738
March
Correspondence
Am. J. Obstet.
15. 197X G~~eu)l.
REFERENCE nun3 Plasma
.
1. Oski, F. A., and Naiman, J. I,.: Hemarologic Problems in the Newborn, ed. 2, Philadelphia, 1972, W. B. Saunders Company.
1.10~ Ery
0,4
i
--i .
Reply to Drs. Schumann and Weitzel Tu the Editors:
I 10
30
20
40
l
Weeks
Fig. 1. An increasing red blood cell count in fetal blood or, vice versa, a decreasing amount of plasma in fetal blood with advancing gestation. (Data of Oski and Naiman.‘)
AFP
T
re/ml
We agree with Drs. Schumann and Weitzel that the four factors change with fetal age. However, in our center, almost all genetic amniocenteses are carried out at I6 weeks’ gestation. Thus, in our paper we discussed the bar at 16 weeks’ gestation in Fig. 2 of Schumann and Weitzel. As this bar assumes a mean feral AFP concentration and the mean fetal red blood cell count of Oski and Naiman (reference 1 in above letter) but does not include any value for volume of amniotic fluid, their illustration gives essentially the same infixmation as the graph in our paper, which was based on dilution of fetal blood in amniotic fluid. Not all amniocenteses can be performed at 16 weeks: in our center there is a variation from 15 to 20 weeks. In the interval from 16 to 20 weeks. the mean fetal hematocrit changes from 35 to 37 per cent, and the mean fetal red blood cell count increases from 2.0 to 2.5 x 10” per cubic millimeter (reference 1 in above letter). The change in fetal red blood cell count is important, and we should consider this in estimating the degree of contamination of blood-stained fluid w,ith fetal AFP. Although we agree that a calculation can give only an estimate of the fetal serum contribution to the total amniotic fluid AFP, we believe that this estimate is useful to the clinician in assessing contamination of an amniotic fluid specimen with fetal blood. T. A. Dorcr~, L. C. Allen, B. B. k’. Piruni, M.B., h’. H. Shumnk,
12
Fig. 2. stained values increase present
16
20
24
Weeks
Change of AFP values in an amniotic fluid sample with fetal blood. Solid columns represent the mean found in amniotic fluid. White columns represent the if 10,000 red blood cells per cubic millimeter are in the sample.
pink, we calculated a change in the shown in Fig. 2. Because there are four factors with that are quite wide, the results of an are uncertain and a high level of AFP stained with fetal blood is not reliable.
AFP values,
as
normal ranges AFP calculation from a sample
K. Schumann, H. Weitzel, Department of Obstetrics and Gynecology School of Medicine Hannover Podbielskistr. 380 ?OOO Hannozw, Federai Republic of Germany
M.D. M.D.
Departmmt.c 4’ 0bstetl-ic.c and Gynaecology, Clinical Biochemistq and Haematology Toronto Generul Hospital Toronto, Onturio, Canada M5G
M.D. Ph.D. Ch.B. M.D.
IL7
Maternal smoking, alcohol consumption, and abruptio placentae To the Editox
Two papers recently published in the JOURNAL by Meyer and Tonascia’ and Naeye and associates’ emphasize the possible etiologic role of maternal smoking in fetal death caused by abruptio placentae. Such a relationship was found in our analysis of a prospective survey of 9,169 women (reference 11 in Meyer and Tonascia’s paper). Naeye and associates rightly point out that the origin of abruptio placentae very often
Correspondence
weight,j and, on the contrary. compc’n~at~~~~ placental hypertrophy is observed with tobacco xrnoL~ng.” Tobacco could have two effects: t,1) Entrauterine growth retardation and (2) intrautel-inr hs poxia. suggested by a higher frequency of nuc-iear- ~:ictmps in rhta perivillous syncytiotrophoblast among sm~)kws, ;I$ rcported by Spira and associates,’ ;is\rGale~ i with a decreased thickness of I he intervillous
Table I. Stillbirth and abruptio placentae related to maternal tobacco use and alcohol consumption
1
Da@ alcohol cmwumption (ml. of absolute alcohol). <45 Nonsmoker Smoker a45 Nonsmoker Smoker
Alcohol effect adjusted for tobacco use Tobacco effect adjusted for alcohol consumption
This
7,551 994
65 21
8.5 20.6
5 4
0.6 4.0
398 94
8 5
19.7 50.5
5.0 20.8
-
*
2 2 *
-
t
*
hypoxia
probably
explain\
rhr
hi:!,hr,t
01‘
yule
of
Ott tll&~rnutri-
tion.
ia. to~.s, alcohol
‘The
fact
that
in our
survey
tht: two
,O the
and tobacco, seem to have a real effect ;Iprecs with the hypothesis of Naeye and associates what ~llldrl.nut:-itiorl and tobacco smoking probablv ;I( t itl(~t,l)(:11d(.rltl\ in rhe genesis
of abrriptio
placentae. J. h1~)“‘d ( l/nt:~A
done by an appropriate by COX.~
I-IS!,
abruptio placentae among smokel~\. Very little is presently known in 1 cqrd alcohol; alcohol use is possibly ielated
tic, .t1.
Adjusted tests have been for small numbers described “p 5 0.01. tp s 0 001.
739
method
remains unexplained. the traditional explanations rep resenting only a small proportion of its etiopathogenesis. We wish to report here some results obtained from our survey mentioned above, carried out in Paris from 1963 to 1969. The women included in the study were interviewed during the third month of pregnancy on their tobacco use and alcohol consumption and were followed up until delivery. Table I takes into account the existing relationship between tobacco smoking and alcohol consumption. It can be seen that each one of these two factors is significantly related to an increased rate of stillbirth when the other is held constant, the risk thus being 2.5 times greater. When the cause of death is considered, there is a very important increase in the frequency of deaths caused by abruptio placentae when these factors are present. The risk is multiplied by six for tobacco smoking and for alcohol consumption and by more than 30 for those women who smoked during pregnancy and consumed daily more than 45 ml. of absolute alcohol. This multiplication of risks suggests that, with some reservation because of the small numbers concerned. the two factors have independent effects. The effects of‘ tobacco and alcohol are probably very different. Tobacco and alcohol both involve fetal hypotrophy+ “; however. hypotrophy produced by alcohol consumption is associated with low placental
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I’Enfnnt 44 Chemin de Ronde i81 IO Le VeGttet, Frccwe Unitk de Rechewhes Statistique\ I6 I-is au. Paul Vaillnnt Couturiri~ 93800 Villqju$ Frclncr REFERENCES
1. Meyer, M. B.. and Tonascia, J. A.: Maternal smoking, pregnancy complications, and perinatal mortality, AM. 2.
3. 4.
5.
6.
7.
J.
128: 494, 1977. Naeye, R. L., Harkness, W. L., and L!rts, J.: Abruptio placentae and perinatal death: A prospective study. AM. J. OESTET.GYNECOL. 128: 740, 1977. Cox, D. R.: Analysis of Binarv Data. 1 ondon, 1970. Methuen and Co.. Ltd. Schwartz, D., Goujard, J., Kaminski, M., and Rumeaw Rouquette, C.: Smoking and pregnancy. Results of a prospective study of 6,989 women, Rev. Eur Erud. Clin. Biol. 17: 867, 1972. Kaminski, M.. Rumeau-Rouquette, C., and Schwartz, D.: Consommation d’alcool chez les fernmen enceintes et issue de la grossesse, Rev. Epidemiol. Med. Sot. Sante Publique 24: 27, 1976. Spira. A., Spira. N., Gouiard, 1.. and Schwartz, D.: Smoking during pregnancy and placental weight. A multivariate analvsis on 3.759 cases. 1. Perinat. Med. 3: 237, 19’75. SpirH, A., Philippe, E., S&ra, N., Drevfus. I., and Schwartr. D’.: Smoking &ring p&gnancv ani plac&tal pathologv. Biomedicine 27: 266, 1977.
OBSTET.GYNECOL.