Volume 165
umber 5, Part 1
for their slightly higher prevalence rates of abnormal
eating behavior. Diagnostic criteria may also influence
these rates: We adhered to the relatively strict criteria
of the American Psychiatric Association Diagnostic and
Statistical Manual ofMental Disorders. 1 We also confirmed
all possible cases identified by the screening instrument
with a clinical interview, and we excluded false positives.
The choice of screening instrument is clearly impor-
tant. We note that other eating disorder investigators
have expressed concern about the BITE," but we have
no experience with that instrument. However, in this
study we did compare the EAT-26 and another com-
mon eating disorder questionnaire, the Eating Disorder
Inventory, which measures pathologic behavior across
a broader range of psychologic and behavioral dimen-
sions associated with eating disorders.' Although these
data were deleted for the sake of brevity in our article,
we found the EAT-26 to be superior to the Eating Dis-
order Inventory in terms of sensitivity, specificity, brev-
ity, and ease of scoring. The main source of error in
both instruments, however, was denial of eating prob-
lems by some patients or false-positive results in over-
weight women who were unhappy, dieting, and preoc-
cupied by food.
We again emphasize that body weight is often a poor
predictor of eating disorders and that careful clinical
inquiry is vital. Our earlier work indicates that women
with eating disorders that remain unresolved before
pregnancy have more problems during pregnancy,'
lower maternal weight gain, and smaller babies with
lower Apgar scores than women whose eating disorders
are in complete remission.' The identification of eating
disorders in reproductive endocrinology clinics is both
cost-effective and an important opportunity for pri-
mary prevention.
D.E. Stewart, MD, D Psych
Departments of Psychiatry and Obstetrics and Gynecology. St.
Michael's Hospital, 30 Bond St... Toronto, Ontaliu, Canada M5B
1W8
REFERENCES
I. American Psychiatric Association. Diagnostic and statistical
manual of mental disorders. 3rd ed. Washington: American
Psychiatric Association. 1987.
2. King M, Williams P. BITE: Self-rating scale for bulimia.
Br J Psychiatry 1987:150:714-5.
3. Garner D, Olmsted M, Polivy J. Development and valida-
tion of a multi-dimensional eating disorder inventory for
anorexia nervosa. Int J Eating Disord 1983;2: 11-20.
4. Stewart DE, MacDonald OL. Hyperemesis gravidarum and
eating disorders in pregnancy. In: Abrahams S. Llewellyn-
Jones D, eds. Eating disorders and disordered eating. Syd-
ney: Ashwood House, 1987:52-5.
5. Stewart DE, Raskin J, Garfinkel PE, MacDonald OL, Rob-
inson GE. Anorexia nervosa, bulimia, and pregnancy. AM
J OBSTET GYNECOL 1987;157:1194-R.
Indomethacin induces hypertensive crisis in
preeclampsia irrespective of prior antihypertensive
drug therapy
To the Editors: Schoenfeld et al. report preeclampsia
being aggravated in two patients treated with 13-adren-
Letters 1577
ergic receptor blockers after ingesting indomethacin;
the authors correlate this hypertensive crisis with an-
tagonism of the f)-adrenergic receptor blockers by in-
domethacin (Schoenfeld A, Freedman S, Hod M, Ova-
dia Y. Antagonism of antihypertensive drug therapy in
pregnancy by indomethacin? AM J OBSTET GYNECOL
1989; 161: 1204-5).
I believe hypertensive crisis can occur in preeclamp-
sia after ingestion of any prostaglandin synthetase in-
hibitor drug (aspirin. indomethacin) irrespective of the
antihypertensive drug regimen, if any. Vasodilatory
prostaglandins produced by the kidneys in the state of
hypoperfusion maintain renal perfusion by dampening
the vasoconstrictive effect of angiotensin on renal ar-
teries.' Indomethacin blocks prostaglandin synthesis
and renders renal vasculature vulnerable to the con-
strictive effect of angiotensin II. Vasoconstriction of
renal arteries results in renal hypo perfusion manifested
by hvpertensive crisis.
Animals given indomethacin and subjected to slight
hemorrhage may have rapidly occurring severe renal
damage.'
Therefore it is wise to avoid all prostaglandin
synthetase inhibitor drugs in women with pre-
eclampsia.
Seid Mostafa Mousavy, MD
P.O. Box 544,81655 Esfahan, Iran
REFERENCE
l. Vander AJ. Renal physiology. 2nd ed. New York: McGraw-
Hill. 1980:60-6.
Reply
To the Editors: We thank Dr. Mousavy for his letter re-
garding our article. We agree with his statement about
the interference with antihypertensive drugs by non-
steroidal antiinflammatory drugs. In our article we
stated that "indomethacin (ami othn) nonsteroidal an-
tiinflammatory drugs vitiate the action of antihyper-
tensive drugs and that in some patients the hyperten-
sive response may be severe."
Dr. Mousavy's hypothesis, which deals with the an-
tiprostaglandin synthesis mechanism, is based on the
work of Vane' and likely explains a good portion of the
action of the nonsteroidal antiinflammatory drugs. We
would like to add that other, recently published 2 • 3
modes of action should be considered.
Alex Schoenfeld, MD
Department of Obstetrics and Gynecology, Beilinsun Medical Center
and Tel Aviv University Medical School, Petah Tiqva, 1smel
49100
REFERENCES
l. Vane JR. Inhibition of PG synthesis as a mechanism of
action for aspirin-like drugs. Nature New Bioi
1971 ;231:232-5.
2. Abramson S, Korchak H, Ludewig R, et al. Modes of action
of aspirin-like drugs. Proc Nat! Acad Sci USA
1985;82:7227-31.
3. Abramson SB, Weissman G. The mechanism of action of
NSAIDS. Arthritis Rheum 1989;342:1-9.