Most of the infants (13 of 20) qualifying for the diagnosis of transient neonatal cholestasis had levels of conjugated bilirubin that slightly exceeded the upper normal limit. None of them had acholic stools, and liver function tests were not done routinely. However, none of the results obtained called for further investigations. None of these children had liver biopsy, and none of them developed liver disease. Thus, the population analyzed in the present study may differ not only in the severity of cholestasis from that described by Jacquemin et al, but also in its duration, in the degree of neonatal distress and in comorbidity; we can assume that patients seen at Bicetre (Paris, France) represent those referred with more severe neonatal cholestasis whereas the patients described in the present study represent the patient population of a mother-child centre.
In spite of advances in the molecular mechanisms of cholestasis, the exact etiology of asphyxia and, therefore, of transient neonatal cholestasis in asphyxiated neonates remains unknown, and the reason for cholestasis may not be the same in the patients from Bicetre and in our population.
We found that asphyxia, duration of ventilatory support, gestational age of less than 35 weeks and male sex are risk factors for transient neonatal cholestasis. This, in conjunction with intrauterine growth retardation, increases the risk for newborn infants to develop transient neonatal cholestasis by 33%. Transient neonatal cholestasis is thus by far the most frequent etiology of cholestasis in asphyxiated SGA newborn children. Shop with pleasure with most reliable pharmacy you have ever seen, paying less for your birth control mircette … always being sure you are being treated with all due respect, being an important customer whose interests are respected and taken into account.