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WISCONSIN MEDICAL

JOURNAL

Hyperemesis Gravidarum:
Literature Review
Binu Philip, DO

ABSTRACT have any cramping, contractions, headaches, or visual


Nausea and vomiting commonly occur in pregnant changes. She had not felt fetal movement.
women. Hyperemesis gravidarum is a severe form of On physical examination she was a thin Hmong
nausea and vomiting rarely occurring in pregnancy. woman, alert and in no acute distress. Vital signs were
Between 0.3% and 2% of all pregnant women suffer as follows: weight 91 pounds (4 pound weight loss),
from hyperemesis gravidarum. The objective of this blood pressure 132/80 mmHg, and pulse 84 bpm. She
paper is to review current literature focusing on the had signs of dehydration, with dry oral mucosa. Neck
definition, incidence, etiology, prognosis, and treat- examination was normal. Auscultation of heart and
ment of hyperemesis gravidarum. A MEDLINE search lungs was normal. The abdominal examination was un-
of the English literature from 1982 through 2001 uti- remarkable for tenderness or fullness. The uterus was
lized the keywords hyperemesis gravidarum, nausea, palpable just above the pubic symphysis.
and pregnancy. Current data pertaining to the epidemi- Fetal heart tones were not audible with doppler.
ology, etiology, clinical presentation, various treatment Transabdominal ultrasound was performed looking for
modalities, and prognosis are presented. Review of the evidence of fetal cardiac motion as well as dating sec-
literature supports that hyperemesis gravidarum is a ondary to a large discrepancy between size and dates.
multifactorial disease. The cause is unknown. Various The ultrasound was described as a “snowstorm” pat-
treatments are recommended although few studies have tern, a characteristic appearance of molar pregnancy.
evaluated effectiveness. A case report of molar preg- (Figure 1) Laboratory data was obtained including a
nancy presenting with hyperemesis gravidarum intro- B-HCG (Beta-human chorionic gonadotropin) level of
duces this literature review. 526,483, and a TSH (thyroid stimulating hormone) of
less than .06. A diagnosis of molar pregnancy was
HYDATIDIFORM MOLE PRESENTING made.
WITH HYPEREMESIS GRAVIDARUM The patient underwent a successful dilation and
Case Report evacuation. Pathology reports supported a complete
L.L. is a 20-year-old Hmong woman who presented hydatidiform mole. She was monitored for resolution
with complaint of excessive vomiting over 1 week. She of her elevated B-HCG levels, which did return to nor-
was a G1P0 female who presented at 19 3/7 weeks ges- mal within 2 months of her treatment. Follow-up TSH
tation based on dating. A urine pregnancy test at the levels were also within normal limits. Chemotherapy
local health care department was positive 10 weeks may have been indicated if the B-HCG levels had
prior to presentation. She did not have any initial pre- reached a plateau or did not fall appropriately. She was
natal care. instructed to avoid conception for at least 6 to 12
Although she admitted to first trimester nausea and months. The hyperemesis in this patient resolved upon
vomiting, her presenting symptoms were significantly treatment of the hydatidiform mole by dilatation and
worse. She denied any lightheadedness or weakness but evacuation.
had not been able to tolerate her normal oral intake.
She denied vaginal bleeding or discharge. She did not BACKGROUND
Hydatidiform mole is characterized by proliferation of
the trophoblast. Molar pregnancies can be complete
(classic) or incomplete (partial). The importance of rec-
Doctor Philip is with the University of Wisconsin, Department of
Family Practice, Eau Claire, Wis. Address reprint requests to Binu
ognizing molar pregnancy is related to its potential for
Philip, DO, 807 S Farwell, Eau Claire, Wis 54701 both gestational trophoblastic disease as well as chorio-

46 Wisconsin Medical Journal 2003 • Volume 102, No.


3
Figure 1.
moles are di- agnosed Treatment should common experience
before 20 weeks of include dilation and affecting 50% to 90%
gestation.1 Cytogenic evacuation of tissue with of all women.3-7
stud- ies show that close tissue analysis for Nausea and vomiting are
complete hydatidiform cell ploidy. Close usually limited to the first
moles are female and that monitoring of B-HCG trimester, but 20% of
all 45 chromosomes are levels after evacuation women have symptoms
paternally derived, likely is ex- tremely important that con- tinue
through dispermy.1 to ensure that no throughout pregnancy.3
Partial hydatidiform trophoblastic tissue The spectrum of nausea
moles are consistent with remains. Follow-up and and vomiting in
embryonic and fetal monitoring along with pregnancy can range
tissue and are usually preven- tion of pregnancy from mild to se- vere and
triploid. Gestational for 6 to 12 months are can involve persistent
choriocarcinoma may recommended. and excessive vomiting.
arise from a mole or Physicians should be Hyperemesis
normal conception. In aware of the possibility gravidarum (HG) is the
carcinoma. Molar the United States and of molar pregnancy in all most severe form of
pregnancies occur in Europe, patients with hyperemesis nausea and vomiting in
approximately 1 in every choriocarcinoma is gravi- darum and be pregnancy and is char-
1500 pregnancies in the found in 1 in 50,000 familiar with the acterized by intractable
United States, 1 per pregnancies and the risk appropriate manage- nausea and vomiting that
1000 pregnancies in the of choriocarcinoma after ment to monitor and leads to dehydration,
United Kingdom, and a complete hydatidiform prevent an often fatal electrolyte and metabolic
are sev- eral-fold more mole is about 3%.1 trophoblas- tic neoplasm. disturbances, and
common in Asian and Micro- scopic findings A proper understanding nutritional deficiency
Latin American include marked edema of the proposed that may require
populations.1 The and enlargement of the mechanism of nausea hospitaliza- tion.3,7-9
incidence is higher in villi along with and vomiting in Hyperemesis gravidarum
both teenagers and proliferation of the pregnancy and the has also been de- fined
women older than 35 trophoblastic lining. knowledge that molar as severe vomiting with
years. The most Pathological specimens pregnancy can present as onset at less than 16
common presentation is usually reveal hydropic hy- peremesis weeks of estimated
vaginal bleeding. Both swelling and a typical gravidarum are crucial gestational age that
hyperemesis gravidarum “grape-like” appearance to recognizing women causes 5% weight loss
and preeclampsia can be of the chorionic villi. at risk. and considerable
presenting features. If molar pregnancy is ketonuria.6,10-13
Hyperemesis suspected, a few tests aid REVIEW OF
in di- agnosis, including I
gravidarum is reported CURRENT n
to occur in as many as quantitative B-HCG, LITERATUR c
26% of molar TSH, and ul- trasound.
E i
pregnancies.2 Increases Likely results include d
D
in the level of serum B- abnormally elevated B- e e
HCG may be the HCG, low TSH, and a f n
mechanism of hy- “snowstorm” appearance i c
on ultrasound. n e
peremesis gravidarum in
i Hyperemesis gravidarum
molar pregnancy as molar
t has an incidence
tis- sue produces
i varying from 0.3% to 2%
markedly elevated B- o of all pregnancies.4-6,8,9,13-
HCG levels. n 15 Although rare, its
The majority of Nausea and vomiting clinical and social impact
patients with complete during pregnancy is a
can be immense. The
socioeconomic impact
of the complete
spectrum of nausea and
vomiting of pregnancy on
time lost from ei- ther
paid employment or
household work is
substan- tial. Deuchar
noted 8.6 million hours
of paid employ- ment
and 5.8 million hours of
housework are lost each
year because of this
condition.3
E
t
i
o
l
o
g
y
The cause of HG is not
well understood but
appears to have both
physiologic and
psychologic components.
Estrogen, progesterone,
adrenal, and pituitary
hor- mones have been
proposed as causes but
currently there is no
conclusive evidence
implicating any of
them. 14
One popular theory is that nausea and vomiting of creased risk of HG has been associated with advanced
pregnancy is related to trophoblastic activity and go- maternal age and cigarette smoking.7 Also, metabolic
nadotropin production, possibly secondary to elevated disorders associated with HG could possibly con-
serum human chorionic gonadotropin (hCG) levels. tribute to an increased risk, including hyperthyroidism,
Schoeneck, in the early 1940s, noted that women with hyperparathyroidism, altered lipid metabolism, and
nausea and vomiting of pregnancy had higher concen- liver dysfunction.3
trations of urinary hCG than asymptomatic pregnant Hyperthyroidism has been found to be associated
women.3 A relationship to the level of hCG has been with HG.21 In fact, decreased thyroid stimulating hor-
postulated because the incidence of hyperemesis gravi- mone (TSH) has been found in patients with HG while
darum is higher in multiple gestation pregnancies as levels of free T3 and free T4 have remained within nor-
well as in molar disease where hCG levels are markedly mal limits. It is thought that there may be a condition
elevated.16 known as transient hyperthyroidism of hyperemesis
Serotonin has a role in emesis in humans as seen by gravidarum (THHG), which is a self-limiting hyper-
its physiological effects in the central nervous system, thyroidism occurring in the context of HG. Diagnosis
gastrointestinal tract, and other sites.17 For this reason, of THHG rests on the following four criteria: (1) ab-
serotonin has been implicated as a cause of HG. How- normal thyroid function tests developing in the context
ever, Borgeat et al found that hyperemesis gravidarum of hyperemesis gravidarum, (2) no evidence of prepreg-
was not associated with an increase of serotonin secre- nancy hyperthyroidism, (3) absence of physical exami-
tion.14 nation findings consistent with hyperthyroidism, and
Recently, Helicobacter pylori infection has been im- (4) negative thyroid antibody titers.
plicated as a possible cause of HG.18,19 In a prospective Another associated risk factor for hyperemesis
study, Helicobacter serum IgG concentrations in pa- gravidarum may be a previous diagnosis of an eating
tients with HG were compared with those in asympto- disorder. Studies have found that occurrence of HG is
matic gravidas matched for week of gestation. Positive greater in women with eating disorders, such as bu-
IgG concentrations were found in 95/105 hyperemesis limia, than in controls.22
patients compared with 60/129 controls. The authors
conclude that infection with H. pylori may cause HG.12 Diagnosis
A question that remains unanswered is whether an in- The diagnosis of HG rests in careful observation of the
creased incidence of nausea and vomiting may lead to signs and symptoms of pregnant patients with excessive
the elevated levels of H. pylori found in these pregnant vomiting. Symptoms of HG typically present during
patients. the first trimester of pregnancy, usually beginning be-
A psychosomatic etiology has been proposed for tween the 4th and 10th weeks of gestation, peaking be-
HG. Zechnich and Hammer reported, “pregnant tween the 8th and 12th week, and resolving by the 20th
women have been shown to have a significantly higher week. In only the rare case, symptoms persist into the
level of anxiety than nonpregnant women and are second half of gestation. Patients usually present with
known to be readily influenced by suggestion and by signs of dehydration, ketosis, electrolyte and acid-base
reassurance.”20 Other authors have suggested that HG disturbances. Weight loss of greater than 5% of body
has been linked to stress and emotional tension and is weight may occur.
found more commonly among “immature, dependent, Work-up must always start with confirmation of a
hysteric, depressed, or anxious” women, although this viable, intrauterine pregnancy. When HG is diagnosed,
has not been studied.17 the associated conditions of multiple gestations and hy-
Other mechanisms that have been proposed for HG datidiform mole should be excluded. Molar pregnan-
include changes in gastrointestinal tract motility, thy- cies and associated cancers can present with FHG in up
roid dysfunction, hypofunction of the anterior pitu- to 30% of cases.3
itary and adrenal cortex, and abnormalities of the cor- The diagnosis of HG should exclude other causes of
pus luteum.9 vomiting, such as gastroenteritis, cholecystitis, acute
pancreatitis, gastric outlet obstruction, pyelonephritis,
Associated Risks primary hyperthyroidism, primary hyperparathy-
Various risk factors have been theorized to be associ- roidism, or liver dysfunction.23
ated with HG. These include increased body weight, Laboratory tests to help with diagnosis and treat-
multiple gestations, trophoblastic disease, HG in a ment may include electrolytes, liver function tests,
prior pregnancy, and nulliparity.3,7 In contrast, a de- amylase, lipase, thyroid function tests, B-HCG, creati-
nine, blood urea vomiting in pregnancy is women with nausea and stores of thiamine,
nitrogen, urinalysis, considered excellent with vomiting of pregnancy or riboflavin, vitamin B6,
and CBC.3 no adverse fetal HG versus women who vitamin A, and retinol-
Ultrasound examination outcome.3 do not vomit during binding protein.
should be considered to Though nausea and pregnancy (4.9 per- cent In selected cases
rule out multiple vomiting are positively instead of 8.6 percent). where greater than 5%
gestation and molar associ- ated with Severe and untreated weight loss and long-
pregnancy. Labora- tory favorable pregnancy HG was found to be term malnourishment
findings at presentation outcomes and lower associated with a poor were of concern, ad-
of HG may include in- risks of spontaneous outcome. In one verse pregnancy
creased ketones and abortions, it is unclear if particular study, the hy- outcomes have been
increased specific gravity HG is as- sociated with peremetic pregnant reported includ- ing low
in urine with an positive pregnancy patients were at severe birth weight, antepartum
associated increase in outcomes. 23 Studies on nutritional risk as the hemorrhage, preterm
blood urea nitrogen. patients suffering from mean dietary intake of delivery, and an
Also, the hematocrit may HG show conflicting most nutrients fell below association with fetal
be elevated indicating a results, with some 50% of the anomalies.6,23
con- tracted fluid reporting adverse effects recommended dietary Poor outcome seems to
volume. Electrolytes on neonatal out- come allowances and differed be related to a lack of
values that may be and others reported a significantly from that of symp- tom control and
associated with HG rather beneficial controls.12 More than inability to correct
include decreased sodium, association with 60% of patients had electrolyte abnor-
potas- sium, and pregnancy outcome.4 A suboptimal biochemical malities.3
chloride, and possibly retrospective analysis re- Prolonged vomiting
increased liver func- tion viewed 193 women who also carries the risk of
tests. developed HG among Wer- nicke’s
P 13,053 pregnant encephalopathy
r patients.23 There were no secondary to thiamine
o differences in preg- nancy (vitamin B1) deficiency.
g outcomes including mean Also, hyponatremia and
n birth weight, mean its rapid rever- sal may
o gestational age, deliveries cause fatal central pontine
s less than 37 weeks, myelinosis.24
i
Apgar scores, perinatal
s T
mortality, or incidence of
The effect of nausea and r
fetal anom- alies in e
vomiting of pregnancy
patients with and a
on ma- ternal and
without HG.23 This t
neonatal outcome has
result was also seen in m
been controversial.
another study that found e
Several studies suggest n
that HG does not seem
that nausea and vomiting t
to have an adverse effect
of pregnancy is a The main treatment of
on the fetus.3 There was
favorable prognostic HG is supportive care.
no significant difference
sign with a de- creased Initially, a diagnosis of
in infants’ gestational
risk of miscarriage, an intrauterine viable
weight or birth weight
stillbirth, fetal mortality, pregnancy must be made,
and no proportion of
preterm delivery, low and associated conditions
stillbirth or spon- taneous
birth weight, perinatal such as multiple gesta-
abortion. In fact, there
mortality, or growth tion and hydatidiform
was found to be a sig-
retardation. Thus the mole must be ruled out.
nificantly decreased risk
outcome of nausea and Various lifestyle and
of fetal loss among
diet changes can help t
patients tolerate oral s
intake. Patients should try .
1
to avoid un- pleasant 3
odors; eat a bland, dry,
In cases that are
carbohydrate diet; eat
refractory to intravenous
small, frequent meals;
fluid treat- ment,
and separate solid and
parentaral nutrition and
liquid foods by at least 2
even feeding tubes have
hours.
been necessary.
Immediate correction
Nutritional support is
of fluid and electrolyte
reserved for pa- tients
deficits and acid-base
who continue to have
disorders must be
25
intractable symptoms
acomplished. If this
and weight loss despite
cannot be done using
appropriate therapy.
oral therapy, intravenous
Without nutri- tional
fluids may be
support, the mother and
considered. The patient
hence the fetus are at sig-
should initially have
nificant nutritional risk.3
nothing by mouth until
Hsu and colleagues report
deficits are corrected.
suc- cessful use of
Once this is done, an
nasogastric tube feeding in
attempt may be made to
the management of HG,
restart oral in- take using
as compared with total
the recommend diet. One
parenteral nutrition. Tube
study found that
feeding is less invasive,
treatment with
carries fewer risks,
intravenous rehydration
provides nutri- tion more
led to cessation of
physiologically, and is
vomiting and increase
easier to use.8
tolerance to oral intake
In a retrospective
within
study of 166 patients
2
with hyper- emesis,
4
27(16.3%) were treated
h with parenteral therapy.
o Patients treated with
u parenteral therapy have a
r marked increase in
s serious complications,
such as venous
i thrombosis, cellulitis,
n line sepsis, bacterial
endocarditis, and
H pneumonia, although
G
exact incidence was not
re-
p
a
t
i
e
n
ported. These data results showed that that daily doses of 1 g of trolled studies found that
suggest that patients treated with a gin- ger extract during P6 acupuncture point
consideration should be droperidol-diphen- a 4-day period was stimu- lation (located
given to less invasive hydramine protocol better than placebo in on the anterior
methods of nutritional compared with other reducing or eliminating forearm, 3 finger-
support.26 antiemetics had symptoms in women breadths proximal to the
The safety of significantly shorter with HG.3,27 wrist) seems to be an
antiemetic therapy is hospitalizations and Unfortunately, no other effective antiemetic
questionable, es- pecially fewer readmissions. 9 follow-up studies have technique. But there did
during the first trimester. Oral corticosteroid been done and safety has not appear to be any
Examples of antiemetics use has been studied in not yet been established. apparent medical benefit
used for treatment of the treat- ment of HG An alternative from the use of P6 acu-
HG include doxy- and may be beneficial.3 treatment that holds little pressure in the
lamine (Unisom), The mechanism by which if no risk to the mother treatment of nausea and
metoclorpramide corticosteroids suppress and fetus involves vomiting of pregnancy.32
(Reglan), promet- hazine the severe vomiting is acupuncture to help Due to a proposed
(Phenergan), probably a direct effect avoid nausea. A review psychosomatic
prochlorperazine on the vomiting center of 12 randomized component of hy-
(Compazine), in the brain.30 A study placebo-con- peremesis, an attempt to
trimethobenzamide by Carlan reported 25 find benefit from brief,
(Tigan), dimenhydrinate patients who were nonin- tensive
(Drama- mine), randomized into two psychotherapy was
droperidol (Inapsine), groups, one that performed by Zechnich
diphenhydramine (Bena- received and Hammer.20 The case
dryl), and ondansetron methylprednisolone and report involved a patient
(Zofran). All the one that received with HG who was treated
aforemen- tioned placebo. Results showed with psychotherapy. The
medications are FDA that a short course of authors sug- gest that
class B (presumed safety methylpred- nisolone in hypnosis and brief
based on animal studies) patients with HG psychotherapy are
or class C (uncertain decreased the likelihood effective in HG
safety as animal studies of a recurrence of treatment.
show an adverse effect vomiting.31 Another
and no human studies randomized, double- P
have been performed). blind controlled study by r
e
Although antiemetics Safari et al comparing
v
are frequently used, there promethazine showed e
have been several oral methylprednisolone n
randomized studies for to be more effective.27 t
their use in the Vitamin B6 has been i
treatment of HG. postulated to have a o
Ylikorkala et al found no beneficial effect on HG n
benefit of intramuscular treatment. Prevention of
adrenocorticotropic Unfortunately, studies hyperemesis has been
hormone with re- spect have not shown a proven studied using oral
to placebo.27 Sullivan et medical benefit.3 multivitamin therapy. A
al found no benefit of Ginger has also been randomized double-
on- dansetron (Zofran) used in HG treatment. A blind con- trolled trial of
compared with dou- ble-blind, peri-conceptional
promethazine randomized, crossover multivitamin supple-
(Phenergan).27-29 In a trial by Fischer- mentation found a
study by Nageotte et al, Ramussen et al reported significant reduction in
the occur- rence of HG, but are potentially safe,
3% in the thus providing additional
supplemented group therapeutic options. In
versus refractory cases,
6.6% in the nutritional supplementa-
unsupplemented group.33 tion becomes life-saving
There was a sig- nificant for both the mother and
decrease in the rate of the fetus.3 Timely
moderate nausea and diagnosis and
vomiting. appropriate management
of HG will reduce
C health risks and
O complications in both
the mother and the fetus.
N
C
R
L
E
U
F
S
E
I
R
O
E
N
N
Hyperemesis gravidarum
C
occurs rarely in the
spectrum of nausea and E
vomiting of pregnancy S
1. Hershman J. Human
but can have sub- stantial chorionic gonadotropin and
effects on the mother and the thyroid:
hyperemesis gravidarum
fetus if left untreated. and trophoblastic tumors.
After confirming a viable Thyroid.
pregnancy and ruling out 1999;9(7):653-657.
2. Glick M, Dick E. Molar
hy- perthyroidism, initial pregnancy presenting
management should be with hypereme- sis
conserva- tive, including gravidarum. J Am
Osteopath Assoc.
reassurance of the
1999;99(3):162-164.
transient nature of the
symptoms and the good
prognosis, in addition to
di- etary modifications.
Pharmacological therapy
is re- served for patients
with persistent
symptoms and is ap-
propriate after discussion
of the risks and benefits
with consideration of
informed consent.
Alternative treat- ments
including psychotherapy
and other non-phar-
macological modalities
are of less proven effect
3. Broussard C, Richter J. Board Fam Pract. 22. Franko D, Spurrell E. 26. Folk J, Leslie H.
Nausea and vomiting of 2000;13(l):35-38. Detection and Hyperemesis
pregnancy. 12. Frigo P, Lang C, management of eating gravidarum: pregnancy
Gastroenterol Clin North Reisenberger K, Kolbl H, disorders during out- comes and
Am. 1998;27(l):123-151. Hirschl A. pregnancy. Obstet complications among
4. Hallak M, Tsalarnandris Hyperemesis Gynecol. women nutritionally
K, Dombrowski K Isada gravidarum associated 2000;95:942-946. sup- ported with and
N, Pryde P, Evans M. with Helicobacter pylori 23. Tsang I, Katz V, Wells without parenteral
Hyperemesis seropositivity. Obstet S. Maternal and fetal therapy. Obstet
gravidarum: effects on Gynecol. outcomes in hy- Gynecol.
fetal out- come. J 1998;91(4):615-617. peremesis gravidarum. 2001;97:42S.
Reprod Med. 13. van Stuijvenberg M, Int J Gynecol Obstet. 27. Safari H, Fassett M,
1996;41(11):871-874. Schabort I, Labadarios 1996;55(3):231-235. Souter I, Alsulyman O,
5. Naef R, Chauhan S, D, Nel J. The nutritional 24. Nelson-Piercy C, de Goodwin T. The efficacy
Roach H, Roberts status and treatment of Swiet M. of methylprednisolone in
W, Travis K, patients with Corticosteroids for the the treatment of
Morrison J. hyperemesis treat- ment of hypereme- sis
Treatment for gravidarum. Am J hyperemesis gravidarum: a
hyperemesis Obstet Gynecol. 1995; gravidarum. Br J randomized, double-
gravidarum in the 172(5):1585-1591. Obstet Gynaecol. blind, controlled study.
home: an alternative 14. Borgeat A, Fathi M, 1994; 10 l(11):1013 Am J Obstet Gynecol.
to hospitalization. J Valiton A. -1015. 1998;179(4):921-924.
Perinatol. 1995; Hyperemesis 25. Godsey R, Newman R. 28. Guikontes E,
15(4):289-292. gravidarum: is Hyperemesis Spantideas A,
6. Safari H, Alsulyman 0, serotonin implicated? gravidarum: a compari- Diakalds J.
Gherman R, Goodwin Am J Obstet Gynecol. son of single and Ondansetron and
T. Experience with oral 1997;176(2):476-477. multiple admissions. J hyperemesis
methylprednisolone in 15. Fitzgerald J. Reprod Med. gravidarum. Lancet.
the treatment of Epidemiology of hyperemesis 1991;36(4):287. 1992;340(8829):1223
refractory hyperemesis gravidarum. .
gravidarum. Am J Lancet. 1956;1:660. 29. Tincello D, Johnstone
Obstet Gynecol. 1998; 16. Chong W, Johnston C. M. Treatment of
178(5):1054-1058. Unsuspected hyperemesis gravi-
7. Abell T, Riely C. thyrotoxicosis and hy- darum with the 5-HT3
Hyperernesis gravidarum. peremesis gravidarum. antagonist
Gastroenterol Postgrad Med J. ondansetron (Zofran).
Clin North Am. 1997;73(858):234-236. Postgrad Med J.
1992;21(4):835-849. 17. Eliakim R, Abulafia O, 1996;72(853):688-
8. Van de Ven C. Sherer D. Hyperemesis 689.
Nasogastric enterel gravidarum: a current 30. la Marca A, Morgante G,
feeding in review. Am J Perinatol. De Leo V. Hyperemesis
hyperemesis 2000;17(4):207-218. gravidarum is not
gravidarum. Lancet. 18. Reymunde A, Santiago associated with
1997;349(9050):445- N, Perez L. hypofunction of the
446. Helicobacter pylori and pituitary-adrenal axis.
9. Nageotte M, Briggs G, severe morning Am J Obstet Gynecol.
Towers C, Asrat T. sickness. Am J 1998; 179(5):1381-1382.
Droperidol and Gastroenterol. 31. Duggar C. The efficacy
diphenhydramine in the 2001;96(7):2279-2280. of methylprednisolone in
management of 19. Hayakawa S, et al. the treat- ment of
hyperemesis gravi- Frequent presence of hyperemesis
darum. Am J Obstet Helicobacter pylori gravidarum: a
Gynecol. genome in the saliva of randomized double-blind
1996;174(6):1801- patients with controlled study. Obstet
1805. hyperemesis gravi- Gynecol. 2001;97:45S.
10. Hershmann J. Human darum. Am J Perinatol. 32. Hoo J.
chorionic 2000;l7(5):243-24. Acupressure for
gonadotropin and the 20. Zechnich 11, Hammer hyperemesis
thy- roid: hyperemesis T. Brief psychotherapy gravidarum. Am J
gravidarum and for hypereme- sis Obstet Gynecol.
trophoblastic tumors. gravidarum. Am Fam 1997;176(6):1395-
Thyroid. Physician. 1397.
1999;9(7):653. 1982;26(5):179-181. 33. Czeizel A. Prevention
11. Caffrey T. Transient 21. Chan N. Thyroid of hyperemesis
hyperthyroidism of function in hyperemesis gravidarum is better
hyperemesis gravi- gravidarum. than treatment. Am J
darum: a sheep in Lancet. Obstet Gynecol.
wolf’s clothing. J Am 1999;353(9171):2243.
1996;174(5):1667.

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