Brenda Vincenzi1, Shannon Stock2, Christina P C Borba3, Sarah M Cleary4, Claire E Oppenheim5, Liana J Petruzzi6, Xiaoduo Fan7, Paul M Copeland8, Oliver Freudenreich9, Corinne Cather10, David C Henderson11. 1. Schizophrenia Clinical and Research Program, Massachusetts General Hospital, 25 Staniford Street, Boston, MA 02114, United States. Electronic address: bvincenzi@partners.org. 2. Department of Mathematics and Computer Science, College of the Holy Cross, Worcester, MA, United States. Electronic address: sstock@holycross.edu. 3. Schizophrenia Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, 25 Staniford Street, Boston, MA 02114, United States. Electronic address: cborba@partners.org. 4. Schizophrenia Clinical and Research Program, Massachusetts General Hospital, 25 Staniford Street, Boston, MA 02114, United States. Electronic address: sarah.m.cleary@gmail.com. 5. Schizophrenia Clinical and Research Program, Massachusetts General Hospital, 25 Staniford Street, Boston, MA 02114, United States. Electronic address: coppenheim@partners.org. 6. Schizophrenia Clinical and Research Program, Massachusetts General Hospital, 25 Staniford Street, Boston, MA 02114, United States. Electronic address: lpetruzzi@partners.org. 7. University of Massachusetts Medical School, UMass Memorial Medical Center, Worcester, MA, United States. Electronic address: xiaoduo.fan@umassmed.edu. 8. Harvard Medical School, Department of Medicine, Massachusetts General Hospital, Boston, MA, United States. Electronic address: pccopeland@partners.org. 9. Schizophrenia Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, 25 Staniford Street, Boston, MA 02114, United States. Electronic address: Freudenreich.Oliver@partners.org. 10. Schizophrenia Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, 25 Staniford Street, Boston, MA 02114, United States. Electronic address: ccather@partners.org. 11. Schizophrenia Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, 25 Staniford Street, Boston, MA 02114, United States. Electronic address: dchenderson@partners.org.
Abstract
OBJECTIVE: The aim of this study was to investigate the role of pravastatin, as an adjunctive therapy, on inflammatory markers, lipid and glucose metabolism, psychopathology, and cognition in subjects with schizophrenia and schizoaffective disorder. METHODS:Schizophrenia or schizoaffective subjects (N=60) were randomized to receive either a 12-week supply of pravastatin 40 mg/day or placebo treatment. Anthropometric measures, lipids and glucose metabolism, inflammatory markers, psychopathology and cognitive performance were assessed at baseline, 6 weeks and 12 weeks. RESULTS:Pravastatin use was associated with a significant decrease in total cholesterol, low density lipoprotein (LDL) cholesterol and LDL particle number levels, but was not associated with any significant changes in cognition or psychopathology in the participants, except a significant decrease in the Positive and Negative Syndrome Scale (PANSS) positive symptom score from baseline to week 6. However, this decrease failed to remain significant at 12 weeks. Interestingly, triglycerides, LDL-cholesterol, total cholesterol, LDL particle number, small LDL particle number, large very low density lipoprotein (VLDL) particle number and C-reactive protein (CRP) followed a similar pattern at 6 and 12 weeks as psychopathology. CONCLUSIONS: These results suggest that a randomized trial with a larger sample size and a higher dosage of pravastatin would be helpful in further evaluating the anti-inflammatory properties of pravastatin, its association with improvements in cognitive symptoms, and its potential to reduce positive and negative symptoms associated with schizophrenia or schizoaffective disorders.
RCT Entities:
OBJECTIVE: The aim of this study was to investigate the role of pravastatin, as an adjunctive therapy, on inflammatory markers, lipid and glucose metabolism, psychopathology, and cognition in subjects with schizophrenia and schizoaffective disorder. METHODS:Schizophrenia or schizoaffective subjects (N=60) were randomized to receive either a 12-week supply of pravastatin 40 mg/day or placebo treatment. Anthropometric measures, lipids and glucose metabolism, inflammatory markers, psychopathology and cognitive performance were assessed at baseline, 6 weeks and 12 weeks. RESULTS:Pravastatin use was associated with a significant decrease in total cholesterol, low density lipoprotein (LDL) cholesterol and LDL particle number levels, but was not associated with any significant changes in cognition or psychopathology in the participants, except a significant decrease in the Positive and Negative Syndrome Scale (PANSS) positive symptom score from baseline to week 6. However, this decrease failed to remain significant at 12 weeks. Interestingly, triglycerides, LDL-cholesterol, total cholesterol, LDL particle number, small LDL particle number, large very low density lipoprotein (VLDL) particle number and C-reactive protein (CRP) followed a similar pattern at 6 and 12 weeks as psychopathology. CONCLUSIONS: These results suggest that a randomized trial with a larger sample size and a higher dosage of pravastatin would be helpful in further evaluating the anti-inflammatory properties of pravastatin, its association with improvements in cognitive symptoms, and its potential to reduce positive and negative symptoms associated with schizophrenia or schizoaffective disorders.
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