Plasma amino acid concentrations in patients with acute myelogenous leukemia

Citation
M. Muscaritoli et al., Plasma amino acid concentrations in patients with acute myelogenous leukemia, NUTRITION, 15(3), 1999, pp. 195-199
Citations number
44
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
NUTRITION
ISSN journal
08999007 → ACNP
Volume
15
Issue
3
Year of publication
1999
Pages
195 - 199
Database
ISI
SICI code
0899-9007(199903)15:3<195:PAACIP>2.0.ZU;2-U
Abstract
Changes in plasma-free amino acid (PFAA) concentrations in the presence of solid tumors have been widely described. Conversely, the PFAA profile in pa tients with acute leukemias is less well defined. The aim of the present st udy was to clarify whether the PFAA profile is altered in patients with acu te myeloid leukemia (AML), whether the profile differs from the PFAA profil e of solid tumors, and whether it may predict outcome of AML. Fasting PFAA were measured in 40 untreated, normally nourished patients with PML (17 mal es, 23 females), ages :22-78 y, with white blood cell (WBC) counts ranging from 1.08 to 276.5 x 10(3)/cm(2), and in 24 healthy volunteers. Plasma conc entrations (mu mol/L, mean +/- SE) of glutamic acid (GLU), free tryptophan (FTRP), ornithine (ORN), and glycine (GLY) were significantly higher in AML (GLU: 90.2 +/- 6.1 versus 37 +/- 8; FTRP: 7.0 +/- 0.6 versus 4.8 +/- 0.3, P < 0.005; ORN: 108.7 +/- 5.8 versus 78 +/- 6, P < 0.001; GLY: 295.0 +/- 14 .8 versus 239 +/- 9, P < 0.01), whereas serine (SER), methionine (MET), and taurine (TAU) were significantly lower in AML than in controls (SER: 109.0 +/- 5.8 versus 130 +/- 4, P < 0.03; MET: 25.5 +/- 1.3 versus 33 +/- 3, P < 0.03; TAU: 46.5 +/- 3.5 versus 81 +/- 2, P < 0.001), and tended to be even lower in patients who had not responded to chemotherapy or had relapsed wi thin 18 mo of enrollment. Such changes were unrelated to age, sex, and WBC count. Changes in PFAA that occur in AML are only in part similar to those observed in solid tumors. The reduction of TAU appears to be a typical feat ure of AML and might be secondary to the deficiency of its precursors SER a nd MET. Further studies are under way aimed at clarifying whether PFAA migh t predict prognosis in AML, whether PFAA is normalized by remission inducti on, and if its correction may be of any benefit for patients with hematolog ic malignancies. Nutrition 1999;15:195-199. (C)Elsevier Science Inc. 1999.