RESUMO
Urinary D-lactate excretion, expressed as the molar D-lactate/creatinine ratio, was measured serially in nine term and premature infants with necrotizing enterocolitis, 15 healthy term infants, and eight term and premature infants sick but without NEC. The mean (+/- SD) uDL/CR of the infants with NEC was 1.63 +/- 1.09, significantly greater than the mean uDL/CR of the healthy infants (0.16 +/- 0.04) or the sick infants without NEC (0.43 +/- 0.32). The uDL/CR of infants with NEC rose coincident with the onset of disease, reached peak values at an average of 5.8 days, and subsided to baseline levels on recovery. Seven of the nine infants with NEC reached or exceeded a peak uDL/CR of 1.47; no infant without NEC reached this ratio. We conclude that uDL/CR is increased in infants with NEC and demonstrates the increased enteric bacterial activity in this disease.
Assuntos
Enterocolite Pseudomembranosa/urina , Lactatos/urina , Creatinina/urina , Feminino , Humanos , Recém-Nascido , Masculino , EstereoisomerismoRESUMO
Methemoglobinemia is an important side effect of dapsone (4,4´-diaminodiphenyl sulfone, DDS) therapy. Previous wirkers had shown a correlation between methemoglobin formation and time of incubation of DDS in a system involving rat liver microsomes and human red cells (RBC). N-Oxidation of ring C labelled DDS by rat liver microsomes was studied both in the presence and absence of RBC. Evidence is presented that in vitro DDS is metabolized to the monohydroxylamine of DDS (DDS-NOH), and maybe to the nitroso (DDS-NO)and azoxy - (azoxy-DDS) analogues of DDS. The latter compunds could also arise from non-microsomal oxidation of DDS-NOH. Specific isotope dilution procedures were employed to measure the N-oxidation of DDS. These involved conversion to azoxy-DDS or the formation of the pentocyanamine ferroate complex of DDS-NOH (and/or DDS-NO). The extent of total N-oxidation of DDS was always less when experiments were carried out in the presence of RBC than in their absence. This suggests that DDS-NOH is enzymatically reduced by RBC. Like other microsomal oxidations, N-Oxidation of DDS was inhibited by SKF-525A. Our studies indicate taht DDS-NOH (and/or DDS-NO) is the cause of the methemoglobinemia observed in dapsone therapy.