IMPACT OF PREGABALIN ON SIGNS AND SYMPTOMS OF GASTROPARESIS
AACE ePoster Library. Umpierrez G. 05/13/15; 97797; 271
Prof. Dr. Guillermo Umpierrez
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Abstract
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Objective: Evaluate our anecdotal experience of dramatic improvement in signs and symptoms of intractable gastroparesis following treatment with pregabalin in patients with long-standing poorly controlled diabetes.
Methods: We conducted a two-center randomized, double-blind, placebo controlled cross-over study to assess the impact of pregabalin on patients with diabetes and documented (by gastric emptying study or GES), symptomatic gastroparesis. Enrolled subjects were started on pregabalin or placebo and doses titrated up to either symptom resolution or a maximum of 300 mg daily over a period of 8 weeks. Following a 1-week washout subjects underwent treatment cross-over and an additional 8 weeks of treatment. Gastroparesis Cardinal Symptom Index (GCSI) score and GES were measured at baseline and at the end of each treatment period. We consented 24 subjects with symptoms suspicious for gastroparesis as per GCSI; 12 subjects had a normal GES.
Results: Twenty patients with data (70% women, 25% type 1 diabetes, 80% on insulin) had the following means (±SD): age 49±10 years, weight 84.3±21.0 kg, BMI 31.6±6.4 kg/m2, A1C 8.3±1.6%. Baseline GCSI (27.7±10.2) improved in both treatment groups with mean change in the pregabalin group (n=4) of -10.5 (95% CI: -18.56, -2.44) and placebo (n=6) of -11.33 (95% CI: -21.44, -1.23). Gastric emptying was evaluated as % of retained Tc-99; mean baseline retention at 1 and 4 hours were 82.7±12.9% and 20.2±20.1%, respectively. The mean change in % retained at 1 and 4 hours was -13.7±15.7% (n=5) and -14.3±28.5% (n=3), respectively, in the pregabalin group (n=5), and -10.7±20.6% and -4.3±28.6%, respectively, in the placebo group (n=4), at the end of the treatment period. Pearson’s correlation coefficients were used to explore the relationship between baseline GCSI and GES (n=20); no significant relationship was found between GCSI and GES (All p>0.05).
Discussion: Despite compelling anecdotal observation, the use of pregabalin in patients with documented symptomatic gastroparesis did not appear to provide additional benefits over placebo. Many of the subjects with suspicious symptomatology on GCSI actually had normal GES.
Conclusion: There was poor correlation between GES results and symptomatology as per GCSI, calling into question the reliability of either assessment in the diagnosis, or management, of gastroparesis in clinical practice. While at this time there is no strong evidence for a beneficial effect of pregabalin on gastroparetic symptomatology, this pilot study might inform additional investigations on a larger sample of affected subjects, or encourage further studies on appropriate diagnostic tools for this condition.
Methods: We conducted a two-center randomized, double-blind, placebo controlled cross-over study to assess the impact of pregabalin on patients with diabetes and documented (by gastric emptying study or GES), symptomatic gastroparesis. Enrolled subjects were started on pregabalin or placebo and doses titrated up to either symptom resolution or a maximum of 300 mg daily over a period of 8 weeks. Following a 1-week washout subjects underwent treatment cross-over and an additional 8 weeks of treatment. Gastroparesis Cardinal Symptom Index (GCSI) score and GES were measured at baseline and at the end of each treatment period. We consented 24 subjects with symptoms suspicious for gastroparesis as per GCSI; 12 subjects had a normal GES.
Results: Twenty patients with data (70% women, 25% type 1 diabetes, 80% on insulin) had the following means (±SD): age 49±10 years, weight 84.3±21.0 kg, BMI 31.6±6.4 kg/m2, A1C 8.3±1.6%. Baseline GCSI (27.7±10.2) improved in both treatment groups with mean change in the pregabalin group (n=4) of -10.5 (95% CI: -18.56, -2.44) and placebo (n=6) of -11.33 (95% CI: -21.44, -1.23). Gastric emptying was evaluated as % of retained Tc-99; mean baseline retention at 1 and 4 hours were 82.7±12.9% and 20.2±20.1%, respectively. The mean change in % retained at 1 and 4 hours was -13.7±15.7% (n=5) and -14.3±28.5% (n=3), respectively, in the pregabalin group (n=5), and -10.7±20.6% and -4.3±28.6%, respectively, in the placebo group (n=4), at the end of the treatment period. Pearson’s correlation coefficients were used to explore the relationship between baseline GCSI and GES (n=20); no significant relationship was found between GCSI and GES (All p>0.05).
Discussion: Despite compelling anecdotal observation, the use of pregabalin in patients with documented symptomatic gastroparesis did not appear to provide additional benefits over placebo. Many of the subjects with suspicious symptomatology on GCSI actually had normal GES.
Conclusion: There was poor correlation between GES results and symptomatology as per GCSI, calling into question the reliability of either assessment in the diagnosis, or management, of gastroparesis in clinical practice. While at this time there is no strong evidence for a beneficial effect of pregabalin on gastroparetic symptomatology, this pilot study might inform additional investigations on a larger sample of affected subjects, or encourage further studies on appropriate diagnostic tools for this condition.
Objective: Evaluate our anecdotal experience of dramatic improvement in signs and symptoms of intractable gastroparesis following treatment with pregabalin in patients with long-standing poorly controlled diabetes.
Methods: We conducted a two-center randomized, double-blind, placebo controlled cross-over study to assess the impact of pregabalin on patients with diabetes and documented (by gastric emptying study or GES), symptomatic gastroparesis. Enrolled subjects were started on pregabalin or placebo and doses titrated up to either symptom resolution or a maximum of 300 mg daily over a period of 8 weeks. Following a 1-week washout subjects underwent treatment cross-over and an additional 8 weeks of treatment. Gastroparesis Cardinal Symptom Index (GCSI) score and GES were measured at baseline and at the end of each treatment period. We consented 24 subjects with symptoms suspicious for gastroparesis as per GCSI; 12 subjects had a normal GES.
Results: Twenty patients with data (70% women, 25% type 1 diabetes, 80% on insulin) had the following means (±SD): age 49±10 years, weight 84.3±21.0 kg, BMI 31.6±6.4 kg/m2, A1C 8.3±1.6%. Baseline GCSI (27.7±10.2) improved in both treatment groups with mean change in the pregabalin group (n=4) of -10.5 (95% CI: -18.56, -2.44) and placebo (n=6) of -11.33 (95% CI: -21.44, -1.23). Gastric emptying was evaluated as % of retained Tc-99; mean baseline retention at 1 and 4 hours were 82.7±12.9% and 20.2±20.1%, respectively. The mean change in % retained at 1 and 4 hours was -13.7±15.7% (n=5) and -14.3±28.5% (n=3), respectively, in the pregabalin group (n=5), and -10.7±20.6% and -4.3±28.6%, respectively, in the placebo group (n=4), at the end of the treatment period. Pearson’s correlation coefficients were used to explore the relationship between baseline GCSI and GES (n=20); no significant relationship was found between GCSI and GES (All p>0.05).
Discussion: Despite compelling anecdotal observation, the use of pregabalin in patients with documented symptomatic gastroparesis did not appear to provide additional benefits over placebo. Many of the subjects with suspicious symptomatology on GCSI actually had normal GES.
Conclusion: There was poor correlation between GES results and symptomatology as per GCSI, calling into question the reliability of either assessment in the diagnosis, or management, of gastroparesis in clinical practice. While at this time there is no strong evidence for a beneficial effect of pregabalin on gastroparetic symptomatology, this pilot study might inform additional investigations on a larger sample of affected subjects, or encourage further studies on appropriate diagnostic tools for this condition.
Methods: We conducted a two-center randomized, double-blind, placebo controlled cross-over study to assess the impact of pregabalin on patients with diabetes and documented (by gastric emptying study or GES), symptomatic gastroparesis. Enrolled subjects were started on pregabalin or placebo and doses titrated up to either symptom resolution or a maximum of 300 mg daily over a period of 8 weeks. Following a 1-week washout subjects underwent treatment cross-over and an additional 8 weeks of treatment. Gastroparesis Cardinal Symptom Index (GCSI) score and GES were measured at baseline and at the end of each treatment period. We consented 24 subjects with symptoms suspicious for gastroparesis as per GCSI; 12 subjects had a normal GES.
Results: Twenty patients with data (70% women, 25% type 1 diabetes, 80% on insulin) had the following means (±SD): age 49±10 years, weight 84.3±21.0 kg, BMI 31.6±6.4 kg/m2, A1C 8.3±1.6%. Baseline GCSI (27.7±10.2) improved in both treatment groups with mean change in the pregabalin group (n=4) of -10.5 (95% CI: -18.56, -2.44) and placebo (n=6) of -11.33 (95% CI: -21.44, -1.23). Gastric emptying was evaluated as % of retained Tc-99; mean baseline retention at 1 and 4 hours were 82.7±12.9% and 20.2±20.1%, respectively. The mean change in % retained at 1 and 4 hours was -13.7±15.7% (n=5) and -14.3±28.5% (n=3), respectively, in the pregabalin group (n=5), and -10.7±20.6% and -4.3±28.6%, respectively, in the placebo group (n=4), at the end of the treatment period. Pearson’s correlation coefficients were used to explore the relationship between baseline GCSI and GES (n=20); no significant relationship was found between GCSI and GES (All p>0.05).
Discussion: Despite compelling anecdotal observation, the use of pregabalin in patients with documented symptomatic gastroparesis did not appear to provide additional benefits over placebo. Many of the subjects with suspicious symptomatology on GCSI actually had normal GES.
Conclusion: There was poor correlation between GES results and symptomatology as per GCSI, calling into question the reliability of either assessment in the diagnosis, or management, of gastroparesis in clinical practice. While at this time there is no strong evidence for a beneficial effect of pregabalin on gastroparetic symptomatology, this pilot study might inform additional investigations on a larger sample of affected subjects, or encourage further studies on appropriate diagnostic tools for this condition.
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