ABSTRACT
BACKGROUND: Remote ischemic preconditioning (RIPC) is a procedure that generates a brief period of ischemia followed by reperfusion. The role of RIPC in protecting myocardial ischemia during hemodialysis is not yet established. The aim of the study was to evaluate RIPC myocardial protection as evaluated by ultrasensitive I troponin in hemodialysis outpatients. PATIENTS AND METHODS: A double-blind randomized trial with two groups: intervention submitted to RIPC and control group without RIPC. Intervention group received RIPC in three consecutive hemodialysis sessions. Blood samples were taken before and after each session. Blood urea nitrogen for calculation of single-pool Kt/v and ultrasensitive I troponin were measured to evaluate dialysis adequacy and myocardial injury. RESULTS: A total of 47 patients were randomized. About 60.8% were men and 54% were diabetic. The mean single-pool Kt/v was 1.51 in the intervention group and 1.49 in control. The ultrasensitive troponin I measured no significant change from the time of collection: before or after dialysis. CONCLUSION: The RIPC applied in three consecutive sessions did not demonstrate superiority to control, therefore another study tested RIPC in 12 consecutive sessions with a positive result in myocardial protection. In our study, more than half of the patients were diabetic. Diabetic patients have a trend to show a lower response to RIPC because of the greater presence of collateral coronary circulation. In summary, in this model there was no interference of RIPC in ultrasensitive troponin I values, but troponin had a high negative predictive value for myocardial infarction in all tested models.
ABSTRACT
BACKGROUND: Fatigue is common in cancer patients receiving adjuvant chemotherapy. To further understand the mechanism of fatigue and search for potential biomarkers, we conducted this prospective study. Methods We enrolled breast cancer (BC) patients before their first adjuvant Adriamycin-based chemotherapy cycle. Patients responded to the brief fatigue inventory (BFI) and Chalder fatigue questionnaires and had their blood drawn for both plasma evaluation and evaluation of the peripheral mononuclear cell fraction (PMNCF) mRNA expression of various biomarkers. We evaluated FSH, LH, estradiol, DHEA, DHEAS, IL6, IL2, ILIRA, IL1ß, CRP, Cortisol in the plasma and IL2, IL10, IL6, TGF-ß, KLRC1, TNF, BTP, SNCA, SOD1, BLNK, PTGS2 and INF γ expression in the PMNCF. RESULTS: 11 patients did not exhibit an increase in their BFI scores and served as controls, whereas 32 patients exhibited an increase in their BFI scores compared with the baseline scores. From the biomarkers we evaluated in the PMNCF, the only one significantly associated with fatigue was TGF-ß (p = 0.0343), while there was a trend towards significance with KLRC1 (p = 0.0627). We observed no evidence of significant associations of any plasma biomarkers with the development of fatigue. However when we analyzed patients with more severe fatigue, plasma IL1-RA levels correlated directly with higher fatigue scores (p = 0.0136). CONCLUSIONS: We conclude that fatigue induced by chemotherapy in BC patients is associated with changes in IL1-ra plasma levels and in TGF-ß lymphocyte expression. Its mechanism may be different than that observed in long-term BC survivors or that induced by radiation therapy. TRIAL REGISTRATION: NCT02041364 [ClinicalTrials.gov].
