Palmitoyl ethanol amide (PEA) is an endogenous substance that plays a role in neuropathic pain. In this article, we evaluated both the safety and the efficacy of ultramicronized PEA (um-PEA) in the treatment of low back pain related to nonsurgical lumbar radiculopathy. In this prospective single-blind study, patients with low back pain related to nonsurgical lumbar radiculopathy received the fixed combination acetaminophen/codeine (500 mg + 30 mg/d) for 7 days, and then it was stopped and changed to um-PEA (1200 mg/d) for 30 days. Patients without an improvement in pain or disability started a second cycle of treatment with um-PEA (600 mg/d in tablets) for 30 days and then acetaminophen/codeine for 30 days. A total of 155 patients were included in the analysis. After the first cycle of treatment we recorded an improvement of pain in all patients with mild pain (visual analog scale score from 3-4 to 1) and in 75% of the patients with moderate pain (visual analog scale score from 5-6 to 2). After the second cycle, we recorded an improvement of pain and disability in all patients with moderate pain (P < .01), but in 26% of patients with severe pain we did not record any improvement in disability (P > .05). In conclusion we evaluated the role of um-PEA in patients with lumbar radiculopathy with a long-term follow-up (24 months) and put in evidence the effectiveness and the safety of this formulation in patients with mild and moderate pain.
It has been suggested that QT dispersion (maximal minus minimal QT interval calculated on a standard 12-lead electrocardiogram) could reflect regional variations of ventricular repolarization and could provide a substrate for reentry ventricular arrhythmias. The present study evaluates QT dispersion in patients with acute myocardial infarction, assessing its relation with early severe ventricular arrhythmias and some clinical features. Three hundred three patients with acute myocardial infarction and a control group of 297 healthy subjects were studied. QT and QTc dispersion were determined on the electrocardiogram taken after 12 hours and on days 3 and 10 after symptoms onset and on the electrocardiogram taken in the control group. The average values of QT and QTc dispersions (ms) were as follows: 70.5 +/- 42.5-87 +/- 45.6 (12th hour), 66.7 +/- 37.6-76.8 +/- 43.6 (day 3), 68.8 +/- 42.7-76.8 +/- 42.8 (day 10), versus 43 +/- 13.2-53.9 +/- 16.2 (control group). There were statistically significant differences between QT and QTc dispersion recorded in normal subjects and in each of the three electrocardiograms taken in patients with infarction. A greater QT dispersion was recorded in patients with anterior infarction (78.9 +/- 38.5 vs 64.9 +/- 42.8 in inferior/lateral infarction). In the first 3 days QT dispersion was not different in patients treated and untreated with thrombolysis, whereas on day 10 it was greater in untreated patients (74.9 +/- 45.3 vs 60.5 +/- 37.2). Creatine kinase peak level did not influence QT dispersion. In the first 72 hours of infarction, 37 patients developed ventricular fibrillation or sustained ventricular tachycardia. Higher early values of QT and QTc dispersion were found in patients who developed severe ventricular arrhythmias (107.8 +/- 62 and 124.8 +/- 67.5 ms) than in patients without serious arrhythmias (62.9 +/- 32.2 and 80.1 +/- 37.9 ms). These data suggest that: (1) QT dispersion increased during acute myocardial infarction. (2) The values were higher in the early hours and fell late after infarction with thrombolysis. (3) Greater QT dispersion is associated with severe ventricular arrhythmias.
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