Gout and Hyperuricemia (2022)

Gout and Hyperuricemia (1)

MARK D. HARRIS, M.D., LORI B. SIEGEL, M.D., AND JEFFREY A. ALLOWAY, M.D.

Am Fam Physician. 1999;59(4):925-934

A more recent article on gout is available.

Gout is a condition characterized by the deposition of monosodium urate crystals in the joints or soft tissue. The four phases of gout include asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout and chronic tophaceous gout. The peak incidence occurs in patients 30 to 50 years old, and the condition is much more common in men than in women. Patients with asymptomatic hyperuricemia do not require treatment, but efforts should be made to lower their urate levels by encouraging them to make changes in diet or lifestyle. Acute gout most commonly affects the first metatarsal joint of the foot, but other joints are also commonly involved. Definitive diagnosis requires joint aspiration with demonstration of birefringent crystals in the synovial fluid under a polarized light microscope. Treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, corticosteroids and analgesics. In patients without complications, NSAID therapy is preferred.

Clinical gout comprises a heterogeneous group of disorders characterized by deposition of monosodium urate crystals in the joints and tendons. Gout progresses through four clinical phases: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout (intervals between acute attacks) and chronic tophaceous gout. Demonstration of intra-articular monosodium urate crystals is necessary to establish a definitive diagnosis of gouty arthritis. Asymptomatic hyperuricemia is common and should not ordinarily be treated. Non-steroidal anti-inflammatory drugs (NSAIDs) are the treatment of choice for acute attacks of gout in most patients. NSAIDs should be used sparingly in elderly patients and should be avoided in patients with renal disease and peptic ulcer disease, and in those receiving concurrent systemic anticoagulation. Corticosteroids are a valuable treatment option for patients in whom NSAID therapy is contraindicated. Acute gouty arthritis and chronic gout require different treatment strategies.

Epidemiology

Gouty arthritis is the most common form of inflammatory joint disease in men older than 40 years.1 The National Health Survey (1983 to 1985) determined the prevalence rate of self-reported gout to be 13.6 cases per 1,000 men and 6.4 cases per 1,000 women. These numbers reflect an approximate threefold increase in the prevalence of gout since 1969.2 In contrast, cases of physician-diagnosed gout suggest a consistently lower prevalence rate—5.0 to 6.6 cases per 1,000 men and 1.0 to 3.0 cases per 1,000 women.3,4

Clinical Features

ASYMPTOMATIC HYPERURICEMIA

Asymptomatic hyperuricemia is the term for an abnormally high serum urate level, without gouty arthritis or nephrolithiasis. Hyperuricemia is defined as a serum urate concentration greater than 7 mg per dL (416 μmol per L), the approximate level at which urate is supersaturated in plasma.5

Although gouty arthritis characteristically occurs in patients with hyperuricemia, it is incorrect to equate hyperuricemia with clinical gout. Researchers from the Normative Aging Study followed 2,046 initially healthy men for 15 years by taking serial measurements of serum urate levels.6 The five-year cumulative incidence rates of gouty arthritis were 2.0 percent for a serum urate level of 8.0 mg per dL (475 μmol per L) or lower, 19.8 percent for urate levels from 9.0 to 10.0 mg per dL (535 to 595 μmol per L) and 30 percent for a serum urate level higher than 10 mg per dL (595 μmol per L).

(Video) Gout - causes, symptoms, diagnosis, treatment, pathology

Hyperuricemia predisposes patients to both gout and nephrolithiasis, but therapy is generally not warranted in the asymptomatic patient. Recognizing hyperuricemia in the asymptomatic patient, however, provides the physician with an opportunity to modify or correct underlying acquired causes of hyperuricemia (Table 1).

Increased urate production
Cause
NutritionalExcess purine, ethanol, fructose consumption
HematologicMyeloproliferative and lymphoproliferative disorders, polycythemia
DrugsEthanol, cytotoxic drugs, vitamin B12 (treatment of pernicious anemia)
MiscellaneousObesity, psoriasis, hypertriglyceridemia
Decreased renal excretion of urate
Cause
DrugsEthanol, cyclosporine (Sandimmune), thiazides, furosemide (Lasix) and other loop diuretics, ethambutol (Myambutol), pyrazinamide, aspirin (low-dose), levodopa (Larodopa), nicotinic acid (Nicolar)
RenalHypertension, polycystic kidney disease, chronic renal failure (any etiology)
Metabolic/endocrineDehydration, lactic acidosis, ketosis, hypothyroidism, hyperparathyroidism
MiscellaneousObesity, sarcoidosis, toxemia of pregnancy

Acute gout is characterized by the sudden onset of pain, erythema, limited range of motion and swelling of the involved joint. Often quoted, the English physician Thomas Sydenham's classic description of his own gouty sufferings is as true today as it was in the 17th century:

“The victim goes to bed and sleeps in good health. About two o'clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep. This pain is like that of dislocation. . . . Then follows chills and shivers and a little fever. The pain, which was at first moderate, becomes more intense. . . . So exquisite and lively meanwhile is the feeling of the part affected, that it cannot bear the weight of bedclothes nor the jar of a person walking in the room. . . .”7

The peak incidence of acute gout occurs between 30 and 50 years of age.8 Approximately 90 percent of first attacks are monoarticular. In more than one half of patients with acute gout, the first metatarsophalangeal joint is the initial joint involved, a condition known as podagra (Figure 1). Joint involvement (in order of decreasing frequency) includes the metatarsophalangeal joint, the instep/forefoot, the ankle, the knee, the wrist and the fingers.

Gout and Hyperuricemia (2)

Gout in women occurs exclusively after menopause. Women develop gout at an older age than men and have twice the prevalence of hypertension, renal insufficiency and exposure to diuretics.9 The onset of gout before age 30 in men or before menopause in women is atypical and raises concern about an associated inherited enzyme defect or renal disease.

INTERCRITICAL GOUT

Following recovery from acute gouty arthritis, the patient reenters an asymptomatic phase of the disease. This phase is referred to as “intercritical gout.” It is during this intercritical phase that the physician should focus on secondary causes of hyperuricemia. Medications should be assessed to identify those that may aggravate the patient's condition (e.g., diuretics) and dietary education regarding purine-rich foods (which contribute to higher serum uric acid levels) should be provided to the patient at this time (Table 2). The patient should also be counseled about limiting alcohol consumption and gradually losing weight, if obese.

High
Best to avoid:
Liver, kidney, anchovies, sardines, herring, mussels, bacon, codfish, scallops, trout, haddock, veal, venison, turkey, alcoholic beverages
Moderate
May eat occasionally:
Asparagus, beef, bouillon, chicken, crab, duck, ham, kidney beans, lentils, lima beans, mushrooms, lobster, oysters, pork, shrimp, spinach
Low
No limitation:
Carbonated beverages, coffee, fruits, breads, grains, macaroni, cheese, eggs, milk products, sugar, tomatoes and green vegetables (including lettuce and excluding vegetables listed above)

RECURRENT GOUTY ARTHRITIS

(Video) Gout

The frequency of subsequent acute attacks of gout usually increases over time. Approximately 60 percent of patients have a second attack within the first year, and 78 percent have a second attack within two years. Only 7 percent of patients do not have a recurrence within a 10-year period.10

Polyarticular involvement also becomes more common over time and can often mimic other forms of arthritis. Gouty arthritis may mimic rheumatoid arthritis, with symmetric small-joint involvement and tophaceous deposits on extensor tendon surfaces that resemble rheumatoid nodules. As many as 30 percent of patients with tophaceous gout also have low titers of rheumatoid factor, adding to the diagnostic confusion.11 Postmenopausal women who are receiving diuretic therapy have a tendency to form tophi in osteoarthritic joints of the hands,12 mimicking inflammatory “erosive osteoarthritis” (Figure 2). These clinical scenarios underscore the need for an accurate diagnosis when evaluating the patient with an acute arthritis. Analysis of synovial fluid is essential to identify monosodium urate crystals. Reliance on clinical presentation, serum hyperuricemia levels or response to NSAID therapy does not replace direct evaluation of synovial fluid and may lead to an inaccurate diagnosis.

Gout and Hyperuricemia (3)

CHRONIC TOPHACEOUS GOUT

Tophi are chalky deposits of sodium urate that are large enough to be seen on radiographs and may occur at virtually any site. The most common sites include the joints of the hands or feet. The helix of the ear, the olecranon bursa and the Achilles tendon are classic, albeit less common, locations for tophi. Articular tophaceous gout can result in a destructive arthropathy and chronic secondary osteoarthritis. The duration of time between the first gouty attack and recognizable tophaceous disease is highly variable and may range from three to 42 years (mean: 11.6 years).13 The rate of urate deposition and, consequently, the rate of tophi formation, correlate with the duration and severity of hyperuricemia.10 Tophaceous disease is more likely to occur in patients with the following: a poly-articular presentation, a serum urate level higher than 9.0 mg per dL (535 μmol per L) and a younger age at disease onset (i.e., 40.5 years or younger).14

It is important to make an accurate diagnosis of gout before beginning therapeutic intervention. A definitive diagnosis requires aspiration and examination of synovial fluid to confirm the presence of monosodium urate crystals. Even the smallest amount of fluid obtained from the shaft or hub of the needle during aspiration can be examined for crystals. Monosodium urate crystals are identified by examination under polarized light microscopy (Figure 3, right). In order to demonstrate the characteristic birefringence, it is necessary to use a microscope with a first-order red compensator and a rotating stage. Urate crystals are bright (strongly birefringent), needle shaped and yellow (negatively birefringent) when lying parallel to the axis of the compensator (an axis reference is usually etched into the housing of the compensator).

Gout and Hyperuricemia (4)

Even if a polarizing microscope is not available, the characteristic needle shape of the monosodium urate crystals, especially when found within white blood cells, can be identified with conventional light microscopy; in this case, they resemble a toothpick pierced through an olive. (Figure 3, left).

Confirmation of the presence of monosodium urate crystals is imperative so that patients with coincidental hyperuricemia and osteoarthritis are not incorrectly diagnosed with gout and unnecessarily treated with allopurinol (Zyloprim).15 Furthermore, rheumatoid arthritis, calcium pyrophosphate dihydrate deposition (pseudogout), spondyloarthropathies and osteoarthritis may also mimic gouty arthritis.16

Therapy

The three general goals of therapy in the management of gout are to terminate the acute painful attack, prevent recurrences and prevent or reverse the complications of urate deposition in joints, kidneys or other involved sites. There is no indication for screening asymptomatic patients for hyperuricemia. Urate-lowering drugs should not be used to treat patients with asymptomatic hyperuricemia. If hyperuricemia is identified, associated factors such as obesity, hypercholesterolemia, alcohol consumption and hypertension should be addressed.

(Video) Gout, Pathophysiology, Causes, Symptoms, Risk Factors, Diagnosis and Treatments, Animation.

ACUTE GOUT

The four treatment options available for the acute gouty attack are NSAIDs, colchicine, corticosteroids and analgesics (Table 3 and Figure 4).

DrugDosageSide effects/comments
NSAIDS (selected)Contraindicated in patients with peptic ulcer disease or systemic anticoagulation; side effects include gastropathy, nephropathy, liver dysfunction, central nervous system dysfunction and reversible platelet dysfunction; may cause fluid overload in patients with congestive heart failure
Indomethacin (Indocin)25 to 50 mg four times daily
Naproxen (Naprosyn)500 mg two times daily
Ibuprofen (Motrin)800 mg four times daily
Sulindac (Clinoril)200 mg two times daily
Ketoprofen (Orudis)75 mg four times daily
Colchicine0.5 to 0.6 mg orally every hour until relief or side effects occur, or until a maximum dosage of 6 mg is reachedDose-dependent gastrointestinal side effects; improper intravenous dosing has caused bone marrow suppression, renal failure and death (see text)
Corticosteroids
OralPrednisone, 0.5 mg per kg on day 1, taper by 5.0 mg each day thereafterFluid retention; impaired wound healing
IntramuscularTriamcinolone acetonide (Kenalog), 60 mg intramuscularly, repeat in 24 hours if necessaryMay require repeat injections; risk of soft tissue atrophy
Intra-articularLarge joints: 10 to 40 mg*Preferable route for monoarticular involvement
Small joints: 5 to 20 mg*
ACTH40 to 80 IU intramuscularly; repeat every 8 hours as necessaryRepeat injections are commonly needed; requires intact pituitary-adrenal axis; stimulation of mineralocorticoid release may cause volume overload
Gout and Hyperuricemia (5)

NSAIDs are the preferred therapy for the treatment of patients without complications. Indomethacin (Indocin) was the first NSAID used for gout, but other NSAIDs, including ibuprofen (Motrin), naproxen (Naprosyn), sulindac (Clinoril), piroxicam (Feldene) and ketoprofen (Orudis) are also effective in the treatment of acute gout.17 Maximum dosages should be given immediately after the onset of symptoms or at the time of diagnosis and continued for 24 hours after complete resolution of the acute attack, then tapered quickly over two to three days.

The most important determinant of therapeutic success is not which NSAID is chosen, but rather how soon NSAID therapy is initiated. In more than 90 percent of patients, complete resolution of the attack occurs within five to eight days of initiation of therapy.18 Unfortunately, the use of NSAIDs is limited by side effects. NSAID therapy should be avoided in patients with peptic ulcer disease, low creatinine clearance, liver disease and poorly compensated congestive heart failure, and in patients receiving anticoagulation therapy.19,20 Side effects of NSAIDs are also more pronounced in elderly patients.21

Colchicine, an antimitotic drug derived from the roots of the herb Colchicum autumnale, is one of the oldest treatments for gout. Although colchicine is effective in treating acute gout, 80 percent of patients experience gastrointestinal side effects, including nausea, vomiting and diarrhea, at therapeutic dosages.22 Furthermore, colchicine is less effective once an acute attack has persisted for a few days. Intravenous colchicine is available but has a narrow therapeutic-toxicity ratio. It should not be used in patients with combined renal and hepatic disease, a creatinine clearance of less than 10 mL per minute (0.17 mL per s) or extrahepatic billiary obstructions, or in patients who have recently received oral colchicine. Improper intravenous colchicine therapy has been associated with bone marrow suppression, renal failure, disseminated intravascular coagulation, tissue necrosis from extravascular extravasation and death.

The systemic toxicity associated with intravenous administration of colchicine has been reviewed.22 Since less toxic therapeutic options are available for the management of patients with complicated gout, intravenous administration of colchicine is generally avoided in favor of corticosteroid or analgesic therapy. However, if intravenous colchicine is used, the initial dosage is 1 to 2 mg in 20 mL of normal saline, infused over one hour into an established venous access. A subsequent dose of 1 mg can be given six hours later if the patient has not experienced relief. Once intravenous colchicine is administered, use of oral colchicine must be discontinued, and no additional colchicine should be taken for one week because of the drug's slow excretion rate.

Corticosteroids, administered intra-articularly, intravenously, intramuscularly or orally, have been shown to be effective in the treatment of acute gout. In cases where one or two accessible joints are involved, intra-articular injection of corticosteroid (in large joints: 10 to 40 mg of triamcinolone hexacetonide [Aristospan Intralesional], triamcinolone acetonide [Kenalog] or methylprednisolone [Medrol]; in small joints: 5 to 20 mg of the previously mentioned agents) can be used with minimal side effects. In almost every case, the joint should be aspirated for diagnosis and synovial fluid cultures before intra-articular steroid administration.

Adrenocorticotropic hormone (ACTH) can also be used in the treatment of acute gout. A dose of 40 IU given intramuscularly and repeated every eight to 24 hours, as needed, is as effective as indomethacin (Indocin) at a dosage of 50 mg three times daily.23,24

Although parenteral ACTH is effective, it may require several repeat injections and cannot be used in patients with recent prior use of systemic steroids, since the action of ACTH requires an unsuppressed adrenal axis. ACTH has not been shown to be any more effective than systemic corticosteroids. In a study25 comparing single intramuscular doses of ACTH (40 IU) with triamcinolone acetonide (60 mg) for the treatment of acute gout, both treatments were found to be effective. Nine of 15 patients receiving ACTH required at least one repeat injection, compared with five of 16 patients receiving triamcinolone acetonide. Triamcinolone acetonide (60 mg) has also been shown to be as effective as indomethacin (50 mg given three times daily) in relieving acute gouty arthritis.26 Triamcinolone acetonide is especially useful in patients with known contraindications to NSAIDs.

A single dose of triamcinolone acetonide is effective in most patients. However, patients with longstanding or polyarticular attacks may require repeat doses. Oral prednisone is an option when repeat dosing is anticipated. A regimen of 0.5 mg per kg of prednisone on day 1 and tapered by 5 mg each day is also very effective. This schedule typically requires about one week of therapy to be effective.

(Video) Best & Worst Foods to Eat with Gout | Reduce Risk of Gout Attacks and Hyperuricemia

INTERCRITICAL GOUT

The use of low-dose colchicine as prophylaxis for the prevention of gouty arthritis was first described in 1936.27 It is common practice among rheumatologists to administer prophylactic or low-dose colchicine (from 0.6 mg to 1.2 mg) at the same time urate-lowering drug therapy is initiated, but this regimen has not been widely embraced by primary care physicians.28,29 Prophylactic therapy is quite effective in patients who tolerate colchicine and is 85 percent effective in preventing acute attacks.30 Colchicine should be used for prophylaxis only with concurrent use of urate-lowering agents. Colchicine alone does not alter urate deposition or tissue damage.31 Low-dose colchicine is used for prophylaxis until the serum urate concentration is stable at the desired level and the patient has been free from acute gouty attacks for three to six months. There is a risk for an acute gouty flare-up when prophylaxis is discontinued. However, most patients are able to remain on urate-lowering agents alone. If patients do not tolerate daily doses of colchicine, a low daily dose of a selected NSAID can be used instead.

URATE-LOWERING AGENTS

After the acute gouty attack is treated and prophylactic therapy is initiated, the issue of ongoing urate deposition should be addressed. A common practice is not to initiate drug therapy aimed at lowering urate levels after the initial attack. Rather, most clinicians prefer to aggressively correct or reverse sources of hyperuricemia in hopes of lowering the serum urate level without the use of medication. Established indications for the use of urate-lowering agents are listed in Table 4.

DrugDosageCost*IndicationsSide effects/comments
Sulfinpyrazone (Anturane)Begin with 50 mg three times daily, gradually titrating upward until the serum urate level is < 6 mg per dL (355 μmol per L); maximum dosage: 800 mg per day$16.75; generic: 12.25Recurrent gout in patients who require antiplatelet therapy; aspirin use may block the effects of probenecidUricosuric agent best used in patients on a regular diet who underexcrete uric acid (i.e., < 800 mg of urate in 24 hours [4.76 mmol per day]); inherent antiplatelet activity
Probenecid (Benemid)Begin with 250 mg twice daily, gradually titrating upward until the serum urate level is < 6 mg per dL (355 μmol per L); maximum dosage: 3 g per day4.50 to 5.25Recurrent gout in patients who are allergic or intolerant to allopurinol; may be combined with allopurinol in select patients with resistant hyperuricemia; for use in patients able to maintain oral hydrationUricosuric agent best used in patients who undersecrete uric acid; creatinine clearance must be > 60 mL per minute (1.00 mL per s); therapeutic effect reversed by high-dose aspirin therapy; avoid concurrent daily aspirin use; contraindicated in patients with a history of urolithiasis; may precipitate gouty attack or renal calculi at start of therapy; rash or gastrointestinal side effects may occur
Allopurinol (Zyloprim)Begin with 50 to 100 mg daily, gradually titrating upward until the serum urate level is < 6 mg per dL (355 μmol per L); typical dosage: 200 to 300 mg daily6.50; generic: 2.50 to 3.00Chronic tophaceous “erosive” gouty arthritis; secondary hyperuricemia related to the use of cytolytics in the treatment of hematologic malignancies; gout complicated by renal disease or renal calculiInhibits uric acid synthesis; best for patients who overproduce uric acid (i.e., those who excrete > 800 mg of urate in 24 hours [4.76 mmol per day]); peak effect in reduction of urate synthesis occurs at two weeks; side effects include rash, gastrointestinal symptoms, headache, urticaria and interstitial nephritis; rare, potentially fatal hypersensitivity syndrome may occur (usually in patients with underlying renal insufficency or concurrent thiazide use)

Determination of 24-hour urine uric acid excretion is essential to identify the most appropriate urate-lowering medication and to check for significant preexisting renal insufficiency. Uricosuric agents should be used in most patients with gout because most are “underexcretors” of uric acid (normal secretion of urate is considered to be 800 mg in 24 hours [4.76 mmol per day] for patients on a regular diet). Patients who have renal insufficiency or a history of nephrolithiasis, or those who might benefit from the cardioprotective effect of low-dose aspirin therapy should not take uricosuric agents.

Inhibitors of uric acid synthesis are more toxic, especially in elderly patients, and should be reserved for use in “overproducers” of urate (i.e., those who excrete more than 800 mg in 24 hours [4.76 mmol per day]). Urate-lowering therapy should not be initiated until the acute attack has completely resolved, since the subsequent rapid decrease in serum urate levels has been shown to exacerbate the gouty attack.

Probenecid (Benemid) is the most frequently used uricosuric medication. Candidates for probenecid therapy must have hyperuricemia attributed to undersecretion of urate (i.e., less than 800 mg in 24 hours [4.76 mmol per day] on a regular diet or less than 600 mg in 24 hours [3.57 mmol per day] on a purine-restricted diet), a creatinine clearance of greater than 60 mL per minute (1.00 mL per s) and no history of nephrolithiasis. Probenecid works at the level of the proximal tubule by blocking reabsorption of filtered uric acid. This action is inhibited by low-dose salicylates; this fact accounts for a significant number of “treatment failures.” Consequently, patients who require low-dose aspirin therapy are not candidates for probenecid therapy. Probenecid should be initiated at a dosage of 250 mg twice daily and increased as needed, up to 3 g per day, to achieve a serum urate level of less than 6 mg per dL (355 μmol per L). The initial side effects of probenecid include possible precipitation of an acute gouty attack and renal calculi. Other common side effects include rash and gastrointestinal problems.

Sulfinpyrazone (Anturane), another uricosuric agent, is preferred by some physicians because of its added antiplatelet effects. Therapy is initiated at a dosage of 50 mg three times a day, which is gradually increased until the serum urate level is lowered. The maximum dosage is 800 mg per day.

Allopurinol (Zyloprim) is currently the only readily available inhibitor of uric acid synthesis. Originally developed as a chemotherapeutic agent, this potent inhibitor of xanthine oxidase-dehydrogenase is the most common drug used in the treatment of hyperuricemia. Allopurinol causes a detectable decrease in the serum urate level within the first 24 hours after administration and an expected maximum reduction within two weeks after initiation of therapy. Indications for the use of allopurinol are listed in Table 4.

Allopurinol may be given in a single daily dose of 300 mg. This is the average effective dosage necessary for patients with normal renal function. Frequently, allopurinol therapy is initiated at a dosage of 100 mg per day and increased in increments of 50 to 100 mg per day every two weeks until the patient's urate level is less than 6 mg per dL (355 μmol per L). Unless the serum urate level is lower than 6.4 mg per dL (380 μmol per L), the concentration at which urate saturates the extra-cellular fluid, crystals will not be absorbed, and tophi will continue to form.

Side effects from allopurinol include rash, gastrointestinal problems, headache, urticaria and interstitial nephritis. The most feared adverse reaction is hypersensitivity syndrome associated with fever, bone marrow suppression, hepatic toxicity, renal failure and a systemic hypersensitivity vasculitis.32 Fortunately, this life-threatening syndrome is rare. It most commonly occurs in elderly patients with renal insufficiency who are receiving concomitant thiazide diuretic therapy.33 Therefore, the maximum dosage of allopurinol should be determined by the creatinine clearance, which can be assessed using a 24-hour urine collection. In patients with a creatinine clearance of 100 mL per minute (1.67 mL per s) or greater, the initial dosage can be up to 300 mg, with a maximum dosage of 600 mg. In patients with a creatinine clearance of 60 mL per minute (1.00 mL per s), the maximum dosage of allopurinol is 200 mg per day. The maximum dosage in patients with a creatinine clearance of 30 mL per minute (0.50 mL per s) is 100 mg per day, and 100 mg every two to three days in patients with a creatinine clearance of 10 mL per minute (0.16 mL per s) or less.

(Video) Gout and Hyperuricemia

Patients for whom allopurinol is indicated who experience side effects with this drug should be referred to a rheumatologist for a possible desensitization protocol or a trial of oxypurinol. Oxypurinol is the major active metabolite of allopurinol and is only available in the United States for use on a compassionate basis.

FAQs

What is the difference between gout and hyperuricemia? ›

Hyperuricemia is a condition characterized by abnormally elevated levels of serum urate (sUA), while gout, the most common form of inflammatory arthritis, arises from the subsequent deposition of urate crystals when concentrations become saturated.

What is the relationship between hyperuricemia and gout? ›

Hyperuricemia is a risk factor for gout. It has been well observed that a large proportion of individuals with hyperuricemia have never had a gout flare(s), while some patients with gout can have a normuricemia. This raises a puzzle of the real role of serum uric acid (SUA) in the occurrence of gout flares.

Is hyperuricemia a symptom of gout? ›

Gout is a condition characterized by the deposition of monosodium urate crystals in the joints or soft tissue. The four phases of gout include asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout and chronic tophaceous gout.

Can you have hyperuricemia without gout? ›

Asymptomatic hyperuricemia is a term traditionally applied to settings in which the serum urate concentration is elevated but in which neither symptoms nor signs of monosodium urate (MSU) crystal deposition disease, such as gout, or uric acid renal disease, have occurred.

What is the most common cause of hyperuricemia? ›

Most of the time, a high uric acid level occurs when your kidneys don't eliminate uric acid efficiently. Things that may cause this slow-down in the removal of uric acid include rich foods, being overweight, having diabetes, taking certain diuretics (sometimes called water pills) and drinking too much alcohol.

What are the three 3 complication for gout? ›

Complications of gout include joint damage, kidney damage, and bone loss. This excess uric acid causes needle-shaped crystals to form around joints, leading to inflammation in and around the joints.

What disease causes hyperuricemia? ›

Acidosis: Types that cause hyperuricemia include lactic acidosis, diabetic ketoacidosis, alcoholic ketoacidosis, and starvation ketoacidosis.

What can cause gout? ›

What causes gout?
  • obesity, high blood pressure and/or diabetes.
  • having a close relative with gout.
  • kidney problems.
  • eating foods that cause a build-up of uric acid, such as red meat, offal and seafood.
  • drinking too much beer or spirits.
29 Sept 2022

What are the three main symptoms of gout? ›

Symptoms
  • Intense joint pain. Gout usually affects the big toe, but it can occur in any joint. ...
  • Lingering discomfort. After the most severe pain subsides, some joint discomfort may last from a few days to a few weeks. ...
  • Inflammation and redness. ...
  • Limited range of motion.

What is the fastest way to get rid of gout? ›

Treatment
  1. Nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs include over-the-counter options such as ibuprofen (Advil, Motrin IB, others) and naproxen sodium (Aleve), as well as more-powerful prescription NSAIDs such as indomethacin (Indocin, Tivorbex) or celecoxib (Celebrex). ...
  2. Colchicine. ...
  3. Corticosteroids.

Can you get rid of hyperuricemia? ›

It is possible to treat hyperuricemia through dietary changes. Consuming fewer foods and drinks that are high in purine can reduce uric acid in the blood. This reduction helps the kidneys to filter out uric acid more effectively again.

What diseases are mistaken for gout? ›

Gout and pseudogout are types of arthritis. They cause pain and swelling in the joints.
...
Gout and pseudogout are sometimes mistaken for other joint conditions, such as:
  • rheumatoid arthritis.
  • osteoarthritis.
  • carpal tunnel syndrome.
  • infectious arthritis.
  • ankylosing spondylitis.
6 Dec 2018

What gets mistaken for gout? ›

Pseudogout is formally known as calcium pyrophosphate deposition disease or CPPD. But the condition is commonly called pseudogout because of its similarity to gout. In both pseudogout and gout, crystal deposits form within a joint, although the type of crystal differs for each condition.

Is lemon good for uric acid? ›

Lemon juice may help balance uric acid levels because it helps make the body more alkaline. This means it slightly raises the pH level of blood and other fluids. Lemon juice also makes your urine more alkaline.

Is coffee good for uric acid? ›

Coffee is thought to reduce gout risk by lowering uric acid levels through several mechanisms . Coffee may lower uric acid levels by increasing the rate that your body excretes uric acid. Coffee is also thought to compete with the enzyme that breaks down purines in the body.

What foods to avoid if you have hyperuricemia? ›

Avoid meats such as liver, kidney and sweetbreads, which have high purine levels and contribute to high blood levels of uric acid. Red meat. Limit serving sizes of beef, lamb and pork. Seafood.

Do bananas trigger gout? ›

Bananas are low in purines and high in vitamin C, which makes them a good food to eat if you have gout. Changing your diet to include more low-purine foods, like bananas, can lower the amount of uric acid in your blood and reduce your risk of recurrent gout attacks.

What fruit is good for gout? ›

Eat: Citrus Fruits

Grapefruit, oranges, pineapples, and strawberries are all great sources of vitamin C, which lowers your uric acid levels and helps prevent gout attacks.

Is Egg good for uric acid? ›

Certain foods, such as red meat, are rich in purines. You should avoid such foods if you have gout or are at a high risk for it. This means you need to choose sources of protein that are low in purines. Eggs are a good option.

Can gout cause kidney failure? ›

These stones are very painful and can hurt the kidneys by: blocking the kidneys from removing wastes, which can cause infection, and. scarring the kidneys with their sharp edges. Both problems can lead to CKD, and even kidney failure.

Does gout do permanent damage? ›

What's the outlook for people with gout? Untreated gout can lead to permanent joint damage. The buildup of uric acid in the joints and soft tissue is called tophus. Some people with gout can also develop other health problems, such as severe arthritis, kidney stones and heart disease.

Can gout affect kidneys? ›

It is a serious disease that requires treatment. Gout happens if a substance called uric acid gets too high in your blood. Having high levels of uric acid in your blood is called hyperuricemia. High levels of uric acid can harm your kidneys and lead to kidney disease or kidney failure.

What drugs raise uric acid levels? ›

Examples of medicines that increase uric acid levels
  • Diuretics (see below)
  • Aspirin low dose (less than 300 mg daily)
  • Nicotinic acid.
  • Levodopa.
  • Ciclosporin.
  • Tacrolimus.
15 Sept 2021

Can hyperuricemia cause back pain? ›

Spinal gout most commonly present as back or neck pain with majority of reported patients with elevated uric acid. The diagnosis of spinal gout is confirmed with the presence of negatively birefringent monosodium urate crystals in tissue.

What does hyperuricemia feel like? ›

Symptoms of Hyperuricemia

This is a disorder where uric acid builds up in the tissues and blood and leads to painful joints, particularly in your big toe. ‌Another common symptom of hyperuricemia is the formation of kidney stones, which can lead to sharp pain in the abdomen or side, nausea, and vomiting.

Can gout be cured? ›

Gout is one of the most common inflammatory arthritides. The disease is due to the deposition of monosodium urate crystals. These deposits are reversible with proper treatment, suggesting that gout is a curable disease.

How do you test for gout? ›

A blood test can check the level of uric acid in your blood. A high level of uric acid could mean you have gout. A uric acid level in the blood between 3.5 and 7.2 milligrams per deciliter (mg/dl) is considered normal for most people.

Can gout be caused by stress? ›

Gout attacks may be triggered by any of the following: Drinking alcohol. Eating a lot of protein-rich foods. Emotional stress.

What is the first stage of gout? ›

Stage 1: High Uric Acid Levels

Also called asymptomatic hyperuricemia, in this beginning stage of gout, uric acid is building up in the blood and starting to form crystals around joints, most often in the foot.

Where is the most common place to get gout? ›

The most common site for a gout attack is what is known as the bunion joint on the big toe. It is typically the first joint affected by gout. As gout worsens, the ankle, mid-foot, knee, and elbow can become common sites of gout attacks.

Does vinegar stop gout? ›

There is no proof that consuming or using apple cider vinegar can help prevent or treat gout. However, certain chemicals in apple cider vinegar, namely acetic acid, may lower the risk of developing conditions that can increase the likelihood of gout, such as obesity, diabetes, and high blood pressure.

How do I get my uric acid back to normal? ›

This article reviews natural ways to help lower uric acid levels.
  1. Limit purine-rich foods. ...
  2. Eat more low purine foods. ...
  3. Avoid medications that raise uric acid levels. ...
  4. Maintain a healthy body weight. ...
  5. Avoid alcohol and sugary drinks. ...
  6. Drink coffee. ...
  7. Try a vitamin C supplement. ...
  8. Eat cherries.
29 Jun 2022

Does exercise reduce uric acid? ›

Studies have shown that exercise can effectively reduce serum uric acid (SUA), but the optimal exercise dose, intensity, and mode of exercise for improving HUA have not been verified in clinical studies.

What autoimmune disease causes gout? ›

Gout is an inflammatory disorder, but it is not an autoimmune condition. Gout is caused by high blood levels of uric acid that the body cannot excrete properly. These uric acid crystals can deposit in the synovial tissues, causing inflammation and pain. RA is an autoimmune inflammatory condition.

Does tumeric help gout? ›

If you have gout, try turmeric as a home remedy. Its most active chemical, curcumin, has potent anti-inflammatory and antioxidant properties. This may help ease gout-related inflammation and pain. When eaten in foods, turmeric is generally safe.

How long does gout take to heal? ›

An attack of gout usually lasts 5 to 7 days, then gets better. It may not cause lasting damage to joints if you get treatment immediately. Ask for an urgent GP appointment or call 111 if: the pain is getting worse.

Can gout go away in 2 days? ›

An acute gout attack will generally reach its peak 12-24 hours after onset, and then will slowly begin to resolve even without treatment. Full recovery from a gout attack (without treatment) takes approximately 7-14 days. An accurate and colorful discription of a gout attack was elegantly written in 1683 by Dr.

Does gout make you tired? ›

Sleep and fatigue

Gout attacks can tend to occur at night. This can cause you to have trouble sleeping. During attacks you may also feel fatigued.

Which exercise is best for uric acid? ›

Exercises that work the body's cardiovascular system are best for managing uric acid levels and help to manage body weight ( 4 ). Examples of these types of exercises include walking, cycling, and swimming.

What is another name for hyperuricemia? ›

Definition. A high uric acid level, or hyperuricemia, is an excess of uric acid in your blood.

What are the two main types of hyperuricemia? ›

Causes of high uric acid levels (hyperuricemia) can be primary (increased uric acid levels due to purine), and secondary (high uric acid levels due to another disease or condition). Sometimes, the body produces more uric acid than it is able to excrete.

What is considered hyperuricemia? ›

Hyperuricemia is an elevated uric acid level in the blood. The normal upper limit is 6.8mg/dL, and anything over 7 mg/dL is considered saturated, and symptoms can occur. This elevated level is the result of increased production, decreased excretion of uric acid, or a combination of both processes.

Is gout and uric acid the same? ›

Gout is caused by a build-up of a substance called uric acid in the blood. If you produce too much uric acid or your kidneys don't filter enough out, it can build up and cause tiny sharp crystals to form in and around joints. These crystals can cause the joint to become inflamed (red and swollen) and painful.

What removes uric acid from the body? ›

Purines are also formed and broken down in your body. Normally, your body filters out uric acid through your kidneys and in urine.

Which is the first line treatment for chronic hyperuricemia? ›

Xanthine oxidase inhibitors (XOIs) still remain the first line of treatment as recommended by all guidelines. Among these, allopurinol is the first-line agent in all but the ACR guidelines, which recommend allopurinol or febuxostat interchangeably.

Does high uric acid mean kidney failure? ›

Uric acid is an independent risk factor for kidney failure in earlier stages of CKD, and has a 'J-shaped' relationship with all-cause mortality in CKD.

Is hyperuricemia a kidney disease? ›

Hyperuricemia may be a major contributor to the development or progression of chronic kidney disease (CKD). Although there is no clear cutoff uric acid (UA) value associated to the risk for kidney damage, it appears to be an increased risk as UA rises.

Can gout destroy bones? ›

Bone erosions, which are associated with long-term damage and disability, are common in patients with gout and have been linked with specific clinical and ultrasound-detected factors, Chinese researchers reported. Among 980 patients with gout, 44% had bone erosions seen on ultrasound, according to Hai B.

What organ is related to gout? ›

Health problem linked to gout go beyond the joints, however. Excess uric acid can also damage kidneys, blood vessels, and other organs, and gout raises the risk for several disorders. These include kidney and cardiovascular disease, as well as diabetes, depression and sleep apnea.

How serious is gout? ›

What's the outlook for people with gout? Untreated gout can lead to permanent joint damage. The buildup of uric acid in the joints and soft tissue is called tophus. Some people with gout can also develop other health problems, such as severe arthritis, kidney stones and heart disease.

Videos

1. Gout - Mechanisms & Treatment
(PhysioPathoPharmaco)
2. Gout and Hyperuricemia. By Dr. Dheyaa Jabbar
(Clinical Pharmacy U.O.B)
3. Gout - Types, Clinical Features and Treatment || Hyperuricemia || Uric Acid || Biochemistry
(Biochemistry Basics by Dr Amit)
4. Hyperuricemia and Gout Disease-Nucleic Acid Metabolism-Biochemistry-B. Pharmacy /BSc./Nursing
(MS Science Academy)
5. Gouty Arthritis (Gout) and Uric Acid
(Medicurio)
6. Gout | Hyperuricemia | Causes and Treatment | Lecture 7
(The Medical Bay)

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