31P NMR spectra were obtained from sera of 22 healthy volunteers and 20 patients with multiple myeloma at the time of diagnosis and repeated up to five times during therapy. All spectra consisted of a Pi peak (used as a reference peak) and two peaks from phospholipids (PL): one peak due to phosphatidylethanolamine and sphingomyelin (PE + SM) and a second peak due to phosphatidylcholine (PC). Prior to therapy, peak intensities of the phospholipids were low relative to Pi. During therapy leading to remission, the resonance from PL progressively increased to approximate the spectral pattern seen in normal sera. By contrast, in non-responders an opposite trend was noted: the intensities of the phospholipid peaks became progressively reduced or remained unchanged. Long-term follow-up studies showed a good correlation between this 31P MRS evaluation of sera and the response of the disease to the therapy. In addition to the correlation with tumor response, our studies also show significant correlations between area, intensities of peaks of PE + SM, PC, and the concentrations of high-density lipoprotein (HDL) (correlation coefficients 0.46, 0.43, 0.59, respectively; p < 0.001). We found that the concentration of HDL in serum of patients with multiple myeloma was significantly reduced. In individuals responding to therapy HDL levels increased to the point where there were no statistically significant differences between them and healthy volunteers. In patients not responding to therapy, HDL concentration did not increase.(ABSTRACT TRUNCATED AT 250 WORDS)
31P spectra were obtained from 22 healthy volunteers and 35 patients with malignant lymphomas. Sera from patients were collected at the time of diagnosis and at several time-points during therapy. Long-term follow-up studies showed a good correlation between the 31P NMR spectra of sera and the clinically evident response of the disease to the chemotherapy. During therapy leading to remission resonance from phospholipids increased progressively resulting in spectra similar to those seen in normal sera. By contrast, in patients who did not respond to therapy the intensities of the phospholipid peaks remained relatively low or became progressively reduced as the disease progressed. To understand the source of the spectral differences, we also examined the concentrations of high-density lipoprotein, low-density lipoprotein, cholesterol, and triglycerides. In individuals responding to the treatment, both high-density lipoprotein and cholesterol increased to the point where they were statistically equivalent to those from healthy volunteers.
Abstract:The aim of this study was to evaluate the phospholipid concentration in acute leukemia (AL) blast cells from peripheral blood (PBMC) and bone marrow (BMMC). In vitro 31 P Nuclear Magnetic Resonance Spectroscopy ( 31 P MRS) was used. The integral intensities of the resonant peaks and the phospholipid concentrations in PBMC and BMMC were analyzed. Differences in the phospholipid concentrations in cells from myeloblastic or lymphoblastic lines were also evaluated. This investigation was carried out on phospholipid extracts from PBMC and BMMC from 15 healthy volunteers and 77 patients with AL (samples taken at the moment of diagnosis). A significant decrease in sphingomyelin (SM) and phosphtidylserine (PS) was observed in the PBMC of patients with AL relative to the results for the healthy volunteers. For ALL, we found a significant decrease in the concentration of phosphatidylcholine plasmalogen (CPLAS), SM, PI+PE (phosphatidylinositol + phosphatidylethanolamine) and PS in comparison with the results for healthy volunteers and patients with AML. Experiments with BMMC cells revealed a significant decrease in the concentration of CPLAS, SM, PI+PE, and PS in ALL relative to AML. Additionally, a significant decrease in phosphatidylcholine (PC) concentration was observed in ALL compared to AML. If the phospholipid extracts were taken simultaneously from the same patient, there were no significant differences in the integral intensities and phospholipid concentrations between PBMC and BMMC.
31P-nuclear magnetic resonance (NMR) spectra were obtained in vitro from sera of 40 healthy volunteers and 30 patients with acute leukemia (AL) at the time of diagnosis and repeated up to 2-13 times during therapy. All spectra consisted of inorganic phosphate (Pi) peak (used as a reference peak) and two peaks from phospholipids (PL): one peak due to phosphatidylethanolamine and sphingomyelin (PE + SM) and second peak due to phosphatidylcholine (PC). Prior to initiation of therapy 31P spectra of sera of patients with acute leukemia differed from spectra of sera of normal individuals. Peak intensities of the PL were low in relation to Pi. During therapy leading to remission, resonance from PL progressively increased approximately to the spectral pattern in normal sera. Contrary to that, in non-responders the intensities of the phospholipids peaks remained unchanged. Long-term follow-up 31P-MRS studies showed not only a good correlation between this 31P-MRS evolution of sera and the response to the therapy but also showed changes in phospholipids' levels in the following days during and after therapy. Moreover, correlations were found between high-density lipoprotein (HDL), cholesterol (CHOL) and low-density lipoprotein (LDL) concentrations measured by conventional techniques and peak intensities of PC and of PE + SM acquired by 31P-MRS.
Abstract:The aim of this investigation was to evaluate the changes in PAF concentrations in the plasma, PBMC and BMMC of patients with acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML). The plasma was from 23 healthy volunteers (HV) and 44 patients with AL (16 ALL, 28 AML). The PBMC were from 15 HV and 55 patients with AL (18 ALL, 37 AML), and the BMMC from 40 patients with AL (11 ALL, 29 AML). Methanol-chloroform phospholipid extraction from 60 x 10 6 cells (PBMC or BMMC) was performed according to a modified version of Folch's method. 31 P MRS data was obtained on an AMX 300 Bruker spectrometer (7.05 T). The PAF concentration in the plasma of the patients with ALL or AML was lower than that for the healthy volunteers. The PAF concentration in the plasma of the patients with ALL did not differ significantly from that of the patients with AML. In the case of both the PBMC and BMMC, the PAF concentration was significantly diminished in patients with ALL relative to the concentration for those with AML and for the healthy volunteers. No differences were observed in the PAF concentrations for the AML patients and the healthy volunteers.
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