eMedicine Specialties > Orthopedic Surgery > Spine
Ankylosing Spondylitis: Treatment & Medication
Updated: May 29, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
- No preventive measure or definitive treatment exists for individuals with AS. Early diagnosis and proper patient education are important.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used to reduce pain and decrease inflammation. Aspirin has been reported to have limited benefit. Oral steroids are not used for long-term management of AS because of the high risk of adverse effects.
- Sulfasalazine has been reported to be effective in some patients with peripheral involvement. Sulfasalazine is also useful in patients with coexisting inflammatory bowel disease.
- Laboratory values, including those of ESR and CRP, are used commonly to monitor the progression of the disease and the effectiveness of treatment.
- After identifying persons with extra-articular manifestations, provide proper treatment or refer them to the appropriate specialist. These extra-articular manifestations include acute iritis, aortitis, heart block, pulmonary fibrosis, amyloidosis, and neurologic deficits, including cauda equina.
- Genetic counseling and patient support groups are useful in further educating patients about the disease process and in identifying individuals at increased risk.
Related Medscape topics:
Resource Center Genomic Medicine
Specialty Site Cardiology
Specialty Site Ophthalmology
Specialty Site Orthopaedics
Specialty Site Pulmonary Medicine
Specialty Site Rheumatology
Surgical Care
- Surgical treatment is geared toward resolution of the complications related to AS. No curative surgical treatment exists.
- Patients with fusion of the cervical or upper thoracic spine may have significant impairment in line of sight, eating, and psychosocial well-being. These patients may benefit from extension osteotomy of the cervical spine.22 This procedure is difficult and hazardous; however, if successful, it allows the patient to return to a more functional life.
- Patients with fusion of the spine secondary to AS who report a change in position of the spine should be cautiously treated and should be considered to have sustained a spinal fracture. Surgical intervention may be necessary to stabilize the fracture and prevent neurologic deficit.23,24
- Note: Patients who develop bowel or bladder dysfunction should be evaluated immediately with MRI to assess for possible cauda equina syndrome secondary to spinal stenosis. The presence of cauda equina syndrome is a surgical emergency requiring decompression within 48 hours to prevent permanent loss of function.
- Patients with significant involvement of the hips may benefit from total hip arthroplasty.25 Following surgery, heterotropic bone formation can be reduced with use of indomethacin or radiation therapy.
Consultations
- Rheumatologist: Consult a rheumatologist for evaluation and management of ongoing medical treatment of patients with AS. Additional coexisting seronegative spondyloarthropathies can be assessed.
- Gastroenterologist: Refer patients with symptoms suggesting coexisting inflammatory bowel disease to a gastroenterologist for evaluation.
- Cardiologist: Refer patients with cardiac involvement, including aortitis or heart block, to a cardiologist for evaluation.
- Physical therapist or physical medicine and rehabilitation specialist: Refer all patients to a physical therapist or rehabilitation specialist. Symptoms of AS are worse with inactivity and are relieved with exercise. As a result, a proper exercise program is a crucial element of treatment.
- Geneticist: Patients may be referred for genetic counseling to assess questions regarding the probabilities of relatives developing the disease.
- Support groups: Many patients benefit from various support groups, which can provide further education on the disease process and available treatment options.
Diet
- Generally, no dietary restrictions are implemented for patients with AS; however, patients with coexisting diseases, such as inflammatory bowel disease, have dietary restrictions.
Related Medscape topic:
Resource Center Nutrition
Activity
- A proper exercise program is a crucial component in the treatment of AS. Patients obtain a significant reduction in symptoms following exercising. Referral to physical therapy or to a rehabilitation specialist is useful in assisting patients to develop an appropriate exercise program.26,27
Medication
Pharmacotherapy is generally aimed at reducing pain and inflammation associated with the disease.
Sieper et al conducted a 12-week randomized, double-blind, controlled study comparing 2 dosages of celecoxib (200 mg once daily [qd] and 200 mg twice daily [bid]) relative to diclofenac SR (75 mg bid) with regard to global pain intensity as well as changes in disease activity, functional and mobility capacities, and adverse events.28 The authors noted that both dosages of celecoxib were comparable to the diclofenac SR dosage with respect to pain. When other parameters were compared, however, celecoxib 200 mg qd was not as effective in reducing certain parameters associated with inflammation as the bid dosages of celecoxib and diclofenac SR.28
At the present time, there are no disease-modifying medications available for the treatment of AS.
Related Medscape topics:
Resource Center Pain Management: Advanced Approaches to Chronic Pain Management
Resource Center Pain Management: Pharmacologic Approaches
Nonsteroidal anti-inflammatory drugs
NSAIDs are useful in reducing the pain and inflammation associated with AS. NSAIDs work by decreasing inflammatory reactions and providing direct pain relief. Numerous choices are available, and they are separated into different families of agents. If an NSAID is ineffective, another agent from a different family can often provide relief. Efficacy and adverse effect profiles differ among agents and families.
Related eMedicine topic:
Toxicity, Nonsteroidal Anti-inflammatory Agents
Related Medscape topic:
Resource Center Adverse Drug Events Reporting
Indomethacin (Indocin, Indochron ER)
Rapidly absorbed. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis.
Adult
25-50 mg PO bid/tid
75 mg SR PO bid; not to exceed 200 mg/d
Pediatric
1-2 mg/kg/d divided PO bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d
Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; GI bleeding; renal insufficiency
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases the risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia exists).
Diclofenac (Voltaren, Cataflam)
Inhibits prostaglandin synthesis by decreasing the activity of the enzyme cyclooxygenase, which, in turn, decreases formation of prostaglandin precursors.
Adult
25 mg PO bid/tid; if well tolerated, increase by 25 mg or 50 mg at weekly intervals until satisfactory response is obtained or total daily dose of 150-200 mg is reached; higher doses generally do not increase effectiveness
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; do not administer into the CNS; do not give to patients with peptic ulcer disease, recent gastrointestinal bleeding or perforation, renal insufficiency, or those at high risk of bleeding
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases the risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia exists.
Naproxen (Aleve, Naprelan, Anaprox)
For relief of mild to moderate pain.
Inhibits inflammatory reactions and pain by decreasing the activity of the enzyme cyclooxygenase, which is responsible for prostaglandin synthesis.
Adult
250-500 mg PO bid; may increase to 1.5 g/d for limited periods
Pediatric
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug.
Aminosalicylic acid derivatives
Aminosalicylic acid derivatives inhibit inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which is responsible for prostaglandin synthesis.
Sulfasalazine (Azulfidine, EN-tabs)
Useful in management of ulcerative colitis. Acts locally in the colon to decrease the inflammatory response. Systemically inhibits prostaglandin synthesis.
Adult
1 g PO tid/qid initially, followed by a maintenance dose of 2 g/d in divided doses
Pediatric
<2 years: Not established
>2 years: 40-60 mg/kg/d PO in 3-6 divided doses; follow with a maintenance dose of 20-30 mg/kg/d divided qid
Decreases the effects of iron, digoxin, and folic acid; conversely, increases the effects of oral anticoagulants, oral hypoglycemic agents, and methotrexate
Documented hypersensitivity; sulfa drugs or any component of sulfa drugs; those diagnosed with gastrointestinal or genitourinary obstruction
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in patients with renal or hepatic impairment, blood dyscrasias, or urinary obstruction
Immunosuppressants
Immunosuppressants inhibit key factors in the immune system that are responsible for inflammatory responses.
Methotrexate (Folex PFS, Rheumatrex)
Unknown mechanism of action in AS; may affect immune function. Effects observed in 3-6 weeks following administration. Ameliorates symptoms (eg, pain, swelling, stiffness) but has no evidence of inducing remission. Adjust dose gradually to attain satisfactory response.
Adult
30-40 mg/m2/wk PO/IM to 100-7500 mg/m2 with leucovorin rescue
Pediatric
5-15 mg/m2/wk PO/IM as single dose or as 3 divided doses given q12h
Oral aminoglycosides may decrease the absorption and blood levels of concurrent oral methotrexate (MTX); charcoal lowers the MTX levels; coadministration with etretinate may increase the hepatotoxicity of MTX; folic acid or its derivatives contained in some vitamins may decrease the response to MTX; probenecid, NSAIDs, salicylates, procarbazine, and sulfonamides (including TMP-SMZ) can increase the MTX plasma levels; may decrease phenytoin plasma levels; may increase the plasma levels of thiopurines
Documented hypersensitivity; alcoholism; hepatic insufficiency; documented immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia); renal insufficiency
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Monitor CBC counts monthly, and monitor liver and renal function q1-3 mo during therapy (monitor more frequently during initial dosing, during dose adjustments, or when the risk of elevated MTX levels [eg, dehydration] exists); MTX has toxic effects on hematologic, renal, gastrointestinal, pulmonary, and neurologic systems; discontinue if a significant drop in blood counts occur; fatal reactions reported when administered concurrently with NSAIDs
Tumor necrosis factor (TNF) inhibitors
TNF is a cytokine of which 2 forms have been identified with similar biologic properties. TNF-α or cachectin is produced predominantly by macrophages, and TNF-β or lymphotoxin is produced by lymphocytes. TNF is but one of many cytokines involved in the inflammatory cascade that may contribute to the symptoms of AS.
Infliximab (Remicade)
Neutralizes cytokine TNF-alpha and inhibits its binding to the TNF-alpha receptor. Mix in 250 mL normal saline for infusion over 2 h. Must use with low-protein – binding filter (£ 1.2 µm). Indicated to reduce the signs and symptoms of active AS.
Adult
5 mg/kg IV infusion at 0, 2, and 6 wk as induction regimen, then 5 mg/kg q6wk for maintenance.
IV infusion must be administered over at least 2 h; must use infusion set with in-line, sterile, nonpyrogenic, low-protein – binding filter (pore size £ 1.2 µm)
Pediatric
Not established
None reported
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
TNF-alpha modulates cellular immune responses; anti-TNF therapies, such as infliximab, may adversely affect normal immune responses and allow the development of superinfections; more cases of lymphoma were observed in TNF alpha-blockers compared with control groups; may increase the risk of reactivation of tuberculosis in patients with particular granulomatous infections
More on Ankylosing Spondylitis |
| Overview: Ankylosing Spondylitis |
| Differential Diagnoses & Workup: Ankylosing Spondylitis |
 Treatment & Medication: Ankylosing Spondylitis |
| Follow-up: Ankylosing Spondylitis |
| Multimedia: Ankylosing Spondylitis |
| References |
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Further Reading
Keywords
AS, Marie-Strumpell disease, von Bechterew disease, rheumatoid spondylitis, seronegative spondyloarthropathy, reactive arthritis, psoriasis, juvenile-onset spondylitis, juvenile chronic arthritis, ulcerative colitis, Crohn disease, Crohn's disease, human leukocyte antigen B27, HLA-B27, spondylodiscitis, Andersson lesions, anulus fibrosus
