Gout And Hyperuricemia

Content

• How Is Gout Treated?
• How Gout Treatment Prevents Disease Progression
• Asymptomatic Hyperuricemia
• Management Of Chronic Gout And Prevention Of Flares
• How Can I Manage My Gout And Improve My Quality Of Life?

Gout is a kind of arthritis caused by a buildup of uric acid crystals in the joints. Uric acid is a breakdown product of purines that are part of many foods we eat. Gout has the unique distinction of being one of the most frequently recorded medical illnesses throughout history. Untreated gout may cause deposits of urate crystals to form under the skin in nodules called tophi (TOE-fie). Tophi can develop in several areas, such as your fingers, hands, feet, elbows or Achilles tendons along the backs of your ankles.

Hard lumps of uric acid deposits, called tophi, can build up near the soft tissue lining the joint and are extremely painful. The joint that gets an attack of the gout is "predisposed", already "upset" and arthritic, even if it never bothered you before the first gout attack. When it gets "attacked", the uric acid crystals deposit inside and around the joint tissues causing the body to reject the uric acid, which in-turn causes a much bigger increase in inflammation. AND, the uric acid crystals which have sharp knife-like edges cut the joint tissues in which they are deposited, causing then more damage and even more inflammation.

How Is Gout Treated?

The kidneys are the portal through which uric acid is eliminated and if they can’t do it fast enough, uric acid build-up occurs. Several medical conditions, including blood and metabolism disorders, sometimes cause gout by lowering uric acid excretion from the body. 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). The pathology is characterized by monosodium urate crystals deposition in periarticular soft tissues. The crystals are needle-shaped and are strongly birefringent in plane-polarized light 10.

These medications decrease the total amount of uric acid in the body and lower the serum uric acid level. For most patients, the goal of uric-acid-lowering medication is to achieve a serum uric acid level of less than 6 mg/dl. These medications also are effective treatments to decrease the size of tophi, with the ultimate goal of eradicating them. Uric-acid-lowering medications include allopurinol , febuxostat , probenecid, and pegloticase . Why some people with high uric acid levels will develop gout and others won’t is unknown.

How Gout Treatment Prevents Disease Progression

There is no cure for gout, but it can be controlled quite well with medication. Proper treatment can help you entirely avoid attacks and long-term joint damage. After an acute attack, skin overlying the affected joint may peel and shed. If this occurs on a toe joint, the area may be more likely to develop a fungal infection (athlete's foot).

In most people with gout, the kidneys do not excrete uric acid adequately while in a minority of people with gout, too much uric acid is produced. Chronically high levels of uric acid in the blood form crystals, which are then deposited in joints, and sometimes tendons and skin as well. These deposits can cause pain-often severe-and swelling in the affected area or areas.

Also, macrophages clear the cellular apoptotic remnants to help stop the inflammatory cascade. Additionally, macrophages secrete TGF-β that eliminates IL-1, another key player in enhancing the inflammatory process . Inside the synovium, the abundance of chemotactic factors such as leukotrienes, platelet activating factor and interleukins mainly IL-8 is responsible for 90% of neutrophils activation and exacerbation of acute inflammation. Accordingly, targeting IL-8 can be promising for stopping the acute attack of gout . Once a doctor has diagnosed gout, there are several simple, effective methods to help manage the symptoms.

What is a Morton's toe?

Plain film radiography may be used to evaluate gout; however, radiographic imaging findings generally do not appear until after at least 1 year of uncontrolled disease. The classic radiographic finding of gout late in disease is that of punched-out or rat-bite erosions with overhanging edges and sclerotic margins.

This observation shows that cartilage damage resulting from OA induces formation of MSU crystals. Interestingly, UA crystals seem to affect the cartilage from its outer surface. Accumulation of UA crystals in the joint results from decreased vascularity and susceptibility of the synovial membrane to pass the crystals. Thus, gout tends to affect peripheral joints such as the big toe . This occurs by removal and phagocytosis of crystals by macrophages, hence suppressing cellular and chemokine activation.

In addition, because CPPD disease and gout can coexist, MSU crystals might be observed. White cell counts can range from a few thousand cells up to 80,000 to 100,000 per high-power field. It is advisable to start probenecid at a low dose and increase the dose gradually until reaching the target serum urate level.

Will gout show up on xray?

A uric acid test measures the amount of uric acid in the body. Uric acid is a chemical that's produced when your body breaks down purines.
How is a uric acid urine test performed? 1. On day 1, urinate into the toilet after waking up.
2. After that, take note of the time and collect all urine for the remaining 24 hours.

In certain circumstances with atypical presentation of gout such as in multiple joint affection or atypical joint distribution, identification of MSU is mandatory to differentiate gout from other diagnoses. Elevated levels of SUA associated with typical joint involvement such, as podagra is usually a straightforward diagnosis. However, according to the EULAR recommendations, synovial fluid analysis is still advised to exclude other causes mainly septic arthritis . Gout has a predilection for lower extremities such as the first MTP, which is the commonest site for acute gout known as podagra . Other joints that can be affected are the tarsal and metatarsal joints, ankles, knees, wrists, MCPs as well as interphalangeal joints of the hands.

Uric acid crystals can also collect in soft tissues and form lumps called tophi, most typically on the hands, fingers, elbows, and ears. accumulates in your body, it can form needle-like crystals in your joints or the surrounding connective tissue and cause a painful attack of gout. 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.

Reduce your intake of fats, alcohol and foods that are more likely to increase the amount of uric acid in the body. Cutting back on alcohol, especially beer can also be helpful. Steroids are commonly used to battle the painful form or arthritis. Just like the medications described above, steroids help combat pain and inflammation. Steroids can either be taken orally or be injected directly into the joint. Common symptoms include bone thinning, weaker immune systems and poor wound healing.