User login
Childhood alopecia areata: What treatment works best?
IT’S UNCLEAR; there are no validated effective treatments for alopecia areata (AA). Topical immunotherapy (squaric acid dibutylester [SADBE] and diphenylcyclopropenone [DPCP]) induces the most signifi cant short-term hair regrowth in children with severe AA (strength of recommendation [SOR]: C, 4 small individual cohort studies and 1 moderately sized retrospective case review). Intralesional steroids can induce hair regrowth greater than 50% in children with limited AA (SOR: C, 1 retrospective cohort study).
Other commonly used treatments—topical and oral corticosteroids, topical cyclosporine, photodynamic therapy, and topical minoxidil—have no benefit over placebo (SOR: A, 14 randomized controlled trials [RCTs] and 3 within-patient studies).
Evidence summary
AA is a common inflammatory condition that causes hair loss and subsequent social consequences. Spontaneous remission occurs in 34% to 50% of patients within 1 year.1 Many trials of commonly used AA treatments have identified no significant patient benefits. A 2008 Cochrane review that examined 17 studies (14 RCTs and 3 within-patient studies) of AA interventions in 540 participants found no clinically significant hair regrowth (>50%) when patients were treated with topical corticosteroids, cyclosporine, minoxidil, photodynamic therapy, or oral corticosteroids.2
Documenting patient outcomes is problematic because of spontaneous resolution and frequent relapses.2 Moreover, few quality-controlled trials have studied children, and no long-term, randomized outcome trials of AA treatments exist.
Intralesional steroids and SADBE show results
In a moderately sized retrospective cohort study in Singapore (392 patients <16 years), 57% of patients experienced more than 50% improvement after 12 weeks of intralesional steroids for limited AA, and 75% showed similar improvement after 24 weeks. Of 43 children treated with anthralin, only 10 with limited AA showed more than 50% clinical improvement within 6 months.3 Fifty-four patients with extensive AA received SADBE; 74% experienced greater than 50% hair regrowth at 6 months.3
SADBE effects aren’t long-lived
A 1996 individual cohort study of 33 children (6*#8211;14 years of age) with extensive AA who were treated with SADBE once a week for a year showed a complete regrowth rate of 30.3%. Only 9% of the children maintained total or partial regrowth during long-term follow-up (mean 6 years), however.4
In another individual cohort study, 28 pediatric patients with extensive AA had mixed results with 2% SADBE used once a week for a year.5 Nine patients (32.1%) showed total or acceptable hair growth; 6 (21.4%) had diffuse regrowth but thinner than normal hair. Eighty-seven percent of patients relapsed within 6 months of discontinuing therapy.5
Studies of DPCP are too small
A 1996 small individual cohort investigation recorded a 40% response rate (90%–100% regrowth) to DPCP in 10 pediatric patients with extensive AA who were treated for an average of 8.6 months. The same study found cosmetically acceptable growth in 27% of patients (4 of 15 patients 4–15 years of age) treated for an average of 9.6 months.6
A small individual study of DPCP reported complete regrowth in 4 of 12 (33%) children with extensive AA; growth persisted at 6 months in 3 of the 4 responders.7 Another cohort study reported a 50% response rate (>80% regrowth) using DPCP in 10 patients (11–14 years of age) with extensive disease.8
Use SADBE and DPCP with caution
SADBE and DPCP are unlicensed treatments that can cause occipital and cervical lymphadenopathy, severe dermatitis (minimized by careful titration), urticaria, and hypo- or hyperpigmentation disorders (especially in racially pigmented patients). These agents shouldn’t be used during pregnancy and should be applied using gloves and aprons to avoid allergic contact dermatitis.
In light of these cautions, and handling and storage limitations, SADBE and DPCP should be reserved for patients with extensive disease (after obtaining signed informed consent). Patients should avoid ultraviolet light for 24 to 48 hours after application to avoid degradation of the medication.
Recommendations
The National Alopecia Areata Foundation and the American Academy of Dermatology recommend corticosteroids, topical minoxidil, and anthralin to treat AA.9,10
The British Association of Dermatologists’ guidelines for managing AA advise using intralesional corticosteroids for limited AA and contact immunotherapy for more extensive disease.1 They also note that intralesional corticosteroids are poorly tolerated and clinicians are reluctant to use contact immunotherapy in children.
Acknowledgements
The opinions and assertions contained herein are the private views of the author and are not to be construed as official, or as reflecting the views of the United States Air Force Medical Service or the US Air Force at large.
1. MacDonald Hull SP, Wood ML, Hutchinson PE, et al. Guidelines for the management of alopecia areata. Br J Dermatol. 2003;149:692-699.
2. Delamere FM, Sladden MJ, Dobbins HM, et al. Interventions for alopecia areata. Cochrane Database Syst Rev. 2008;(2):CD004413.-
3. Tan E, Tay YK, Giam YC. A clinical study of childhood alopecia areata in Singapore. Pediatr Dermatol. 2002;19:298-301.
4. Tosti A, Guidetti MS, Bardazzi F, et al. Long-term results of topical immunotherapy in children with alopecia totalis or alopecia universalis. J Am Acad Dermatol. 1996;35:199-201.
5. Orecchia G, Malagoli P, Santagostino L. Treatment of severe alopecia areata with squaric acid dibutylester in pediatric patients. Pediatr Dermatol. 1994;11:65-68.
6. Schuttelaar ML, Hamstra JJ, Plinck EP, et al. Alopecia areata in children: treatment with diphencyprone. Br J Dermatol. 1996;135:581-585.
7. Hull SM, Pepall L, Cunliffe WJ. Alopecia areata in children: response to treatment with diphencyprone. Br J Dermatol. 1991;125:164-168.
8. Sotiriadis D, Patsatsi A, Lazaridou E, et al. Topical immunotherapy with diphenylcyclopropenone in the treatment of chronic extensive alopecia areata. Clin Exp Dermatol. 2007;32:48-51.
9. National Alopecia Areata Foundation. Treatment recommendations. Available at: www.naaf.org/site/PageServer?pagename=about_alopecia_treatment.html. Accessed December 17, 2010.
10. American Academy of Dermatology. Alopecia areata. Available at: http://www.aad.org/public/publications/pamphlets/common_alopecia.html. Accessed December 17, 2010.
IT’S UNCLEAR; there are no validated effective treatments for alopecia areata (AA). Topical immunotherapy (squaric acid dibutylester [SADBE] and diphenylcyclopropenone [DPCP]) induces the most signifi cant short-term hair regrowth in children with severe AA (strength of recommendation [SOR]: C, 4 small individual cohort studies and 1 moderately sized retrospective case review). Intralesional steroids can induce hair regrowth greater than 50% in children with limited AA (SOR: C, 1 retrospective cohort study).
Other commonly used treatments—topical and oral corticosteroids, topical cyclosporine, photodynamic therapy, and topical minoxidil—have no benefit over placebo (SOR: A, 14 randomized controlled trials [RCTs] and 3 within-patient studies).
Evidence summary
AA is a common inflammatory condition that causes hair loss and subsequent social consequences. Spontaneous remission occurs in 34% to 50% of patients within 1 year.1 Many trials of commonly used AA treatments have identified no significant patient benefits. A 2008 Cochrane review that examined 17 studies (14 RCTs and 3 within-patient studies) of AA interventions in 540 participants found no clinically significant hair regrowth (>50%) when patients were treated with topical corticosteroids, cyclosporine, minoxidil, photodynamic therapy, or oral corticosteroids.2
Documenting patient outcomes is problematic because of spontaneous resolution and frequent relapses.2 Moreover, few quality-controlled trials have studied children, and no long-term, randomized outcome trials of AA treatments exist.
Intralesional steroids and SADBE show results
In a moderately sized retrospective cohort study in Singapore (392 patients <16 years), 57% of patients experienced more than 50% improvement after 12 weeks of intralesional steroids for limited AA, and 75% showed similar improvement after 24 weeks. Of 43 children treated with anthralin, only 10 with limited AA showed more than 50% clinical improvement within 6 months.3 Fifty-four patients with extensive AA received SADBE; 74% experienced greater than 50% hair regrowth at 6 months.3
SADBE effects aren’t long-lived
A 1996 individual cohort study of 33 children (6*#8211;14 years of age) with extensive AA who were treated with SADBE once a week for a year showed a complete regrowth rate of 30.3%. Only 9% of the children maintained total or partial regrowth during long-term follow-up (mean 6 years), however.4
In another individual cohort study, 28 pediatric patients with extensive AA had mixed results with 2% SADBE used once a week for a year.5 Nine patients (32.1%) showed total or acceptable hair growth; 6 (21.4%) had diffuse regrowth but thinner than normal hair. Eighty-seven percent of patients relapsed within 6 months of discontinuing therapy.5
Studies of DPCP are too small
A 1996 small individual cohort investigation recorded a 40% response rate (90%–100% regrowth) to DPCP in 10 pediatric patients with extensive AA who were treated for an average of 8.6 months. The same study found cosmetically acceptable growth in 27% of patients (4 of 15 patients 4–15 years of age) treated for an average of 9.6 months.6
A small individual study of DPCP reported complete regrowth in 4 of 12 (33%) children with extensive AA; growth persisted at 6 months in 3 of the 4 responders.7 Another cohort study reported a 50% response rate (>80% regrowth) using DPCP in 10 patients (11–14 years of age) with extensive disease.8
Use SADBE and DPCP with caution
SADBE and DPCP are unlicensed treatments that can cause occipital and cervical lymphadenopathy, severe dermatitis (minimized by careful titration), urticaria, and hypo- or hyperpigmentation disorders (especially in racially pigmented patients). These agents shouldn’t be used during pregnancy and should be applied using gloves and aprons to avoid allergic contact dermatitis.
In light of these cautions, and handling and storage limitations, SADBE and DPCP should be reserved for patients with extensive disease (after obtaining signed informed consent). Patients should avoid ultraviolet light for 24 to 48 hours after application to avoid degradation of the medication.
Recommendations
The National Alopecia Areata Foundation and the American Academy of Dermatology recommend corticosteroids, topical minoxidil, and anthralin to treat AA.9,10
The British Association of Dermatologists’ guidelines for managing AA advise using intralesional corticosteroids for limited AA and contact immunotherapy for more extensive disease.1 They also note that intralesional corticosteroids are poorly tolerated and clinicians are reluctant to use contact immunotherapy in children.
Acknowledgements
The opinions and assertions contained herein are the private views of the author and are not to be construed as official, or as reflecting the views of the United States Air Force Medical Service or the US Air Force at large.
IT’S UNCLEAR; there are no validated effective treatments for alopecia areata (AA). Topical immunotherapy (squaric acid dibutylester [SADBE] and diphenylcyclopropenone [DPCP]) induces the most signifi cant short-term hair regrowth in children with severe AA (strength of recommendation [SOR]: C, 4 small individual cohort studies and 1 moderately sized retrospective case review). Intralesional steroids can induce hair regrowth greater than 50% in children with limited AA (SOR: C, 1 retrospective cohort study).
Other commonly used treatments—topical and oral corticosteroids, topical cyclosporine, photodynamic therapy, and topical minoxidil—have no benefit over placebo (SOR: A, 14 randomized controlled trials [RCTs] and 3 within-patient studies).
Evidence summary
AA is a common inflammatory condition that causes hair loss and subsequent social consequences. Spontaneous remission occurs in 34% to 50% of patients within 1 year.1 Many trials of commonly used AA treatments have identified no significant patient benefits. A 2008 Cochrane review that examined 17 studies (14 RCTs and 3 within-patient studies) of AA interventions in 540 participants found no clinically significant hair regrowth (>50%) when patients were treated with topical corticosteroids, cyclosporine, minoxidil, photodynamic therapy, or oral corticosteroids.2
Documenting patient outcomes is problematic because of spontaneous resolution and frequent relapses.2 Moreover, few quality-controlled trials have studied children, and no long-term, randomized outcome trials of AA treatments exist.
Intralesional steroids and SADBE show results
In a moderately sized retrospective cohort study in Singapore (392 patients <16 years), 57% of patients experienced more than 50% improvement after 12 weeks of intralesional steroids for limited AA, and 75% showed similar improvement after 24 weeks. Of 43 children treated with anthralin, only 10 with limited AA showed more than 50% clinical improvement within 6 months.3 Fifty-four patients with extensive AA received SADBE; 74% experienced greater than 50% hair regrowth at 6 months.3
SADBE effects aren’t long-lived
A 1996 individual cohort study of 33 children (6*#8211;14 years of age) with extensive AA who were treated with SADBE once a week for a year showed a complete regrowth rate of 30.3%. Only 9% of the children maintained total or partial regrowth during long-term follow-up (mean 6 years), however.4
In another individual cohort study, 28 pediatric patients with extensive AA had mixed results with 2% SADBE used once a week for a year.5 Nine patients (32.1%) showed total or acceptable hair growth; 6 (21.4%) had diffuse regrowth but thinner than normal hair. Eighty-seven percent of patients relapsed within 6 months of discontinuing therapy.5
Studies of DPCP are too small
A 1996 small individual cohort investigation recorded a 40% response rate (90%–100% regrowth) to DPCP in 10 pediatric patients with extensive AA who were treated for an average of 8.6 months. The same study found cosmetically acceptable growth in 27% of patients (4 of 15 patients 4–15 years of age) treated for an average of 9.6 months.6
A small individual study of DPCP reported complete regrowth in 4 of 12 (33%) children with extensive AA; growth persisted at 6 months in 3 of the 4 responders.7 Another cohort study reported a 50% response rate (>80% regrowth) using DPCP in 10 patients (11–14 years of age) with extensive disease.8
Use SADBE and DPCP with caution
SADBE and DPCP are unlicensed treatments that can cause occipital and cervical lymphadenopathy, severe dermatitis (minimized by careful titration), urticaria, and hypo- or hyperpigmentation disorders (especially in racially pigmented patients). These agents shouldn’t be used during pregnancy and should be applied using gloves and aprons to avoid allergic contact dermatitis.
In light of these cautions, and handling and storage limitations, SADBE and DPCP should be reserved for patients with extensive disease (after obtaining signed informed consent). Patients should avoid ultraviolet light for 24 to 48 hours after application to avoid degradation of the medication.
Recommendations
The National Alopecia Areata Foundation and the American Academy of Dermatology recommend corticosteroids, topical minoxidil, and anthralin to treat AA.9,10
The British Association of Dermatologists’ guidelines for managing AA advise using intralesional corticosteroids for limited AA and contact immunotherapy for more extensive disease.1 They also note that intralesional corticosteroids are poorly tolerated and clinicians are reluctant to use contact immunotherapy in children.
Acknowledgements
The opinions and assertions contained herein are the private views of the author and are not to be construed as official, or as reflecting the views of the United States Air Force Medical Service or the US Air Force at large.
1. MacDonald Hull SP, Wood ML, Hutchinson PE, et al. Guidelines for the management of alopecia areata. Br J Dermatol. 2003;149:692-699.
2. Delamere FM, Sladden MJ, Dobbins HM, et al. Interventions for alopecia areata. Cochrane Database Syst Rev. 2008;(2):CD004413.-
3. Tan E, Tay YK, Giam YC. A clinical study of childhood alopecia areata in Singapore. Pediatr Dermatol. 2002;19:298-301.
4. Tosti A, Guidetti MS, Bardazzi F, et al. Long-term results of topical immunotherapy in children with alopecia totalis or alopecia universalis. J Am Acad Dermatol. 1996;35:199-201.
5. Orecchia G, Malagoli P, Santagostino L. Treatment of severe alopecia areata with squaric acid dibutylester in pediatric patients. Pediatr Dermatol. 1994;11:65-68.
6. Schuttelaar ML, Hamstra JJ, Plinck EP, et al. Alopecia areata in children: treatment with diphencyprone. Br J Dermatol. 1996;135:581-585.
7. Hull SM, Pepall L, Cunliffe WJ. Alopecia areata in children: response to treatment with diphencyprone. Br J Dermatol. 1991;125:164-168.
8. Sotiriadis D, Patsatsi A, Lazaridou E, et al. Topical immunotherapy with diphenylcyclopropenone in the treatment of chronic extensive alopecia areata. Clin Exp Dermatol. 2007;32:48-51.
9. National Alopecia Areata Foundation. Treatment recommendations. Available at: www.naaf.org/site/PageServer?pagename=about_alopecia_treatment.html. Accessed December 17, 2010.
10. American Academy of Dermatology. Alopecia areata. Available at: http://www.aad.org/public/publications/pamphlets/common_alopecia.html. Accessed December 17, 2010.
1. MacDonald Hull SP, Wood ML, Hutchinson PE, et al. Guidelines for the management of alopecia areata. Br J Dermatol. 2003;149:692-699.
2. Delamere FM, Sladden MJ, Dobbins HM, et al. Interventions for alopecia areata. Cochrane Database Syst Rev. 2008;(2):CD004413.-
3. Tan E, Tay YK, Giam YC. A clinical study of childhood alopecia areata in Singapore. Pediatr Dermatol. 2002;19:298-301.
4. Tosti A, Guidetti MS, Bardazzi F, et al. Long-term results of topical immunotherapy in children with alopecia totalis or alopecia universalis. J Am Acad Dermatol. 1996;35:199-201.
5. Orecchia G, Malagoli P, Santagostino L. Treatment of severe alopecia areata with squaric acid dibutylester in pediatric patients. Pediatr Dermatol. 1994;11:65-68.
6. Schuttelaar ML, Hamstra JJ, Plinck EP, et al. Alopecia areata in children: treatment with diphencyprone. Br J Dermatol. 1996;135:581-585.
7. Hull SM, Pepall L, Cunliffe WJ. Alopecia areata in children: response to treatment with diphencyprone. Br J Dermatol. 1991;125:164-168.
8. Sotiriadis D, Patsatsi A, Lazaridou E, et al. Topical immunotherapy with diphenylcyclopropenone in the treatment of chronic extensive alopecia areata. Clin Exp Dermatol. 2007;32:48-51.
9. National Alopecia Areata Foundation. Treatment recommendations. Available at: www.naaf.org/site/PageServer?pagename=about_alopecia_treatment.html. Accessed December 17, 2010.
10. American Academy of Dermatology. Alopecia areata. Available at: http://www.aad.org/public/publications/pamphlets/common_alopecia.html. Accessed December 17, 2010.
Evidence-based answers from the Family Physicians Inquiries Network
Does spinal manipulation relieve back pain?
YES, spinal manipulation therapy (SMT) reduces lower back pain and improves the ability to perform everyday activities more than sham therapies (strength of recommendation [SOR]: A, multiple randomized controlled trials [RCTs] and systematic reviews), but it’s no more or less effective than pain medication, physical therapy, exercise, back school, or care given by a general practitioner (SOR: A, meta-analysis).
Insufficient evidence exists to conclude that the effectiveness of SMT varies with the presence or absence of radiating pain or the profession or training of the manipulator.
Evidence summary
Low back pain, defined as pain between the thoracic cage and proximal thighs, is the fifth most common reason for physician visits in the United States.1,2 The pain can be characterized by its duration: acute, <4 weeks; subacute, >4 weeks but <3 months; and chronic, >3 months.1,3
Pharmacologic treatments for low back pain include nonsteroidal anti-inflammatory agents, opioids, and muscle relaxants.2,3 Nonpharmacologic options comprise exercise, physical therapy, massage, acupuncture, and yoga.2,3 Self-care includes handouts, books, heat, cognitive-behavioral therapy, and interdisciplinary rehabilitation. Traction, corsets, bed rest, home care, and diathermy are considered harmful.3
How SMT compares with other treatments
A 2004 Cochrane meta-analysis of 39 RCTs with a total of 5486 patients concluded that SMT was superior to placebo and as effective as all other treatments in reducing low back pain.3 SMT wasn’t more helpful than other forms of treatment.1,3 Neither the professional training of the SMT provider nor the patient’s level of radiating pain was associated with better outcomes.3
Compared with patients who received sham therapy for acute low back pain, SMT-treated patients showed a 10-mm improvement in pain on a visual analog scale (VAS) (95% confidence interval [CI], 2-17 mm) and no statistically significant difference in function on the Roland-Morris Disability Questionnaire (RMDQ).3 No significant clinical or statistical differences were noted between SMT and conventional care/analgesics, physical therapy/exercise, and back school.
SMT patients reported only slightly more pain reduction (4 mm on a 100-mm scale [95% CI, 1-8 mm]) and no significant improvement in function compared with patients treated with nonbeneficial modalities, such as traction, bed rest, or topical gel.
Patients with chronic low back pain showed a 19-mm improvement in pain on the VAS (95% CI, 3-35 mm) and functional gains of 3.3 mm on the RMDQ (95% CI, 0.6-6.0 mm) compared with patients receiving sham therapy.
Complications from SMT are rare
The American Pain Society (APS) and the American College of Physicians (ACP) recently published a comprehensive review of RCTs published from 2000 to 2006 that examined nonpharmacologic treatments for low back pain.2 They evaluated 69 trials in 10 systematic reviews of the efficacy of SMT. Five higher-quality reviews reached conclusions consistent with the Cochrane review—there was no difference between SMT and other effective therapies. Two lower-quality reviews (based on 1-3 trials with low numbers) found SMT superior to other effective treatments.1,2
Based on a review of more than 70 controlled trials, the APS and ACP concluded that the risk of a serious complication from SMT (worsening lumbar disk herniation or cauda equina syndrome) is rare, less than 1 per 1 million patient visits.2
Recommendations
The APS and ACP guidelines recommend adding nonpharmacologic therapies such as SMT for acute, subacute, and chronic low back pain when patients don’t improve with self-care.4
Acknowledgement
The opinions and assertions contained herein are the private views of the authors and not to be construed as official or as reflecting the views of the US air Force medical Service or the US air Force at large.
1. Chou R, Huffman LH. Nonpharmacologic therapies for acute and chronic low back pain: a review of the evidence for an American Pain Society/American College of Physicians Clinical Practice Guideline. Ann Intern Med. 2007;147:492-504.
2. Kinkade S. Evaluation and treatment of acute low back pain. Am Fam Physician. 2007;75:1181-1188.
3. Assendelft WJ, Morton SC, Yu EI, et al. Spinal manipulative therapy for low-back pain. Cochrane Database Syst Rev. 2004;(1):CD000447.-
4. Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007;147:478-491.
YES, spinal manipulation therapy (SMT) reduces lower back pain and improves the ability to perform everyday activities more than sham therapies (strength of recommendation [SOR]: A, multiple randomized controlled trials [RCTs] and systematic reviews), but it’s no more or less effective than pain medication, physical therapy, exercise, back school, or care given by a general practitioner (SOR: A, meta-analysis).
Insufficient evidence exists to conclude that the effectiveness of SMT varies with the presence or absence of radiating pain or the profession or training of the manipulator.
Evidence summary
Low back pain, defined as pain between the thoracic cage and proximal thighs, is the fifth most common reason for physician visits in the United States.1,2 The pain can be characterized by its duration: acute, <4 weeks; subacute, >4 weeks but <3 months; and chronic, >3 months.1,3
Pharmacologic treatments for low back pain include nonsteroidal anti-inflammatory agents, opioids, and muscle relaxants.2,3 Nonpharmacologic options comprise exercise, physical therapy, massage, acupuncture, and yoga.2,3 Self-care includes handouts, books, heat, cognitive-behavioral therapy, and interdisciplinary rehabilitation. Traction, corsets, bed rest, home care, and diathermy are considered harmful.3
How SMT compares with other treatments
A 2004 Cochrane meta-analysis of 39 RCTs with a total of 5486 patients concluded that SMT was superior to placebo and as effective as all other treatments in reducing low back pain.3 SMT wasn’t more helpful than other forms of treatment.1,3 Neither the professional training of the SMT provider nor the patient’s level of radiating pain was associated with better outcomes.3
Compared with patients who received sham therapy for acute low back pain, SMT-treated patients showed a 10-mm improvement in pain on a visual analog scale (VAS) (95% confidence interval [CI], 2-17 mm) and no statistically significant difference in function on the Roland-Morris Disability Questionnaire (RMDQ).3 No significant clinical or statistical differences were noted between SMT and conventional care/analgesics, physical therapy/exercise, and back school.
SMT patients reported only slightly more pain reduction (4 mm on a 100-mm scale [95% CI, 1-8 mm]) and no significant improvement in function compared with patients treated with nonbeneficial modalities, such as traction, bed rest, or topical gel.
Patients with chronic low back pain showed a 19-mm improvement in pain on the VAS (95% CI, 3-35 mm) and functional gains of 3.3 mm on the RMDQ (95% CI, 0.6-6.0 mm) compared with patients receiving sham therapy.
Complications from SMT are rare
The American Pain Society (APS) and the American College of Physicians (ACP) recently published a comprehensive review of RCTs published from 2000 to 2006 that examined nonpharmacologic treatments for low back pain.2 They evaluated 69 trials in 10 systematic reviews of the efficacy of SMT. Five higher-quality reviews reached conclusions consistent with the Cochrane review—there was no difference between SMT and other effective therapies. Two lower-quality reviews (based on 1-3 trials with low numbers) found SMT superior to other effective treatments.1,2
Based on a review of more than 70 controlled trials, the APS and ACP concluded that the risk of a serious complication from SMT (worsening lumbar disk herniation or cauda equina syndrome) is rare, less than 1 per 1 million patient visits.2
Recommendations
The APS and ACP guidelines recommend adding nonpharmacologic therapies such as SMT for acute, subacute, and chronic low back pain when patients don’t improve with self-care.4
Acknowledgement
The opinions and assertions contained herein are the private views of the authors and not to be construed as official or as reflecting the views of the US air Force medical Service or the US air Force at large.
YES, spinal manipulation therapy (SMT) reduces lower back pain and improves the ability to perform everyday activities more than sham therapies (strength of recommendation [SOR]: A, multiple randomized controlled trials [RCTs] and systematic reviews), but it’s no more or less effective than pain medication, physical therapy, exercise, back school, or care given by a general practitioner (SOR: A, meta-analysis).
Insufficient evidence exists to conclude that the effectiveness of SMT varies with the presence or absence of radiating pain or the profession or training of the manipulator.
Evidence summary
Low back pain, defined as pain between the thoracic cage and proximal thighs, is the fifth most common reason for physician visits in the United States.1,2 The pain can be characterized by its duration: acute, <4 weeks; subacute, >4 weeks but <3 months; and chronic, >3 months.1,3
Pharmacologic treatments for low back pain include nonsteroidal anti-inflammatory agents, opioids, and muscle relaxants.2,3 Nonpharmacologic options comprise exercise, physical therapy, massage, acupuncture, and yoga.2,3 Self-care includes handouts, books, heat, cognitive-behavioral therapy, and interdisciplinary rehabilitation. Traction, corsets, bed rest, home care, and diathermy are considered harmful.3
How SMT compares with other treatments
A 2004 Cochrane meta-analysis of 39 RCTs with a total of 5486 patients concluded that SMT was superior to placebo and as effective as all other treatments in reducing low back pain.3 SMT wasn’t more helpful than other forms of treatment.1,3 Neither the professional training of the SMT provider nor the patient’s level of radiating pain was associated with better outcomes.3
Compared with patients who received sham therapy for acute low back pain, SMT-treated patients showed a 10-mm improvement in pain on a visual analog scale (VAS) (95% confidence interval [CI], 2-17 mm) and no statistically significant difference in function on the Roland-Morris Disability Questionnaire (RMDQ).3 No significant clinical or statistical differences were noted between SMT and conventional care/analgesics, physical therapy/exercise, and back school.
SMT patients reported only slightly more pain reduction (4 mm on a 100-mm scale [95% CI, 1-8 mm]) and no significant improvement in function compared with patients treated with nonbeneficial modalities, such as traction, bed rest, or topical gel.
Patients with chronic low back pain showed a 19-mm improvement in pain on the VAS (95% CI, 3-35 mm) and functional gains of 3.3 mm on the RMDQ (95% CI, 0.6-6.0 mm) compared with patients receiving sham therapy.
Complications from SMT are rare
The American Pain Society (APS) and the American College of Physicians (ACP) recently published a comprehensive review of RCTs published from 2000 to 2006 that examined nonpharmacologic treatments for low back pain.2 They evaluated 69 trials in 10 systematic reviews of the efficacy of SMT. Five higher-quality reviews reached conclusions consistent with the Cochrane review—there was no difference between SMT and other effective therapies. Two lower-quality reviews (based on 1-3 trials with low numbers) found SMT superior to other effective treatments.1,2
Based on a review of more than 70 controlled trials, the APS and ACP concluded that the risk of a serious complication from SMT (worsening lumbar disk herniation or cauda equina syndrome) is rare, less than 1 per 1 million patient visits.2
Recommendations
The APS and ACP guidelines recommend adding nonpharmacologic therapies such as SMT for acute, subacute, and chronic low back pain when patients don’t improve with self-care.4
Acknowledgement
The opinions and assertions contained herein are the private views of the authors and not to be construed as official or as reflecting the views of the US air Force medical Service or the US air Force at large.
1. Chou R, Huffman LH. Nonpharmacologic therapies for acute and chronic low back pain: a review of the evidence for an American Pain Society/American College of Physicians Clinical Practice Guideline. Ann Intern Med. 2007;147:492-504.
2. Kinkade S. Evaluation and treatment of acute low back pain. Am Fam Physician. 2007;75:1181-1188.
3. Assendelft WJ, Morton SC, Yu EI, et al. Spinal manipulative therapy for low-back pain. Cochrane Database Syst Rev. 2004;(1):CD000447.-
4. Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007;147:478-491.
1. Chou R, Huffman LH. Nonpharmacologic therapies for acute and chronic low back pain: a review of the evidence for an American Pain Society/American College of Physicians Clinical Practice Guideline. Ann Intern Med. 2007;147:492-504.
2. Kinkade S. Evaluation and treatment of acute low back pain. Am Fam Physician. 2007;75:1181-1188.
3. Assendelft WJ, Morton SC, Yu EI, et al. Spinal manipulative therapy for low-back pain. Cochrane Database Syst Rev. 2004;(1):CD000447.-
4. Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007;147:478-491.
Evidence-based answers from the Family Physicians Inquiries Network