Objectives: Our objective was to evaluate the efficacy of probiotics and prebiotics in patients with Parkinson disease (PD) and constipation. Methods: We conducted a tertiary setting, randomized, double-blind, placebo-controlled trial in patients with PD with Rome III–confirmed constipation based on 2-week stool diary data at baseline. Patients (n = 120) were randomly assigned (2:1) to either a fermented milk, containing multiple probiotic strains and prebiotic fiber, or placebo, once daily for 4 weeks. The primary efficacy endpoint was the increase in the number of complete bowel movements (CBMs) per week. The key secondary endpoints were 3 or more CBMs and an increase by one or more CBMs per week during weeks 3 and 4. Results: For the primary endpoint, the consumption of a fermented milk containing probiotics and prebiotics resulted in a higher increase in the number of CBMs (mean 1.2, 95% confidence interval [CI] 0.8–1.6) than placebo (0.1, 95% CI −0.4% to 0.6%) (mean difference 1.1, 95% CI 0.4–1.8; p = 0.002). For the key secondary endpoints, a higher number of patients in the probiotics–prebiotics group vs the placebo group reported 3 or more CBMs (p = 0.030; 58.8% vs 37.5%; odds ratio = 2.4, 95% CI 1.1–5.2) and an increase by one or more CBMs (p = 0.004; 53.8% vs 25.0%; odds ratio = 3.5, 95% CI 1.8–8.1) during weeks 3 and 4. Conclusions: The consumption of a fermented milk containing multiple probiotic strains and prebiotic fiber was superior to placebo in improving constipation in patients with PD. ClinicalTrials.gov identifier: NCT02459717. Classification of evidence: This study provides Class I evidence that for patients with PD who have constipation, fermented milk containing probiotics and prebiotics increases the frequency of CBMs.

The most efficient therapeutic approach for immunoglobulin light chain amyloidosis (AL) is autologous stem cell transplantation (ASCT); however, the toxicity of ASCT limits its feasibility to a minority of patients. Patients ineligible for ASCT are usually treated with standard oral melphalan and prednisone, but the response rate to this regimen is unsatisfactory, and time to response is long. High-dose dexamethasone provides a rapid response time in patients with AL. We evaluated the combination of oral melphalan and high-dose dexamethasone (M-Dex) in 46 patients with AL ineligible for ASCT. Thirty-one (67%) achieved a hematologic response and 15 (33%) a complete remission. In 22 (48%) of the responsive patients functional improvement of the organs involved was observed. Five patients (11%) experienced severe adverse events, 3 required hospitalization, and no treatment-related deaths were observed. M-Dex represents a feasible and effective therapeutic option for patients with advanced AL who are ineligible for ASCT.

OBJECTIVE: Diabetes has been associated with chronic neurodegeneration. We performed a systematic review and meta-analysis to assess the relationship between pre-existing diabetes and Parkinson’s disease (PD). RESEARCH DESIGN AND METHODS: Original articles in English published up to 10 May 2011 were searched for in electronic databases (PubMed, Embase, and Scopus) and by reviewing references of eligible articles. Prospective cohort and case-control studies providing risk and precision estimates relating to pre-existing diabetes and PD were considered eligible. RESULTS: Nine studies/1,947 citations (cohort, N = 4; case-control, N = 5) fulfilled inclusion criteria for meta-analysis. In prospective studies, the onset of diabetes before onset of PD was found to be a risk factor for future PD (relative risk [RR] = 1.37 [95%CI 1.21–1.55]; P < 0.0001). This association was confirmed by secondary analyses based on estimates derived after the exclusion of participants who had vascular disease at baseline and/or who developed vascular disease during follow-up (RR = 1.34 [1.14–1.58]; P < 0.001) and by sensitivity analyses addressing the association with diabetes at baseline or during follow-up. However, the association found for case-control studies was not significant (odds ratio [OR] 0.75 [95%CI 0.50–1.11]; P = 0.835). Sensitivity analysis based on estimates adjusted for BMI confirmed the lack of a relationship between PD and diabetes (OR 0.56 [0.28–1.15]; P = 0.089). CONCLUSIONS: Although data from cohort studies suggest that diabetes is a risk factor for PD, there is no conclusive evidence on this association. Further prospective studies focused on putative pathogenic pathways and taking a broad range of confounders into account is required to clarify this relationship.