The ‘enthesis’ is the region of insertion of a tendon, ligament, capsule, or fascia into bone. The enthesis is now understood to be a complex structure that extends into the bone and marrow cavity.¹³ Recent work suggests that the entheseal fibrocartilage is the major target of the immune response and the primary site of the immunopathology.¹⁴ The bone marrow demonstrates edema and contains cellular infiltrates. T lymphocytes are abundant in these areas with a preponderance of CD8+ cells.¹⁵ Pathologic studies have demonstrated inflammatory infiltration and destruction which affect the whole anulus fibrosus, not just the enthesis of the intervertebral disc.¹⁶

Synovitis

Patients with spondyloarthropathy may have peripheral arthritis, typically mono- or oligoarticular, and often affecting one or both knees. Microscopic analysis reveals fibrin, synovial cell proliferation, lymphocytes, and plasma cells in the synovium.¹⁷ A more recent hypothesis suggests that bacterial antigens and microorganisms in a susceptible HLA-B27-postitive patient may interact to produce inflammation and arthritis in ankylosing spondylitis.¹⁸ It is well established in reactive arthritis that synovial fluid demonstrates bacteria-specific T-cell responses to the bacterium that causes the arthritis.^19,²⁰

Sacroiliitis

Studies of the sacroiliac joint reveal evidence of synovitis, osteitis, and enthesitis. Biopsy and autopsy specimens demonstrate pannus formation, myxoid marrow, superficial cartilage destruction, intra-articular fibrous strands, new bone formation, and bony ankylosis. Biopsy samples demonstrate cellular infiltrates of T lymphocytes, with both CD4+ and CD8+ cells.^21,²² Contrast-enhanced magnetic resonance imaging (MRI) studies of the sacroiliac joints in inflammatory back pain can demonstrate the following: sacroiliitis is more often bilateral in AS (84%) than in undifferentiated SpA (48%); the dorsocaudal parts of the synovial joint and the bone marrow are the most frequently inflamed structures early in the disease; in contrast, the entheses and ligaments are more commonly involved in later stages.²³

DIAGNOSIS

Ankylosing spondylitis

The classification criteria for AS were reassessed in 1984 and are referred to as the ‘modified New York criteria for ankylosing spondylitis.’ The criteria include both clinical and radiographic categories.^25,²⁶ The three clinical criteria include:

• Low back pain and stiffness of longer than 3 months’ duration, improved with exercise but not relieved by rest;

• Limitation of motion of the lumbar spine in both the sagittal and frontal planes; and

• Limitation of chest expansion relative to normal values corrected for age and sex.

The two radiologic criteria include:

• Sacroiliitis with more than minimum abnormality bilaterally; and

• Sacroiliitis of unequivocal abnormality unilaterally.

‘Definite AS’ is present in the presence of one clinical criterion and one radiologic criterion. ‘Probable AS’ is diagnosed if three clinical criteria are present or one radiologic criterion.

Clinical features

Clinical features of AS are heralded by chronic low back pain and stiffness as the initial symptoms in 75% of patients.²⁷ Often, the symptoms develop spontaneously and progress insidiously. Buttock pain that radiates into the thigh may be erroneously blamed on sciatica. This pain may reflect involvement of the sacroiliac joints.^28,²⁹ A history of nocturnal back pain, diurnal variation with prolonged morning stiffness, and improvement with exercise should raise the suspicion of an inflammatory etiology to chronic back pain. A good response to nonsteroidal antiinflammatory drug (NSAID) therapy and an age younger than 40 also increase the likelihood of inflammatory back pain.³⁰ Another, less common presentation of AS may be enthesitis or peripheral arthritis, mono- or oligoarticular.³¹ The enthesitis may involve the Achilles or plantar tendon insertions. The knee is often involved in the arthritis. These findings are not unique to AS. The differential diagnosis may include Reiter’s syndrome or reactive arthritis.

Physical examination

The earliest physical examination finding is often tenderness in the region of the sacroiliac joints or pain on provocative test maneuvers such as hip hyperextension and sacral compression tests. The two most sensitive maneuvers are pressure over the anterior-superior iliac spines and pressure over the lower half of the sacrum.³² As the disease progresses, physical examination findings will reflect restricted ranges of motion. As an example, reduced chest expansion is measured from maximal exhalation to maximal inhalation at the level of the fourth intercostal space. An expansion of less than 2.5 cm is considered abnormal.²⁷ The restricted motion reflects fusion of the costovertebral joints.

Schober’s test and finger-to-floor test will also become abnormal. The Schober’s test is performed by marking the fifth lumbar vertebra and a point in the midline 10 cm above. The patient is then asked to flex forward maximally while maintaining the knees straight. The distance between the two points exceeds 15 cm in normal individuals.¹

Laboratory studies

Laboratory studies in AS are often non-specific. Acute-phase reactants such as erythrocyte sedimentation rate and C-reactive protein are often elevated, but are not specific for AS and do not necessarily reflect disease activity.^33,³⁴ A mild normochromic normocytic anemia may be present. Serologic tests for lupus and rheumatoid arthritis should be negative.

HLA-B27 is present in approximately 90% of Caucasian patients and 50–60% of African-American patients with AS.³ It is present in only 6% of the general population.

Undifferentiated spondyloarthropathy, Reiter’s syndrome, and reactive arthritis

The spondyloarthropathy family of diseases share common features. As a spine specialist, it is most important to diagnose the presence of a spondyloarthropathy, rather than the specific type.

The classification criteria for SpA is based on clinical features, as there are no specific confirmatory blood tests. There are two sets of clinical criteria that have been developed and validated in Europe and are used widely. These are the European Spondyloarthropathy Study Group (ESSG) and the multiple-entry criteria by Bernard Amor.¹

The European Spondyloarthropathy Study Group criteria

To consider the diagnosis of spondyloarthropathy according to the ESSG criteria, a patient must demonstrate one of two entry criteria:

• Inflammatory spinal pain; or

• Synovitis, either asymmetric or predominantly in the lower limbs.

Indications for the designation of spinal pain as ‘inflammatory’ are:

• Onset before 40 years of age;

• Insidious onset;

• Duration longer than 3 months;

• Morning stiffness; and

• Improvement with exercise.

Indications for the designation of synovitis are:

• Soft tissue swelling;

• Warmth over a joint;

• Joint effusion;

• Decreased active and passive range of motion; and

• Symptoms are worse after rest.

There are other features which can be considered if a patient has one or two of the entry criteria. These include:

• Positive family history;

• Psoriasis;

• Inflammatory bowel disease;

• Urethritis, cervicitis, acute diarrhea;

• Alternating buttock pain;

• Enthesopathy; and

• Sacroiliitis.

The ESSG criteria have been evaluated in many studies, including those in Europe, Brazil, and Alaska.³⁵^–³⁸

The Amor criteria

The Amor criteria are a series of items which are weighted with a point scoring system.^1,^39,⁴⁰

In order to qualify for a diagnosis of spondyloarthropathy, a patient must score a total of at least six from among the list of features detailed in Table 35.2.

Table 35.2 Clinical features scored in the Amor classification

	Feature	Score
CLINICAL
	Night pain or morning stiffness of the thoracic or lumbar spine	1
	Asymmetrical oligoarthritis	2
	Buttock pain (uni- or bilateral)	1 or 2
	Sausage-like toe or digit	2
	Heel pain	2
	Iritis	2
	Nongonococcal urethritis or cervicitis within 1 month prior to arthritis	1
	Acute diarrhea within 1 month prior to arthritis	1
	Presence or h/o psoriasis, balanitis, inflammatory bowel disease	2
RADIOLOGIC
	Sacroiliitis (grade >2 if bilateral; grade >3 if unilateral)	2 or 3
GENETIC
	HLA-B27 present and/or family h/o spondyloarthropathy	2
RESPONSE TO TREATMENT
	Clear-cut response to NSAIDs	2

Specific diagnoses

The Amor and ESSG criteria are for the diagnosis of spondyloarthropathy in general. The criteria for the subtypes of spondyloarthropathy are less well defined.

Reactive arthritis

Inflammatory arthritides developing after a distant infection are labeled reactive.⁴¹ Inciting organisms may be: Chlamydia, Yersinia, Salmonella, Shigella, Campylobacter, Clostridium difficile, Brucella, and Giardia.⁴² The infection should have occurred within 6 weeks of clinical presentation of the arthritis. The presence of HLA-B27 renders the host susceptible; however, there is an interplay between HLA-B27 and environmental/infectious triggers in the development of reactive arthritis.⁴³

Reiter’s syndrome

Reiter’s syndrome represents one example of reactive arthritis. The classic triad of uveitis, urethritis, and arthritis defines Reiter’s syndrome. The pathogenesis is similar to reactive arthritis since both are triggered by an infectious agent and are more common in those patients with the HLA-B27 gene.⁴⁴

Not all patients present with all three features of the triad. The American College of Rheumatology requires peripheral arthritis (longer than 1 month’s duration) in association with urethritis or cervicitis.⁴⁵

Undifferentiated spondyloarthropathy

Among patients who meet ESSG or Amor criteria for spondyloarthropathy, there is a large group that does not fit into the above discrete categories. These patients are labeled as undifferentiated spondyloarthropathy.¹ In a recent study from Spain,⁴⁶ 68 patients with the diagnosis of undifferentiated spondyloarthropathy (uSpA) were followed for 2 years. At the end of this period, 75% retained the diagnosis of uSpA; disease remission occurred in 13%; ankylosing spondylitis 10%; and psoriatic arthritis 2%. In addition, a subset of patients with uSpA may be found to have reactive arthritis.⁴⁷

Arthritis associated with psoriasis

Psoriasis is a chronic autoimmune disorder affecting the skin and can be associated with inflammatory arthritis. Ten to forty percent of patients with psoriasis develop a chronic inflammatory arthritis. Psoriatic arthritis (PSA) occurs as a result of interplay of genetic, immunologic, and environmental factors.^48,⁴⁹ Clinically, PSA may resemble RA, except that PSA patients are seronegative and express cytokines preferentially at the enthesis in addition to the synovium. The most common presentation is either oligoarthritis or symmetric polyarthritis. There are several proposed subtypes: monoarthritis and oligoarthritis, polyarthritis, arthritis of distal interphalangeal joints with nail changes, arthritis mutilans, and spondylitis.^6,⁵⁰ This is often associated with flexor tenosynovitis. Axial spinal involvement of sacroiliitis and spondylitis does occur in PSA but usually occurs after years of illness, and is not a common presenting complaint.⁸

Enteropathic arthritis

Enteropathic arthritis refers to inflammatory arthritis in association with inflammatory bowel disease, ulcerative colitis, or Crohn’s disease.⁵¹ Conversely, two-thirds of patients with spondyloarthropathy show subclinical histologic signs of gut inflammation and approximately 6% will go on to develop inflammatory bowel disease.⁵² In a study by de Vlam et al.,⁵³ 39% of 103 consecutive patients followed in a gastroenterology clinic for ulcerative colitis or Crohn’s disease had enteropathic arthritis. Ninety percent met criteria for spondyloarthropathy, while 10% fulfilled criteria for ankylosing spondylitis. An additional 18% had asymptomatic sacroliliitis.⁶ Approximately 25% of patients with enteropathic arthritis have axial disease. Peripheral joint arthritis occurs more frequently in patients with enteropathic colitis compared with AS.

Please refer to Table 35.3 which represents a summary of some of the key clinical aspects of the differential diagnosis of systemic causes of arthritis. This may clarify the recognition of systemic arthritis for the practicing spine specialist.¹

Table 35.3 Differential diagnosis of some systemic causes of arthritis

Radiographic imaging in spondyloarthropathies

Seronegative spondyloarthropathies including ankylosing spondylitis, psoriatic arthritis, reactive arthritis, Reiter’s syndrome, enteropathic arthritis, and undifferentiated spondyloarthropathy share common clinical and radiographic features. Synovial joint inflammation and enthesitis may involve the axial or appendicular skeleton, or both.

The main musculoskeletal features include: sacroiliitis, spondylitis, and peripheral joint lesions. Sacroiliitis is the hallmark feature which unifies the group.⁵⁴ The distribution of joint involvement may give a clue to diagnosis. For example, ankylosing spondylitis primarily involves the axial joints and enthesis, with less consistent findings in the appendicular skeleton,⁵⁵ and psoriatic arthritis distinctively may involve the interphalageal joints.⁵⁶ Multiple imaging modalities are available to assess seronegative spondyloarthropathies, provide early diagnosis, and possibly follow disease activity.

Radiographic assessment

Standard radiographs are still the appropriate first images to obtain in practice. Radiographic features common to all spondyloarthropathies include: erosion, periostitis, bone proliferation at the entheses, and normal bone mineralization.⁵⁴ Radiographic analysis of early sacro-iliitis may demonstrate erosions on the iliac side of the joint. Late-stage radiographic appearance is one of SI fusion and ankylosis.⁵⁷ The shortcomings of plain radiography for the diagnosis of sacroiliitis include the large variability in interpretation among radiologists, and the relative insensitivity in early sacroiliitis.⁵⁸

Scintigraphy (bone scan)

Bone scanning is well documented as a modality to identify hyperemia and joint inflammation that may not be apparent radiographically. Quantitative bone scanning has approximately 80% predictability for detection of active sacroiliitis. This compares to 100% for MRI.⁵⁹ Periarticular radionuclide uptake around peripheral joints and at the entheses are demonstrated with bone scan.⁶⁰ The problem with scintigraphy is that it is non-specific and must be correlated with other clinical and radiologic investigations. Single photon emission computed tomography (SPECT) has improved localization of areas of increased uptake and may be a useful supplement.⁵⁴

Computed tomography

Computed tomography (CT) scanning is superior to plain radiography for visualization of early sacroiliac erosions and sclerosis.⁶¹ The true synovial sacroiliac joint is the inferior two-thirds, with the superior one-third being ligamentous. Comparison of CT with MRI scanning suggests that CT is superior for evaluation of chronic bone changes in the ligamentous portion of the joint; however, it is insensitive for detection of inflammatory changes in the subchondral bone.⁶² In addition, CT should be considered if further information about spinal fracture or bony canal stenosis is needed. A recent study demonstrates efficacy of CT-guided sacroiliac injections for treatment of sacroiliitis.⁶³

Magnetic resonance imaging

Magnetic resonance imaging (MRI) has emerged as a sensitive and detailed modality for imaging of spondyloarthropathy. MRI is excellent at depicting the normal sacroiliac joint and clearly separates the synovial and ligamentous compartments. The tissue resolution permits visualization and evaluation of bone marrow, synovium, articular cartilage, ligaments, tendons, muscles, entheses, and various stages of inflammation. MRI can identify joint effusion, synovitis, bone marrow edema, and bone erosions.⁵⁴ In patients with a high clinical likelihood of spondyloarthropathy and negative standard radiography, MRI (especially with gadolinium enhancement) provides excellent radiation-free evidence of sacroiliitis and enthesitis.⁶⁴

Musculoskeletal ultrasound

Currently, ultrasound is best applied to the evaluation of small peripheral joints since they are superficial and accessible. Early enthesitis may be demonstrated on ultrasound.⁵⁴

DIAGNOSIS OF SPONDYLOARTHROPATHIES

As an overview, there are four basic steps to follow if a clinician suspects the diagnosis of spondyloarthropathy (Fig. 35.1):

1. Suspect the disease if back pain characteristics are ‘inflammatory;’

2. Take additional history, physical examinations, labs;

3. Check specialized tests of chest expansion and lumbar range of movement; and

4. Take specific imaging.

Fig. 35.1 An algorithm of the four basic steps to follow if a clinician suspects the diagnosis of spondyloarthropathy.

Systemic features of spondyloarthropathies

One of the distinguishing features of the spondyloarthropathies is their systemic nature. In contrast to other etiologies of back pain, patients with spondyloarthropathies may experience systemic symptoms such as fever, malaise, and weight loss. Patients may have increased levels of inflammatory markers such as an erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Moreover, they may have extra-articular manifestations of their disease. Below is a discussion of the most common extra-articular findings in patients with spondylitis.

Ocular

Eye involvement can occur in all of the spondylotic variants. The most common finding is uveitis, and this can be seen in 25–40% of patients who have ankylosing spondylitis.⁶⁵ Symptoms include eye pain, blurred vision, and photosensitivity. The eye can appear red and injected. In cases in which uveitis is suspected, patients should immediately be referred to an ophthalmologist, as the diagnosis can only be made by slit-lamp examination. The treatment generally includes topical nonsteroidal eye drops or steroid drops. In severe or refractory cases, systemic immunosuppression and aggressive treatment with disease-modifying agents is necessary. While most patients will recover, severe cases can result in visual loss. A less common ocular manifestations of the spondylotic variants includes Sjögren’s syndrome and optic neuritis.⁶⁶

Gastrointestinal

Gastrointestinal involvement, in particular bowel inflammation and ulceration, can be seen in all of the spondylotic variants. Up to 44% of patients with ankylosing spondylitis have gastrointestinal involvement.⁶⁷ Gut inflammation in patients with ankylosing spondylitis is histologically similar to the lesions found in Crohn’s disease.⁶⁸ Moreover, in one series subclinical sacroiliitis was found in 24% of patients with inflammatory bowel disease.⁶⁹ Therefore, patients with spondylitis should be monitored for symptoms suggestive of occult inflammatory bowel disease and, conversely, patients with documented inflammatory bowel disease should be monitored for spondylitis.

Patient management

The management of patients with spondylotic variants should first include a functional evaluation. Treatment modalities include physical therapy, pharmacologic agents, spinal injections, surgery, and complementary therapies.

Functional assessment

This functional evaluation should include a functional assessment and an evaluation of how much fixed damage has been done to the spine and the joints. Patients with spondylitis can develop functional impairment leading to long-term disability. Various assessment tools can be used but the most common are the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), the Bath Ankylosing Spondylitis Functional Index (BASFI) and the Dougados Functional Index (DFI).⁷⁷ More recently, the World Health Organization Disability Assessment Schedule II (WHODAS II) was shown to be useful for evaluating functional capacity in patients with ankylosing spondylitis.⁷⁸ The BASDAI focuses on pain, joint involvement, and swelling while the BASFI, DFI, and the WHODAS II assess functional impairment.

Prognostic indicators

In addition to functional assessment, various disease characteristics portend prognostic outcome. In particular, worse outcome is found in persons who have disease onset prior to age 16, hip joint involvement, peripheral joint involvement (in particular a sausage digit), decreased range of motion of the lumbar spine, high ESR, and poor response to nonsteroidal antiinflammatory drugs.⁷⁹

One should examine patients for active inflammation of the peripheral joints. Laboratory testing should include ESR and CRP, CBC with differential, platelet count, and an assessment of baseline renal and liver function. The renal and liver function should be assessed because of the potential of hepatorenal toxicity of many of the medications in use. An elevated ESR and CRP suggest that ongoing active inflammation is occurring.

Physical therapy

One of the mainstays of therapy for spondylitis is exercise and physical therapy. The theory is that even in cases of spinal fusion and severe restriction in range of motion of the spine, physical therapy and exercise can maximize function and maintain as much mobility as possible. In Europe, spa therapy is included as part of the treatment regimen.⁸⁰

Unfortunately, there are few well-designed studies that clearly demonstrate long-term efficacy of physical therapy. In one meta-analysis, group physical therapy was better than home exercise in decreasing pain and stiffness.⁸¹ In another study, recreational exercise for longer than 200 minutes a week was shown to decrease pain and stiffness, but not to improve HAQ scores in patients with disease for less than 15 years. In patients with longer-standing disease, 5–7 days a week of back exercises decreased pain and had a modest improvement of HAQ scores.⁸²

Pharmacologic management

For many years, treatment of the spondylotic variants, in particular ankylosing spondylitis and Reiter’s syndrome, was almost exclusively limited to nonsteroidal antiinflammatory drugs, analgesics, and occasionally steroids. Other disorders that present with spondylitis as part of the disease, such as inflammatory bowel disease and psoriatic arthritis, were more likely to be treated with systemic agents for the extraspinal manifestations. Occasionally, disease-modifying antirheumatic drugs such as sulfasalazine and methotrexate were used, but with limited enthusiasm. More recently, however, with the advent of biologics, there has been interest in being more aggressive with the treatment of the spondylotic variants. There is growing evidence that these agents may arrest the progression of these disorders. Below is a discussion of the treatment of spondylotic disorders with NSAIDs, sulfasalazine, methotrexate, biologics, and the more experimental therapies such as palidronate and thalidomide.

Nonsteroidal antiinflammatory drugs and COX-2 inhibitors

Historically, the most commonly used NSAID has been indometacin.⁸³ This was based upon the sense that this medication was more effective than other antiinflammatory agents although controlled studies have failed to substantiate this finding.⁸⁴ In general, any of the nonsteroidals may be used to treat the pain and inflammation of the spondylotic variants. Phenylbutazone was once used with high frequency in patients with ankylosing spondylitis but is no longer used secondary to its high toxicity. In those patients who are intolerant of NSAIDs or who have had gastrointestinal toxicity from NSAIDs, the COX-2 inhibitors can be used. Both the NSAIDs and the COX-2 inhibitors can unmask occult colitis in these patients, so the treating healthcare provider should be aware of the potential for gastrointestinal toxicity. Moreover, the COX-2 inhibitors have been associated with increased risk of cardiovascular disease and should be used judiciously.

Sulfasalazine

Sulfasalazine has been used for many years in the treatment of inflammatory bowel disease and for rheumatoid arthritis. The data on its utility in spondylitis are murkier. While inflammatory markers such as the C-reactive protein clearly improve with sulfasalazine it is unclear whether the spondylitis and those symptoms benefit. It is particularly beneficial for patients who have extraspinal manifestations of spondylitis such as psoriatic arthritis, peripheral arthritis, and inflammatory bowel disease. Dosing is in the range of 2000–3000 mg a day. The major toxicity is bone marrow or liver toxicity.⁸⁵

Methotrexate

Methotrexate was approved in the early 1980s for use in rheumatoid arthritis. It has also been used for the treatment of inflammatory bowel disease and psoriatic arthritis. The efficacy of this medication in spondylitis is less clear. In one double-blind, placebo-controlled study of ankylosing spondylitis, there was no benefit of methotrexate treatment compared with placebo.⁸⁶

Tumor necrosis factor-alpha antagonists

The new biologic agents, especially those directed against tumor necrosis factor-alpha, have only been used recently for the treatment of spondylotic variants but represent a large advance in the pharmacologic therapy of ankylosing spondylitis. Those that are approved include etanercept, infliximab, and adalimumab. These agents have been shown to be effective in the treatment of patients with ankylosing spondylitis. Both infliximab and etanercept have been shown to cause a rapid and significant improvement in BASDAI scores and improvement in morning stiffness, spinal pain, and inflammatory markers such as the ESR and CRP.^87,⁸⁸ As these agents are used with greater frequency and earlier in the course of the disease, it will be interesting to see whether they can impact disease outcome.

They do have significant toxicities including either the exacerbation of underlying demyelinating processes or the reactivation of tuberculosis, including atypical forms.

Pamidronate has been studied in a few open label trials. Long-lasting improvement in pain, stiffness, and function were found although several patients developed arthralgias and myalgias after the infusions. Further studies need to be done before accepting the utility of this medication in treating spondylitis.⁹²

Complementary therapy

There are limited data on the use of complementary therapy in the treatment of spondylitis. In one case study, chiropractic manipulation was helpful in a patient with advanced ankylosing spondylitis. However, given the degree of fusion found in patients’ spines, caution should be used.⁹³

Surgery

Some patients with spondylotic variants will require surgery. Hip arthroplasty and spinal surgery are the most common. Risks particular to persons with ankylosing spondylitis are postoperative heterotopic ossification.

Spinal surgery is rarely used for the treatment of ankylosing spondylitis because the auto-fusion the patients experience circumvents the benefit of many spinal surgical procedures. In the case of instability, fusion has been used.

Persons presenting for evaluation of lower back pain, especially in the area of the sacroiliac joints, may be presenting with spondylitis. Morning stiffness and systemic symptoms may be present. Once the diagnosis of spondylitis is suspected, patients should be monitored for extra-articular manifestations. While standard therapy has included physical therapy and nonsteroidal antiinflammatory drugs, more recently the biologics and other agents are being evaluated. These newer therapies may hopefully lead to earlier treatment that will circumvent the spinal fusion that can be so debilitating in these disorders.

CASE STUDIES

Case study 1

A 28-year-old male who has a 10-year history of ankylosing spondylitis comes to the office. He has ongoing pain in his neck and the feeling of malaise. He has shortness of breath with walking short distances. He also has new onset of eye pain and blurry vision. His family history is notable for a mother with AS. On exam, Schober’s reveals an expansion of 1 mm, chest expansion is 1 cm, and he has minimal rotation (30° in either direction) of his neck. He is currently taking nonsteroidals but is wondering about other treatment options. Laboratory testing reveals an elevated ESR and CRP.

What further work-up needs to be done?

This case illustrates the systemic nature of ankylosing spondylitis and the spondylotic variants. The key features of his presentation are the shortness of breath and eye symptoms. These should prompt further work-up. He needs to have a chest X-ray to rule out pulmonary fibrosis and possibly pulmonary function tests. He also needs to be referred to an ophthalmologist for a slit-lamp examination because of the risk of uveitis. After these extraspinal conditions are ruled out, one could consider therapy with a disease-modifying agent such as sulfasalazine or tumor necrosis factor blockade.

Case study 2

A 33-year-old woman is referred for pain in her lumbar area. The pain is not radiating and she has no neurological symptoms. She feels that after she gets up in the morning and showers, she loosens up. She feels better as the day goes on and she moves around. She is concerned because she is recently married and would like to start a family and she is not sure that she would be able to handle an infant with her current level of pain. On examination, her Schober’s test shows her lumbar spinal extension is 3 cm, chest expansion is normal, and she has no peripheral joint involvement. Plain radiographs of her back are negative.

What should the next diagnostic work-up be?

MRI of the sacroiliac joints is more sensitive than plain radiographs in detecting erosions. In this case, her history of profound morning stiffness and improvement with activity in conjunction with the findings on physical examination are quite suggestive of a spondylotic variant. This patient should have MRI of her sacroiliac joints.

SUMMARY

Spondyloarthropathies are a family of disorders that frequently manifest with back and spine complaints. These disorders are associated with psoriasis and inflammatory bowel disease. Other systemic symptoms are seen, including uveitis and lung disease. Practitioners who treat patients with spine disorders should be aware of these diseases and consider them in the differential diagnosis of patients who present with back pain. Systemic symptoms, the presence of an elevated CRP and ESR, and a positive HLA-B27 can be helpful in diagnosing these disorders. Imaging studies such as radiographs and magnetic resonance imaging may be helpful in establishing the ankylosing spondylitis. These patients may be treated with traditional NSAIDs and, in some cases, patients may benefit from rheumatic disease-modifying antirheumatic drugs.

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SPONDYLOARTHROPATHIES
	AS Reiter’s syndrome (reactive arthritis) Psoriatic arthritis Inflammatory bowel disease Acne-associated arthritis or SAPHO syndrome Intestinal bypass arthritis

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