BRIEF COMMUNICATIONS

Our patient had 2 vaginal deliveries. Over elective cesarean delivery,

we prefer early epidural anesthesia, combined with regular inhalation
analgesia as needed, for women with myotonia congenita. If a cesarean
delivery is necessary, the epidural solution can be strengthened or the
epidural anesthesia can be replaced by spinal anesthesia [5].
References

63

[2] Butwick AJ, Riley ET. Successful spinal blockade in a parturient with myotonia
congenita [letter]. Int J Obstet Anaesth 2007;16(3):2923.
[3] Chrestian N, Puymirat J, Bouchard JP, Dupre N. Myotonia congenita: a cause of
muscle weakness and stiffness. Neurol 2006;2(7):3939.
[4] Chang TY, Kuo HC, Hsiao KM, Huang CC. Phenotypic variability of autosomal
dominant myotonia congenita in a Taiwanese family with muscle chloride channel
(CLCN1) mutation. Acta Neurol Taiwan 2007;16(4):2149.
[5] Howell PR, Douglas MJ. Lupus anticoagulant, paramyotonia congenital and
pregnancy. Can J Anaesth 1992;39(9):9926.

[1] Farrow C, Carling A. Successful spinal blockade in a parturient with myotonia

congenita. Int J Obstet Anaesth 2007;16(2):8990.

0020-7292/$ see front matter 2009 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ijgo.2009.01.031

Helicobacter pylori and hyperemesis gravidarum

Ghada M. Mansour a,, Ehab H. Nashaat b
a
b

Department of Obstetrics and Gynecology, Ain Shams University, Cairo, Egypt

Department of Internal Medicine, Ain Shams University, Cairo, Egypt

a r t i c l e

i n f o

Article history:
Received 29 September 2008
Received in revised form 6 February 2009
Accepted 6 March 2009
Keywords:
Helicobacter pylori
Hyperemesis gravidarum

Helicobacter pylori is a common bacterial infection worldwide that

is known to cause chronic active gastritis (type B). A majority of
patients will have chronic supercial gastritis persisting throughout
life, whereas others may develop either a duodenal or a gastric ulcer
[1].
Hyperemesis gravidarum is a complication affecting 0.3%2.0% of
all pregnancies. It is dened as vomiting during pregnancy that is
severe enough to cause weight loss, dehydration, acidosis from starvation, alkalosis from loss of hydrochloric acid, and hypokalemia. Mild
to moderate ketonuria may be detected by urine analysis. The cause of
hyperemesis gravidarum is unknown, but hypotheses include hormonal mechanisms, emotional factors, and H. pylori infection.
The increased serum steroid and human chorionic gonadotropin
levels that cause changes in the pH of the gastrointestinal tract in
addition to pregnancy-induced gastrointestinal tract dysmotility and
altered humoral and cell-mediated immunity in pregnancy all favor
activation of H. pylori infection.
The aim of the present study was to evaluate the role of H. pylori in
the pathogenesis of hyperemesis gravidarum, and to assess the value
of using a nonteratogenic regimen for treating H. pylori infection in
intractable cases.
Fifty women with hyperemesis gravidarum and between 10 and
16 weeks of pregnancy were recruited to the study group between
January 2004 and January 2008. Fifty women without hyperemesis
gravidarum who were between the same weeks of pregnancy as the
study group were recruited to the control group. The study was
Corresponding author. Tel.: +233 20 8113773.
E-mail address: sopareaddo@yahoo.com (H.S. Opare-Addo).

approved by the ethics committee and informed consent was obtained

from all participants.
The inclusion criteria for the study group consisted of severe
vomiting (more than 3 times per day without any other obvious
cause), weight loss, and the presence of ketonuria. A full history was
taken to exclude peptic ulcer, long-term use of nonsteroidal antiinammatory drugs (NSAIDs), hyperthyroidism, psychological disorders, hepatic disorders, urinary tract infection, Addison disease,
vestibular disease, pancreatitis, bowel disease, and intracranial
disorders. Patients who had received antibiotics, H2 blockers, or
proton pump inhibitors in the preceding month were excluded from
the study.
After general and local examination, an ultrasound examination
was performed for the women with hyperemesis gravidarum to
exclude obstetric causes, such as twin pregnancy, molar pregnancy, or
missed abortion. Urine analysis for ketones was performed to detect
starvation ketosis. Serum H. pylori immunoglobulin G antibody titer
was measured using enzyme-linked immunosorbent assay for both
groups of women. This widely accepted noninvasive test has a
sensitivity of 97.1% and a specicity of 98.6% [2].
The women with hyperemesis gravidarum included 39 primigravida
and 11 multigravida. Eight multigravida had a history of hyperemesis in
previous pregnancies and 3 of these women had undergone previous
induced abortions for severe intractable vomiting. The control group
included 28 primigravida and 22 multigravida, with no previous history
of hyperemesis.
Data were analyzed using SPSS software, version 11.0 (SPSS,
Chicago, IL, USA). The Pearson 2 test was used for nominal values and
the paired t test and analysis of variance were used for numerical
values. P b 0.05 was considered statistically signicant.
There was no signicant difference in mean maternal age between
the study and control groups (28.04 2.96 years [range 2535 years]
vs 25.8 2.2 years [range 2331 years], respectively). No statistical
differences were observed for gravidity, parity, and fetal biometry.
The H. pylori serum antibody test was positive for 42 out of 50
(84%) women in the study group and for 18 out of 50 women (36%) in
the control group.
Among the 50 women with hyperemesis gravidarum, 3 patients
had severe symptoms that did not respond to treatment with
intravenous uids, electrolyte replacement, anti-emetics, and vitamin

64

BRIEF COMMUNICATIONS

supplements. These 3 women had a history of previous abortion due

to severe intractable vomiting. One of them experienced hematemesis; an upper endoscopy revealed severe antral gastritis.
These 3 patients were at more than 12 weeks of pregnancy and
they gave consent for treatment with a twice daily dose of 150 mg of
ranitidine (Zantac; GlaxoSmithKline, UK), 500 mg of metronidazole
(Flagyl; Pzer, USA), and 500 mg of ampicillin for 2 weeks. Ampicillin
and ranitidine were given parenterally and metronidazole rectally
until the patients could receive oral therapy. They showed marked
improvement and a reduction in the number of vomiting incidences
and a reduction of epigastric pain. This improvement continued until
delivery. It should be noted that the treatment in the present study
was given in the 3 complicated cases, and although a signicant
response was noticed, further studies with larger numbers are needed
to corroborate the results.
The incidence of H. pylori was signicantly higher in the women with
hyperemesis gravidarum in the present study and this nding is in

agreement with results of other studies [3,4]. H. pylori should, therefore,

be considered as one of the causes of hyperemesis gravidarum.
Screening for H. pylori should be added to the investigations for
hyperemesis gravidarum especially in prolonged conditions that are
refractory to conventional management and in cases that extend to the
second trimester. Appropriate therapeutic regimens for treatment of H.
pylori may be considered in intractable cases.
References
[1] Hunt H. The role of Helicobacter pylori in pathogenesis: the spectrum of clinical
outcomes. Scand J Gastroenterol Suppl 1996;220:39.
[2] Veenendaal RA, Gtz JM, Schroijen V, Kurban F, Bernards AT, Veselic M, et al.
Diagnosis of Helicobacter pylori infection by specic gastric mucosal IgA and IgG
pylori antibodies. J Clin Pathol 1995;48(11):9903.
[3] Frigo P, Lang C, Reisenberger K, Kolbl H, Hirschl AM. Hyperemesis gravidarum
associated with Helicobacter pylori seropositivity. Obstet Gynecol 1998;91(4):6157.
[4] Jacoby EB, Porter KB. Helicobacter pylori infection and persistent hyperemesis
gravidarum. Am J Perinatol 1999;16(2):858.

0020-7292/$ see front matter 2009 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ijgo.2009.03.006

Enzyme replacement therapy for Gaucher disease in twin pregnancy

Vra Malinov a,, Helena Pouptov b, Lenka Dvokov b, Ji Zeman a,b
a
b

Department of Pediatrics, First Faculty of Medicine, Charles University, Prague, Czech Republic
Institute for Inherited Metabolic Disorders, First Faculty of Medicine, Charles University, Prague, Czech Republic

a r t i c l e

i n f o

Article history:
Received 5 January 2008
Received in revised form 2 February 2009
Accepted 26 February 2009
Keywords:
Enzyme replacement therapy
Gaucher disease
Twin pregnancy

Pregnancy may present a signicant physiological burden for

women with Gaucher disease if they are untreated [1]. Existing
disease manifestations (anemia, thrombocytopenia, increased bleeding risk, hepatosplenomegaly) may deteriorate and new symptoms
may appear [2]. The present study reports a retrospective comparison
of the outcomes in 2 women with type 1 Gaucher disease and a twin
pregnancy. Patient 1 received enzyme replacement therapy before
and throughout pregnancy. Patient 2, who was not diagnosed before
pregnancy, was untreated.
Gynecological records for patient 1 reported menarche at 15 years
of age. Menses were regular and lasted 67 days with hypermenorrhea. From 10 years of age the patient had nosebleeds, frequent
hematomas, and intermittent bone pain in the lower limbs. Hepatosplenomegaly was recognized at 14 years of age. Gaucher disease was
suspected following liver biopsy and detection of lysosomal storage at
20 years of age and was conrmed by glucocerebrosidase assay

Corresponding author. First Faculty of Medicine, Charles University, Prague, Czech

Republic. Tel.: +420 224967794; fax: +420 224967713.
E-mail address: malinovaV@seznam.cz (V. Malinov).

(3.7 nmol/mg protein/hour, reference range 7.516 nmol/mg) and

genotyping (N370S/RecNcil). Magnetic resonance imaging (MRI)
revealed metabolic bone disease with storage in the bone marrow in
the long bones of the lower limbs and vertebrae, and compression
fractures of L2, L3, and L5.
The patient began treatment with 1938 units/kg of imiglucerase
(Cerezyme; Genzyme, Cambridge, UK) every two weeks. Menorrhagia improved, hemoglobin concentration and platelet count
normalized, biomarkers of disease (chitotriosidase, acid phosphatase, and angiotensin-1-converting enzyme) improved, and spleen
and liver volumes decreased (Table 1). At 26 years of age the patient
underwent cholecystectomy for cholelithiasis. The patient conceived
twins at 30 years of age and, with informed consent, continued
imiglucerase treatment throughout pregnancy. Bone parameters were
stable before pregnancy. Hemoglobin concentration and platelet count
remained stable during pregnancy. A mild temporary increase in
chitotriosidase activity (14%) suggested some impact of pregnancy on
disease status. The patient was delivered at 37 weeks of gestation by
cesarean. Pregnancy, delivery, and the postpartum period were
uncomplicated. Both neonates weighed 2600 g at birth, had normal
early postnatal adaptation, and growth and development appropriate
for gestational age. Compression fractures of vertebrae L5 and T8 were
observed in the patient 1 year after delivery. MRI demonstrated stable
bone inltration.
Menarche occurred at 13 years of age in patient 2. Menses were
regular and lasted 1011 days with hypermenorrhea. From 12 years
of age the patient had nosebleeds, frequent hematomas, low back
pain, and pain in the lower limbs. Although splenomegaly was
apparent at 15 years of age and compression fractures of vertebrae L1
and L2 were detected at 18 years, Guacher disease was not
diagnosed. The patient conceived twins at 26 years of age and
pregnancy was complicated by cholestatic jaundice, back pain, and
HELLP syndrome (hemolytic anemia, elevated liver enzymes, and