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Does prophylactic azithromycin reduce the number of COPD exacerbations or hospitalizations?
EVIDENCE SUMMARY
A randomized, placebo-controlled trial including 1142 patients with COPD (forced expiratory volume in one second [FEV1] <70%, postbronchodilator FEV1 <80%) found that daily azithromycin 250 mg reduced acute exacerbations more than placebo over one year.1 Researchers recruited patients who were using supplemental oxygen, had required glucocorticoids, or had been hospitalized for an acute exacerbation in the last year. Patients with asthma, resting heart rate >100 beats/min, prolonged QTc interval (or on prolonging medications), or hearing impairment were excluded.
Azithromycin increased the median time to first exacerbation (defined as increase or new onset of cough, sputum, wheeze, and chest tightness for 3 days requiring antibiotics or systemic steroids) compared with the placebo group (266 days vs 174 days; P<.001) and reduced the risk of an acute exacerbation per patient year (hazard ratio [HR]=0.73; 95% confidence [CI], 0.63-0.84). It also reduced the rate of acute exacerbations per patient year (1.83 vs 1.43; P=.01; rate ratio=0.83; 95% CI, 0.72-0.95). The number needed to treat to prevent one exacerbation was 2.86.
No differences in death from any cause (3% vs 4%; P=.87), death from respiratory cause (2% vs 1%; P=.48), or death from cardiovascular cause (0.2% vs 0.2%; P=1.0) were found between azithromycin and placebo. Nor did rates of hospitalizations for acute exacerbations differ.
The groups also showed no significant difference in serious adverse events leading to discontinuation of medication. Notably, more patients in the azithromycin group had audiogram-confirmed hearing loss (25% vs 20%; P=.04), although the authors state that their criteria for hearing loss may have been too stringent because hearing improved on repeat testing whether or not the study drug was discontinued. In addition, more patients in the placebo group developed nasopharyngeal colonization with methicillin-resistant Staphylococcus aureus (31% vs 12%; P<.001).
Older ex-smokers on long-term O2 benefit most from the antibiotic
A retrospective subgroup analysis of the RCT identified patients who benefited most from daily azithromycin therapy.2 Compared with placebo, azithromycin decreased the time to first exacerbation in patients >65 years (542 patients; HR=0.59; 95% CI, 0.47-0.74), but not patients ≤65 years (571 patients; HR=0.84; 95% CI, 0.68-1.04).
The azithromycin group also demonstrated decreased time to first exacerbation in ex-smokers (867 patients; HR=0.65; 95% CI, 0.55-0.77) and patients on long-term oxygen (659 patients; HR=0.66; 95% CI, 0.55-0.80) but not current smokers (246 patients; HR=0.99; 95% CI, 0.71-1.38) or patients not using long-term oxygen (454 patients; HR=0.80; 95% CI, 0.62-1.03).
Azithromycin administration decreased exacerbations in patients with GOLD stages II (292 patients; HR=0.55; 95% CI, 0.40-0.75) and III (451 patients; HR=0.71; 95% CI, 0.56-0.90), but not stage IV (370 patients; HR=0.84; 95% CI, 0.65-1.08). The significance of the results is limited because the study was not originally powered for this level of subgroup analysis.
Continue to: Smaller study shows similar results
Smaller study shows similar results
A smaller RCT of 92 patients that evaluated exacerbation rates with azithromycin and placebo recruited patients with at least 3 acute COPD exacerbations in the previous year.3
Compared with placebo, oral azithromycin 500 mg 3 times a week (Monday, Wednesday, and Friday) increased the time between exacerbations over a 12-month period (59 days vs 130 days; P=.001). It also reduced the exacerbation rate per person per year (1.94 vs 3.22; risk ratio=0.60; 95% CI, 0.43-0.84) but didn’t change the hospitalization rate (odds ratio=1.34; 95% CI, 0.67-2.7).
No difference in serious adverse events was found between the azithromycin and placebo groups (3 patients vs 5 patients; P=NS), but an increase in diarrhea (9 patients vs 1 patient; P=.015) was noted.
RECOMMENDATIONS
An evidence-based guideline by the American College of Chest Physicians and Canadian Thoracic Society recommends long-term macrolide therapy to prevent acute exacerbations in patients >40 years with moderate or severe COPD and a history of ≥1 moderate or severe exacerbation in the previous year despite maximized inhaler therapy (Grade 2A, weak recommendation, high-quality evidence).4 The guideline also states that the duration and optimal dosages are unknown.
1. Albert RK, Connett J, Bailey WC, et al. Azithromycin for prevention of exacerbations of COPD. N Engl J Med. 2011;365:689-698.
2. Han M, Tayob N, Murray S, et al. Predictors of chronic obstructive pulmonary disease exacerbation reduction in response to daily azithromycin therapy. Am J Resp Crit Care. 2014;189:1503-1508.
3. Pomares X, Montón C, Espasa M, et al. Long-term azithromycin therapy in patients with severe COPD and repeated exacerbations. Int J Chron Obstruct Pulmon Dis. 2011;6:449-456.
4. Criner GJ, Bourbeau J, Diekemper RL, et al. Prevention of acute exacerbations of COPD: American College of Chest Physicians and Canadian Thoracic Society Guideline. Chest. 2015;147:894-942.
EVIDENCE SUMMARY
A randomized, placebo-controlled trial including 1142 patients with COPD (forced expiratory volume in one second [FEV1] <70%, postbronchodilator FEV1 <80%) found that daily azithromycin 250 mg reduced acute exacerbations more than placebo over one year.1 Researchers recruited patients who were using supplemental oxygen, had required glucocorticoids, or had been hospitalized for an acute exacerbation in the last year. Patients with asthma, resting heart rate >100 beats/min, prolonged QTc interval (or on prolonging medications), or hearing impairment were excluded.
Azithromycin increased the median time to first exacerbation (defined as increase or new onset of cough, sputum, wheeze, and chest tightness for 3 days requiring antibiotics or systemic steroids) compared with the placebo group (266 days vs 174 days; P<.001) and reduced the risk of an acute exacerbation per patient year (hazard ratio [HR]=0.73; 95% confidence [CI], 0.63-0.84). It also reduced the rate of acute exacerbations per patient year (1.83 vs 1.43; P=.01; rate ratio=0.83; 95% CI, 0.72-0.95). The number needed to treat to prevent one exacerbation was 2.86.
No differences in death from any cause (3% vs 4%; P=.87), death from respiratory cause (2% vs 1%; P=.48), or death from cardiovascular cause (0.2% vs 0.2%; P=1.0) were found between azithromycin and placebo. Nor did rates of hospitalizations for acute exacerbations differ.
The groups also showed no significant difference in serious adverse events leading to discontinuation of medication. Notably, more patients in the azithromycin group had audiogram-confirmed hearing loss (25% vs 20%; P=.04), although the authors state that their criteria for hearing loss may have been too stringent because hearing improved on repeat testing whether or not the study drug was discontinued. In addition, more patients in the placebo group developed nasopharyngeal colonization with methicillin-resistant Staphylococcus aureus (31% vs 12%; P<.001).
Older ex-smokers on long-term O2 benefit most from the antibiotic
A retrospective subgroup analysis of the RCT identified patients who benefited most from daily azithromycin therapy.2 Compared with placebo, azithromycin decreased the time to first exacerbation in patients >65 years (542 patients; HR=0.59; 95% CI, 0.47-0.74), but not patients ≤65 years (571 patients; HR=0.84; 95% CI, 0.68-1.04).
The azithromycin group also demonstrated decreased time to first exacerbation in ex-smokers (867 patients; HR=0.65; 95% CI, 0.55-0.77) and patients on long-term oxygen (659 patients; HR=0.66; 95% CI, 0.55-0.80) but not current smokers (246 patients; HR=0.99; 95% CI, 0.71-1.38) or patients not using long-term oxygen (454 patients; HR=0.80; 95% CI, 0.62-1.03).
Azithromycin administration decreased exacerbations in patients with GOLD stages II (292 patients; HR=0.55; 95% CI, 0.40-0.75) and III (451 patients; HR=0.71; 95% CI, 0.56-0.90), but not stage IV (370 patients; HR=0.84; 95% CI, 0.65-1.08). The significance of the results is limited because the study was not originally powered for this level of subgroup analysis.
Continue to: Smaller study shows similar results
Smaller study shows similar results
A smaller RCT of 92 patients that evaluated exacerbation rates with azithromycin and placebo recruited patients with at least 3 acute COPD exacerbations in the previous year.3
Compared with placebo, oral azithromycin 500 mg 3 times a week (Monday, Wednesday, and Friday) increased the time between exacerbations over a 12-month period (59 days vs 130 days; P=.001). It also reduced the exacerbation rate per person per year (1.94 vs 3.22; risk ratio=0.60; 95% CI, 0.43-0.84) but didn’t change the hospitalization rate (odds ratio=1.34; 95% CI, 0.67-2.7).
No difference in serious adverse events was found between the azithromycin and placebo groups (3 patients vs 5 patients; P=NS), but an increase in diarrhea (9 patients vs 1 patient; P=.015) was noted.
RECOMMENDATIONS
An evidence-based guideline by the American College of Chest Physicians and Canadian Thoracic Society recommends long-term macrolide therapy to prevent acute exacerbations in patients >40 years with moderate or severe COPD and a history of ≥1 moderate or severe exacerbation in the previous year despite maximized inhaler therapy (Grade 2A, weak recommendation, high-quality evidence).4 The guideline also states that the duration and optimal dosages are unknown.
EVIDENCE SUMMARY
A randomized, placebo-controlled trial including 1142 patients with COPD (forced expiratory volume in one second [FEV1] <70%, postbronchodilator FEV1 <80%) found that daily azithromycin 250 mg reduced acute exacerbations more than placebo over one year.1 Researchers recruited patients who were using supplemental oxygen, had required glucocorticoids, or had been hospitalized for an acute exacerbation in the last year. Patients with asthma, resting heart rate >100 beats/min, prolonged QTc interval (or on prolonging medications), or hearing impairment were excluded.
Azithromycin increased the median time to first exacerbation (defined as increase or new onset of cough, sputum, wheeze, and chest tightness for 3 days requiring antibiotics or systemic steroids) compared with the placebo group (266 days vs 174 days; P<.001) and reduced the risk of an acute exacerbation per patient year (hazard ratio [HR]=0.73; 95% confidence [CI], 0.63-0.84). It also reduced the rate of acute exacerbations per patient year (1.83 vs 1.43; P=.01; rate ratio=0.83; 95% CI, 0.72-0.95). The number needed to treat to prevent one exacerbation was 2.86.
No differences in death from any cause (3% vs 4%; P=.87), death from respiratory cause (2% vs 1%; P=.48), or death from cardiovascular cause (0.2% vs 0.2%; P=1.0) were found between azithromycin and placebo. Nor did rates of hospitalizations for acute exacerbations differ.
The groups also showed no significant difference in serious adverse events leading to discontinuation of medication. Notably, more patients in the azithromycin group had audiogram-confirmed hearing loss (25% vs 20%; P=.04), although the authors state that their criteria for hearing loss may have been too stringent because hearing improved on repeat testing whether or not the study drug was discontinued. In addition, more patients in the placebo group developed nasopharyngeal colonization with methicillin-resistant Staphylococcus aureus (31% vs 12%; P<.001).
Older ex-smokers on long-term O2 benefit most from the antibiotic
A retrospective subgroup analysis of the RCT identified patients who benefited most from daily azithromycin therapy.2 Compared with placebo, azithromycin decreased the time to first exacerbation in patients >65 years (542 patients; HR=0.59; 95% CI, 0.47-0.74), but not patients ≤65 years (571 patients; HR=0.84; 95% CI, 0.68-1.04).
The azithromycin group also demonstrated decreased time to first exacerbation in ex-smokers (867 patients; HR=0.65; 95% CI, 0.55-0.77) and patients on long-term oxygen (659 patients; HR=0.66; 95% CI, 0.55-0.80) but not current smokers (246 patients; HR=0.99; 95% CI, 0.71-1.38) or patients not using long-term oxygen (454 patients; HR=0.80; 95% CI, 0.62-1.03).
Azithromycin administration decreased exacerbations in patients with GOLD stages II (292 patients; HR=0.55; 95% CI, 0.40-0.75) and III (451 patients; HR=0.71; 95% CI, 0.56-0.90), but not stage IV (370 patients; HR=0.84; 95% CI, 0.65-1.08). The significance of the results is limited because the study was not originally powered for this level of subgroup analysis.
Continue to: Smaller study shows similar results
Smaller study shows similar results
A smaller RCT of 92 patients that evaluated exacerbation rates with azithromycin and placebo recruited patients with at least 3 acute COPD exacerbations in the previous year.3
Compared with placebo, oral azithromycin 500 mg 3 times a week (Monday, Wednesday, and Friday) increased the time between exacerbations over a 12-month period (59 days vs 130 days; P=.001). It also reduced the exacerbation rate per person per year (1.94 vs 3.22; risk ratio=0.60; 95% CI, 0.43-0.84) but didn’t change the hospitalization rate (odds ratio=1.34; 95% CI, 0.67-2.7).
No difference in serious adverse events was found between the azithromycin and placebo groups (3 patients vs 5 patients; P=NS), but an increase in diarrhea (9 patients vs 1 patient; P=.015) was noted.
RECOMMENDATIONS
An evidence-based guideline by the American College of Chest Physicians and Canadian Thoracic Society recommends long-term macrolide therapy to prevent acute exacerbations in patients >40 years with moderate or severe COPD and a history of ≥1 moderate or severe exacerbation in the previous year despite maximized inhaler therapy (Grade 2A, weak recommendation, high-quality evidence).4 The guideline also states that the duration and optimal dosages are unknown.
1. Albert RK, Connett J, Bailey WC, et al. Azithromycin for prevention of exacerbations of COPD. N Engl J Med. 2011;365:689-698.
2. Han M, Tayob N, Murray S, et al. Predictors of chronic obstructive pulmonary disease exacerbation reduction in response to daily azithromycin therapy. Am J Resp Crit Care. 2014;189:1503-1508.
3. Pomares X, Montón C, Espasa M, et al. Long-term azithromycin therapy in patients with severe COPD and repeated exacerbations. Int J Chron Obstruct Pulmon Dis. 2011;6:449-456.
4. Criner GJ, Bourbeau J, Diekemper RL, et al. Prevention of acute exacerbations of COPD: American College of Chest Physicians and Canadian Thoracic Society Guideline. Chest. 2015;147:894-942.
1. Albert RK, Connett J, Bailey WC, et al. Azithromycin for prevention of exacerbations of COPD. N Engl J Med. 2011;365:689-698.
2. Han M, Tayob N, Murray S, et al. Predictors of chronic obstructive pulmonary disease exacerbation reduction in response to daily azithromycin therapy. Am J Resp Crit Care. 2014;189:1503-1508.
3. Pomares X, Montón C, Espasa M, et al. Long-term azithromycin therapy in patients with severe COPD and repeated exacerbations. Int J Chron Obstruct Pulmon Dis. 2011;6:449-456.
4. Criner GJ, Bourbeau J, Diekemper RL, et al. Prevention of acute exacerbations of COPD: American College of Chest Physicians and Canadian Thoracic Society Guideline. Chest. 2015;147:894-942.
EVIDENCE-BASED ANSWER:
Yes for exacerbations, no for hospitalizations. Prophylactic azithromycin reduces the number of exacerbations by about 25%. It also extends the time between exacerbations by approximately 90 days for patients with moderate-to-severe chronic obstructive pulmonary disease (COPD). Azithromycin benefits patients who are >65 years, patients with Global Initiative for Obstructive Lung Disease (GOLD) stage II or III COPD, former smokers, and patients using long-term oxygen; it doesn’t benefit patients ≤65 years, patients with GOLD stage IV COPD, current smokers, or patients not using oxygen (strength of recommendation [SOR]: B, randomized controlled trials [RCTs]).
Prophylactic azithromycin doesn’t reduce hospitalizations overall (SOR: B, single small RCT).
Do trigger point injections effectively treat fibromyalgia?
Possibly. Trigger point injections appear effective in reducing pain and increasing pressure thresholds in patients with fibromyalgia and myofascial trigger points (strength of recommendation [SOR]: B, small randomized controlled trials [RCTs]).
Consensus guidelines suggest that trigger point injections may have a role in the treatment of fibromyalgia (SOR: C, expert opinion).
Active injections produce sustained improvement
A 2011 double-blind RCT randomized 68 female patients with both fibromyalgia and myofascial trigger points to either active trigger point injections with 1 mL 0.5% bupivacaine or placebo-like needle penetration with no medication to an area near the trigger point.1 Patients were evaluated for both local and generalized fibromyalgia symptoms at 4 and 8 days (trial period) and after 30 days (follow-up). Injections occurred on Days 1 and 4, with an option of additional injections on Days 8 and 11.
Compared to baseline (7 days before the injection), patients receiving active trigger point injections had decreased myofascial pain episodes 7 days after the injection (5.6 vs 0.97 episodes; P<.001), decreased pain intensity (62 vs 19/100 mm Visual Analog Scale score; P<.001), and increased pressure threshold at the trigger point (1.5 vs 2.9 kg/cm2; P<.0001), whereas the control group showed no differences.
During Days 1 to 8, patients receiving active trigger point injections required less acetaminophen (0.2 vs 2.7 tablets/d; P<.0001). At Day 8, no patients in the active trigger point injection group requested additional injections, whereas all the patients in the control group requested an injection (P<.0001).
At Day 8, patients also had significantly decreased intensity of fibromyalgia pain, fewer tender points, and higher tender point pressure thresholds; none of these differences were statistically significant in the placebo injection group (data presented graphically). The improvements persisted at 30 days of follow-up (data presented graphically).
Small study shows improvement with injections after 2 weeks
An uncontrolled prospective before-after study in 1996 evaluated the effectiveness of 0.5% lidocaine trigger point injections in 9 patients with myofascial trigger points plus fibromyalgia compared with 9 patients with myofascial trigger points alone.2
Immediately after injection, patients with fibromyalgia had a nonsignificant worsening in pain intensity (pain scale 8.1 to 8.4/10; P>.1), but there was a significant improvement at 2 weeks (5.9; P<.01). The pressure threshold also decreased initially (1.7 to 1.4 kg/cm2; P>.1), but significantly increased at 2 weeks (2.4 kg/cm2; P<.01). In comparison, patients without fibromyalgia showed immediate improvement in all domains, which persisted at 2 weeks (P<.01).
What the guidelines say
Recent Canadian Fibromyalgia Guidelines discuss trigger point injections in the section on “off-label” medications, stating that they “may have some place in treatment of fibromyalgia.”3
1. Affaitati G, Costantini R, Fabrizio A, et al. Effects of treatment of peripheral pain generators in fibromyalgia patients. Eur J Pain. 2011;15:61-69.
2. Hong CZ, Hsueh TC. Difference in pain relief after trigger point injections in myofascial pain patients with and without fibromyalgia. Arch Phys Med Rehabil. 1996;77:1161-1166.
3. Fitzcharles MA, Ste-Marie PA, Goldenberg DL, et al. 2012. Canadian Guidelines for the diagnosis and management of fibromyalgia syndrome: executive summary. Pain Res Manag. 2013;18:119-126.
Possibly. Trigger point injections appear effective in reducing pain and increasing pressure thresholds in patients with fibromyalgia and myofascial trigger points (strength of recommendation [SOR]: B, small randomized controlled trials [RCTs]).
Consensus guidelines suggest that trigger point injections may have a role in the treatment of fibromyalgia (SOR: C, expert opinion).
Active injections produce sustained improvement
A 2011 double-blind RCT randomized 68 female patients with both fibromyalgia and myofascial trigger points to either active trigger point injections with 1 mL 0.5% bupivacaine or placebo-like needle penetration with no medication to an area near the trigger point.1 Patients were evaluated for both local and generalized fibromyalgia symptoms at 4 and 8 days (trial period) and after 30 days (follow-up). Injections occurred on Days 1 and 4, with an option of additional injections on Days 8 and 11.
Compared to baseline (7 days before the injection), patients receiving active trigger point injections had decreased myofascial pain episodes 7 days after the injection (5.6 vs 0.97 episodes; P<.001), decreased pain intensity (62 vs 19/100 mm Visual Analog Scale score; P<.001), and increased pressure threshold at the trigger point (1.5 vs 2.9 kg/cm2; P<.0001), whereas the control group showed no differences.
During Days 1 to 8, patients receiving active trigger point injections required less acetaminophen (0.2 vs 2.7 tablets/d; P<.0001). At Day 8, no patients in the active trigger point injection group requested additional injections, whereas all the patients in the control group requested an injection (P<.0001).
At Day 8, patients also had significantly decreased intensity of fibromyalgia pain, fewer tender points, and higher tender point pressure thresholds; none of these differences were statistically significant in the placebo injection group (data presented graphically). The improvements persisted at 30 days of follow-up (data presented graphically).
Small study shows improvement with injections after 2 weeks
An uncontrolled prospective before-after study in 1996 evaluated the effectiveness of 0.5% lidocaine trigger point injections in 9 patients with myofascial trigger points plus fibromyalgia compared with 9 patients with myofascial trigger points alone.2
Immediately after injection, patients with fibromyalgia had a nonsignificant worsening in pain intensity (pain scale 8.1 to 8.4/10; P>.1), but there was a significant improvement at 2 weeks (5.9; P<.01). The pressure threshold also decreased initially (1.7 to 1.4 kg/cm2; P>.1), but significantly increased at 2 weeks (2.4 kg/cm2; P<.01). In comparison, patients without fibromyalgia showed immediate improvement in all domains, which persisted at 2 weeks (P<.01).
What the guidelines say
Recent Canadian Fibromyalgia Guidelines discuss trigger point injections in the section on “off-label” medications, stating that they “may have some place in treatment of fibromyalgia.”3
Possibly. Trigger point injections appear effective in reducing pain and increasing pressure thresholds in patients with fibromyalgia and myofascial trigger points (strength of recommendation [SOR]: B, small randomized controlled trials [RCTs]).
Consensus guidelines suggest that trigger point injections may have a role in the treatment of fibromyalgia (SOR: C, expert opinion).
Active injections produce sustained improvement
A 2011 double-blind RCT randomized 68 female patients with both fibromyalgia and myofascial trigger points to either active trigger point injections with 1 mL 0.5% bupivacaine or placebo-like needle penetration with no medication to an area near the trigger point.1 Patients were evaluated for both local and generalized fibromyalgia symptoms at 4 and 8 days (trial period) and after 30 days (follow-up). Injections occurred on Days 1 and 4, with an option of additional injections on Days 8 and 11.
Compared to baseline (7 days before the injection), patients receiving active trigger point injections had decreased myofascial pain episodes 7 days after the injection (5.6 vs 0.97 episodes; P<.001), decreased pain intensity (62 vs 19/100 mm Visual Analog Scale score; P<.001), and increased pressure threshold at the trigger point (1.5 vs 2.9 kg/cm2; P<.0001), whereas the control group showed no differences.
During Days 1 to 8, patients receiving active trigger point injections required less acetaminophen (0.2 vs 2.7 tablets/d; P<.0001). At Day 8, no patients in the active trigger point injection group requested additional injections, whereas all the patients in the control group requested an injection (P<.0001).
At Day 8, patients also had significantly decreased intensity of fibromyalgia pain, fewer tender points, and higher tender point pressure thresholds; none of these differences were statistically significant in the placebo injection group (data presented graphically). The improvements persisted at 30 days of follow-up (data presented graphically).
Small study shows improvement with injections after 2 weeks
An uncontrolled prospective before-after study in 1996 evaluated the effectiveness of 0.5% lidocaine trigger point injections in 9 patients with myofascial trigger points plus fibromyalgia compared with 9 patients with myofascial trigger points alone.2
Immediately after injection, patients with fibromyalgia had a nonsignificant worsening in pain intensity (pain scale 8.1 to 8.4/10; P>.1), but there was a significant improvement at 2 weeks (5.9; P<.01). The pressure threshold also decreased initially (1.7 to 1.4 kg/cm2; P>.1), but significantly increased at 2 weeks (2.4 kg/cm2; P<.01). In comparison, patients without fibromyalgia showed immediate improvement in all domains, which persisted at 2 weeks (P<.01).
What the guidelines say
Recent Canadian Fibromyalgia Guidelines discuss trigger point injections in the section on “off-label” medications, stating that they “may have some place in treatment of fibromyalgia.”3
1. Affaitati G, Costantini R, Fabrizio A, et al. Effects of treatment of peripheral pain generators in fibromyalgia patients. Eur J Pain. 2011;15:61-69.
2. Hong CZ, Hsueh TC. Difference in pain relief after trigger point injections in myofascial pain patients with and without fibromyalgia. Arch Phys Med Rehabil. 1996;77:1161-1166.
3. Fitzcharles MA, Ste-Marie PA, Goldenberg DL, et al. 2012. Canadian Guidelines for the diagnosis and management of fibromyalgia syndrome: executive summary. Pain Res Manag. 2013;18:119-126.
1. Affaitati G, Costantini R, Fabrizio A, et al. Effects of treatment of peripheral pain generators in fibromyalgia patients. Eur J Pain. 2011;15:61-69.
2. Hong CZ, Hsueh TC. Difference in pain relief after trigger point injections in myofascial pain patients with and without fibromyalgia. Arch Phys Med Rehabil. 1996;77:1161-1166.
3. Fitzcharles MA, Ste-Marie PA, Goldenberg DL, et al. 2012. Canadian Guidelines for the diagnosis and management of fibromyalgia syndrome: executive summary. Pain Res Manag. 2013;18:119-126.
Evidence-based answers from the Family Physicians Inquiries Network