Antitumor Necrosis Factor-α Drugs and Disease-Modifying Antirheumatic Drugs for Low Back Pain

Abstract Background: In recent years, convincing evidence has emerged implicating tumor necrosis factor α as a causative factor in radiculopathy and discogenic back pain. But although preliminary open-label studies demonstrated promising results for the treatment of low back pain with tumor necrosis factor-α inhibitors, early optimism has been tainted by a controlled study showing no significant benefit in sciatica. To determine whether outcomes might be improved by a more direct route of administration, the authors evaluated escalating doses of intradiscal etanercept in 36 patients with chronic lumbosacral radiculopathy or discogenic low back pain. Methods: A double-blind, placebo-controlled pilot study was conducted whereby six patients received 0.1, 0.25, 0.5, 0.75, 1.0, or 1.5 mg etanercept intradiscally in each pain-generating disc. In each escalating dose group of six patients, one received placebo. A neurologic examination and postprocedure leukocyte counts were performed in all patients at 1-month follow-up visits. In patients who experienced significant improvement in pain scores and function, follow-up visits were conducted 3 and 6 months after the procedure. Results: At 1-month follow-up, no differences were found for pain scores or disability scores between or within groups for any dose range or subgroup of patients. Only eight patients remained in the study after 1 month and elected to forego further treatment. No complications were reported, and no differences were noted between preprocedure and postprocedure leukocyte counts. Conclusions: Although no serious side effects were observed in this small study, a single low dose of intradiscal etanercept does not seem to be an effective treatment for chronic radicular or discogenic low back pain.

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Confirmation of administrative claims-identified opportunistic infections and other serious potential adverse events associated with tumor necrosis factor α antagonists and disease-modifying antirheumatic drugs

Arthritis & Rheumatism ◽

10.1002/art.22544 ◽

2007 ◽

Vol 57 (2) ◽

pp. 343-346 ◽

Cited By ~ 17

Author(s):

J. R. Curtis ◽

C. Martin ◽

K. G. Saag ◽

N. M. Patkar ◽

J. Kramer ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Opportunistic Infections ◽

Administrative Claims ◽

Disease Modifying Antirheumatic Drugs ◽

Antirheumatic Drugs ◽

Disease Modifying ◽

Factor Α ◽

Necrosis Factor

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The Expression of Tumor Necrosis Factor-α and CD68 in High-Intensity Zone of Lumbar Intervertebral Disc on Magnetic Resonance Image in the Patients With Low Back Pain

Spine ◽

10.1097/brs.0b013e3181dfce9e ◽

2011 ◽

Vol 36 (6) ◽

pp. E429-E433 ◽

Cited By ~ 18

Author(s):

Ren Dongfeng ◽

Shuxun Hou ◽

Wenwen Wu ◽

Huadong Wang ◽

Weilin Shang ◽

...

Keyword(s):

Low Back Pain ◽

Back Pain ◽

Magnetic Resonance Image ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Low Back ◽

Lumbar Intervertebral Disc ◽

High Intensity Zone ◽

Factor Α ◽

Necrosis Factor

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Intradiscal Administration of Tumor Necrosis Factor-α Inhibitor, Etanercept, Clinically Improves Intractable Discogenic Low Back Pain

Global Spine Journal ◽

10.1055/s-0034-1376544 ◽

2014 ◽

Vol 4 (1_suppl) ◽

pp. s-0034-1376544-s-0034-1376544 ◽

Cited By ~ 2

Author(s):

T. Sainoh ◽

S. Orita ◽

K. Yamauchi ◽

Y. Sakuma ◽

G. Kubota ◽

...

Keyword(s):

Low Back Pain ◽

Back Pain ◽

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Low Back ◽

Discogenic Low Back Pain ◽

Factor Α ◽

Necrosis Factor

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Biologic disease-modifying antirheumatic drugs in the treatment of major monogenic autoinflammatory diseases: literature review and clinical observation

Modern Rheumatology Journal ◽

10.14412/1996-7012-2021-6-95-100 ◽

2021 ◽

Vol 15 (6) ◽

pp. 95-100

Author(s):

S. O. Salugina ◽

E. S. Fedorov

Keyword(s):

High Efficiency ◽

Interleukin 1 ◽

Autoinflammatory Diseases ◽

Disease Modifying Antirheumatic Drugs ◽

Antirheumatic Drugs ◽

Disease Modifying ◽

Factor Α ◽

Genetically Determined ◽

Late Stages

Autoinflammatory diseases (AIDs) are a heterogeneous group of rare genetically determined conditions, the main manifestations of which are episodes of fever in combination with other signs of systemic inflammation: skin rashes, musculoskeletal and neurological disorders, damage to the organs of vision, hearing, etc., as well as acute phase markers and the absence of autoantibodies. The use of biological therapy, especially inhibitors of interleukin 1 (iIL1), in most common monogenic AIDs (mAID) – FMF, TRAPS, HIDS/MKD, CAPS – has shown its high efficiency and led to significant progress in the treatment of these patients. Currently, iIL1 are the first-line drugs for mAIDs therapy, primarily CAPS. In the case of their ineffectiveness or intolerance in certain situations, other biologic disease-modifying antirheumatic drugs can also be used – inhibitors of tumor necrosis factor α and iIL6, but this issue needs further investigation. The article describes a patient with mAID, in whom the diagnosis was made more than 40 years after the onset; administration of targeted therapy even in the late stages of the disease led to a significant improvement in many symptoms and quality of life.

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Circulating Adipokines in Predicting the Transition from Acute to Persistent Low Back Pain

Pain Medicine ◽

10.1093/pm/pnaa052 ◽

2020 ◽

Vol 21 (11) ◽

pp. 2975-2985 ◽

Cited By ~ 1

Author(s):

David M Klyne ◽

Paul W Hodges

Keyword(s):

Low Back Pain ◽

Back Pain ◽

Depressive Symptoms ◽

Repeated Measurements ◽

Low Back ◽

Reactive Protein ◽

Acute Low Back Pain ◽

Pain Disability ◽

Inflammation Cytokines ◽

Necrosis Factor

Abstract Objectives Cytokines such as tumor necrosis factor (TNF) contribute to the transition from acute to persistent pain. Despite increasing incidence of obesity and its linkage with chronic pain and inflammation, cytokines predominantly produced by adipose tissue (adipokines) have received little attention. Here we aimed to explore the longitudinal trajectory of adipokines from the onset of acute low back pain (LBP) and identify combinations of adipokines and/or other features that predict outcome. Methods Individuals with acute LBP (less than two weeks after onset) who had either recovered (no pain, N = 15) or remained unrecovered (no reduction/increase in pain, N = 13) at six months and 15 controls were retrospectively selected from a larger prospective cohort. Participants provided blood for the measurement of TNF, interleukin-6 (IL-6), resistin, visfatin, adiponectin, leptin, and C-reactive protein (CRP), and completed questionnaires related to pain/disability, depression, and sleep at baseline. LBP participants repeated measurements at six months. Results Compared with controls, acute LBP individuals had higher TNF and CRP but lower adiponectin. In LBP, unrecovered individuals had higher TNF at both time points, but lower CRP at baseline and leptin at six months. Although combined low CRP, high TNF, and depressive symptoms at baseline predicted poor recovery, the primary adipokines leptin, resistin, visfatin, and adiponectin did not. Conclusions Primary adipokines did not add to the prediction of poor LBP outcome that has been identified for the combination of low CRP, high TNF, and depressive symptoms in acute LBP. Whether adipokines play a role in LBP persistence in overweight/obese individuals requires investigation.

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