Journals / Journal of Turkish Spinal Surgery / 2018 / Cilt: 29 - Sayı: 2

THE IMPORTANCE OF C-REACTIVE PROTEIN IN DISCOGENIC LOW BACK PAIN: THE ANALYSIS OF 444 PATIENTS

Pages
115–118
DOI
—
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AI Summary & Key Takeaways

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⚡ TL;DR(Too Long; Didn't Read)

All patients were assessed in terms of CRP positivity at the first admission and whether surgery is recommended or not.

📌 3 Key Takeaways

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Objective & Hypothesis:Background: Low back complaint is the most common health problem.
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Key Findings & Data:Material and Methods: 444 patients with discogenic low back pain were assessed in three groups.
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Conclusion & Impact:All patients were assessed in terms of CRP positivity at the first admission and whether surgery is recommended or not.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Background: Low back complaint is the most common health problem. Recent studies point out the role of inflammation on discogenic back pain. In this study, we intended to examine the importance of C-reactive protein (CRP) level in discogenic low back pain. Material and Methods: 444 patients with discogenic low back pain were assessed in three groups. The first group (n=229) consisted of patients who appealed to outpatient clinic and who were recommended medical therapy. In the second group (n=15), there were patients who appealed to outpatient clinic and who were offered operation but who did not accept surgery. As for the third group (n=200) included patients who were operated because of single level lumbar discopathy. All patients were assessed in terms of CRP positivity at the first admission and whether surgery is recommended or not. Results: Positivity of CRP was significantly higher in the group to whom surgery is recommended (n=215) than in medical treatment recommended patients (17.8 % vs. 3.1 %, p < 0.0001, OR=6.8, 95 % CI: 2.9-15.6). Furthermore, the positivity of CRP was found significantly higher in the third group compared to the first group (18 % vs. 3.1 %, p < 0.0001, OR= 6.9, 95 % CI: 3.1-16.1). However, it was relatively higher in the second group than in the first group (13.3 % vs. 3.1 %, p=0.0626, OR=4.9, 95% CI: 0.9-25.9). Conclusion: Discogenic low back pain is caused by both mechanical and inflammatory factors. Preoperative CRP values can be predictive for inflammatory process in lomberdiscopathy. For more accurate results further studies are needed.

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Cite This Article

DURDAĞ, E., ALBAYRAK, S., ATCI, İ. B., ÇİVİ, S., KARDEŞ, Ö., KOCA, S. S. (2018). THE IMPORTANCE OF C-REACTIVE PROTEIN IN DISCOGENIC LOW BACK PAIN: THE ANALYSIS OF 444 PATIENTS. Journal of Turkish Spinal Surgery, Cilt: 29 - Sayı: 2, 115–118. https://ajindex.com/articles/196411

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References (17)

  1. Anderson G. Epidemiologic features of chronic low back pain. Lancet 1999; 354: 581-585. Benoist M. The natural history of lumbar degenerative spinal stenosis. Joint Bone Spine 2002; 69 (5): 450-457.
  2. Bobechko WE, Hirsch C. Auto-immune response to nucleus pulposus in the rabbit. J Bone Joint Surg 1965; 47-B: 574-580.
  3. Chang CW, Lai PH, Yip CM, Hsu SS. Spontaneous regression of lumbar herniated disc. J Chin Med Assoc 2009; 72(12): 650-603.
  4. Demir NA, Ural O. Serum interleukin-8 levels may predict relapse in brucellosis. Turk J Med Sci 2012; 42(5): 796-801.
  5. Emch TM, Modic MT. Imaging of lumbar degenerative disk disease: history and current state. Skeletal Radiol 2011; 40(9): 1175-1189.
  6. Elves MW, Bucknill T, Sullivan MF. In vitro inhibition of leukocyte migration in patients with intervertebral disclesions. Orthop Clin North Am 1975; 6: 59-65.
  7. Gertzbein SD, Tait JH, Devlin SR. The stimulation of lymphocytes by nucleus pulposus in patients with degenerative disk disease of the lumbar spine. Clin Orthop 1977; 123: 149-154.
  8. Gertzbein SD, Tyle M, Gross A. Autoimmunity in degenerative disc disease of the lumbar spine. Orthop Clin North Am 1975; 6: 67-73.
  9. Genevay S, Finckh A, Payer M, Mezin F, Tessitore E, Gabay C, Guerne PA. Elevated levels of tumor necrosis factor-alpha imperiradicular fat tissue in patients with radiculopathy from herniated disc. Spine 2008; 33(19): 2041-2046.
  10. Goupille P, Jayson MI, Valat JP. The role of inflammation in disk herniation-associated radiculopathy. Semin Arthritis Rheum 1998; 28(1): 60-67.
  11. Guinto FC Jr, Hashim H, Stumer M. CT demonstration of disk regression after conservative therapy. Am J Neuroradiol 1984; 5: 632-633.
  12. Hamamoto H, Miyamoto H, Doita M, Takada T, Nishida K, Kurosaka M. Capability of non-degenerated and degenerated discs in producing inflammatory agents with or without macrophage interaction. Spine 2012, 37(3): 161-167.
  13. Komori H, Shinomiya K, Nakai O, Yamaura I, Takeda S, Furuya K. The natural history of Herniated Nucleus Pulposus with radiculopathy. Spine 1996; 15; 225-229
  14. Marshall L, Trethewie ER. Chemical irritation of nerve root in disc prolapse. Lancet 1973; 2: 230-234.
  15. Marshall LL, Trethewie ER, Curtain CC. Chemical radiculitis: a clinical, physiological and immunological study. Clin Orthop 1977; 129: 61-67.
  16. Miyamoto H, Saura R, Doita M, Kurosaka M, Mizuno K. The role of cyclooxygenase-2 in lumbar disc herniation. Spine 2002; 15; 27(22): 2477-2483.
  17. Mulleman D, Mammou S, Griffoul I, Watier H, Goupille P. Pathophysiol