RESUMO
The term "late metabolic acidosis" is generally used to define a population of apparently healthy LBW infants who fail to grow and have a base deficit in excess of 5 mEq/l (CO2TOT less than 21 mM). A relationship between hypobasemia and the lack of appropriate growth was postulated. This conclusion was reached, however, in the absence of adequate information regarding the distribution of acid-base variables in healthy LBW infants. The results of this study demonstrate that the CO2TOT of LBW infants (n = 114) rises between birth and three weeks of life from a mean of 18.6 to 20.3 mM. The frequency distribution of CO2TOT values did not show any significant deviations from normality, and 2 SD included values as low as 14.5 mM. No difference in the rate of growth was detected between "hypobasemic" infants given a solution of bicarbonate calculated to bring their blood CO2TOT to greater than 21 mM and those given similar amounts of isotonic saline solution. The ability of the LBW infants to excrete an ammonium chloride load was not related to their acid-base status and was comparable to that of term infants. It is apparent that the definition of late metabolic acidosis needs to be reconsidered.
Assuntos
Acidose/epidemiologia , Doenças do Prematuro/epidemiologia , Peso Corporal , Dióxido de Carbono/sangue , Estudos de Avaliação como Assunto , Crescimento , Humanos , Recém-Nascido de Baixo Peso , Recém-NascidoRESUMO
Among 195 nephrotic children, ten developed resistance to prednisone therapy after responding to this drug on one or more occasions (late nonresponders). All were found to have "minimal lesions" on renal biopsy. Nine of these patients went into remission: one responded to further prednisone therapy, one went into remission while receiving azathioprine, and the remaining seven children responded to cyclophosphamide. Five of these seven patients subsequently relapsed; three of them have continued to respond to prednisone. The other two eventually became steroid resistant a second time, but in both instances a second course of cyclophosphamide again induced a remission. These nine patients have been followed for periods ranging from 6 months to 9.5 years (median = 53 months); all are doing well and have normal renal function. The tenth patient died from sepsis four months after the onset of steroid resistance.