eMedicine Specialties > Emergency Medicine > Rheumatology

Gout and Pseudogout: Follow-up

Author: Joseph Kaplan, MD, MS, FACEP, Attending Physician, Department of Emergency Medicine, Martin Army Community Hospital, Fort Benning, Georgia
Contributor Information and Disclosures

Updated: Aug 27, 2009

Follow-up

Further Outpatient Care

  • Patients should be followed up to ensure that the gouty attack resolves and no secondary infection appears. Patients on diuretics that may have been stopped during the initial attack should be evaluated, and, if used for hypertension, losartan, which has a low uricosuric potential, should be considered. Prophylactic measures such as allopurinol should be begun.

Deterrence/Prevention

  • No prophylactic or deterrent regimen for patients with idiopathic pseudogout is known. If an underlying metabolic problem is responsible for pseudogout, the arthritis may be cured when the underlying problem is addressed.
  • Consumption of purine-rich foods increases the frequency of attacks in patients with gout. Alcohol, yeasty foods, oily fish, and liver have been implicated in gout attacks. A consultation with a dietitian may be helpful for such patients.
  • Gout prophylaxis may be carried out with allopurinol (100-300 mg/d) or with a combination of colchicine (0.6 mg qd/bid) with probenecid (250-500 mg bid). Increasing dosage of or starting patients on probenecid and allopurinol is contraindicated during an acute attack of gouty arthritis. Long-term continuation is controversial.

Complications

  • Gout patients who have a 24-hour urinary excretion of uric acid above 1100 mg have a 50% risk of developing urate and oxalate kidney stones. Those with a measured urate excretion greater than 800 mg per 24 hours may benefit from allopurinol prophylaxis to prevent urate nephropathy.
  • Severe degenerative arthritis
  • Secondary infections
  • Recurrent painful episodes
  • Carpal tunnel syndrome (rare)
  • Urate or uric acid nephropathy
  • Nerve or spinal cord impingement

Prognosis

  • Gout
    • With early treatment, total control usually is attained.
    • If attacks recur, successful uric acid adjustment (requiring lifelong use of uricosuric or allopurinol medication) usually is effective.
    • During the first 6-24 months of uricosuric or allopurinol therapy, acute gout may occur.
  • Pseudogout
    • Acute attacks usually resolve within 10 days. Prognosis for resolutions of acute attacks is excellent.
    • Some patients experience progressive joint damage with functional limitation.

Patient Education

  • Advise patients to begin a low-purine diet.
  • For excellent patient education resources, visit eMedicine's Arthritis Center. Also, see eMedicine's patient education article Gout.

Miscellaneous

Medicolegal Pitfalls

  • Failure to diagnose a septic joint in a patient with what is assumed to be an acute crystal-induced arthritis
  • Failure to inform patient of the risks associated with medication used to treat crystal-induced arthritis

Special Concerns

  • Posterior interosseous nerve syndrome has been reported because of elbow inflammation causing compression of the nerve. In patients presenting with a swollen elbow and inability to extend the fingers actively, this should be considered. Treatment with intra-articular steroids has led to resolution of the nerve palsy in a case report.9
  • Allopurinol is a drug that is a hypoxanthine analog. It is not used in acute gouty arthritis but is a competitive inhibitor of xanthine oxidase at low doses and is a noncompetitive inhibitor at high doses. This decreases the amount of uric acid produced. However, it is not innocuous and is associated with allopurinol hypersensitivity syndrome. It is also associated with the drug rash with eosinophilia and systemic symptoms (DRESS) syndrome.
    • Allopurinol hypersensitivity syndrome occurs in 2% of those on the drug.10 It entails a slight rash, which will usually resolve with discontinuation of the drug.
    • DRESS syndrome affects the liver, kidney, and skin. It is a delayed-hypersensitivity response occurring 6-8 weeks after beginning allopurinol. The underlying mechanism is thought to be a cell-mediated immunity to allopurinol and its metabolites. Although occurrence is 0.4 %, the rate of organ failure and death is high. Treatment is with intravenous N- acetyl cystine and steroids.
    • Accumulation of allopurinol and its metabolite oxypurinol is felt to increase the risk of hypersensitivity reaction. Dosing guidelines are being developed to decrease their accumulation based on creatinine clearance while decreasing the amount of serum uric acid.
  • Because of the hypersensitivity syndromes associated with allopurinol, other uricosuric drugs have been investigated. These include probenecid, sulfinpyrazone, and benzbromarone. Although probenecid (1-2 g/d) and sulfinpyrazone were shown not to be as effective in lowering uric levels as allopurinol, they are not associated with DRESS syndrome. However, they cannot be used in patients with renal impairment. Benzbromarone can significantly reduce uric acid levels but is associated with hepatic problems and, in some cases, hepatic failure. For this reason, its use is restricted in the United States.
  • Research has indicated that the lipid-lowering drug fenofibrate, a fibric acid derivative, will lower serum uric acid levels while reducing very-low-density lipoprotein (VLDL), total cholesterol, and triglyceride levels.11 However, the creatinine level increases, and all effects are negated once the drug has been discontinued.
 


More on Gout and Pseudogout

Overview: Gout and Pseudogout
Differential Diagnoses & Workup: Gout and Pseudogout
Treatment & Medication: Gout and Pseudogout
Follow-up: Gout and Pseudogout
References
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References

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Further Reading

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Keywords

calcium pyrophosphate disease, CPPD, peripheral arthritis, sodium urate crystals, monosodium urate monohydrate crystals, MSU crystals, calcium pyrophosphate crystals, CPP crystals, podagra, hyperuricemia, primary gout, secondary gout, intermediate gout, late-phase gout, pseudogout, tophi, gouty nephropathy, gouty arthritis, first metatarsophalangeal joint pain, uric acid, increased serum uric acid, arthritis nodosa, arthritis uratica, foot pain, edema of the foot, crystal-induced arthritis, joint edema, acute arthritis, lysis of polymorphonuclear white blood cells, inflammatory crystalline arthritis, acute septic arthritis, pseudogout arthritis, carpal tunnel syndrome, arthrocentesis

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Contributor Information and Disclosures

Author

Joseph Kaplan, MD, MS, FACEP, Attending Physician, Department of Emergency Medicine, Martin Army Community Hospital, Fort Benning, Georgia
Joseph Kaplan, MD, MS, FACEP is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Edward A Michelson, MD, Program Director, Associate Professor, Department of Emergency Medicine, University Hospital Health Systems in Cleveland
Edward A Michelson, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gino A Farina, MD, Program Director, Associate Professor of Clinical Emergency Medicine, Department of Emergency Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine
Gino A Farina, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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