The 15-Minute Visit

A guide to patient encounters in the real world of office practice

Chronic gouty arthritis

PROBLEM

A 61-year-old man presents with a nodule on his elbow that he has had for several years but that has become more bothersome over the past year as it has slowly increased in size. He reports episodic attacks of joint pain.

APPROACH

The physical examination revealed a swollen olecranon bursa containing a rounded, subcutaneous nodule that was slightly tender and rubbery to the touch. Also noteworthy was a subcutaneous nodule at the left second metacarpal-phalangeal joint (MCP), as well as synovial proliferation or swelling of the left wrist and the bilateral second and third MCP joints.

The differential diagnosis for this patient includes gout, pseudogout, and rheumatoid arthritis. Other forms of inflammatory arthritis, including psoriatic, hepatitis-C-associated, and spondyloarthropathy, could cause similar joint findings but would not be expected to cause nodules. In the elderly, gout may often be misdiagnosed as rheumatoid arthritis, since the acute attacks may have been occurred years before, and the patient may now be experiencing a chronic arthritis associated with subcutaneous tophaceous deposits on the fingers, toes, and elbows. Conversely, since hyperuricemia occurs more often than clinical gout, a flare pain from osteoarthritis of the metarsophalangeal (MTP) joint of the big toe in a patient with hyperuricemia can lead the unwary practitioner into applying the wrong diagnostic label of gouty arthritis.

Calcium pyrophosphate dihydrate crystal deposition disease (CPPD) may also resemble gout and occurs concomitantly in up to 40% of patients with gout. Typically, CPPD may involve a different anatomic distribution from gout in early disease, with greater frequency of wrist involvement and much less podagra. CPPD is associated with joint-space narrowing. Additionally, the absence of erosions and tophi further distinguishes CPPD from gout. Since gout and calcinosis can coexist, chondrocalcinosis on radiography does not exclude gout. The diagnosis of gout is confirmed by finding monosodium urate or pseudogout crystals in the aspirated fluid of a joint or subcutaneous tophus of gout).

With radiograph findings of punched-out lesions in the MTP joint with overhanging edges, a diagnosis of chronic gouty arthritis was suspected in this patient and later confirmed with joint aspiration. As the most common inflammatory arthritis, gout is more prevalent in men than in premenopausal women, and its peak incidence is seen in patients 30 to 50 years old. The main predisposing factors for gout in men are a family history, genetic predisposition, obesity, alcohol (beer and liquor) intake (particularly in a binge pattern), and a high purine diet.

Tophi may form almost anywhere. Older patients, particularly women taking diuretics, may to have gout in the small distal joints of the fingers. Tophi and inflammation may also gradually erode cartilage and bone, ultimately destroying the joint.

Potential causes

Is the prevalence of gout increasing because of the popularity of high-protein diets? A recently published 12-year study found that men in whom gout developed were more likely to be in the highest quintile of meat intake. In addition, the increased intake of a greater variety of dietary products was associated with a decreased incidence of gout. Increased urate levels have been epidemiologically linked to obesity, high cholesterol levels, insulin resistance, and hypertension. In addition, several studies have suggested an association between coronary heart disease (CHD) and gout. One study concluded that gout was an independent risk factor for CHD.

Clinical course

In some patients, flares of gout can be triggered by events surrounding hospitalization, joint injury, surgery, certain drug treatments, and overindulgence in alcohol or purine-rich foods. According to some studies, symptoms occur more frequently in the spring (with the peak in April). Most often, symptoms are initially monoarticular. Gout can be conceptualized as having 4 clinical stages: asymptomatic, acute, intercritical, and chronic.

Asymptomatic hyperuricemia, the first stage of gout, occurs when urate deposition is initiated as a result of elevated uric acid levels. This stage lasts many years (seemingly shorter in transplant patients taking cyclosporine). Although chronic hyperuricemia virtually always precedes gout, it does not inevitably lead to it. In fact, the full-blown arthritic disease develops in less than a quarter of the hyperuricemic population.

Acute gouty arthritis occurs when the symptoms of gout appear. Sometimes gout is heralded by brief twinges of pain in affected joints, which can precede the full-blown condition by several years. In many cases, the attack occurs late at night or early in the morning and wakes the patient from sleep. Localized swelling may extend beyond the joint, an indication of the intense inflammatory response. The skin over the affected area is often red, shiny, and tense and may start to peel after a few days.

Intercritical gout refers to the asymptomatic periods between attacks. Crystals may still be found in asymptomatic joints at this time. The first attack is usually followed by a complete remission of symptoms but, if left untreated, gout nearly always recurs at some point. One study found that 62% of untreated subjects experienced at least 1 further attack within 1 year. At the end of 2 years, 78% of patients experienced a recurrence. After 10 years, 93% of the patients had had repeat attacks.

Chronic tophaceous gout occurs when gout is unsuccessfully treated and the intercritical periods become shorter. Though sometimes less intense, the attacks may last longer. Over many years, gout may become a disorder characterized by constant low-grade joint pain, stiffness, and inflammation. Gout may eventually affect additional joints, including, in rare cases, the shoulders, hips, or spine.

TREATMENT

In recent years, some of the standard treatment recommendations for acute and chronic gout have undergone revision. For example, IV colchicine use is rarely advocated for treatment of routine acute gout. Likewise, hourly administration of oral colchicine is rarely used. NSAIDs are the first-line therapy for acute gout and should be given in full dosages unless there is a history of peptic ulcer disease, a background of renal impairment, significant hypertension, or cardiac failure. The NSAIDs used in the treatment of acute gout include ibuprofen, indomethacin (Indocin, Indochron E-R), ketoprofen (Orudis, Oruvail), naproxen, and sulindac (Clinoril). Intra-articular corticosteroids (if infection is excluded) and systemic corticosteroids are useful in older patients and in those with impaired renal function.

This patient was prescribed indomethacin, 50 mg tid. When his pain and inflammation significantly decreased by day 2, the dosage was decreased to 25 mg tid until his symptoms fully resolved on day 7. One month after his acute attack, the patient was put on long-term prophylaxis with allopurinol (Zyloprim). Allopurinol is the chronic therapy of choice for patients with tophi. The patient was started at a low dosage of 50 mg/d of allopurinol, which was increased over 3 to 4 weeks, titrated to the dosage that lowered the serum uric acid level to less than 6 mg/dL. (Note that an allopurinol dosage of 300 mg/d may accomplish this in only about 50% of patients.) The hypouremic drugs used for gout can also precipitate acute gout symptoms and thus should not be used until symptoms have clearly subsided.

 

What would you do if . . . 1. The patient never responds completely after adequate initial treatment with indomethacin? 2. The patient's medical history contraindicates NSAIDs and colchicine? Answers 1. The NSAID dosage may have been insufficient because the duration of treatment was too short. If the dosage of indomethacin cannot be increased, prescribe a corticosteroid in moderately high dosages until the attack subsides. 2. Start the patient on a high dosage of an oral corticosteroid. When the attack resolves completely, taper the dosage slowly over 7 to 10 days if the attack was severe.

ADVISOR

KARL SINGER, MD, general internist and family physician in private practice in Exeter, NH; and the Medical Director of Patient Care.

REVIEWER

BRIAN F. MANDELL, MD, PhD, Education Program Director, Rheumatic and Immunologic Diseases, Cleveland Clinic Foundation, Cleveland, Ohio.