Differential Diagnosis of Polyarticular GEORGE G.A. PUJALTE, MD, Mayo Clinic Health System, Waycross, Georgia SHIRLEY A. ALBANO-ALUQUIN, MD, Pennsylvania State University College of Medicine, Hershey, Pennsylvania

Polyarticular arthritis is commonly encountered in clinical settings and has multiple etiologies. The first step is to distinguish between true articular pain and nonarticular or periarticular conditions by recognizing clinical patterns through the history and physical examination. Once pain within a joint or joints is confirmed, the next step is to clas- sify the pain as noninflammatory or inflammatory in origin. Noninflammatory arthritis, which is mostly related to , has a variable onset and severity and does not have inflammatory features, such as warm or swollen joints. Osteoarthritis usually presents with less than one hour of morning stiffness and pain that is aggravated by activity and improves with rest. A review of systems is usually negative for rashes, oral ulcers, or other internal organ involvement. In contrast, inflammatory arthritis generally causes warm, swollen joints; prolonged morning stiffness; and positive findings on a review of systems. Once inflammatory arthritis is suspected, possible diagnoses are sorted by the pattern of joint involvement, which includes number and type of joints involved, symmetry, and onset. The suspicion for inflammatory arthritis should be confirmed by the appropriate serologic/tissue and/or imaging studies in the clinical setting or in consultation with a subspecialist. (Am Fam Physician. 2015;92(1):35-41. Copyright © 2015 American Academy of Family Physicians.)

CME This clinical content hen a patient presents with considered chronic after two weeks. The conforms to AAFP criteria pain in multiple joints, the pattern of chronic symptoms should be for continuing medical pain can originate from the classified as intermittent or constant (fluctu- education (CME). See CME Quiz Questions on joint (true arthritis); the ating from mild, moderate, or severe) to help page 16. Wadjacent structures, such as bone, tendon, identify the behavior of the inflammatory Author disclosure: No rel- or bursa; or from psychogenic/metabolic process, possible triggers, and concurrent evant financial affiliations. factors, such as depression or hypothyroid- problems. ism. Once arthritis is suspected, physicians The pattern of joint involvement is pro- should distinguish between noninflamma- filed by assessing symmetry, and number tory and inflammatory forms of arthritis and types of joints involved. A symmet- while recognizing potentially disabling and ric pattern affects both sides of the body as life-threatening problems. opposed to an asymmetric pattern, which Conditions with polyarthritis are often has a spotty distribution. Possible condi- accompanied by synovitis. On the other tions are classified based on number of hand, conditions that cause pain outside of joints affected: pauciarticular pattern (two the joints are considered when there is no to four joints) vs. polyarticular pattern (five apparent joint . Nearly 50% or more joints). The of patients with polyarticular pain will have are classically pauciarticular, whereas rheu- unclassifiable conditions; these patients may matoid arthritis (RA) is usually polyarticu- not need medications and may go into remis- lar. However, spondyloarthropathies, such sion within one year.1 However, patients with as , may also present in a unclassifiable conditions may benefit from polyarticular manner, whereas RA may ini- medications for symptomatic relief. tially affect just a few joints. The size and kind of joints involved Patient History also provide major diagnostic clues. For The first step in the diagnosis is to determine instance, spondyloarthropathies often the onset and timing (acute vs. chronic) involve the spine, including sacroiliac joints of symptoms. Acute symptoms last from and medium/large joints, such as the shoul- hours to two weeks, whereas symptoms are ders, hips, knees, and ankles. Smaller joint

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SORT: KEY RECOMMENDATIONS FOR PRACTICE

Evidence Clinical recommendation rating References

Joint swelling, erythema, prolonged morning stiffness (more than one hour), and symmetric pain even at C 3-6 rest are suggestive of inflammatory conditions. Noninflammatory and inflammatory conditions can be differentiated with C-reactive protein and erythrocyte C 7, 8 sedimentation rate tests; however, in the acute phase, erythrocyte sedimentation rate is less reliable than C-reactive protein. In the diagnosis of , a high serum uric acid level has little diagnostic value. The standard of diagnosis is C 14, 15 the presence of intracellular monosodium urate crystals on polarized microscopy. Osteoarthritis is noninflammatory; is typically pauciarticular; and often involves the spine and weight-bearing C 3-6 joints, such as the hips and knees.

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort. involvement, such as the wrists, fingers, and toes, is more a neurologic cause of pain might be combined with a consistent with RA and lupus. Table 1 summarizes clini- rheumatologic cause, leading to mixed characteristics. cal patterns that are helpful in the diagnosis of polyar- Extra-articular symptoms can help narrow the diag- ticular arthritis.2-6 nostic options. For example, weakness may be a sign of neuromuscular disease, whereas dry mouth, dry eyes, INFLAMMATORY AND NONINFLAMMATORY ARTHRITIS Raynaud phenomenon, pleuritic chest pain, nasal ulcers, Arthritis can be divided into two broad categories: oral ulcers, alopecia, adenopathy, or rash might suggest inflammatory and noninflammatory (degenerative systemic inflammatory rheumatologic conditions. Con- arthritis). The presence of joint swelling, erythema, stitutional symptoms such as weight loss, night sweats, prolonged morning stiffness (more than one hour), and fever, and fatigue are also more common with systemic symmetric pain even at rest is suggestive of inflamma- illnesses. tory conditions.3-6 On the other hand, weight bearing Patient history, including social history, can provide and movement worsens the pain of noninflammatory further insight into the patient’s physiologic state. This arthritis conditions, such as osteoarthritis. Noninflam- includes identifying comorbid conditions that might matory arthritis typically causes less than one hour of increase the pain burden, such as diabetes mellitus with morning stiffness. Weight-bearing joints in the lower complications of neuropathy; depression; polypharmacy extremities are likewise more commonly involved in an and use of medications that can cause arthritis, such as asymmetric pattern. A symmetric presentation suggests in drug-induced lupus arthritis; exposure to ticks that an underlying inflammatory arthritis condition.2 can cause Lyme disease in an endemic area; or exposure Signs of systemic inflammation include rashes (e.g., to hepatitis C, parvovirus, or human immunodeficiency psoriasis, photosensitivity), oral and genital ulcerations, virus, which can lead to viral arthritis.3 The history Raynaud phenomenon, serositis with pleurisy and peri- should also include surgical procedures, fractures, and carditis, sicca symptoms of dry eyes and dry mouth, trauma. The patient’s exercise capabilities or ability to eye inflammation, bowel inflammation, neurologic perform activities of daily living should be assessed. symptoms, and ischemic symptoms (including stroke). These signs are integral in correctly diagnosing systemic EMERGENT CONDITIONS inflammatory . In general, emergent conditions involving the joints present acutely and should be recognized promptly. OTHER CAUSES OF JOINT PAIN typically involves a large joint such as Neurologic causes of pain may be determined by char- the knee,3 but can affect several joints and is accompa- acterization; apart from numbness and burning pain, the nied by malaise, weight loss, fever, and swollen and/or pain is unlikely to worsen with joint movement and is warm joints.3 Other conditions include neuropathies, likely to worsen at night. Combinations of causes might radiculopathies, or myelopathies, which cause numb- make characterization of pain difficult. For example, ness or a burning pain, (e.g., cauda equina syndrome);

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compartment syndrome, with joint pain exceeding what polyarthritis who tests negative for the antibodies. would be expected based on physical examination find- Conversely, many rheumatic conditions can be associ- ings; and sepsis or infection. ated with antinuclear antibodies; therefore, a positive test result does not always correlate with SLE, especially Physical Examination in a patient who lacks other specific clinical criteria.2,3 The presence of the cardinal signs of inflammation on The higher the titer of antinuclear antibodies, the greater physical examination, such as erythema, warmth, swell- the chance of autoimmune disease. A diagnosis of SLE ing, and tenderness, confirms inflammatory arthritis.3,4 becomes more likely when a high ANA titer is accom- Noninflammatory arthritis may also present with swell- panied by more specific autoantibodies for lupus, such ing and tenderness, but does not cause erythema or as anti–double-stranded DNA and anti-Smith antibod- warmth. Periarthritis in the contiguous structures, such ies. Sjögren syndrome may be present with any autoim- as the tendons, ligaments, and bursa, should also be dif- mune illness, or it may be the primary diagnosis with ferentiated using physical examination findings. Nonar- dry eyes, dry mouth, and titers positive for anti–Sjögren ticular conditions, such as muscular injuries, tendinitis, syndrome A and B antibodies.3 or bursitis, present with a normal passive range of motion and reduced active range of motion, with the latter usu- ERYTHROCYTE SEDIMENTATION RATE AND C-REACTIVE PROTEIN ally caused by pain. On the other hand, joint abnormali- ties, synovitis, and soft tissue (e.g., frozen Noninflammatory and inflammatory conditions can be shoulder) present with reduced passive and active range differentiated using C-reactive protein and erythrocyte of motion. Increased pain with active or resisted range sedimentation rate (ESR) tests, which are nonspecific for of motion also suggests processes that involve the mus- inflammation.7 Rheumatic, malignant, and infectious cles, tendons, and bursa. During evaluation of range of conditions, and allergic reactions might cause these lev- motion, crepitation without warmth or erythema sug- els to be elevated; therefore, these tests are not diagnos- gests a degenerative process, such as osteoarthritis. tic.7 Because abnormal red cells might affect the ESR, it Systemic autoimmune diseases are associated with is less reliable in the acute phase than the C-reactive pro- organ system involvement in addition to arthritis. For tein test.8,9 Other noninflammatory conditions, includ- instance, fine inspiratory rales suggest interstitial lung ing dysproteinemia, hyperlipoproteinemia, diabetes, disease, a complication of RA; pleuropericardial friction and kidney problems, can lead to an elevated ESR and rubs occur with lupus; and parotid gland enlargement should be considered.7 The ESR level varies between men accompanies Sjögren syndrome.3 Mucocutaneous dis- and women, and increases with age. The normal upper orders, sarcoidosis, cancer, pseudogout, gout, podagra, limit for ESR is calculated as age plus 10 divided by two systemic (SLE), vasculitis, Still dis- for women, and age divided by two for men. ease, post–enteric infection , and infec- A normal ESR also does not preclude rheumatic dis- tious arthritis may all present with fever.3 ease. In one series, 3% of patients with RA had normal Once the history and physical examination are com- ESR findings.10 However, when clinical presentation and plete, the clinician can usually establish whether the pain physical examination findings point to a specific diagno- is truly articular and whether the condition is inflam- sis, an ESR result that is compatible with that diagnosis matory or noninflammatory. Further management may help support an inflammatory diagnosis. For exam- should be directed toward refining the specific arthritis ple, a markedly increased ESR in an older individual with diagnosis, instituting therapy, and possibly facilitating shoulder and hip pain might lead to a diagnosis of poly- subspecialty consultations (i.e., orthopedic surgery, reha- myalgia rheumatica; however, the diagnosis should not bilitation, neurology, or ). Rheumatology be discounted entirely if the ESR is within normal limits. consultation may be appropriate even for nonclassifiable conditions because seronegative inflammatory arthritis RHEUMATOID FACTOR AND ANTI–CITRULLINATED PEPTIDE ANTIBODIES is fairly common, and identifying these conditions in the primary care setting may be challenging. Anti–citrullinated peptide antibody levels are more spe- cific for RA and correlate with erosive disease. Rheuma- Laboratory Tests toid factor is a nonspecific immunoglobulin that is also ANTINUCLEAR ANTIBODY detected in chronic infections, such as hepatitis C, tuber- SLE without antinuclear antibodies comprises less than culosis, and infective endocarditis, and in autoimmune 2% of cases; therefore, SLE is unlikely in a patient with disorders such as paraproteinemias, vasculitis, or SLE

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Table 1. Clinical Patterns of Polyarticular Arthritis

Autoimmune connective tissue disease Spondyloarthritis Infectious arthritis Crystal arthritis

Inflammatory Rheumatoid Systemic lupus Vasculitis (including polymyalgia Ankylosing Psoriatic Reactive bowel disease Calcium pyrophosphate Characteristic arthritis erythematosus rheumatica, ) spondylitis arthritis arthritis arthritis Bacterial Viral Gout deposition disease Osteoarthritis

Symmetry Symmetric + + + + Asymmetric ++ ++ + + + + + +

Inflammatory + + + + + + + + + + +

Noninflammatory +

Number Pauciarticular + + + + + + + + Polyarticular + + + +

Joint involvement Spine-cervical/ + ++ + + + + + thoracic/lumbar Sacroiliac joint + ++ ++ + + +

Small joints Wrists + + + + + ++ + Carpometacarpals ++ Metacarpophalangeals ++ + + + Proximal ++ + + + + interphalangeals Distal interphalangeals ++ ++ Ankle + ++ ++ ++ + + + + + Metatarsophalangeals + ++ + + ++ +

Medium and large joints Shoulders + + + + + + ++ + Elbows + + + + + + + Hips/knees + + + + + + ++ ++ ++

Systemic features Fevers, uveitis, Malar rash, oral ulcers, Rash, gangrene, stroke, headache, Uveitis, Psoriasis, Uveitis, urethritis, Crohn disease, Fever Fever, rash Tophi, uric Preexisting osteoarthritis; nodules, pleurisy wrist drop, hemoptysis, pneumonitis uveitis enteritis ulcerative acid stones Wilson disease, pneumonitis gastrointestinal tract bleeding, colitis ochronosis, proteinuria, hematuria hemochromatosis

Laboratory tests Rheumatoid Antinuclear antibodies, Erythrocyte sedimentation rate Human Testing for Tissue biopsy Lyme disease Hepatitis B Serum uric Calcium pyrophosphate factor, double-stranded > 50, antineutrophil cytoplasmic leukocyte Chlamydia, testing, surface antigen, acid, uric crystals in joint fluid; anti-cyclic DNA, anti-Smith antibody, temporal artery or antigen B27 Gonorrhea, joint/blood hepatitis C virus acid crystals measurements of thyroid- citrullinated antibodies, urinalysis other tissue biopsy, urinalysis Salmonella, culture antibody, human in joint fluid stimulating hormone, peptide with proteinuria and with proteinuria and hematuria and Shigella immunodeficiency parathyroid hormone, hematuria, serum titers virus, human iron, magnesium, or C3/C4 parvovirus B19 phosphorus

Radiographic findings Erosions No erosions Pulmonary infiltrates/nodules, Sacroiliitis Erosions, Effusions Erosions, , angiography: dilatation and sacroiliitis overhanging joint space stenosis edges narrowing

NOTE: Classical patterns of joint involvement, systemic features, and laboratory and radiographic findings can differentiate among main groups of polyarthritis and serve as a useful tool for clinicians. + = possibly present; ++ = usually present; blank = none. Information from references 2 through 6. Polyarticular Arthritis

Table 1. Clinical Patterns of Polyarticular Arthritis

Autoimmune connective tissue disease Spondyloarthritis Infectious arthritis Crystal arthritis

Inflammatory Rheumatoid Systemic lupus Vasculitis (including polymyalgia Ankylosing Psoriatic Reactive bowel disease Calcium pyrophosphate Characteristic arthritis erythematosus rheumatica, polyarteritis nodosa) spondylitis arthritis arthritis arthritis Bacterial Viral Gout deposition disease Osteoarthritis

Symmetry Symmetric + + + + Asymmetric ++ ++ + + + + + +

Inflammatory + + + + + + + + + + +

Noninflammatory +

Number Pauciarticular + + + + + + + + Polyarticular + + + +

Joint involvement Spine-cervical/ + ++ + + + + + thoracic/lumbar Sacroiliac joint + ++ ++ + + +

Small joints Wrists + + + + + ++ + Carpometacarpals ++ Metacarpophalangeals ++ + + + Proximal ++ + + + + interphalangeals Distal interphalangeals ++ ++ Ankle + ++ ++ ++ + + + + + Metatarsophalangeals + ++ + + ++ +

Medium and large joints Shoulders + + + + + + ++ + Elbows + + + + + + + Hips/knees + + + + + + ++ ++ ++

Systemic features Fevers, uveitis, Malar rash, oral ulcers, Rash, gangrene, stroke, headache, Uveitis, Psoriasis, Uveitis, urethritis, Crohn disease, Fever Fever, rash Tophi, uric Preexisting osteoarthritis; nodules, pleurisy wrist drop, hemoptysis, pneumonitis uveitis enteritis ulcerative acid stones Wilson disease, pneumonitis gastrointestinal tract bleeding, colitis ochronosis, proteinuria, hematuria hemochromatosis

Laboratory tests Rheumatoid Antinuclear antibodies, Erythrocyte sedimentation rate Human Testing for Tissue biopsy Lyme disease Hepatitis B Serum uric Calcium pyrophosphate factor, double-stranded > 50, antineutrophil cytoplasmic leukocyte Chlamydia, testing, surface antigen, acid, uric crystals in joint fluid; anti-cyclic DNA, anti-Smith antibody, temporal artery or antigen B27 Gonorrhea, joint/blood hepatitis C virus acid crystals measurements of thyroid- citrullinated antibodies, urinalysis other tissue biopsy, urinalysis Salmonella, culture antibody, human in joint fluid stimulating hormone, peptide with proteinuria and with proteinuria and hematuria and Shigella immunodeficiency parathyroid hormone, hematuria, serum titers virus, human iron, magnesium, or C3/C4 parvovirus B19 phosphorus

Radiographic findings Erosions No erosions Pulmonary infiltrates/nodules, Sacroiliitis Erosions, Effusions Erosions, Chondrocalcinosis Osteophytes, angiography: dilatation and sacroiliitis overhanging joint space stenosis edges narrowing

NOTE: Classical patterns of joint involvement, systemic features, and laboratory and radiographic findings can differentiate among main groups of polyarthritis and serve as a useful tool for clinicians. + = possibly present; ++ = usually present; blank = none. Information from references 2 through 6. Polyarticular Arthritis

and should prompt consideration for these entities in the absence of a typical RA joint BEST PRACTICES IN RHEUMATOLOGY: pattern.11,12 The diagnostic value of rheuma- RECOMMENDATIONS FROM THE CHOOSING WISELY CAMPAIGN toid factor testing may be limited by its spec- Sponsoring ificity; however, it should be used when signs Recommendation organization and symptoms of inflammatory arthritis are Do not test antinuclear antibody subserologies American College present. In the clinical setting of symmetric without a positive antinuclear antibody test result of Rheumatology polyarthritis, a high rheumatoid factor titer and clinical suspicion of immune-mediated disease. is associated with poor outcomes and high Do not test for Lyme disease as a cause of American College predictive value for diagnosing RA.13 musculoskeletal symptoms without an exposure of Rheumatology history and appropriate examination findings. SERUM URIC ACID Source: For more information on the Choosing Wisely Campaign, see http:// A high serum uric acid level is commonly www.choosingwisely.org. For supporting citations and to search Choosing seen in the general population and is not Wisely recommendations relevant to primary care, see http://www.aafp.org/afp/ recommendations/search.htm. diagnostic of gout.14 Gout is diagnosed by aspiration of joint fluid and demonstration of intracellular monosodium urate crystals on polarized tests are expensive, are unnecessary unless clinically microscopy. In most patients with gout, serum uric acid indicated, and can result in high false-positive rates.18 levels are elevated in the intercurrent period.15 During a gout attack, the serum uric acid level may be normal Imaging or even low, and is best measured during the intercur- Polyarticular require imaging if the cli- rent period and every three to six months to monitor nician is looking for concurrent fracture, erosions, response to uric acid–lowering therapy with a goal of osteoarthritis, or osteomyelitis. The best approach is to keeping levels below 6 mg per dL (357 µmol per L).14,15 evaluate the joints that are commonly affected by spe- cific conditions. For example, radiographs of the feet, SYNOVIAL FLUID TESTS hands/wrists, and cervical spine will provide changes Crystal-induced synovitis and bacterial infections should most useful for the diagnosis of RA by demonstrating be confirmed by joint aspiration and synovial fluid tests erosions in the metatarsophalangeal, wrist, and meta- for Gram stain and culture, cell count, and crystals. carpal joints, or C1-C2 articulations suggestive of atlan- Febrile patients with a joint effusion should be treated for toaxial instability.19 septic arthritis until it can be ruled out.3,16 Superimposed In new-onset bursitis, tendinitis, gout, SLE, or RA, septic arthritis should be ruled out in patients with known radiography may not be helpful because of limited diag- arthritis who present with fever. Synovial fluid is consid- nostic specificity. In seronegative , ered noninflammatory if the white blood cell count is less such as , sacroiliac joint radio- than 2,000 per mm3 (2.0 × 109 per L), typically with less graphs can show early abnormalities best confirmed by than 75% polymorphonuclear leukocytes. Infection is magnetic resonance imaging.19,20 confirmed and best treated with a positive Gram stain Small erosions are more visible on ultrasonography or with confirmed growth of bacteria or other pathogen on magnetic resonance imaging.19 Erosions associated with culture. Gout is confirmed by findings of intracellular RA do not have the overhanging edge caused by repair negatively birefringent crystals on polarized microscopy, changes that may be seen on imaging in chronic gout.3 whereas pseudogout or calcium deposition disease is con- When calcified, tophaceous deposits are easily visible on firmed with positively birefringent crystals.17 radiographs. If not, an arc of crystals on the cartilagi- nous surface may be seen more easily on ultrasonogra- TESTS FOR INFECTION phy.21 Paget disease, infection, malignancy, and disease Testing for the presence of Borrelia burgdorferi, involving the sacroiliac and hip joints are sometimes hepatitis B, hepatitis C, or parvovirus antibodies can diagnosed more easily through imaging with specific lead to the diagnosis and specific treatment. It must be procedures or radionuclide scans.2 noted that parvovirus immunoglobulin M (IgM) must be present to indicate acute infection; IgG indicates past Biopsy exposure. However, these tests should be ordered only Tissue biopsies are essential for diagnosing giant cell when there is clinical suspicion and not routinely. These arteritis (temporal artery biopsy), cutaneous lupus or

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skin vasculitis (skin biopsy), glomerulonephritis (kid- 6. West S. Musculoskeletal signs and symptoms B. Polyarticular joint dis- ease. In: Klippel JH, et al., eds. Primer on the Rheumatic Diseases. 13th ney biopsy), and pulmonary vasculitis (lung biopsy). A ed. New York, NY: Springer; 2008:47-57. synovial biopsy may help in elusive cases, such as granu- 7. Sox HC Jr, Liang MH. The erythrocyte sedimentation rate. Guidelines for lomatous diseases (e.g., sarcoidosis, fungal infection, rational use. Ann Intern Med. 1986;104(4):515-523. ), hemochromatosis, Whipple disease, and 8. Kushner I. C- reac tive protein in rheumatology. Arthritis Rheum. 1991; 2 34(8):1065-1068. rheumatoid nodules. 9. Miller A, Green M, Robinson D. Simple rule for calculating normal eryth- Data Sources: A PubMed search was completed in Clinical Queries. rocyte sedimentation rate. Br Med J (Clin Res Ed). 1983;286(6361):266. using the key terms polyarticular, arthritis, polyarthritis, joint pain, and 10. Pinals RS. with a normal erythrocyte sedimenta- joint inflammation. The search included meta-analyses, randomized tion rate. J Rheumatol. 1978;5(3):272-274. controlled trials, clinical trials, and reviews. Also searched were the 11. Nishimura K, Sugiyama D, Kogata Y, et al. Meta-analysis: diagnostic Cochrane database, Essential Evidence Plus, UpToDate, and DynaMed. accuracy of anti-cyclic citrullinated peptide antibody and rheumatoid Search dates: December 2013 through March 2014. factor for rheumatoid arthritis. Ann Intern Med. 2007;146(11):797-808. 12. Whiting PF, Smidt N, Sterne JA, et al. Systematic review: accuracy of anti-citrullinated peptide antibodies for diagnosing rheumatoid arthri- The Authors tis. Ann Intern Med. 2010;152(7):456-464, W155-66. 13. Shmerling RH, Delbanco TL. How useful is the rheumatoid factor? Arch GEORGE G.A. PUJALTE, MD, is a sports medicine physician in the Pri- Intern Med. 1992;152(12):2417-2420. mary Care and Orthopedics Divisions of the Mayo Clinic Health System 14. Hadler NM, Franck WA, Bress NM, Robinson DR. Acute polyarticular in Waycross, Ga. He is also part of the sports medicine team at the Mayo gout. Am J Med. 1974;56(5):715-719. Clinic and is an assistant professor of family medicine at the Mayo Medical 15. Schlesinger N, Norquist JM, Watson DJ. Serum urate during acute School in Jacksonville, Fla. gout [published correction appears in J Rheumatol. 2009;36(8):1851]. SHIRLEY A. ALBANO-ALUQUIN, MD, is an assistant professor of medicine J Rheumatol. 2009;36(6):1287-1289. at Pennsylvania State University College of Medicine in Hershey, and a 16. Shmerling RH, Delbanco TL, Tosteson AN, Trentham DE. Synovial fluid rheumatologist at Pennsylvania State Hershey Medical Center. tests. What should be ordered? JAMA. 1990;264(8):1009-1014. 17. Klippel JH, et al., eds. Primer on the Rheumatic Diseases. 13th ed. New Address correspondence to George G.A. Pujalte, MD, 1921 Alice York, NY: Springer; 2008:241, 249-57. St., Mayo Clinic Health System, Waycross, GA 31501 (e-mail: pujalte. 18. Juby A, Johnston C, Davis P. Specificity, sensitivity and diagnostic pre- [email protected]). Reprints are not available from the authors. dictive value of selected laboratory generated autoantibody profiles in patients with connective tissue diseases. J Rheumatol. 1991;18(3): 354-358. REFERENCES 19. Baillet A, Gaujoux-Viala C, Mouterde G, et al. Comparison of the effi- cacy of sonography, magnetic resonance imaging and conventional 1. Pinals RS. Polyarthritis and fever. N Engl J Med. 1994;330 (11):769-774. radiography for the detection of bone erosions in rheumatoid arthritis 2. Shmerling RH. Evaluation of the adult with polyarticular pain. UpTo- patients. Rheumatology (Oxford). 2011;50 ( 6):1137-1147. Date. http://www.uptodate.com/contents/evaluation-of-the-adult-with- 20. Mandl P, Navarro-Compán V, Terslev L, et al. EULAR recommenda- polyarticular-pain (subscription required). Accessed February 25, 2014. tions for the use of imaging in the diagnosis and management of 3. American College of Rheumatology Ad Hoc Committee on Clinical spondyloarthritis in clinical practice [published ahead of print April 2, Guidelines. Guidelines for the initial evaluation of the adult patient with 2015]. Ann Rheum Dis. http://ard.bmj.com/content/early/2015/04/02/ acute musculoskeletal symptoms. Arthritis Rheum. 1996;39(1):1-8. annrheumdis-2014-206971.long. Accessed April 24, 2015. 4. El-Gabalawy HS, Duray P, Goldbach-Mansky R. Evaluating patients with 21. Howard RG, Pillinger MH, Gyftopoulos S, et al. Reproducibility of mus- arthritis of recent onset. JAMA. 2000;284(18):2368-2373. culoskeletal ultrasound for determining monosodium urate deposition. 5. Mies Richie A, Francis ML. Diagnostic approach to polyarticular Arthritis Care Res (Hoboken). 2011;63 (10 ):1456-1462. joint pain [published corrections appear in Am Fam Physician. 2006; 73(7):1153, and Am Fam Physician. 2006;73(5):776]. Am Fam Physician. 2003;68(6):1151-1160.

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