Differences in Acute Phase Reactants between Gout and Pseudogout

DOI: 10.4236/ijcm.2013.412A2003   PDF   HTML     7,242 Downloads   9,505 Views   Citations


Objectives: To define clinical differences in the acute phase response and serum acute phase reactants between gout, pseudogout and crystal-induced arthritis in the presence of non-articular infections (CAI). Patients and Methods: Eleven patients with definite gout, 12 patients with pseudogout and 5 patients with CIA were included in the study. Results: The erythrocyte sedimentation rate (ESR) was significantly different between gout (68.2 ± 49.9 mm/Hr) and CIA (113.8 ± 37.2 mm/Hr) but not between gout and pseudogout (83.9 ± 45.6 mm/Hr) or between pseudogout and CIA. The C-reactive protein (CRP) was significantly increased between gout (10.1 ± 7.9 mg/dL) and pseudogout (18.9 ± 9.8 mg/dL), gout and CIA (36.5 ± 12.4 mg/dL) as well as between pseudogout and CIA. The peripheral white cell count was significantly different between gout (9.27 ± 3.7 k/μL) and CIA (16.5 ± 6.8 k/μL), and between pseudogout (8.9 ± 3.2 k/μL) and CIA. Conclusions: Measurement of ESR and CRP are helpful in crystal-induced arthritis. The CRP has more discriminating utility than the ESR in distinguishing between gout, pseudogout and CIA. Peripheral wbc is most useful for differentiating crystal-induced arthritis from CIA.

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C. Tagoe and Y. Raza, "Differences in Acute Phase Reactants between Gout and Pseudogout," International Journal of Clinical Medicine, Vol. 4 No. 12B, 2013, pp. 13-19. doi: 10.4236/ijcm.2013.412A2003.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] C. M. Wise, “Crystal-Associated Arthritis in the Elderly,” Rheumatic Disease Clinics of North America, Vol. 33, No. 1, 2007, pp. 33-55.
[2] A. J. Elliot, K. W. Cross and D. M. Fleming, “Seasonality and Trends in the Incidence and Prevalence of Gout in England and Wales 1994-2007,” Annals of the Rheumatic Diseases, Vol. 68, No. 11, 2009, pp. 1728-1733.
[3] P. Richette, T. Bardin and M. Doherty, “An Update on the Epidemiology of Calcium Pyrophosphate Dihydrate Crystal Deposition Disease,” Rheumatology (Oxford), Vol. 48, No. 7, 2009, pp. 711-715.
[4] E. Roddy and M. Doherty, “Epidemiology of Gout,” Arthritis Research & Therapy, Vol. 12, 2010 p. 223.
[5] Y. Zhu, B. J. Pandya and H. K. Choi, “Prevalence of Gout and Hyperuricemia in the US General Population: The National Health and Nutrition Examination Survey 2007-2008,” Arthritis & Rheumatism, Vol. 63, No. 10, 2011, pp. 3136-3141. http://dx.doi.org/10.1002/art.30520
[6] L. Trieste, I. Palla, F. Fusco, et al., “The Economic Impact of Gout: A Systematic Literature Review,” Clinical and Experimental Rheumatology, Vol. 30, No. 4, 2012, pp. S145-S148.
[7] N. Busso and A. So, “Microcrystals as DAMPs and Their Role in Joint Inflammation,” Rheumatology (Oxford), Vol. 51, No. 7, 2012, pp. 1154-1160.
[8] S. L. Wallace, H. Robinson, A. T. Masi, J. L. Decker, D. J. McCarty and T. F. Yu, “Preliminary Criteria for the Classification of the Acute Arthritis of Primary Gout,” Arthritis & Rheumatism, Vol. 20, No. 3, 1977, pp. 895-900. http://dx.doi.org/10.1002/art.1780200320
[9] D. J. McCarty, “Calcium Pyrophosphate Dihydrate Crystal Deposition Disease: Nomenclature and Diagnostic Criteria,” Annals of Internal Medicine, Vol. 87, No. 2, 1977, pp. 241-242.
[10] W. Zhang, M. Doherty, T. Bardin, et al., “European League against Rheumatism Recommendations for Calcium Pyrophosphate Deposition. Part I: Terminology and Diagnosis,” Annals of the Rheumatic Diseases, Vol. 70, No. 4, 2011, pp. 563-570.
[11] M. E. Margaretten, J. Kohlwes, D. Moore and S. Bent, “Does This Adult Patient Have Septic Arthritis?” JAMA, Vol. 297, No. 13, 2007, pp. 1478-1488.
[12] T. Neogi, “Clinical Practice. Gout,” New England Journal of Medicine, Vol. 364, No. 5, 2011, pp. 443-452.
[13] F. Martinon, V. Petrilli, A. Mayor, A. Tardivel and J. Tschopp, “Gout-Associated Uric Acid Crystals Activate the NALP3 Inflammasome,” Nature, Vol. 440, No. 7081, 2006, pp. 237-241. http://dx.doi.org/10.1038/nature04516
[14] R. Liu-Bryan and F. Liote, “Monosodium Urate and Calcium Pyrophosphate Dihydrate (CPPD) Crystals, Inflammation, and Cellular Signaling,” Joint Bone Spine, Vol. 72, No. 3, 2005, pp. 295-302.
[15] P. A. Guerne, R. Terkeltaub, B. Zuraw and M. Lotz, “Inflammatory Microcrystals Stimulate Interleukin-6 Production and Secretion by Human Monocytes and Synoviocytes,” Arthritis & Rheumatism, Vol. 32, No. 11, 1989, pp. 1443-1452. http://dx.doi.org/10.1002/anr.1780321114
[16] R. Liu, M. O’Connell, K. Johnson, K. Pritzker, N. Mackman and R. Terkeltaub, “Extracellular Signal-Regulated Kinase 1/Extracellular Signal-Regulated Kinase 2 Mitogen-Activated Protein Kinase Signaling and Activation of Activator Protein 1 and Nuclear Factor KappaB Transcription Factors Play Central Roles in Interleukin-8 Expression Stimulated by Monosodium Urate Monohydrate and Calcium Pyrophosphate Crystals in Monocytic Cells,” Arthritis & Rheumatism, Vol. 43, No. 5, 2000, pp. 1145-1155.
[17] O. Gross, A. S. Yazdi, C. J. Thomas, et al., “Inflammasome Activators Induce Interleukin-1Alpha Secretion via Distinct Pathways with Differential Requirement for the Protease Function of Caspase-1,” Immunity, Vol. 36, No. 3, 2012, pp. 388-400.
[18] F. S. di Giovine, S. E. Malawista, E. Thornton and G. W. Duff, “Urate Crystals Stimulate Production of Tumor Necrosis Factor Alpha from Human Blood Monocytes and Synovial Cells. Cytokine mRNA and Protein Kinetics, and Cellular Distribution,” The Journal of Clinical Investigation, Vol. 87, No. 4, 1991, pp. 1375-1381.
[19] W. J. Martin, O. Shaw, X. Liu, S. Steiger and J. L. Harper, “Monosodium Urate Monohydrate Crystal-Recruited Noninflammatory Monocytes Differentiate into M1-Like Proinflammatory Macrophages in a Peritoneal Murine Model of Gout,” Arthritis & Rheumatism, Vol. 63, No. 5, 2011, pp. 1322-1332. http://dx.doi.org/10.1002/art.30249
[20] A. W. Taylor, N. O. Ku and R. F. Mortensen, “Regulation of Cytokine-Induced Human C-Reactive Protein Production by Transforming Growth Factor-Beta,” The Journal of Immunology, Vol. 145, No. 8, 1990, pp. 2507-2513.
[21] G. Tosato and K. D. Jones, “Interleukin-1 Induces Interleukin-6 Production in Peripheral Blood Monocytes,” Blood, Vol. 75, No. 6, 1990, pp. 1305-1310.
[22] A. Desgeorges, C. Gabay, P. Silacci, et al., “Concentrations and Origins of Soluble Interleukin 6 Receptor-Alpha in Serum and Synovial Fluid,” The Journal of Rheumatology, Vol. 24, No. 8, 1997, pp. 1510-1516.
[23] K. Schroder and J. Tschopp, “The Inflammasomes,” Cell, Vol. 140, No. 6, 2010, pp. 821-832.
[24] H. Tsutani, N. Yoshio and T. Ueda, “Interleukin 6 Reduces Serum Urate Concentrations,” The Journal of Rheumatology, Vol. 27, No. 2, 2000, p. 554.
[25] N. Busso and H. K. Ea, “The Mechanisms of Inflammation in Gout and Pseudogout (CPP-Induced Arthritis),” Reumatismo, Vol. 63, No. 4, 2011, pp. 230-237.
[26] L. Punzi, F. Oliviero and R. Ramonda, “Transforming Growth Factor-Beta Levels in Synovial Fluid of Osteoarthritis with or without Calcium Pyrophosphate Dihydrate Crystals,” The Journal of Rheumatology, Vol. 30, No. 2, 2003, p. 420.
[27] B. Söderquist, I. Jones, H. Fredlund and T. Vikerfors, “Bacterial or Crystal-Associated Arthritis? Discriminating Ability of Serum Inflammatory Markers,” Scandinavian Journal of Infectious Diseases, Vol. 30, No. 6, 1998, pp. 591-596. http://dx.doi.org/10.1080/00365549850161151

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