Should Patients Who Develop Hyperuricemia With Hydrochlorothiazide Be Started On Allopurinol?

Content

• Take On Chronic Pain Where It Lives
• What Are Side Effects Associated With Using Allopurinol?
• Mar Vista Animal Medical Center

Although the absolute rates of gout and distribution of vitamin C intake may not be representative of a random sample of US men, the biological effects of vitamin C on gout should be similar. Given the potential effect of female hormones on the risk of gout in women41 and an increased role of dietary effect on uric acid levels in patients with existing gout,42 prospective studies of these populations would be valuable. Gout often is associated with high blood pressure, heart and kidney disease, or the use of medications that increase uric acid levels.

It's best not to take aspirin for pain and inflammation because aspirin can raise the uric acid level in the bloodstream. Note that taking a low-dose aspirin for prevention of heart disease or stroke has little effect on gout. The use of diuretics (furosemide, thiazides etc.) may increase uric acid levels and interfere with the function of allopurinol.

Take On Chronic Pain Where It Lives

Talk to your healthcare provider or pharmacist before taking any new medicine. Along with its needed effects, your medicine may cause some unwanted side effects. Some side effects may go away as your body adjusts to the medicine. Tell your healthcare provider if you have any side effects that continue or get worse. Your blood pressure should be checked regularly, and blood tests should be done occasionally.

Retrospective analysis with heterogeneous populations and uncontrolled confounding factors should be interpreted with caution by the clinicians. In this study, individuals were significantly more hyperuricemic and the mean SUA levels were significantly higher in the thiazide group. Allopurinol has rare but potentially fatal adverse effects involving the skin. The most serious adverse effect is a hypersensitivity syndrome consisting of fever, skin rash, eosinophilia, hepatitis, and worsened renal function. Allopurinol is one of the drugs commonly known to cause Stevens–Johnson syndrome and toxic epidermal necrolysis, two life-threatening dermatological conditions.

What Are Side Effects Associated With Using Allopurinol?

Your primary-care physician can diagnose gout in most cases. You may also be referred to a rheumatologist, a specialist in the diagnosis, treatment and long-term management of arthritis and related rheumatic diseases, which includes gout. Diet and exercise are risk factors you can control – but you may need a little help to make those changes stick. Your doctor is your partner in managing your gout and preventing long- term problems, but other members of your healthcare team, such as nurses, physical therapists, nutritionists and others, can play a major role as well.

Mar Vista Animal Medical Center

In this article, learn about eight natural ways to lower uric acid levels. A drug called colchicine is sometime used to treat gout, but it often causes unpleasant side effects before it eases pain and swelling. Mostly, in veterinary medicine, allopurinol is used in dogs but it can also be used in birds where gout is a problem. In dogs, a therapeutic diet low in purines is generally prescribed.

Gout attacks usually last for several days, but the pain is most intense during the first 24 to 36 hours. More than half of people who have had one attack of gout will have a second, usually within six months to two years. Whether the problem is natural inability to produce allantoin , inability to get uric acid into liver cells for conversion to allantoin or excessive purine intake , the goal in this situation is to reduce uric acid production. In conclusion, there are strong evidences to support both results - diuretics increase SUA levels and do not have an impact on SUA levels. This sheds lights on the urgent need to design robust prospective, longitudinal case-control trials to establish concrete evidence regarding this correlation.

Many drugs have been found to alter these processes and induce a state of hyperuricemia. Diuretic-induced hyperuricemia is probably the single most common form of hyperuricemia seen in clinical practice. In most cases, the uric acid level returns to normal after the removal of the offending drug provided there has not been any drug-induced renal injury. Elevated uric acid levels may produce kidney problems, or none at all.

Can furosemide affect hearing?

In small studies, furosemide use has been associated with sudden sensorineural hearing loss that is usually reversible but can be permanent 11–13. The hearing loss is more likely to occur following intravenous drug administration but can also occur after oral dosing 11, 13.

Several strengths and potential limitations of this study deserve comment. This study was substantially larger than previous studies concerning gout.1,29-34 Also, dietary data, including vitamin C information, were prospectively collected and validated. Potential biased recall of diet was avoided in this study because the intake data were collected before the diagnosis of gout. Because dietary consumption was self-reported by questionnaire, some misclassification of exposure is inevitable. However, the food frequency questionnaire has been extensively validated in a subsample of this cohort, and any remaining misclassification would have likely biased the results toward the null.

Moreover, hyperuricemia is the leading risk factor for gout . The association of thiazide diuretic use and gout was first noted in case series from the medical literature . In trials and observational studies, diuretic use was associated with an increased risk of gout .

Asymptomatic Hyperuricemia

Acute gout flares typically manifest with a severely painful big toe and occur most often in men following triggers such as alcohol consumption. Diagnosis is based on clinical presentation and, ideally, by the demonstration of negatively birefringent monosodium urate crystals on synovial fluid analysis. Acute attacks are treated with corticosteroids, NSAIDs (e.g., naproxen, indomethacin), or colchicine. The management of chronic gout includes lifestyle modifications and urate-lowering medications (e.g., allopurinol) to control hyperuricemia. In humans, urate is the final breakdown product of purine nucleotides, constituents of cellular energy stores such as ATP, and of DNA and RNA both internal or, to a lesser extent, ingested.

However, there was insufficient data – only 22 cases of gout among those with CHF, of whom only 4 were exposed to a diuretic – to examine the association of diuretic use with incident gout among those participants with CHF. We could not rule out the possibility that serum urate is a confounder and not a mediator of this association. However, it is unlikely that physicians would be selectively prescribing a diuretic to those with elevated serum urate, as this would be the source of the confounding. Although serum urate has been found to predict the onset of hypertension, a randomized controlled trial would be necessary to determine the directionality of the uric acid and hypertension association. Our analysis was not designed to test whether the urate level was a consequence of changing blood pressure levels. However, in new initiators with hypertension, those who initiated a diuretic experienced, on average, a greater escalation in serum urate levels than those who did not initiate a diuretic.

Given orally or by injection into the muscle, these medicines can be very effective in treating gout attacks. If only one or two joints are involved, your doctor can inject a corticosteroid directly into your joint. Gout is often diagnosed upon the finding of uric acid based crystals. The physician may use a needle to extract fluid from an affected joint and will study that fluid under a microscope to find whether urate crystals are present. Crystals also can be found in deposits that can appear under the skin.

These changes include eating a diet that is low in fat and salt, maintaining a healthy weight, exercising at least 30 minutes most days, not smoking, and using alcohol in moderation. Before taking any type of NSAID, tell your doctor if you drink alcohol or take blood thinners , ACE inhibitors, lithium or furosemide. Also report any sensitivity or allergy to aspirin or similar drugs. All non-aspirin NSAIDs may cause an increased risk of serious blood clots, heart attack and stroke, which can be fatal. This risk can occur as early as the first weeks using an NSAID and increases with dose and duration of use. Patients who have or who are at risk for cardiovascular disease are at greater risk for these complications than someone without cardiovascular disease or its risk factors.

Clinical Presentation

In contrast, hypertension patients taking calcium channel blockers or losartan may have a lower risk of gout. Gout flares often can occur when you first start to use medications that lower blood uric acid levels. Patients can help prevent flares when starting these medications by also using low‐dose colchicine or NSAIDs. Often, doctors advise patients to keep taking colchicine in a low, preventive dose together with the uric acid-lowering medicine for at least six months.

In other people, attacks may become more frequent over time. In conclusion, the results of this study, which can change our clinical practice, consisting of a retrospective and heterogeneous population, should be interpreted with caution. We believe that, as the authors emphasize, there is a need for prospective well-designed studies about the effects of diuretics on the necessary doses of ULDs to achieve the targeted SU level.