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. It appears that tophi shrink more quickly with this agent than with any other agent used to treat gout. An earlier Phase II trial 13 and two essentially identical Phase III trials a study of at least moderate size that compares a new treatment with the current standard of care in patients , Gout 1 and Gout 2 have been presented.
There were also allergic-type events and events where patients dropped their blood pressure while this intravenous agent was running into them. None of these episodes of drop in blood pressure led to death or long-term problems for the patients, however, and the blood pressure returned to baseline in these cases.
The drop in blood pressure is still a concern, and this medication must be used in a setting where treatment of the drop in blood pressure can be managed. Pegloticase may be especially useful in patients with very large collections of uric acid tophi , especially if these are draining to the skin. More recent data has looked at ways to reduce the body forming antibodies to pegloticase. If we can prevent antibody formation, it has been shown that infusion reactions are dramatically decreased, and the effectiveness of pegloticase is also much better maintained.
A larger trial with methotrexate and pegloticase is in progress. If a patient is allergic to allopurinol, there are often limited options. If the rash was relatively mild, one option is an oral desensitization regimen for that agent. Although at times the rash will reoccur during this process, often a patient can be desensitized in this way and subsequently tolerate allopurinol.
Although some patients develop a mild rash to allopurinol that remains mild over time, or respond to antihistamines, continuing the allopurinol despite a rash is not advised, since the rash can worsen unpredictably. If none of the above options is possible or successful, physicians often seek a clinical trial of a new agent for gout, if available, for their patient to enter. See section 7 below for a discussion of agents presently under study for gout. Online resources, such as ClinicalTrails. Cherry juice , which has long been an alternative remedy and which had anecdotal support, now has been studied.
At the American College of Rheumatology meeting in November data available there were two studies looking at cherry juice. It appears that cherry juice may have a small effect in decreasing production of uric acid. It also, possibly through its Vitamin C content, can increase the excretion of uric acid by the kidney. In separate earlier study, Vitamin C itself did appear to increase uric acid excretion. However, the effect using mg a day dosing was small--only a drop in blood uric acid level of about 0.
These early studies of cherry juice are interesting, and might be relevant for a patient who was "almost there" in their uric acid goal, but a gout sufferer should be very careful about trusting to cherry juice to manage their uric acid. Based on the data, the result is likely not going to be sufficient. Diet has been discussed in more detail above, and gout is clearly one of the rheumatic diseases where diet is unequivocally important. 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. The disease should be diagnosed and treated by a doctor or a team of doctors who specialize in care of gout patients.
This is important because the signs and symptoms of gout are not specific and can look like signs and symptoms of other inflammatory diseases. Doctors who specialize in gout and other forms of arthritis are called rheumatologists. To find a provider near you, visit the database of rheumatologists external icon on the American College of Rheumatology website.
Once a rheumatologist has diagnosed and effectively treated your gout, a primary care provider can usually track your condition and help you manage your gout. Gout can be effectively treated and managed with medical treatment and self-management strategies. Your health care provider may recommend a medical treatment plan to. In addition to medical treatment, you can manage your gout with self-management strategies.
Self-management is what you do day to day to manage your condition and stay healthy, like making healthy lifestyle choices. The self-management strategies described below are proven to reduce pain and disability, so you can pursue the activities important to you.
Gout affects many aspects of daily living, including work and leisure activities. Fortunately, there are many low-cost self-management strategies that are proven to improve the quality of life of people with gout. This could be because they affect the way the kidneys filter urate, or because they cause more urate to be produced in the first place.
Several things can cause the crystals to shake loose into your joint cavity, triggering an attack. These include:. Diagnosing gout is usually straightforward, especially if you have typical symptoms of the condition - for example, if you have an attack in your big toe. But gout can sometimes be more difficult to diagnose. High urate levels in blood tests can suggest that you have gout, but this will need to be considered alongside your symptoms.
Ultrasound and CT scans can be good at spotting joint damage, crystals in the joints and early signs of gout. X-rays are generally used to pick up the bone and joint damage caused by having gout for a long time. The fluid is then examined under a microscope for urate crystals. If you have tophi, doctors can take a sample from one of those instead.
Attacks can vary from person to person. Some people only have an attack every few years, while others have attacks every few months. If you take medication to lower your urate levels, and have a healthy diet and lifestyle, most of the damage and complications caused by gout can be stopped. Treatments for gout are incredibly successful. There are two main parts to treating gout, which are:. The treatment helps you to manage your symptoms when an attack happens.
But your preference is also taken into consideration — many people with gout quickly learn what works best for them. Attacks of gout are often treated with NSAID tablets, which can help with pain and reduce some of your inflammation.
Your doctor may let you keep a supply so you can start taking them at the first signs of an attack. They can also interact with other drugs, so make sure you talk to a doctor before starting on any new medication. To reduce the risk of this happening and to protect your stomach, your doctor will also prescribe a proton pump inhibitor. As with NSAIDs, colchicine tablets should be taken as soon as you notice an attack coming on, or it may not work as well.
Your doctor will probably recommend keeping a supply at home. Colchicine can interact with several other drugs, including statins taken for high cholesterol. However, they can also be taken as an injection into a muscle or joint affected by gout. This can be particularly helpful if gout is affecting only one joint. There are drugs available that can lower urate levels, prevent new crystals from forming and dissolve away the crystals in your joints. They are called urate lowering therapies or ULTs for short.
It can take a few months or years for the drugs to completely clear your body of urate crystals. You could actually have more attacks within the first six months of starting them.
As the drugs start dissolving the crystals, they become smaller and are more likely to get into the joint cavity, triggering an attack. ULTs are usually life-long treatments and require yearly check-ups to monitor your urate levels. Try not to miss or skip any of your doses, especially in the first year or two of starting treatment.
This could cause your urate levels to go up and down, which could trigger an attack. Allopurinol is the most commonly used ULT. Allopurinol is broken down and removed from the body through your kidneys, so if you have a problem with your kidneys, it may not be suitable for you. Your doctor might decide to start you on an even lower dose and increase slowly, or suggest that you try febuxostat instead. Febuxostat is a newer drug that reduces the amount of urate made in the body in the same way that allopurinol does.
Febuxostat is more likely to trigger gout attacks than allopurinol when you first start treatment. Uricosuric drugs, which include sulfinpyrazone, benzbromarone and probenecid, work by flushing out more urate than normal through your kidneys.
This is because, by encouraging your kidneys to filter more urate, they also increase the risk of developing kidney stones. Uricosuric drugs are usually used on their own.
If your gout has caused damage to your joints, then the treatments available will be the same as those used for osteoarthritis. They include:. Visit our osteoarthritis page to find out more about treatments available for joint damage.
This will then decrease the chances of you having attacks of gout. Exercise is extremely important, not only to reduce the chances of an attack, but also for your general health and wellbeing. Exercises that get you out of breath are particularly good for burning calories.
You could try dancing, walking in hilly countryside or doubles tennis. It helps to find a sport or exercise which you enjoy and will keep doing. Some people find joining a leisure centre or sports club to be really fun and motivational. You should avoid exercising during a flare up of gout, as it could make your pain worse.
You should try to have a well-balanced diet that is low in fats and added sugars, but high in vegetables and fibre. Extreme weight loss or starvation diets increase cell breakdown in your body, which can raise urate levels. However, you should be OK to do some daytime fasting - for example, during Ramadan.
The NHS has a good diet and exercise plan which can help you lose weight in a healthy way over 12 weeks. You should try to avoid eating large quantities of foods that are high in purines. Protein is an important part of your diet, but you can get it from sources other than just meat and fish.
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