strategies for the time being. We have studied 200 VLBW infants with vancomycin or teicoplanin prophy- laxis without any case of sepsis, side effects, or an increased M IC in isolates of Gram-positive cocci.

References 1 . MBller JC. Nachtrodt G, Richter A, Tegtmeyer FK. Prophylactic

vancomycin t o prevent staphylococcal septicaemia in very-low- birth-weight infants. Lancet 1992;340:424

2. Gerhardt T. BPD-diagnosis, etiology, epidemmiology, prognosis. Piidiatr Grenzgeb 1994;33:299 300

3. Mdler JC, Nachtrodt G , Tegtmeyer F K , Richter A, Gortner L. Prophylactic low-dose vancomycin treatment in very-low-birth weight inliints. Dev Pharmacol Ther 1992; 19: 178-82

4. Kacia MA, Horgan MJ, Ochoa L, Sandler R, Lepow ML. Vrnezia RA. Prevention of Grdm-poSitiVe sepsis in neonates weighing less than 1500 grams. .I Pediatr 1994;125:253-8

5 . Spafford PS, Sinkin RA, Cox C, Reubens L, Powell KR. Preven- tion of central venous catheter-related coagulase negative staphy- lococcal sepsis in neonates. J Pediatr 1994;125:259 63

6. Tarral E. Jehl F, Tarral A, et al. Pharmacokinetics ofteicoplanin in children. J Antimicrob Chemother 1988;21 Suppl A:47 51

7. Gortner L, Bernsau U, Brand, M, et al. Drug utilization in very premature infants in neonatal intensive care units. Dev Pharmacol Ther 1991;17:167 71

Early breastfeeding linked to higher intelligence quotient scores

Sir, We are indebted to Dr Shirley Ratcliffe for bringing to our attention some misleading information in Tables 2 and 3 of our previously published article (Riva, Agostoni, Biasucci, Trojan, Luotti, Fiori, Giovannini) "Early breastfeeding is linked to higher intelligence quotient scores in dietary treated phenylketonuric child- ren" (Acta Paediatr 1996;85:56-8). The entries in the Maternal education group are transposed. The tables are reprinted here as they should be.

This confirms the weak relationship of IQ to maternal education, as reported in the text.

( ' d o Ago.s/oni. Di~purtiirent of'Pediofrics, Universiiy ofMilan, Thr San Puolo Hionicdicul Institute, 8 Via A . cli Ruclini. 1-20142 Milan, Italy

Table 2. Unadjusted overall IQ (WISC-R scale) in PKU subjects by type of early feeding, social category and maternal education.

Groups Mean (SD) Advantage

scores (95"h CI)

Feeding type ( n ) Breastfed ( 1 3) 105.8 (10.2) 14.0 (2.7, 25.3) Bottle-fed (13) 91.8(16.8) p = 0.01

Upper ( 1 5 ) 103.6 (14.2) I I .4 (-0.5. 23.3) Lower (1 1) 92.2 ( I 5.0) p = 0.06

Social category (n)

Maternal education (n ) Secondary and further (9) 106.1 (16.9) 1 1 . 1 (-1.4. 23.6) Elementary (17) 95.0 (8.95) p = 0.08

CI, confidence interval

Tuhle 3. ANCOVA analysis by type of early feeding. social category and maternal education.

Groups Adjusted advantage

F-ratio p > F (95% CI)

Feeding type ( n ) Breastfed (1 3) versus formula fed (1 3 ) 6.21 0.02 12.9 ( I .6, 24.3)

Social category (n) Upper ( I 5 ) versus lower (1 1) 1.63 0.21 7.5 (-4.4. 19.5)

Maternal education ( n ) Secondary and further (9) versus elementary (I 7) 1.10 0.30 6.4(-6.l, 18.9)

C1, confidence interval.

Derangement of pyruvate dehydrogenase activity in circulating lymphocytes of a newborn with fetal alcohol syndrome

Sir, Robinson et al. ( I ) pointed out that the marked simila- rities in phenotype of fetal alcohol syndrome (FAS) babies and of pyruvate dehydrogenase (PDH) complex deficient patients suggest a common mechanism of tera- togenesis. Acetaldehyde, the most important product of ethanol breakdown, is elevated in blood of alcoholic mothers of FAS children and is considered an inhibitor of the PDH complex in animal tissues. Accordingly, acetaldehyde could lower the PDH complex activity in utero, thereby mimicking the inherited enzyme deficiency.

Basal PDHa and PDHt and enzyme activity after exposure to insulin 5 and 50pU/ml were assayed i n circulating lymphocytes as previously described (2) in a normoglycaemic and normoinsulinaemic FAS baby and in seven normal newborn controls. PDH activity assay and insulin incubation procedures were per- formed according to already reported methods (3) and PDH activity is expressed in terms of the reaction pro- ducts acetylCoA (nmol acetylCoA/lO' cells/h).

At 8 days of life, in the FAS baby PDHa and PDHt activities (17.3 and 30.3 respectively) were lower 0, < 0.001) than in controls (34.1 f 6 and 46.2 f 6), but enzyme activities after in vitro cell exposure to 5 pU/ml insulin rose significantly (FAS baby: 30.3 and 40.2; controls: 37.6 * 5 and 48.4 i 6). After exposure to insu- lin at 50 pU/mI, PDHa and PDHt activation occurred (FAS baby: 27.5 and 38.1) instead of inhibition (con- trols: 18.8 314 and 31.8318). At 30 days in the baby, both PDHa and PDHt levels were within the normal range (26.5 and 40.1 respectively), though the enzyme response to insulin 50 pU/ml remained abnormal (PDHa: 30.1; PDHt: 45.9); at 62 days this response also normalized with PDH inhibition (PDHa: 23; PDHt: 33.7).

PDHa activity in circulating lymphocytes of the baby was low, possibly indicating a quantitative enzyme defi- ciency; however, because PDHa and PDHt activities in cells exposed to 5pU/ml insulin are not that much below those of similarly treated cells of controls, this conclusion may not be justified.

As in various cell types, mediators with activating and inhibiting effects on PDH, responsible for trans- ferring the insulin message to PDH, are well docu- mented (4), it might be speculated that in lymphocytes from normal subjects PDH activation or inhibition result from the generation of specific mediators. If so, in this case PDH activation with insulin at 50pU/ml suggests that generation of mediators is not affected, but the ability to recognize this insulin concentration is. Low enzyme activity and altered PDH response to insulin at 50 pU/ml were no longer seen in this subject beyond two months of life. This gradual recovery could follow restored membrane function of previously damaged cells no longer exposed to ethanol, or alter- natively a renewal of cell population. If PDH activity derangement seen in circulating lymphocytes is common to other cells and tissues and if recovery only proceeds through the renewal of cell population, negative implications should follow for perennial tissues exposed to ethanol. Greater case series and follow up will highlight these points.

References 1. Robinson BH, MacMillan H. Petrova-Benedict R, Shewood G.

Variable clinical presentation in patients with dcfectivc E I compo- nent of pyruvate dehydrogenase complex. J Pedintr 1987; I I I : 525-33

2. Curto M , Piccinini M, Bruno R, Mostert M. Rinaudo MT. Insulin modulation of pyruvate dchydrogenase i n human circulating lym- phocytes. Int J Biochem 1988;20:121 I -7

3. Wieland OH. The mammalian pyruvate dehydrogenase complex: structure and regulation. Rev Physiol Biochcm Pharinacol 1983:96: 126-70

4. Cheng K, Galasko G, Kellogg J , Larner J . Studies of the insulin mediator-11. Separation of two antagonistic biologically active materials from fraction 11. Diabetes I980;29:659 61