Participants could continue concomitant medications including analgesics throughout the study, given the stipulations stated above. Such concomitant medications were closely monitored and recorded as part of the case report form. The primary outcome was leg pain intensity using the visual analog scale VAS. Participants were asked to rate their average leg pain during the last 24 hours out of 10, with 0 representing no leg pain and 10 representing the worst pain imaginable.
The key secondary outcome was the Oswestry Disability Index ODI questionnaire 4 to assess disability in which scores range from 0 to , with higher scores indicating greater disability. The clinically important difference is represented by 10 points. Details of AEs were collected throughout the course of the trial and were noted as a description including a score of 0 to 10 for frequency and severity, whereby an increasing number denotes a higher frequency or severity.
Outcomes were assessed at baseline, then at weeks 4, 8, 10, 14, and Baseline and weeks 8, 10, and 18 were considered the primary times for the primary outcome that represented the start and finish of each medication. Data collection was conducted by the study researchers from telephone, email, or online. Week 10 data collection served as the crossover secondary baseline for the purpose of analysis. Data were entered into case report forms by dedicated trained staff.
Adherence to study medication was documented through a self-reported daily medication diary and by counting the returned medicine. These assumptions included an SD of the difference between the 2 same values for the same patient of 1. No formal stopping rules were used owing to the lack of previous head-to-head data enabling the presetting of boundaries. Instead, the investigators and independent trial monitor would make a judgment based on AEs and outcomes in the primary measure.
Missing data were handled by a single imputation method whereby the last observation is carried forward and used as a surrogate for the missing value. This is the favored approach for replacing missing data as it is conservative, yields an appropriate estimate of variation in outcome, and is unlikely to bias toward the alternative hypothesis. Data were deidentified prior to interim statistical analysis and performed on an intention-to-treat basis.
Unadjusted means SDs were calculated and presented for descriptive statistics of the population. Normality of data distribution was assessed, and the appropriate t tests performed for between-groups differences including repeated measures linear models.
Statistical significance was set at a 2-sided P value of less than. The frequency and severity of AEs were reported descriptively with calculated mean SD based on unadjusted mean scores of patients. Twenty participants underwent randomization from March to March This equated to 40 drug and patient episodes. Two patients were excluded. After randomization, 2 patients were excluded from analysis. One patient did not collect study medication and was subsequently lost to follow-up.
More than half of the population 10 [ When the per-patient—recorded AEs were clustered based on body system affected into central nervous system, respiratory, gastrointestinal, and genitourinary, both GBP and PGB demonstrated predominantly central nervous system AEs eTable 1 in Supplement 3.
However, ODI severity was not significant by crossover Table 4. The predetermined criteria for stopping the trial was a significant difference in recurrence rates or incidence of AEs between groups. Simultaneously, the trial would have considered to be stopped if any superiority was observed between the medications. After consultation in March , the independent data monitor made a recommendation to the investigators that stopping the trial early was justified.
This predetermined interim analysis of this randomized clinical trial showed that while PGB and GBP were both significantly efficacious in reducing pain intensity in patients with CS, GBP was superior when compared head to head. This clinical trial was adequately powered to detect a conservative difference between medications of 0. We acknowledge the current clinically important treatment effect of 1. Compliance with the medication regimen was high based on patient diaries and pill containers returned at each visit.
Our selection criteria were based on an established definition of CS with 1 specialist neurosurgeon involved in screening and recruitment for consistency. The dose of the medications were adjusted using an increasing titration schedule with AE monitoring according to National Formulary recommendations.
The crossover method chosen for this trial provides many advantages and particularly strengthens the study findings. In clinical trials, a crossover design should be limited to a disease that is long-term and stable and for which treatments should not result in a total cure but, instead, only alleviate the condition.
This clinical trial therefore achieves a more efficient comparison of treatments than is possible with a parallel trial design. Any potential disadvantage relating to a carryover effect between medications in sequence was obviated by having set the washout period to more than 6 half-lives of either PGB or GBP effectively, 1 week. There are limitations of this study.
The low recruitment frequency reflects the difficulty associated with recruiting patients with CS who have not already been prescribed either PGB or GBP by practitioners in primary or tertiary care. Another limitation is the effects of treatment duration. Suboxone vs Methadone: Main Differences Looking for a prescription? Search now! Type your drug name.
Neuropathic pain from diabetic peripheral neuropathy Postherpetic neuralgia Adjunctive therapy for partial onset seizures Fibromyalgia. Postherpetic neuralgia Adjunctive therapy for partial onset seizures. Yes Pregabalin. Gabapentin is the generic name. Gabapentin Price. Hydrocodone Morphine Antacids containing magnesium and aluminum hydroxide Maalox.
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Lyrica vs. Medically reviewed by Neal Patel, Pharm. Ingredients of Lyrica and gabapentin. Uses of Lyrica vs. Dosage, forms, and administration. Switching between Lyrica and gabapentin. Cost of Lyrica vs. Side effects of Lyrica vs. Effectiveness of Lyrica vs. Warnings of Lyrica and gabapentin.
Based on these values, pregabalin was estimated to be about 2. One study analyzed data from phase 2 trials of gabapentin and pregabalin and created a pharmacodynamic model. Pregabalin also exhibited a steeper dose-response curve than gabapentin. For clinicians who wish to convert patients from gabapentin to pregabalin, there are a few studies that reviewed such a conversion. One cohort study reviewed the utility of switching patients with neuropathic pain due to peripheral neuropathy from gabapentin to pregabalin.
The authors also stratified the pregabalin group further into those who responded well or poorly to gabapentin, with gabapentin stopped after the nighttime dose and pregabalin started the following morning. The authors found that those who responded well to gabapentin and those who did not showed additional benefit with decreased pain when they were switched to pregabalin.
Patients taking pregabalin also had improved pain control compared with those who remained on gabapentin. Switching to pregabalin resulted in improved pain relief and also fewer adverse events. This was particularly true for patients who previously responded to gabapentin. Patients who experienced adverse events with gabapentin were more likely to also experience adverse events with pregabalin. These patients were also more likely to discontinue use of pregabalin than those who responded well to both gabapentin and pregabalin.
Another small trial compared the degree of pain relief with gabapentin to pregabalin in patients with postherpetic neuralgia in order to more closely determine equivalent dosing between the 2 medications. Patients were switched from gabapentin to pregabalin using one-sixth the dose of gabapentin with unchanged dosage frequency. After switching medications, patients reported similar pain relief and side effects, with the exception of an increased incidence of peripheral edema in the pregabalin group.
The authors concluded that the analgesic effect of pregabalin was about 6 times that of gabapentin. Other studies have looked at methods for converting gabapentin to pregabalin. One such trial used population pharmacokinetic models to examine 2 possible scenarios for converting gabapentin to pregabalin, using a ratio of gabapentin to pregabalin.
The first scenario involved discontinuing gabapentin and immediately starting pregabalin at the next scheduled dosing period. The other option included a gradual transition from gabapentin to pregabalin. After this time, gabapentin was discontinued and pregabalin was increased to full desired dose. The model looked at transitioning patients from gabapentin to pregabalin at various doses, including:.
Both scenarios were quick and seamless, so the authors concluded that either technique could be an effective method to switch patients between the medications. Though pregabalin and gabapentin have somewhat similar pharmacokinetic and pharmacodynamic profiles, there are clearly significant differences.
Overall, pregabalin has more predictable pharmacokinetics, and it also shows a stronger binding affinity to its target receptor, increased potency, and a steeper dose-response curve in neuropathic pain that does not plateau over recommended dosing levels.
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