factor for developing gout. Purines are found in certain high-protein foods and some drinks. It used to be thought that gout was caused only by lifestyle and diet, but new research has found that's not true; instead, gout is thought to have a genetic link.

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. It is largely managed in primary care but treatment is often suboptimal. Acute gout causes attacks of excruciating joint pain requiring rapid treatment. In primary care, treatment is most frequently with non-steroidal anti-inflammatory drugs which are effective but have frequent gastrointestinal, cardiovascular and renal side-effects, particularly in the elderly. Oral colchicine has been used to treat acute gout for many years although high-doses can cause intolerable gastrointestinal side-effects.

Liu R, Aupperle K, Terkeltaub R. Src family protein tyrosine kinase signaling mediates monosodium urate crystal-induced IL-8 expression by monocytic THP-1 cells. Wigley FM, Fine IT, Newcombe DS. The role of the human synovial fibroblast in monosodium urate crystal-induced synovitis. di Giovine FS, Malawista SE, Thornton E, Duff GW. Urate crystals stimulate production of tumor necrosis factor alpha from human blood monocytes and synovial cells. Cytokine mRNA and protein kinetics, and cellular distribution. Ryckman C, Gilbert C, De Medicis R, Lussier A, Vandal K, Tessier PA. Monosodium urate monohydrate crystals induce the release of the proinflammatory protein S100A8/A9 from neutrophils. Abramson S, Hoffstein ST, Weissmann G. Superoxide anion generation by human neutrophils exposed to monosodium urate.

What Does Gout Look Like?

If you do have a high uric acid level during a gout attack, it is likely that the level was even higher before the attack. To help diagnose gout, your doctor may check your blood uric acid levels in between attacks to see if they run high. Long term management of gout focuses on lowering urate levels, aiming for levels under 0.36 mmol/L, or better still, under 0.30 mmol/L. These medicines can prevent attacks of gouty arthritis and prevent MSU crystals from being deposited in the tissues. Medicines that lower urate levels should not be started during an acute attack of gout; instead they should be started a few weeks after the attack has resolved. In addition to lifestyle changes, medications play a vital role in gout treatment.

Although the frequency is only is 0.4%, the rate of organ failure and death is high. Less frequently (1% of cases), patients taking allopurinol can develop severe allopurinol hypersensitivity syndrome, which carries a mortality of 20-30%. Features of this syndrome include fever, toxic epidermal necrolysis, bone marrow suppression, eosinophilia, leukocytosis, kidney failure, liver failure, and vasculitis. Corticosteroids are often used to treat severe allopurinol hypersensitivity syndrome.

Key Points About Gout

Since cells contain DNA, and DNA contains purines, anything that increases the breakdown of cells in the body can lead to more uric acid and gout. For example, if a patient is receiving chemotherapy for a tumor, as the treatment kills the tumor cells a gout attack or kidney stone can develop as a result of the breakdown of the purines from those cells. Gout is considered when a patient reports a history of repeated attacks of painful arthritis, especially at the base of the toes or in the ankles and knees. The most reliable test for gout is detecting uric acid crystals in the joint fluid obtained by joint aspiration. This common office procedure is performed with topical local anesthesia.

Uric acid is produced in the body during the breakdown of purines – chemical compounds that are found in high amounts in certain foods such as meat, poultry, and seafood. It takes a long time without treatment to reach the stage of chronic tophaceous gout – around 10 years. It is very unlikely that a patient receiving proper treatment would progress to this stage. Finally, doctors can search for urate crystals around joints or within a tophus using ultrasound scan.

Researchers have reported that meat or seafood consumption increases the risk of gout attacks, while dairy consumption seemed to reduce this risk. Weight reduction can be helpful in lowering the risk of recurrent attacks of gout. Corticosteroids are an appropriate alternative for patients who cannot tolerate NSAIDs or colchicine.22 Patients with diabetes mellitus can be given corticosteroids for short-term use with appropriate monitoring for hyperglycemia. To reduce the risk of a rebound flare, preventive treatment and initiation of a tapered course of corticosteroids over 10 to 14 days is recommended after resolution of symptoms. After treating the pain and inflammation of a gout flare up, it is important to decrease your uric acid levels to prevent future gout attacks and joint damage. Your rheumatologist will work with you to find a balance of medications and lifestyle changes to help lower your uric acid levels.

In spite of these effective treatment modalities, question arises on their safety profile. Newer treatment options are being extensively studied especially interleukin-1 (IL-1) inhibitors but their approval is still pending. The quest for an optimally designed drug with desirable efficacy and acceptable safety profile is still on.

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