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66 How to Differentiate Chronic Widespread Pain in Order to Reduce Misdiagnosis…
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must be explored to ensure that the medication’s adverse effect is not the cause of the pain complaint. Medications that should be considered include lipid-lowering agents in statins, aromatase inhibitors, bisphosphonates, and paradoxically even opioids. Therefore a history of current medication use is obligatory. Physical exam­ination: A physical examination is required specically to examine for evidence of structural joint abnormality, muscle weakness, neurological abnormality, or evi­dence of endocrine disease. The physical examination should be within normal limits for the patient’s age. Clues that may point to a diagnosis of FM are soft tissue and generalized body tenderness. Although the tender point examination was used in the past to establish a diagnosis of FM, this nding is no longer incorporated into the physical examination because of poor validity and poor reproducibility. Some patients may demonstrate dysesthesia on light touch, myofascial induration, or joint hypermobility. Additional testing: No conrmatory blood tests, imaging, or histological analysis is available for FM.A limited number of laboratory tests will allow for screening for medical conditions that can mimic FM symptoms. The 2016 criteria require a widespread pain index (WPI) of between four (2011 required three) and six pain sites and symptom severity (SS) score of ≥9. In addition, gen­eralized pain, as dened by pain occurring in at least four of ve body regions except for the face and the abdomen, should be present [19]. The Fibromyalgia Survey Questionnaire (also called polysymptomatic distress scale, PSD) capturing the 2011 (21) and 2016 (21) diagnostic criteria of FM can be completed by the patient to further complement the clinical assessment and can be used to give some indication of the severity of the condition. In most cases, a denite diagnosis can be effectively established based on the history, a physical examination that demon­strates general tenderness, the absence of some other pathology that could explain pain and fatigue, and normal basic laboratory tests. The standards of good medical practice state that the physician must always consider a differential diagnosis for any patient presenting with a diffuse pain complaint. This has been covered in the section on misdiagnosis of FM. FM may coexist with other pain syndromes. Patients diagnosed with FM may also experience other painful conditions that are mostly distinct from FM and are generally classied as overlapping pain condi­tions. Notably, the 2011 [20] and 2016 [20] criteria include headache and abdomi- nal pain in the somatic symptom score, increasing the probability that patients with migraine or tension headaches or irritable bowel syndrome will meet FM criteria. Even when the ACR 1990 classication criteria [21] are used for diagnosis, many patients with FM meet the criteria of some other function. Recent studies have demonstrated that treatment of visceral pain comorbidities (endometriosis, IBS, primary dysmenorrhea) reduced FM pain [14–16]. Therefore, FM patients should be screened for other pain syndromes, and a questionnaire that captures somatic symptom burden, such as the Patient Health Questionnaire (PHQ) [15, 18–20]. The coexistence of FM with some other medical condition that could act as a pain gen­erator may inuence the outcome of the other condition in particular and the global health outcome in general. There are two considerations when FM coexists with some other condition: rstly, the underlying condition should be treated according to best practice, e.g., for osteoarthritis or mechanical back pain; secondly, there
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must be an appreciation that concomitant FM may affect the outcome of the under­lying condition. This has been shown for a surgical outcome that is less favorable for patients with osteoarthritis of the knee and comorbid FM [20]. FM may coexist with mental health disorders. Depression is another FM symptom identied in the somatic symptom scale of the Fibromyalgia Symptom Questionnaire. Depending on the clinical setting, up to 80% of FM patients meet the criteria of depressive and anxiety disorder. FM’s severity (number and intensity of symptoms and degree of disability) is substantially determined by comorbid mental disorders [5]. A screen­ing of FM patients for psychological distress either by questions such as “Over the last 2 weeks, how often have you been feeling down, depressed, or hopeless” and “Feeling nervous, anxious or on edge” or questionnaires (e.g., PHQ 4) [21] is rec­ommended by some FM guidelines. Severe comorbid mental disorders require the inclusion of a mental health specialist in the management of FM [19]. The severity of FM as a chronic disorder for patients with the full expression of FM are at the end of a continuum of multiple pain sites and other somatic and psychological symptoms [20]. As for other diseases dened by continuous variables, such as hypertension, diabetes, or depression, there is currently no absolute point dening where FM begins. Cutoff points for diagnosing continuum disorders are dened by expert consensus and based on clinical studies. The higher the cutoff point for a diagnosis, the lower the prevalence. The 2016 diagnostic criteria for FM [21] increased the requirements needed to meet the widespread pain criterion compared to the 2011 diagnostic criteria [21]. Thus, potential FM cases in the general German population decreased from 2.1% [21] to 1.9% (Wolfe 2018, submitted). In addi­tion, longitudinal studies of patients with CWP and/or bromyalgia have demon­strated that some patients report uctuation in symptoms over time and thus oscillate around the cutoff points, at times being FM positive or FM negative [19–
21]. FM’s waxing and waning nature might explain some discrepancies between
the prevalence of criteria identied FM and clinical FM.There is no internationally accepted grading of the severity of FM, but clinical wisdom requires the treating physician to assess severity to direct treatment options [4]. Most gradings suggest a distinction between mild, moderate, and severe forms of FM based on the inten­sity of symptoms and the degree of limitation in daily functioning. It, therefore, follows that a stepwise management approach can be based on the severity of FM. Mild forms require primarily education and advice (regular physical and social activities) with perhaps the occasional use of drug therapy for episodes of exacerbation and can be managed in primary care. More severe forms require mul­ticomponent (exercise, psychological therapies, drugs) and multidisciplinary thera­pies [12, 18]. Therefore, for the follow-up of patients diagnosed with FM, a “continuum” assessment, e.g., by questions about general well-being (e.g., on a 0–10 scale or a Likert scale of “the same,” “better,” or “worse”) or by symptom questionnaires such as the PSD [20] or the PHQ 15 [21], might be more appropriate [19] than the determination of whether a patient meets FMS criteria or not at a particular time point [21].
66 How to Differentiate Chronic Widespread Pain in Order to Reduce Misdiagnosis…
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Plan ofAction, Pitfalls toAvoid, andPearls ofKnowledge toConsider
1. Know all the clinical manifestations of FM.
2. Incorporate a multisystemic approach when diagnosing FM.
3. Create a plan of action when doing an examination of a new patient.
4. Avoid coming into the examination with an idea of diagnosis.
5. Review current up-to-date criteria for diagnosing FM.
6. Have the patient ll appropriate questionnaires when there is CWP.
7. Consider mental distress as a possible indicator of FM not just CWP.

Conclusion

Fibromyalgia syndrome (FM) is an enigma. Even with the gradual acceptance of the validity of FM, it has continued to be misdiagnosed by clinicians. Evidence-based interdisciplinary guidelines have presented a comprehensive clinical assessment to avoid misdiagnosis. A patient with chronic pain should be screened for CWP.Those with CWP should be examined for presence of additional major symptoms of FM: unrefreshed sleep and fatigue. A complete medical history and complete physical examination are mandatory in the evaluation of a patient with CWP in order to con­clude the diagnosis of FM.Mild and limited simple laboratory testing is recom­mended to screen for possible other diseases. When taking into consideration of the differential diagnosis of FM, special attention should be paid to the presence of other chronic pain that is overlapping conditions and of mental disorders. FM on its own as a diagnosis is rare, as almost all patients with FM meet criteria for other overlapping pain conditions or mental disorders. The intensity of FM should be assessed in order to direct treatment approaches and help inform the likely outcome for an individual patient.

References

1. Häuser W, Fitzcharles MA. Facts and myths pertaining to bromyalgia. Dialogues Clin Neurosci. 2018;20:53–62.
2. Talotta R, Bazzichi L, DI Franco M etal. One year in review 2017: bromyalgia. Clin Exp Rh.
3. Wolfe F.Fibromyalgia wars. J Rheumatol. 2009;36:671–8.
4. Wolfe F.Criteria for bromyalgia? What is bromyalgia? Limitations to current concepts of bromyalgia and bromyalgia criteria. Clin Exp Rheumatol. 2017;35(Suppl 105):S3–5.
5. Agarwal A, Oparin Y, Glick L, et al. Attitudes toward and management of bromyalgia: a National Survey of Canadian rheumatologists and critical appraisal of guidelines. J Clin Rheumatol. 2018;24:243–9.
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6. Häuser W, Ablin J, Fitzcharles MA, etal. Fibromyalgia. Nat Rev Dis Primers. 2015;1:15022.
7. Shir Y, Fitzcharles MA. Should rheumatologists retain ownership of bromyalgia? J Rheumatol. 2009;36:667–70.
8. Perrot S, Choy E, Petersel D, Ginovker A, Kramer E.Survey of physician experiences and perceptions about the diagnosis and treatment of bromyalgia. BMC Health Serv Res. 2012;12:356.
9. Briones-Vozmediano E, Vives-Cases C, Ronda-Pérez E, Gil-González D.Patients’ and profes­sionals’ views on managing bromyalgia. Pain Res Manag. 2013;18:10–24
10. Choy E, Perrot S, Leon T, etal. A patient survey of the impact of bromyalgia and the journey to diagnosis. BMC Health Serv Res. 2010;10:102.
11. Häuser W, Zimmer C, Felde E, Köllner V.What are the key symptoms of bromyalgia? Results of a survey of the German Fibromyalgia Association. Schmerz. 2008;22:176–83.
12. Petzke F, Brückle W, Eidmann U, et al. General treatment principles, coordination of care and patient education in bromyalgia syndrome: Updated guidelines 2017 and overview of systematic review articles. Schmerz. 2017;31:246–54.
13. Fitzcharles MA, Esdaile JM. The overdiagnosis of bromyalgia syndrome. Am J Med. 1997;103:44–50.
14. Fitzcharles MA.BOULOS P: inaccuracy in the diagnosis of bromyalgia syndrome: analysis of referrals. Rheumatology (Oxford). 2003;42:263–7.
15. di Franco M, Iannuccelli C, Bazzichi L et al. Misdiagnosis in bromyalgia: a multicentre study. Clin Ex.
16. Walitt B, Katz RS, Bergman MJ, Wolfe F.Three-quarters of persons in the US population reporting a clinical diagnosis of bromyalgia do not satisfy bromyalgia criteria: the 2012 National Health Interview Survey. PLoS One. 2016;11:e0157235.
17. Album D, Johannessen LEF, Rasmussen EB.Stability and change in disease prestige: a compar­ative analysis of three surveys spanning a quarter of a century. Soc Sci Med. 2017;180:45–51.
18. Fitzcharles MA, Ste-Marie PA, Goldenberg DL, etal. Canadian Pain Society and Canadian rheumatology association recommendations for rational care of persons with bromyalgia: a summary report. J Rheumatol. 2013;40:1388–93.
19. MacFarlane GJ, Kronisch C, Atzeni F, et al. EULAR recommendations for management of bromyalgia. Ann Rheum Dis. 2017;76:e54.
20. Nakamura I, Nishioka K, Usui C, etal. An epidemiologic internet survey of bromyalgia and chronic pain in Japan. Arthritis Care Res (Hoboken). 2014;66:1093–101.
21. Marschall U, Arnold B, Häuser W.Treatment and healthcare costs of bromyalgia syndrome in Germany: analysis of the data of the Barmer health insurance (BEK) from 2008-2009. Schmerz. 2011;25(402–4):406–10.
K. Geslaghi and B. Krout
Chapter 67
Rheumatoid Arthritis Misdiagnosed asGout
KoshaGeslaghi andBrandonKrout
Learning Objectives
By the end of this presentation, the clinician should be able to:
1. Correctly differentiate between gout and rheumatoid arthritis.
2. Discuss how to correctly identify radiographic images of gout in patients.
3. Explain the symptomatology of gout and rheumatoid arthritis.
4. Summarize the effects of diuretics in patients who may be presenting with the same clinical manifestations of gout.

Introduction

Rheumatoid arthritis (RA) is a chronic inammatory disease with an etiology that is not well understood. RA is characterized by symmetric polyarthritis, the most com­mon form being chronic and inammatory [1, 2, 4, 6–8]. Since active RA often ends in articular cartilage and bone destruction and functional disability, it is crucial to diagnose and treat this disease early before damage ensues [1, 2, 4, 9]. As RA is a systemic disease, if left untreated, it may also lead to a variety of articular symptoms and subcutaneous nodules, including fatigue, lung involvement, peripheral neuropa­thy, pericarditis, vasculitis, and hematologic abnormalities [1, 2, 4, 5].
A different, metabolic disease that is often a cause for misdiagnosis in RA patients is gout. The most prevalent demographic for patients with gout and RA overlap which can lead to misdiagnosis, i.e., a middle-aged to elderly males or
K. Geslaghi (*) · B. Krout St. Martinus University Faculty of Medicine, Willemstad, Curacao e-mail: kosha.geslaghi@martinus.edu; brandon.krout@martinus.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 H. Tohid et al. (eds.), The Misdiagnosis Casebook in Clinical Medicine,
https://doi.org/10.1007/978-3-031-28296-6_67
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postmenopausal females. Gout is a metabolic disease with a main demographic of middle- aged to elderly men and postmenopausal women. Gout results from an increase of urate with hyperuricemia [1, 2, 4]. It is identied by episodic acute arthritis or chronic arthritis caused by deposition of monosodium urate crystals in joints and connective tissue tophi [2, 4]. There is the risk for deposition of monoso­dium urate crystals in kidney interstitium or uric acid nephrolithiasis [1, 2, 4].
In recent years, the atypical presentation of gout in the elderly has started to be acknowledged in greater frequency [1, 2]. Gout observed in older patients is often a subacute, symmetric polyarthritis missing in classic podagra [1–4]. Early develop­ment of tophi in a patient with symmetric gouty arthritis can lead to the misdiagnosis of rheumatoid arthritis with rheumatoid nodules; this results in inappropriate manage­ment of a condition that is generally treated with very positive results [1, 2]. The crystals found in gout are that of a buildup of uric acid which crystallizes in the syno­vial uid; however, RA being an autoimmune disorder, there is a buildup of granu­lated tissue in the synovial spaces. The following case will demonstrate these points as well as the challenging clinical problems frequently encapsulating the effective diagnosis and treatment of gout in the most common demographic: that of the elderly.

Clinical Case Presentation

A 74-year-old elderly woman arrived into the emergency room after 10days of weakness, diarrhea, and anorexia. She described 4years of arthritis, occurring rst in her ankles and later progressing to knees and hands, with the development of deformities and soft tissue nodules [1, 2]. There were no signs of morning stiffness and acute attacks of arthritis. The patient’s past medical history was signicant for hypertension, two myocardial infarctions, and renal insufciency [10–13]. A diag­nosis of rheumatoid arthritis had been made [1, 2]. Treatment with nonsteroidal anti-inammatory agents (NSAIDS) was initiated. Two weeks prior to admission, she noted increasing pain in all joints, swelling of hands and knees, and resultant inability to ambulate [1, 2]. Her medications included prazosin, diltiazem, furose­mide, indomethacin, and acetaminophen with codeine. System review revealed no cough, chest pain, or fever. She did note recent weight gain.
On examination the patient was fully oriented, with BP 200/100mm Hg, pulse 104, respirations 28, and temperature 102F.Soft tissue nodules were present on the ngers and were prominent around the proximal and distal interphalangeal joints. Cardiopulmonary exam showed a diffuse ventricular impulse and lowered breath sounds with left basilar egophony [1, 2]. No evident nodules were present on the olecranon or pinnae. Joint exam revealed warm knees with a 3+ effusion on the right limiting exion and a 1+ effusion on the left with crepitance [1, 2]. Destruction of the metacarpophalangeal joint and proximal interphalangeal joints had caused a right hand exion contracture and an asymmetric left hand deformity with ulnar deviation (Fig. 67.1). Bilateral hallux valgus deformities of the rst metacarpophalangeal joints were present. Laboratory exam revealed Hgb 8.5g/dL, WBC 11,500/mm3,
67 Rheumatoid Arthritis Misdiagnosed asGout
Fig. 67.1 Hands of a 74-year-old woman in full extension, asymmetric deformities of proximal interphalangeal and metacarpophalangeal joints, ulnar deviation, and exion contractures on the right
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Fig. 67.2 Radiographs of patient’s left hand in Fig.67.1: preserved joint space in noninvolved joints and characteristic para-articular gout erosion with overhanging margin in the middle proxi­mal interphalangeal
BUN 58mg/dL, creatinine 3.0mg/dL, uric acid 9.4mg/dL, rheumatoid factor 1: l O by latex xation, normal cardiac isoenzymes, age-indeterminate infarction by ECG, cardiomegaly with cephalization of blood ow, and a predominant left lower lobe inltrate on chest X-ray [1, 2]. Echocardiogram revealed a hypokinetic left ventricle with ejection fraction of 13%. On knee radiographs, changes of the patellofemoral compartment and a right knee effusion were present, without overt chondrocalcino­sis or erosions. On left hand lm, a soft tissue deformity and eccentric cortical ero­sion with overhanging margins of the involved proximal interphalangeal joint were present (Fig.67.2) [1, 2]. Arthrocentesis of the right knee yielded copious opalescent uid with a thick slurry of visible white particles [1, 2]. Polarizing microscopy
502
revealed a mass of needle-shaped crystals with both negative and positive birefrin­gence. Intracellular crystals were present. When diluted 10× the synovial uid revealed concentrations of uric acid 13.1mg/dL, calcium 1.2 mg/dL, and glucose 10mg/dL, conrming the predominant presence of monosodium urate crystals. The patient was treated on admission for congestive failure, hypertension, azotemia, and suspected pneumonia using erythromycin, prazosin, diltiazem, and azotemia; oral colchicine was begun without loading.
The diagnosis of gout rests on the identication of negatively birefringent intra­cellular crystals from synovial uid or tophi [1, 2]. Supporting evidence, as in this case, may also include asymmetric joint involvement, soft tissue tophi, and periar­ticular osteolysis or classical marginal erosions outside the joint capsule.
K. Geslaghi and B. Krout

Differential Diagnosis

1. Septic Arthritis—A joint infection that causes severe pain, swelling, erythema,
warmth, and loss of function of the affected joint. Also frequently causes sys­temic signs such as fever. This condition is marked by its trademark fever prior to the onset of arthritis.
2. Osteoarthritis—A condition characterized by degeneration of the articular carti-
lage and the underlying bone as a result of chronic wear and tear. Usually occurs in the elderly but can be accelerated in patients with an underlying joint pathol­ogy and increased or abnormal biomechanical forces on the joint, including elevated body mass index. While this condition appears to be the same as RA, the risk factors of obesity differ from that of RA.
3. Psoriatic Arthritis—A seronegative inammatory arthritis found in patients with
psoriasis. In 60–80% of patients, psoriasis precedes the arthritis; in 15–20% of patients, arthritis appears before psoriasis. Other common symptoms include enthesitis particularly where the Achilles tendon attaches to the calcaneus, dac­tylitis, and nail changes.
4. Pseudogout—The acute form of calcium pyrophosphate crystal deposition dis-
ease. Manifests similarly to an acute gout are, with sporadic episodes of mono­articular synovitis affecting large joints. Unlike gout, it can last for months and may be associated with systemic symptoms.
What WasMisdiagnosed inThis Case andWhy?
Diuretic gout was misdiagnosed as RA.The reason for this misdiagnosis was the diagnosing physician did not consider the effects of diuretics in patients with hyper­tension; the side effects of the aforementioned diuretic lead to accumulation of uid in the proximal interphalangeal joints leading medical professionals to believe that it was RA caused by an autoimmune etiology.
67 Rheumatoid Arthritis Misdiagnosed asGout
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Discussion

RA is known as a chronic inammatory disease and its etiology is unknown. RA is characterized by polyarthritis and is the most prevalent form of inammatory arthri­tis. Gout, however, causes arthritis-like pain but it is not an inammatory disease. Gout occurs in response to the presence of monosodium urate (MSU) crystals in the joints.
The prole of the elderly gout patient has been classied as a thin 75-year-old woman with Heberden’s nodes who is a teetotaler and uses diuretics [12, 13]. Accompanying this new prole for gout is the clinical history of a polyarticular arthritis involving both the upper and lower extremities, with subacute or no acute attacks [10, 11]. Gout in the elderly is strongly associated with diuretic use; the association reaches levels of 85%, 95%, and 100% in reports on gout in elderly women. All women were on diuretics and presented after the fth decade with sub­acute attacks and often exuberant tophi, warranting the new label of diuretic-induced gout. A study emphasized renal insufciency in 90% of all elderly gout patients, underscoring decrease in urate excretion as the cause of their gout [12]. Polyarticular gout in the setting of mild renal insufciency and diuretic use may be the predomi­nant form of gout in women. Early tophi are a unique characteristic of diuretic gout, often occurring within the rst or second year of disease [1, 2, 13]. Urate deposition in the elderly shows a predilection for the sites of osteoarthritis in hand interphalan­geal (IP) joints known as Heberden’s and Bouchard’s nodes. Several authors have demonstrated by crystal analysis that attacks of previously classied “inammatory osteoarthritis,” with clinical inammation and erosive changes, are actually epi­sodes of gouty arthritis in osteoarthritic IP joints. Development of tophi at osteoar­thritic IP joints or in the soft tissue of the distal ngerpad may predate all attacks of gouty arthritis. It is therefore critical for the diagnosing physician to consider the side effects of medication on the patient population as the source for the current pathophysiology. This knowledge, combined with a focused physical exam, imag­ing, and synovial uid analysis, is needed for a comprehensive medical workup of the presenting patient.
Plan ofAction, thePoints Clinician Should Consider, Pitfalls toAvoid, andPearls ofKnowledge toConsider
1. Create a framework when meeting new or referred patients.
2. Know all possible side effects of medication of patients, especially long-term
medications.
3. Always refer to radiographic images before making diagnosis as well as clinical
manifestations.
4. Running tests to conrm diagnosis may be invasive, but it would save the
patient’s time and energy in early diagnosis.
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Conclusion

Rheumatoid arthritis is a very common diagnosis in the elderly patient population. As such, there are chances for error in assuming that a presenting patient who is elderly with symmetric polyarticular joint pain and nodules is suffering from rheu­matoid or systemic arthritis. There must be a consideration of medication side effects, especially diuretics, for the proper patient workup. Diuretics can potentially lead to an increase of monosodium urate crystals in the kidneys and joint spaces, with resulting tophi formation and pain. A complete workup should include a detailed history, including medication review, physical examination, imaging, and serum studies. By using the various modalities offered to modern physicians, the misdiagnosis of gout can be signicantly limited.

References

1. Acute polyarticular gout. Am J Med. 1974;56(5):A112. https://doi.
org/10.1016/0002- 9343(74)90655- x
2. Doherty M, Dieppe P. Crystal deposition disease in the elderly. Clin Rheum Dis. 1986;12(1):97–116. https://doi.org/10.1016/s0307- 742x(21)00622- 6.
3. Doherty M, Dieppe P, Watt I.Low incidence of calcium pyrophosphate dihydrate crystal depo­sition in rheumatoid arthritis, with modication of radiographic features in coexistent disease. Arthritis Rheum. 1984;27(9):1002–9. https://doi.org/10.1002/art.1780270906.
4. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J.Harrison’s principles of internal medicine, vol. 1, 2. 12th ed. McGraw-Hill Education / Medical; 2018.
5. Lally EV. The clinical spectrum of gouty arthritis in women. Arch Intern Med. 1986;146(11):2221–5. https://doi.org/10.1001/archinte.146.11.2221.
6. Lally EV, Zimmermann B Jr, G.H., & Kaplan, S. R. Urate-mediated inammation in nodal osteoarthritis: clinical and roentgenographic correlations. Arthritis Rheum. 1989;32(1):86–90.
https://doi.org/10.1002/anr.1780320115.
7. MacFarlane DG, Dieppe PD. Diuretic-induced gout in elderly women. Rheumatology. 1985;24(2):155–7. https://doi.org/10.1093/rheumatology/24.2.155.
8. Serum uric acid. Its association with other risk factors and with mortality in coronary heart disease. J Chronic Dis. 1976;29(9):557–69. https://doi.org/10.1016/0021- 9681(76)90003- 5.
9. Sewell KL, Petrucci R, Keiser HD.Misdiagnosis of rheumatoid arthritis in an elderly woman with gout. J Am Geriatr Soc. 1991;39(4):403–6. https://doi.org/10.1111/j.1532- 5415.1991.
tb02909.x.
10. ter Borg EJ, Rasker JJ.Gout in the elderly, a separate entity? Ann Rheum Dis. 1987;46(1):72–6.
https://doi.org/10.1136/ard.46.1.72.
11. Trentham DE. Chronic synovitis in gout simulating rheumatoid arthritis. JAMA. 1976;235(13):1358. https://doi.org/10.1001/jama.1976.03260390044030.
12. Virshup AM. Coexistent rheumatoid arthritis and gout. Arthritis Rheum. 1985;28(2):238.
https://doi.org/10.1002/art.1780280228.
13. Vukmir RB, Weiss L, Verdile VP. Polyarticular symmetric tophaceous joint inamma­tion as the initial presentation of gout. Am J Emerg Med. 1990;8(1):43–5. https://doi.
org/10.1016/0735- 6757(90)90294- a.