Inflammatory back pain (IBP) is a condition of pain localized to the axial spine and sacroiliac joints that is chronic and is differentiated from mechanical back pain by a set of key diagnostic features. Inflammatory back pain is associated strongly with, but not diagnostic of, several inflammatory conditions that may have both axial and peripheral pain features. Pain in inflammatory back pain is more often localized to the lumbar spine and may be associated with buttock pain that alternates from one side to another; though, it is patient characteristics, chronicity, and pain progression that set IBP apart from other causes. The classic association of inflammatory back pain symptoms is with ankylosing spondylitis; however, IBP may also be present in other seronegative spondyloarthropathies such as psoriatic arthritis, enteropathic arthropathy, juvenile idiopathic arthritis, and reactive arthritis. The cause of inflammatory back pain may also be undifferentiated given the absence or combination of diagnostic features of any of these conditions.
The identification of seronegative spondyloarthropathies can follow the presentation of inflammatory back pain. The etiology of these conditions is complex, but in general, is associated with a precipitating systemic inflammatory response to a known or unknown source. This systemic inflammation causes local tissue alterations that can persist in the local joint environment. The persistence of inflammation through pathways that are continuing to be identified and described, such as interleukin-17 and tumor necrosis factor, mediates a cycle of ongoing unbalanced bone remodeling and resulting axial bone loss. These inflammatory and resulting structural changes, demonstrated classically on imaging by vertebral bone fusion noted in ankylosing spondylitis, suggest a source for the insidious onset of chronic pain noted in patients with IBP and have helped to guide research into avenues of intervention.
The assessment of the prevalence of inflammatory back pain is approximately 5 to 6% in United States adults age 20 to 69. However, a gap exists between the prevalence of IBP and a relatively much lower prevalence of spondyloarthropathies in the U.S. only reaching 0.9 to 1.4%. Studies in Asia demonstrate a very low incidence of ankylosing spondylitis in that population near 0.001%. Further, only 36% of Asian populations with inflammatory back pain also meet criteria for spondyloarthropathy. This gap between the prevalence of inflammatory back pain and seronegative spondyloarthropathy has led some to search for other associated causes or to suggest that IBP may be a unique condition separate from other inflammatory immune-mediated conditions.
On eUK study noted variability of findings with a prevalence of inflammatory back pain ranging from 3% to as high as 7% depending on the diagnostic criteria employed, and one study in Mexico found the prevalence of inflammatory back pain to be 3.0% in that population. Findings of the frequency of IBP in populations vary greatly depending on diagnostic criteria employed; however, the prevalence in most studies does not exceed 8%.
Inflammatory back pain is more prevalent among non-Hispanic white persons than non-Hispanic black persons (5.9% vs. 3.3%) in at least one large study. Little evidence exists to demonstrate a significant difference in rates of IBP across gender or by age group.
Inflammatory back pain is a chronic pain condition typically associated with an insidious onset of pain localized to the lower back and buttocks. Its pathophysiology is thought to stem from a systemic inflammatory response to some insult with inflammatory mediators that localize to the axial skeletal joints and induce pro-inflammatory intracellular changes. This chronic inflammatory condition results in a cycle of unbalanced bone remodeling associated with bone loss and possible bone fusion.
Inflammatory back pain correlates with the onset of pain before age 40, the persistence of pain for 3 or more months, morning stiffness that improves with mobility or exercise, and an insidious presentation of pain symptoms.
Though not a diagnostic criterion, inflammatory back pain has been demonstrated to be a sentinel condition to seronegative spondyloarthropathies. Histopathologic study of patients with spondyloarthropathies, when compared to patients with rheumatoid arthritis, shows increased vascularity, the proliferation of CD163+ macrophages, and increased levels of polymorphonuclear leukocytes.
Inflammatory back pain is differentiated from mechanical back pain by its insidious onset, improvement with exercise, lack of improvement with rest, and pain at night that improves with rising and movement. Given its association with seronegative spondyloarthropathies, IBP may be preceded by an inciting illness or systemic inflammatory process.
Inflammatory back pain, if differentiated from other causes of back pain by accepted diagnostic criteria, may be useful as a referral criterion for rheumatologic evaluation if a positive HLA-B27 laboratory test along with sacroiliitis confirmed by imaging accompany the pain criteria.
As high as 50% of patients with axial spondyloarthropathy will have increased acute phase response with elevations in erythrocyte sedimentation rate and C-reactive protein. However, elevations in these values are also typically associated with rheumatoid arthritis.
Following a diagnosis of inflammatory back pain by accepted criteria, referral to a rheumatologic specialist may be indicated in the setting of positive HLA-B27 testing and confirmation of sacroiliitis by imaging.
Initial treatment for inflammatory back pain begins with patient education as to the nature and expected course of their condition. The patient should be informed regarding the possibility of associated conditions and further investigation to be taken into an underlying cause such as laboratory evaluation and imaging. It is important to advise patients to stop smoking. Furthermore, sources of psychosocial support should be a topic of discussion with the patient. A consultation with physical therapy is likely necessary as inflammatory back pain, and its associated inflammatory illnesses, respond favorably to exercise and movement therapies.
Initial pharmacologic therapy for inflammatory back pain whether or not it is considered symptomatic of an axial spondyloarthropathy is a trial of NSAID therapy, which may often require a maximum dose. Initial treatment should extend for two to four weeks with evaluation for effectiveness. Upon determining an effective medication, this medication may be useful as needed for control of symptoms.
If NSAID therapy proves ineffective for control of symptoms in patients with known axial spondyloarthropathy, the next line medications include TNF-inhibitors or an alternative secukinumab. These classes of medications compromise patients’ immune response and require careful consideration of immune function, diagnosis of malignancy, heart health, or coexisting demyelinating diseases.
Indications for surgical intervention in the setting of inflammatory back pain with axial spondyloarthritis include severe hip involvement with persistent pain or severe limitation in mobility and quality of life, atlantoaxial subluxation with neurologic impairment, and severe flexion deformities with impaired ability to look in a forward direction.
The differential diagnosis of inflammatory back pain includes mechanical, non-mechanical, and visceral sources. It is particularly important to rule out pain sources from cancer or vertebral body compression fractures. Recall that the characteristic features of IBP are an age of onset less than 40 years, duration of back pain greater than 3 months, insidious onset, morning stiffness, and improvement with exercise. Causes of mechanical back pain tend to worsen with movement and exercise and tend to correlate with injury and more acute onset.
Patients should undergo assessment for neurologic deficits that may suggest compression of the spinal cord or cauda equina syndrome. Further, patients with high clinical suspicion of vertebral osteomyelitis or epidural abscess warrant immediate MRI.
A recent study evaluating the effectiveness of various findings traditionally thought to suggest cancer as the cause of back pain found that history of malignancy and strong clinical suspicion for cancer were most useful in directing toward evaluation for a cancerous cause of back pain.
Non-steroidal anti-inflammatory pharmacotherapy is part of the first line treatment for seronegative spondyloarthropathies and has been shown to demonstrate significant improvement in inflammatory back pain. Further, NSAIDs have been demonstrated to improve patient’s duration of morning stiffness and chest expansion in related arthropathies. These medications in association with other interventions shown to be effective, such as exercise and physical therapy can significantly improve the quality of life in patients with inflammatory back pain.
While little or no data exists directly linking inflammatory back pain and increased risk of mortality. Ankylosing spondylitis and other spondyloarthropathies involving the axial spine have correlations with a 36 to 76% increase in risk for the acute coronary syndrome and a 50% increased risk of venous thromboembolism. Of note, female patients with psoriatic arthritis have been shown to have nearly double the risk of ACS compared to the general population. However, given the relatively young age of presentation of these diseases and associated inflammatory back pain, the absolute risks of ACS, VTE, or stroke in these populations are modest.
The immunologically mediated process associated with inflammatory back pain also correlates with a cycle of unbalanced bone remodeling which leads to osteoporosis that is notable within the first 10 years of diagnosis. Patients with ankylosing spondylitis are twice as likely to experience vertebral fracture as the general population, most commonly with extension in the cervical region. Spinal cord injury is 11 times more common in AS, and patients with long-standing disease are at increased risk of cauda equine syndrome. Further, patients with axial spondyloarthropathy may be at higher risk of renal disease with an 8% increase in abnormal urinalysis compared to the general population.
Chronic use of non-steroidal anti-inflammatory drugs for patients with inflammatory back pain carry associations with a variety of possible complications. NSAIDs have links with exacerbation of peptic ulcer disease, increased risk of cardiovascular events in at-risk populations, incitement of renal injury or failure, and exacerbation of existing reactive airway disease. Administration of NSAIDs should commence in consideration for patients’ underlying disease process associated with inflammatory back pain, other comorbid illness, and other medications they are taking, particularly glucocorticoids, anticoagulants, diuretics, and SSRIs.
Following the diagnosis of inflammatory back pain by accepted criteria, referral to a rheumatologic specialist may be indicated in the setting of positive HLA-B27 testing and confirmation of sacroiliitis by imaging.
Initial treatment intervention for patients with inflammatory back pain should begin with education regarding the expected course of their condition along with expectation for further evaluation for a possible source of the inflammatory process. Patients instruction should include advice to stop smoking, as this can worsen symptoms, and they receive a referral to sources of psychosocial support. Physical therapy is an essential target of referral for those with inflammatory back pain, as exercise and postural training may greatly benefit them in the course of this disease.
Inflammatory back pain is a chronic condition characterized by insidious onset at an age less than 40 years, persisting for three months or more, associated with morning stiffness, and improving with exercise. It is strongly associated with, but not diagnostic of, spondyloarthropathies that involve the axial skeleton. As a chronic back pain condition it shares similarities with treatment with mechanical back pain; however, identification of the characteristic profile of symptoms of inflammatory back pain should prompt further evaluation of HLA-B27 and imaging, particularly by MRI. With positive lab values and/or presence of sacroiliitis by imaging, consultation or referral to a rheumatologic specialist would be appropriate.
Patients with inflammatory back pain either in isolation or associated with a diagnosed spondyloarthropathy have shown symptomatic relief with NSAID therapy. Physical therapy has also been shown to improve symptoms of inflammatory back pain, and this should be part of a multi-system approach to treatment.
While inflammatory back pain may occur independent of a diagnosed spondyloarthropathy, it may serve as a sentinel to identify associated conditions such as ankylosing spondylitis, psoriatic arthritis, inflammatory bowel disease, or reactive arthritis creating a bridge to complete therapy in treating an underlying illness. Appropriate consultation, patient education by the primary care provider and nurse practitioner, pharmacotherapy, and physical therapy can significantly improve patient outcomes and quality of life. [Level I]
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|Weisman MH, Inflammatory back pain: the United States perspective. Rheumatic diseases clinics of North America. 2012 Aug; [PubMed]|
|Braun J,Inman R, Clinical significance of inflammatory back pain for diagnosis and screening of patients with axial spondyloarthritis. Annals of the rheumatic diseases. 2010 Jul; [PubMed]|
|Thomas GP,Duan R,Pettit AR,Weedon H,Kaur S,Smith M,Brown MA, Expression profiling in spondyloarthropathy synovial biopsies highlights changes in expression of inflammatory genes in conjunction with tissue remodelling genes. BMC musculoskeletal disorders. 2013 Dec 15; [PubMed]|
|Zhao J,Chen J,Yang TH,Holme P, Insights into the pathogenesis of axial spondyloarthropathy from network and pathway analysis. BMC systems biology. 2012; [PubMed]|
|Chyuan IT,Chen JY, Role of Interleukin- (IL-) 17 in the Pathogenesis and Targeted Therapies in Spondyloarthropathies. Mediators of inflammation. 2018; [PubMed]|
|Hamilton L,Macgregor A,Warmington V,Pinch E,Gaffney K, The prevalence of inflammatory back pain in a UK primary care population. Rheumatology (Oxford, England). 2014 Jan; [PubMed]|
|Weisman MH,Witter JP,Reveille JD, The prevalence of inflammatory back pain: population-based estimates from the US National Health and Nutrition Examination Survey, 2009-10. Annals of the rheumatic diseases. 2013 Mar; [PubMed]|
|Tam LS,Wei JC,Aggarwal A,Baek HJ,Cheung PP,Chiowchanwisawakit P,Dans L,Gu J,Hagino N,Kishimoto M,Reyes HM,Soroosh S,Stebbings S,Whittle S,Yeap SS,Lau CS, 2018 APLAR axial spondyloarthritis treatment recommendations. International journal of rheumatic diseases. 2019 Feb 28; [PubMed]|
|Baeten D,Kruithof E,De Rycke L,Boots AM,Mielants H,Veys EM,De Keyser F, Infiltration of the synovial membrane with macrophage subsets and polymorphonuclear cells reflects global disease activity in spondyloarthropathy. Arthritis research [PubMed]|
|Brandt HC,Spiller I,Song IH,Vahldiek JL,Rudwaleit M,Sieper J, Performance of referral recommendations in patients with chronic back pain and suspected axial spondyloarthritis. Annals of the rheumatic diseases. 2007 Nov; [PubMed]|
|Rudwaleit M,van der Heijde D,Landew� R,Listing J,Akkoc N,Brandt J,Braun J,Chou CT,Collantes-Estevez E,Dougados M,Huang F,Gu J,Khan MA,Kirazli Y,Maksymowych WP,Mielants H,S�rensen IJ,Ozgocmen S,Roussou E,Valle-O�ate R,Weber U,Wei J,Sieper J, The development of Assessment of SpondyloArthritis international Society classification criteria for axial spondyloarthritis (part II): validation and final selection. Annals of the rheumatic diseases. 2009 Jun; [PubMed]|
|van der Heijde D,Ramiro S,Landew� R,Baraliakos X,Van den Bosch F,Sepriano A,Regel A,Ciurea A,Dagfinrud H,Dougados M,van Gaalen F,G�her P,van der Horst-Bruinsma I,Inman RD,Jongkees M,Kiltz U,Kvien TK,Machado PM,Marzo-Ortega H,Molto A,Navarro-Comp�n V,Ozgocmen S,Pimentel-Santos FM,Reveille J,Rudwaleit M,Sieper J,Sampaio-Barros P,Wiek D,Braun J, 2016 update of the ASAS-EULAR management recommendations for axial spondyloarthritis. Annals of the rheumatic diseases. 2017 Jun; [PubMed]|
|Smolen JS,Sch�ls M,Braun J,Dougados M,FitzGerald O,Gladman DD,Kavanaugh A,Landew� R,Mease P,Sieper J,Stamm T,Wit M,Aletaha D,Baraliakos X,Betteridge N,Bosch FVD,Coates LC,Emery P,Gensler LS,Gossec L,Helliwell P,Jongkees M,Kvien TK,Inman RD,McInnes IB,Maccarone M,Machado PM,Molto A,Ogdie A,Poddubnyy D,Ritchlin C,Rudwaleit M,Tanew A,Thio B,Veale D,Vlam K,van der Heijde D, Treating axial spondyloarthritis and peripheral spondyloarthritis, especially psoriatic arthritis, to target: 2017 update of recommendations by an international task force. Annals of the rheumatic diseases. 2018 Jan; [PubMed]|
|Wahl EC,Smith D,Sesto M,Boissonnault W, Differential diagnosis of a patient with low back and toe pain. The Journal of manual [PubMed]|
|Verhagen AP,Downie A,Maher CG,Koes BW, Most red flags for malignancy in low back pain guidelines lack empirical support: a systematic review. Pain. 2017 Oct; [PubMed]|
|Wong JJ,Côté P,Sutton DA,Randhawa K,Yu H,Varatharajan S,Goldgrub R,Nordin M,Gross DP,Shearer HM,Carroll LJ,Stern PJ,Ameis A,Southerst D,Mior S,Stupar M,Varatharajan T,Taylor-Vaisey A, Clinical practice guidelines for the noninvasive management of low back pain: A systematic review by the Ontario Protocol for Traffic Injury Management (OPTIMa) Collaboration. European journal of pain (London, England). 2017 Feb; [PubMed]|
|Kroon FP,van der Burg LR,Ramiro S,Landewé RB,Buchbinder R,Falzon L,van der Heijde D, Non-steroidal anti-inflammatory drugs (NSAIDs) for axial spondyloarthritis (ankylosing spondylitis and non-radiographic axial spondyloarthritis). The Cochrane database of systematic reviews. 2015 Jul 17; [PubMed]|
|Wang R,Ward MM, Epidemiology of axial spondyloarthritis: an update. Current opinion in rheumatology. 2018 Mar; [PubMed]|
|Moltó A,Etcheto A,van der Heijde D,Landewé R,van den Bosch F,Bautista Molano W,Burgos-Vargas R,Cheung PP,Collantes-Estevez E,Deodhar A,El-Zorkany B,Erdes S,Gu J,Hajjaj-Hassouni N,Kiltz U,Kim TH,Kishimoto M,Luo SF,Machado PM,Maksymowych WP,Maldonado-Cocco J,Marzo-Ortega H,Montecucco CM,Ozgoçmen S,van Gaalen F,Dougados M, Prevalence of comorbidities and evaluation of their screening in spondyloarthritis: results of the international cross-sectional ASAS-COMOSPA study. Annals of the rheumatic diseases. 2016 Jun; [PubMed]|
|Mundwiler ML,Siddique K,Dym JM,Perri B,Johnson JP,Weisman MH, Complications of the spine in ankylosing spondylitis with a focus on deformity correction. Neurosurgical focus. 2008; [PubMed]|
|Chaudhary SB,Hullinger H,Vives MJ, Management of acute spinal fractures in ankylosing spondylitis. ISRN rheumatology. 2011; [PubMed]|
|Lee SH,Lee EJ,Chung SW,Song R,Moon JY,Lee SH,Lim SJ,Lee YA,Hong SJ,Yang HI, Renal involvement in ankylosing spondylitis: prevalence, pathology, response to TNF-a blocker. Rheumatology international. 2013 Jul; [PubMed]|
|Walker C,Biasucci LM, Cardiovascular safety of non-steroidal anti-inflammatory drugs revisited. Postgraduate medicine. 2018 Jan; [PubMed]|
|Shim YK,Kim N, [Nonsteroidal Anti-inflammatory Drug and Aspirin-induced Peptic Ulcer Disease]. The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi. 2016 Jun 25; [PubMed]|
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