[Decreased peripheral nerve conduction velocity may be associated with lower-serum level of vitamin E in patients with infantile hepatitis syndrome].

OBJECTIVE: To explore the influence of vitamin E (VitE) concentration in serum on peripheral nerve conduction in patients with infantile hepatitis syndrome (IHS).

METHODS: A retrospective study was carried out in 58 infants suffered from IHS without congenital biliary atresia and 31 of them were followed up. Thirty-two healthy infants were as control. The level of VitE in serum was detected with high performance liquid chromatography and nerve conduction was tested with surface electrodes along the nerves of limbs. The relationship between the level of VitE or total bilirubin (TB) or direct bilirubin (DB) and the nerve conduction velocity was analyzed comparatively.

RESULTS: (1) The serum level of VitE was below the lower limit of 90% the normal value (13.78 micromol/L) in 71% (41/58) of patients, and was below the lower limit of 99% the normal level (9.17 micromol/L) in 48% (28/58) of patients. (2) The level of DB was more than 25.7 micromol/L in 86% (50/58) of the patients and was more than 102.6 micromol/L in 47% (27/58) of patients. Severe conjugated hyperbilirubinemia with cholestasis was demonstrated in most patients. (3) At least one abnormal parameter in nerve conduction test was found in 86% (50/58) patients. In 144 nerves tested, 60.4% (87/144) had at least one abnormal parameter. (4) Analysis for the association between bilirubin levels and VitE concentration in serum: in groups of DB > or = 25.7 micromol/L and DB < 25.7 micromol/L, the percentage of decreased VitE concentrations was 78% (39/50) and 25% (2/8), respectively, and the difference was significant (P < 0.01). Similar association between low VitE concentration and increased level of TB in serum could not be demonstrated. (5) Analysis for the association between abnormal nerve conduction and VitE concentration in serum: in the two groups with low and normal level of VitE, the percentage of abnormal nerve conduction was 93% (38/41) and 71% (12/17), respectively (chi(c)(2) = 4.93, P < 0.05). (6) Analysis for the association between abnormal nerve conduction and bilirubin in serum: There was no significant association between abnormal nerve conduction and serum level of either DB or TB. (7) Eight patients died and 9 patients had motor development delay in 31 patients during follow up. In these 17 patients with poor outcome, 88% (15/17) had very low VitE levels (< 9.17 micromol/L), which was markedly higher than the proportion of cases (43%, 6/14) with better prognosis (chi(c)(2) = 7.235, P < 0.01).

CONCLUSIONS: (1) Low VitE serum levels were found in excess of the two thirds of patients with IHS and severely decreased levels in nearly a half of them. (2) A conjugated hyperbilirubinemia with cholestasis could be found in most patients (86%) suffered from IHS without congenital biliary atresia and about a half of them had serious cholestasis. (3) Conjugated hyperbilirubinemia with cholestasis could be the predominant cause of decreased serum VitE level in this study. (4) Abnormality of nerve conduction in patients with IHS might be related to VitE deficiency.