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Functional defects in growth hormone (GH) secretion and its efficacy as a complementary treatment have been suggested for fibromyalgia. This study investigated the efficacy and safety of low-dose GH as an add-on therapy in patients with both severe FM and low insulin-like growth factor 1 levels. A total of 120 patients were enrolled in a multicenter, placebo-controlled study for 18 months. They were randomly assigned to receive either 0.006 mg/kg/day of GH subcutaneously (group A, n=60) or placebo (group B, n=60) for 6 months (blind phase). The placebo arm was switched to GH treatment from month 6 to month 12 (open phase), and a follow-up period after GH discontinuation was performed until month 18. Standard treatment for fibromyalgia (selective serotonin re-uptake inhibitors, opioids, and amitriptyline) was maintained throughout the study. Number and intensity of tender points, Fibromyalgia Impact Questionnaire (FIQ) with its subscales, and EuroQol 5 dimensions test (EQ5D) with visual analogue scale (VAS) were assessed at different time points. At the end of the study, 53% of group A patients obtained fewer than 11 positive tender points, vs 33% of group B patients (P<.05). 39.1% vs 22.4% reached more than 50% improvement in VAS (P<.05). Group A patients showed significantly improved FIQ scores (P=.01) compared with group B. Although GH discontinuation worsened all scores in both groups during follow-up, impairment in pain perception was less pronounced in the GH-treated group (P=.05). In this largest and longest placebo-controlled trial performed in FM (NCT00933686), addition of GH to the standard treatment is effective in reducing pain, showing sustained action over time.

FM patients show a high prevalence of GH axis dysfunction. A significant number of patients show biochemical patterns of GH deficiency as well as some degree of GH resistance and might be potential candidates for substitution treatment.

Left ventricular contractility was assessed before and during the peak effect of ketamine in eight canine right heart bypass preparations. Myocardial contractility was defined in terms of maximum left ventricular dp/dt, the ejection fraction, and left ventricular end-diastolic and left atrial pressures at constant heart rate and cardiac inflow. Ketamine produced significant decreases in contractility and there were some indications of a dose-response pattern. The action of ketamine was dependent partly on changes in arterial pressure, as the drug caused a mild but sustained vasodilatation which was not dose-dependent. These data offer further evidence of a small and transient negative inotropic effect of ketamine.

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