Repeated bouts of gout can lead to gouty arthritis, a worsening form of arthritis. There is no cure for gout, but you can effectively treat and manage the condition with medication and self-management strategies.
Gout flares start suddenly and can last days or weeks. These flares are followed by long periods of remission—weeks, months, or years—without symptoms before another flare begins. Gout usually occurs in only one joint at a time. It is often found in the big toe. Along with the big toe, joints that are commonly affected are the lesser toe joints, the ankle, and the knee. Top of Page. Gout is caused by a condition known as hyperuricemia, where there is too much uric acid in the body.
The body makes uric acid when it breaks down purines, which are found in your body and the foods you eat. When there is too much uric acid in the body, uric acid crystals monosodium urate can build up in joints, fluids, and tissues within the body. Hyperuricemia does not always cause gout, and hyperuricemia without gout symptoms does not need to be treated. A medical doctor diagnoses gout by assessing your symptoms and the results of your physical examination, X-rays, and lab tests.
Gout can only be diagnosed during a flare when a joint is hot, swollen, and painful and when a lab test finds uric acid crystals in the affected joint. Share on: Facebook Twitter. Show references Gout. Centers for Disease Control and Prevention. Accessed Dec. Goldman L, et al. Crystal deposition diseases. In: Goldman-Cecil Medicine. Elsevier; Ferri FF. In: Ferri's Clinical Advisor American College of Rheumatology. Caffo AL. Clinical manifestations and diagnosis of gout.
Gout or pseudogout adult. Mayo Clinic. Gloperba prescribing information. Food and Drug Administration. It is important that damage to bone from gout be diagnosed, since documented damage is a clear indication for long-term therapy see below. If the blood level is reduced, then the joint level of uric acid will gradually decrease as well. This leads to gout attacks diminishing or completely ceasing over time, and to tophi getting reabsorbed and shrinking or fully disappearing.
Different approaches can be taken to lowering total body uric acid. The production of uric acid can be decreased in the body for example, by allopurinol, see below or the excretion of uric acid can be increased for example, by probenecid, see below.
The crystals can also be broken down in the body see 7a below, re: Rasburicase, and 7b below, re: pegylated uricase. Figure Gout of the Base of the 1st Toe. Figure Gout of the Distal Finger Joints. The red and hot joints, coupled with rapid acceleration of joint pain, strongly suggest gout, and identifying tophi, if present see Figures help further.
Special effort should be made to distinguish gout from the other crystal-induced types of arthritis. For example, pseudogout , caused by a different type of crystal calcium pyrophosphate , causes the same type of hot, red joint, and the same rapid acceleration of pain as does gout.
Pseudogout can be distinguished by seeing calcium deposits within the joints on X-ray, which deposits in a different way than it does in gout.
When fluid is examined from an inflamed joint in pseudogout, the specific causative crystal can be seen. A third type of crystal-induced arthritis, hydroxyapatite deposition disease , has a type of crystal that needs special studies one such study is electron microscopy for identification.
The management of an acute attack of gout is very different from the prevention of subsequent attacks. See Figure 4 for overall approach to treatment and prevention of gout. Treatments used for prevention, such as allopurinol see below can actually make things worse if given during an attack, and so need to be held back until the attack has resolved for several weeks. There are a number of measures that can help resolve an attack of gout. See Table 2 for summary of treatment strategies for acute gout.
One principle is that treatment for an attack of gout should be instituted quickly, since quick treatment can often be rewarded with a quick improvement. If an attack of gout is allowed to last more than a day or so before treatment is started, the response to treatment may be much slower. It is important to get off the foot if the gout attack is in the lower extremity.
Trying to ignore the attack can lead to a more prolonged duration. Local ice has been shown to help for not more than 10 minutes at a time, to avoid skin damage. Leg elevation is helpful for some. Diet plays a key role diet in gout prevention: Since foods can directly set off gout attacks, patients with gout should receive counseling as to which foods are more likely to induce attacks.
Losing weight is often also helpful. However, as important as diet is in gout, for most people with gout diet, and even weight loss, are not enough, and medications will be needed to get to their uric acid goal.
Dietary control may be sufficient in a patient with mildly elevated uric acid, for example, 7. For those with a higher level, for example, The cutoff where patients with gout seem to dramatically reduce their number of attacks is when their uric acid level is taken below 6. With the above qualifications, attention to diet in gout patients is helpful, and especially so when first starting medication to lower the uric acid which may, paradoxically, initially set off gout attacks. There are a few basic principles of diet in gout which have stood up to a variety of studies: limit red meat and meat gravies, limit shellfish, and limit alcohol, especially beer.
All types of alcohol cause more uric acid to be reabsorbed by the kidneys, raising blood uric acid levels, but beer has its own high purine level and so contributes to blood uric acid elevation in two different ways. Vegetable protein is broken down to purine, but does not seem to be a significant contributing factor in gout. Low fat dairy products, despite mild protein being broken down to purine, likewise seems not to contribute to gout risk and may even be protective.
Along with diet, physical activity can help with weight loss, and gout has been associated with being overweight. An exercise program combined with diet in gout can reduce risk for attacks.
Clues to an attack of gout coming on include local swelling, heat, redness, and tenderness in a joint, especially in the foot, ankle, or knee. Some patients have fever and chills as the first warning that an attack of gout is coming on. When used as one or two tablets a day 0. Some physicians would start colchicine after one very severe or two moderately severe attacks of gout, and beyond that, use allopurinol. If a patient has two attacks of gout within the same 12 months, it is generally recommended that they be treated with a medication to lower the uric acid, which colchicine does not accomplish.
See below for discussion of the uric acid-lowering agents, allopurinol and probenecid. There is a rare effect on the nerves and muscles with long-term use of colchicine, and a blood test from the muscle CPK is monitored at approximately six-month intervals in patients taking colchicine on a regular basis. Colchicine also has a major role when patients are beginning therapy with allopurinol see below to prevent the increase in gout attacks that can happen when allopurinol is begun.
The colchicine, in that case, is often withdrawn at about six months, assuming no gout attacks have occurred. Allopurinol : This agent is presently the most commonly used drug for the prevention of gout. Allopurinol is effective in preventing gout no matter what the mechanism of the elevated uric acid was. Within a week after taking a dose, uric acid is significantly lowered by allopurinol.
The most common adverse reaction to allopurinol is an increase in gout attacks early in therapy. Ampicillin, an antibiotic, seems to cause more rashes in patients already taking allopurinol. A rare but very serious side-effect is the allopurinol hypersensitivity syndrome, which can present with severe rash along with severe liver and blood cell abnormality.
This syndrome has been reported to be more likely if the patient has abnormal kidney function. The level of uric acid in these patients is followed closely, and the level of uric acid is used as a guide as the allopurinol dose is slowly increased. The severity of the allopurinol hypersensitivity syndrome is a reminder that specific criteria must be used to decide which patients should be treated with allopurinol See Table 4: Reasons to Use Medication to Lower Uric Acid.
It works similarly to allopurinol in that it inhibits xanthine oxidase, a key enzyme in the pathway that produces uric acid, and thereby reduces total body uric acid level. Like allopurinol, the most common side-effect of febuxostat is causing gout to flare after this drug is started. As with allopurinol, it is reasonable whenever possible to add a preventative medication, such as colchicine, for at least the first six months after starting febuxostat to help avoid gout flares. Later on, as the total body uric acid decreases, this will generally no longer be needed.
One potential advantage of febuxostat is that it is structurally quite different from allopurinol, and therefore likely can be used in patients who are allergic to allopurinol.
Only a limited number of patients who were allergic to allopurinol have been studied to date, but the drug was tolerated in those patients. Another advantage is that its excretion is handled more by the liver than the kidney, unlike allopurinol, and febuxostat may thus have some advantage in patients with kidney dysfunction. Febuxostat is approved by the FDA to start at 40mg daily, and if the uric acid has not reached goal less than 6.
Rheumatologists often adjust allopurinol doses higher than mg when needed to reach uric acid goal, although the literature on higher doses of allopurinol is limited. Patients with controlled uric acid level and doing well on allopurinol would seem to have no reason to switch to this new agent, in view of allopurinol's lower cost and 40 year history of an overall very good safety record see "Allopurinol" discussion above.
In March of , a study of allopurinol versus febuxostat heart safety was published. This study, the CARES trial, looked at patients, all of whom had some cardiovascular disease history, either heart attack, stroke, min-stroke or need for urgent heart surgery for coronary disease. The study looked at whether a combination of cardiovascular outcomes heart attack, stroke, cardiac death, mini-stroke, urgent heart surgery for coronary disease were more common in the allopurinol or the febuxostat group.
For the combination of these outcomes, the two medications were the same. However, cardiac death was higher in the febuxostat group. There were some problems with interpreting the study, since almost all the patients who died had already stopped their gout medication, whether allopurinol or febuxostat.
There was also a high drop-out rate in the 5 year study. Many rheumatologists do not think this is a definitive study, and there is other data that does not show increased heart risk with febuxostat. However, the FDA has interpreted this study and put a warning on febuxostat that it should be used second line, after allopurinol. Now that the FDA has put this warning on febuxostat, even in people with kidney abnormality we would be likely to start allopurinol first. For people already on febuxostat who never took allopurinol, it is an individual case decision about whether to switch to allopurinol.
Allopurinol has a higher risk of severe skin reaction in people with kidney function abnormality, and people with this abnormality are often the ones on febuxostat. After considering all this data, many patients in this situation have chosen to stay on febuxostat, but each person, with their physician, makes this decision.
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.
It is generally agreed that we have no evidence that febuxostat is a negative for the heart, just the question of the CARES trial as to whether it is not as protective as allopurinol.
The FAST trial challenges this, and it may well be that they are equally protective. Probenecid : This medication increases the amount of uric acid that is excreted in the urine, by decreasing the amount that gets reabsorbed by the kidney. Medications that can cause more uric acid to come out in the urine are called uricosuric agents. Probenecid is the main such agent used in the U.
Probenecid can be successful in bringing the blood uric acid below 6. Like allopurinol, an increased number of gout attacks can occur when probenecid is started, and for this reason colchicine is often given for the first six months of therapy.
Unlike allopurinol, however, early in therapy probenecid can increase urinary uric acid, which could lead to the development of a kidney stone. If the result is borderline, at a minimum the patient is advised to drink extra fluids, to help prevent kidney stones early on in treatment. There are also medications that can change the acidity of the urine, and by alkalinizing the urine in such a case the risk of kidney stone can be decreased uric acid is more soluble in alkaline medium, so less likely to crystallize.
Probenecid can also cause a rash, but seems less likely than allopurinol to cause a very severe hypersensitivity reaction. Probenecid is not effective if a patient has kidney dysfunction [creatinine greater than 2. Because of the above limitations, allopurinol is often used as the drug of choice in a patient where lowering uric acid is the goal, but there remains a place for probenecid in the armamentarium against gout.
This once-a-day oral medication increases the amount of uric acid that comes out in the urine, a mechanism it shares with probenecid see iv above. This medication was approved for gout by the FDA in , to be used together with either allopurinol or febuxostat to help get patients to their goal uric acid of less than 6.
It is not approved to be used alone for gout. This medication was generally well-tolerated in studies. Kidney function is thus checked before and during treatment. Lesinurad is taken once a day, so more convenient than probenecid.
In theory this medication, like probenecid, can increase the risk of uric acid-induced kidney stones, but this was minimal risk in published studies and the combination with either allopurinol or probenecid likely dramatically reduces this risk. Lesinurad is now available in combination with allopurinol, allowing a person taking both medications to take a single pill a day.
It was approved in late for use in gout patients who have failed or were intolerant to both allopurinol and febuxostat.
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