Liver disease in pregnancy

Lucy Mackillop,
1
Catherine Williamson
2
ABSTRACT
Pregnancy is a time of great maternal physiological and
metabolic changes. This affects the biochemical and
haematological parameters used in the assessment of
liver disease, and it is important to appreciate the
different reference ranges in pregnancy to facilitate
recognition of liver disorders in pregnancy. Due to the
increased physiological and metabolic stress of
pregnancy, liver disorders that have previously been
subclinical may become symptomaticdfor example,
primary biliary cirrhosis. Gallstone disease is a common
problem in women of childbearing age, and pregnancy
promotes their formation. The viral hepatidides constitute
a huge disease burden worldwide and the pregnant state
confers particular concerns for the mother and her baby.
In particular, hepatitis E has a predilection for the
pregnant population and confers a particularly poor
prognosis. In addition certain pregnancy specic
disordersdfor example, haemolysis, elevated liver
enzymes, low platelets syndrome, acute fatty liver of
pregnancy, and obstetric cholestasisdaffect primarily
the liver. It is important to know how to diagnose and
manage these conditions and distinguish them from non-
pregnancy specic conditions as this will change the
timing and management of affected women and their
babies, some of whom can be seriously ill. We propose an
approach to the investigation and management of the
pregnant patient with abnormal liver function tests.
INTRODUCTION
The physiological and metabolic changes seen in
pregnancy affect all organ systems and the liver is
no exception. Therefore, pregnant women with
pre-existing liver disease may present with specic
symptoms or complications in pregnancy. In addi-
tion, there are a collection of pregnancy specic
disorders that affect the liver. This article presents
a review of the current knowledge of liver disorders
specic to pregnancy and discusses other liver
disorders that may present atypically in pregnancy
or have a predilection for the pregnant population.
Finally, we propose an approach to the investiga-
tion and management of the pregnant patient with
abnormal liver function tests (LFTs).
LIVER PHYSIOLOGY AND FUNCTION IN NORMAL
PREGNANCY
The size of the liver and the absolute blood ow to
the liver is unchanged in normal pregnancy.
However, there is an increase in venous pressure
1
and clinical signs that are suggestive of liver disease
outside pregnancy, such as spider nevi, palmar
erythema and oedema, may be normally found in
pregnancy.
Liver function tests, including aspartate trans-
aminase, alanine transaminase, g-glutamyl transferase
(g-GT) and bilirubin, are markers of hepatocyte
damage and their normal range changes in pregnancy
(table 1). The reduction in the upper end of the normal
range for most tests is in part a consequence of
haemodilution secondary to the increased circulating
volume in pregnancy. In contrast, serum alkaline
phosphatase (ALP) increases steadily through preg-
nancy, reaching up to 300% of the non-pregnant value
by term. This is due to the production of a placental
isoenzyme. Occasionally women present with
notably raised ALP (>1000 u/l). This is almost
invariably of placental origin and isoenzymes maybe
tested to conrm it is not from hepatic origin.
There is an increase in hepatic synthesis of
coagulation factors VII, VIII, X and brinogen. The
range for prothrombin time (PT) and activated
partial thromboplastin time (APTT) remain the
same as for the non-pregnant woman. Therefore
prolonged PT, in particular, may be a good early
marker of synthetic dysfunction. There is a fall in
serum albumin concentrations such that a value of
30 g/l is considered normal and not a sign of
abnormal hepatic synthetic function.
Hypercholesterolaemia and hypertriglyceridaemia
are normal ndings in pregnancy with concentra-
tions increased by 50% and 300%, respectively.
2
Following delivery the normal range for some liver
function test alters. In particular the aspartate
transaminase, alanine transaminase and g-GTrise by
60e150% in women without hepatic impairment.
3
PREGNANCY SPECIFIC LIVER DISORDERS
There are several disorders that are conned to
pregnancy that affect the liver and are therefore
a common cause of abnormal liver function in
pregnancy. Ultimately, the only cure for these
disorders is delivery; however, medical management
has a role in ameliorating symptoms which may
allow the pregnancy to continue if the womans
and her babys clinical condition allows. It is also
appropriate to use medical management immedi-
ately before delivery to stabilise and optimise the
woman for delivery.
Haemolysis, elevated liver enzymes, low platelets
syndrome
This is a syndrome that is part of the spectrum of
pre-eclampsia and complicates 10e21%
4 5
of severe
pre-eclampsia cases. It most commonly occurs
antenatally (70%) but can occur postnatally in up to
30% of cases. Haemolysis, elevated liver enzymes,
low platelets (HELLP) syndrome often presents
with non-specic symptoms (box 1) and is further
difcult to diagnose as, despite being a variant of
pre-eclampsia, a proportion of women will not have
hypertension or proteinuria at the time of onset of
signs and symptoms (box 2). It is an important
diagnosis to make, however, as HELLP is attributed
1
Oxford Radcliffe Hospitals NHS
Trust, Womens Centre, John
Radcliffe Hospital, Oxford, UK
2
Obstetric Medicine, Imperial
College, Hammersmith Campus,
Institute of Reproduction and
Developmental Biology, London,
UK
Correspondence to
Dr Lucy Mackillop, Oxford
Radcliffe Hospitals NHS Trust,
Womens Centre, John Radcliffe
Hospital, Headley Way, Oxford
OX3 9DU, UK;
lucymackillop@hotmail.com
Received 17 August 2009
Accepted 6 December 2009
160 Postgrad Med J 2010;86:160e164. doi:10.1136/pgmj.2009.089631
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to a high maternal (1e24%)
6 7
and perinatal (7e34%)
8 9
mortality rate.
The diagnosis of HELLP is discussed below. Patients with
HELLP should be managed on a high dependency obstetric unit.
Management involves optimising the health of the mother and
fetus before delivery. This includes: careful monitoring of the
platelet count, liver function tests and clotting; adequately
controlling the blood pressure; and management of uid balance
to optimise kidney function. Correction of coagulopathy with
fresh frozen plasma and platelets maybe required before delivery.
Treatment with magnesium sulfate should also be considered
due to the increased risk of eclamptic seizures in women with
HELLP.
10
Steroids for fetal lung maturity may be indicated for
delivery at early gestations. There is no proven benet to
outcome of giving high dose steroids to women with HELLP. It is
important to remember the maternal condition may continue to
deteriorate after delivery so these management steps should
continue to be performed postnatally in conjunction with close
surveillance to ensure there is no evidence of clinical and
biochemical deterioration.
There is an increased risk of both pre-eclampsia and HELLP in
a subsequent pregnancy. A US study looked at 161 subsequent
pregnancies in 481 women with a diagnosis of HELLP in their
rst pregnancy. The investigators found an increased risk of
complications in the subsequent pregnancies with 43% of
women having pre-eclampsia, and recurrent HELLP occurring in
19e27%, depending on the diagnostic criteria.
11
Acute fatty liver of pregnancy
Acute fatty liver of pregnancy (AFLP) is a rare but dangerous
disorder with maternal case mortality reported between 2e18%
and neonatal mortality 7e58%.
12 13
Again, it may present with
non-specic symptoms and is sometimes difcult to differentiate
from HELLP syndrome (table 2). Typically the liver trans-
aminases, bilirubin, serum creatinine, and white blood cell count
are higher, although they may be raised in both conditions.
Furthermore, hypoglycaemia and coagulopathy are generally
much more evident in AFLP and both need to be monitored
carefully and corrected immediately. A recent prospective study
conrmed the diagnostic criteria for AFLP (box 3). AFLP is
a recognised cause of liver failure, and management should
include involvement of a hepatologist at an early stage to facili-
tate timely transfer to a liver transplant centre if required. It is
important to aim to deliver women with AFLP promptly once
the diagnosis has been made and any serious maternal
biochemical or haematological abnormalities have been
corrected. Most women stabilise after delivery. Affected women
and their offspring should be screened for disorders of b fatty acid
oxidation as AFLP occurs more commonly in heterozygous
mothers who are carrying fetuses that are homozygous for these
disorders.
14
Obstetric cholestasis
Obstetric cholestasis (OC), also called intrahepatic cholestasis of
pregnancy, affects 0.5e1.5% of pregnant Europeans, but is more
common in women of South Asian and South American origin.
The aetiology is complex, but most commonly there is a genetic
predisposition such that studies have reported a 20-fold increased
risk in the rst degree relative of an affected woman.
15
There
Table 1 Liver function tests in normal pregnancy
21
Non-pregnant 1st trimester 2nd trimester 3rd trimester
AST (u/l) 7e40 10e28 11e29 11e30
ALT (u/l) 0e40 6e32 6e32 6e32
Bilirubin (mmol/l) 0e17 4e16 3e13 3e14
g-GT (u/l) 11e50 5e37 5e43 5e41
ALP u/l 30e130 32e100 43e135 130e418
ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase;
g-GT, g-glutamyl transferase.
Box 1 Symptoms and signs in pregnancy that may repre-
sent liver dysfunction
<
New onset nausea and vomiting in the second or third
trimester
<
Itchdespecially (but not exclusively) over palms and soles
and worse at night
< Jaundice
< Polyuria and polydipsia
<
Upper abdominal/epigastric pain
<
Shoulder tip pain
< Dark urine
Box 2 Diagnosis and investigation of haemolysis, elevated
liver enzymes, low platelets (HELLP) syndrome
<
Haemolysis
Peripheral blood lm
Raised unconjugated bilirubin
Raised lactate dehydrogenase (LDH)
< Elevated liver enzymes
Raised alanine aminotransferase (ALT)
Raised aspartate aminotransferase (AST)
Raised LDH
< Low platelets (<100310
9
/l)
<
Ultrasound scan:
Liver (exclude cholecystitis, gallstones, hepatic haema-
toma)
Fetal (check growth, umbilical artery and cord Dopplers,
liquor volume)
Table 2 Differential diagnosis of HELLP syndrome and AFLP (adapted
from C Nelson-Piercy. Handbook of obstetric medicine. Informa
Healthcare; 2006.)
Symptoms/presentation HELLP AFLP
Epigastric pain ++ +
Vomiting 6 ++
Hypertension ++ +
Proteinuria ++ +
Elevated liver enzymes + ++
Hypoglycaemia 6 ++
Hyperuricaemia + ++
Elevated creatinine 6 +
DIC + ++
Thrombocytopenia (without DIC) ++ 6
[White blood cell count + ++
Ultrasound/CT Normal/hepatic haematoma See text
Multiple pregnancy +
Primiparous ++ +
Male fetus 50% 70% (M:F3:1)
AFLP, acute fatty liver of pregnancy; CT, computed tomography; DIC, disseminated
intravascular coagulopathy; HELLP, haemolysis, elevated liver enzymes, low platelets.
Postgrad Med J 2010;86:160e164. doi:10.1136/pgmj.2009.089631 161
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appears to be a cholestatic effect of raised oestrogens and/or
progesterone in susceptible individuals, and this is supported by
evidence that OC is more common in twin pregnancies (where
oestrogen concentrations are higher) and OC symptoms are
sometimes seen in women given exogenous oestrogens and
progesteronesdfor example, the contraceptive pill. OC compli-
cating pregnancy is more common in women with pre-existing
liver disease. However, pre-existing liver disease may not have
been diagnosed before the pregnancy, therefore it is important to
screen for viral causes and autoimmune causes of liver disease in
a woman presenting clinically with OC.
OC is diagnosed in pregnant women with pruritus and
impaired liver function. The specic liver function test abnor-
mality used varies in different studies. Classically affected
women have raised serum bile acids and the authors recommend
that this test should be used to diagnose OC. However, the liver
transaminases are also raised in the majority of cases. Serum
bilirubin and g-GT values are raised in approximately 10% and
30% of cases, respectively. The management of OC involves
careful monitoring of maternal liver function tests and serum
total bile acids, together with assessment of fetal wellbeing and
timely delivery. It is important to diagnose OC as it is associated
with increased fetal complications including spontaneous
preterm labour, meconium stained amniotic uid, fetal distress,
and sudden intrauterine death.
16 17
However, despite improved
fetal monitoring, it is very difcult to predict which babies will
be affected.
Several drug treatments have been proposed for the treatment
of OC.
18
Ursodeoxycholic acid (UDCA) is the most effective drug
at improving maternal symptoms and biochemical abnormali-
ties. Vitamin K administration may protect against postpartum
haemorrhage, and aqueous cream with 1% menthol improves
maternal pruritus.
Perinatal mortality has improved over the last 40 years, but it
is difcult to know the extent to which this is related to
improved perinatal outcome generally over this time; the use of
UDCA to reduce bile acids; improved fetal monitoring; or judi-
cious and often early delivery with improved neonatal outcome
over this time. A retrospective study showed that 90% of intra-
uterine deaths occurred at 37 weeks gestation or later, and this
may explain why many units electively induce women with
proven OC at 37e38 weeks of gestation.
17
A Swedish study
demonstrated that in their population, the fetal complications
listed above did not occur in cases where serum fasting total bile
acids were below 40 mmol/l. However, there was a 1e2% increase
in these complications for every 1 mmol/l rise in bile acids above
this threshold.
16
This study raises the possibility that there may
be a threshold level of serum bile acids above which OC preg-
nancies have high rates of fetal complications, and below which
intervention may not be necessary, and additional studies are
currently assessing this in more detail.
Hyperemesis gravidarum
Hyperemesis gravidarum (HG) occurs when prolonged or severe
vomiting leads to uid, electrolyte and nutritional disturbance in
a pregnant woman. Abnormal liver function tests may occur in
up to 50% of cases and liver failure has been described in asso-
ciation with HG. However, abnormal LFTs in the rst trimester
with or without HG should precipitate a search for another
cause, and HG associated deranged LFTs should be a diagnosis of
exclusion (table 3). Abnormal LFTs should resolve as the HG
improves. Other biochemical abnormalities that occur in HG are
hyponatraemia and hypokalaemia, both of which must be
corrected with care. The condition may also be associated with
biochemical thyrotoxicosisdthat is, raised free tri-iodothyronine
(T3) and thyroxine (T4) and suppressed thyroid stimulating
hormone (TSH) in the absence of clinical hyperthyroidism. This
should not be treated unless there are signs of maternal thyro-
toxicosis as it usually resolves with treatment of the hyperemesis.
Most conventional antiemetic drugs are safe to use in preg-
nancy. In particular there is no evidence for teratogenicity
following treatment with dopamine antagonists (metoclopra-
mide, domperidone), phenothiazines (chlorpromazine,
prochlorperazine), anticholinergics (dicyclomine), or antihista-
mine H
1
receptor antagonists (promethazine, cyclizine), and one
of these should be tried in the rst instance.
LIVER DISEASE INCIDENTAL TO PREGNANCY
Liver disease coincident to pregnancy is an important diagnosis
to make as it has important implications on the mother and
fetus future health; diagnosis may allow safe continuation of the
pregnancy and thus ameliorates the sequelae of premature
delivery on the neonate. Below is a discussion of some of the
more common hepatobiliary conditions encountered in preg-
nancy. For women on maintenance therapy for a chronic liver
condition, it is important to facilitate pre-pregnancy advice to
optimise the medical management of the patient through her
pregnancy.
Box 3 Criteria for the diagnosis of acute fatty liver of
pregnancy (AFLP)
22
Six or more of the following features in the absence of another
explanation:
<
Vomiting
< Abdominal pain
< Polyuria/polydipsia
<
Encephalopathy
< Elevated bilirubin (>14 mmol/l)
< Hypoglycaemia (<4 mmol/l)
<
Elevated urate (>340 mmol/l)
<
Leucocytosis (>113109/l)
< Ascites or bright liver on ultrasound
<
Elevated transaminases (ALT, AST >42 IU/l)
<
Elevated ammonia (>47 mmol/l)
< Renal impairment (creatinine >150 mmol/l)
<
Coagulopathy (prothrombin time >14 s or activated partial
thromboplastin time >34 s)
< Microvascular steatosis on liver biopsy
Table 3 Investigations for abnormal liver function tests
Test Associated diagnosis
Viral hepatitis screendhepatitis A, B, and
C. It may be appropriate to test for E also;
HIV, CMV, EBV, HSV, VZV
Evidence of acute infection (IgM) with any
of these viruses. The viral load is also of
clinical signicance
Liver autoimmune screendANA, anti-
LKM, anti-mitochondrial, anti-SM
Autoimmune hepatitis; primary biliary
cirrhosis; autoimmune sclerosing
cholangitis
Serum copper and caeruloplasmin Wilsons disease
Ferritin Haemochromatosis
Liver ultrasound Gall stones, fatty liver, cirrhotic changes
ANA, antinuclear antibodies; CMV, cytomegalovirus; EBV, EpsteineBarr virus; HIV, human
immunodeciency virus; HSV, herpes simplex virus; LKM, liver/kidney microsomal; SM,
smooth muscle; VZV, varicella zoster virus.
162 Postgrad Med J 2010;86:160e164. doi:10.1136/pgmj.2009.089631
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Viral hepatitis
Hepatitis B and C, in particular, are a worldwide health problem,
together affecting at least 5% of the world population.
19
In
many countries there is now routine screening for hepatitis B as
well as HIV in pregnancy. Therefore, asymptomatic women
newly found to be hepatitis B virus surface antigen positive
(signifying chronic carrier status) are regularly encountered,
depending on the population. It is important to screen for the
other hepatitis viruses as co-infection can affect maternal prog-
nosis and risk of the neonate contracting the disease. Neonatal
infection rates are high (70e90%) in hepatitis B e-antigen
(HBeAg) positive mothers compared to 5e10% in HBeAg nega-
tive mothers. Caesarean section and avoidance of breast feeding
is not protective and the only proven benet to reduce neonatal
transmission is to identify the infected mothers and treat the
neonate immunoprophylactically, with hepatitis B immuno-
globulin immediately after birth followed by the hepatitis B
vaccine.
Hepatitis C seropositivity occurs in approximately 1 in 500
women in the UK. In the absence of co-infection with HIV,
vertical transmission rates are low. Vaginal delivery and breast
feeding do not increase the risks of vertical transmission.
It is important to mention hepatitis E which appears to have
a predilection for the pregnant population and confers a partic-
ularly poor prognosis. It is most prevalent in Asia, Africa and
South America and is transmitted through the faecaleoral route.
It does not progress to chronicity and usually causes a self
limiting illness. However, in the pregnant population, acute liver
failure is reported in up to 20% of women with acute hepatitis E
with high rates of maternal and fetal morbidity and mortality in
this group.
Finally, of note is herpes simplex virus (HSV) which is a rare
cause of hepatitis in pregnancy. Primary HSV infection must be
considered in a pregnant woman with signicant neurological
and/or hepatitic impairment. The classical mucocutaneous
lesions may often be absent. Intravenous acyclovir should be
administered to patients in whom this diagnosis is suspected.
Gall bladder disease
Pregnancy predisposes to gallstone formation and gall bladder
disease is the most common non-obstetric reason for hospital
admission in the year following delivery.
20
It is important,
therefore, to perform an ultrasound scan to rule out the diagnosis
in a woman presenting with symptoms and/or evidence of liver
dysfunction. Magnetic resonance cholangio-pancreatography
(MRCP) is the diagnostic preference, and endoscopic retrograde
cholangio-pancreatography (ERPC) the therapeutic preference,
for extra-hepatic ductal stones in pregnancy. Cholecystitis should
be treated aggressively and may predispose to preterm labour.
Gallstone pancreatitis is a rare but serious complication.
Management is as for the non-pregnant population and, if rst
presentation is in the rst or second trimester, consideration of
antenatal cholecystectomy should be made as there is a high
incidence of recurrence.
Primary biliary cirrhosis and primary sclerosing cholangitis
While rare, boththese conditions affect womenof childbearing age
and may present or symptoms may worsen in pregnancy. Primary
sclerosing cholangitis (PSC) is oftenassociated withinammatory
bowel disease (IBD), and new itch in pregnancy in a woman with
IBD should prompt investigation for this condition (table 3). The
mainstay of treatment for both these conditions is UDCA and
cholestyramine which may be continued during pregnancy. Bile
acids should be monitored as with obstetric cholestasis, and the
dose of UDCA may need to be increased to keep bile acid
concentrations down and symptoms at a minimum.
DIAGNOSIS AND MANAGEMENT OF ABNORMAL LIVER
FUNCTION IN PREGNANCY
Transient mildly deranged LFTs, in the absence of any history,
signs or symptoms, are a common nding within and outside of
pregnancy. However, this nding should precipitate a clinical
and biochemical reassessment at the earliest opportunity.
A transient drug induced (eg, co-amoxyclav (amox-
icillineclavulanic acid)) hepatitis, while usually clinically insig-
nicant, is a common nding. Therefore a careful history should
be taken to elicit this possibility. The majority of liver disorders
specic to pregnancy affect women in the second half of preg-
nancy and are more common the later the gestation, with the
exception of HG. Therefore abnormal liver function in the rst
half of pregnancy should precipitate a hunt for non-pregnancy
specic causes. Anyone with a history of abnormal liver function
or OC in a previous pregnancy should have LFTs checked in early
pregnancy. If abnormal, and in addition to careful history and
examination, investigations suggested in table 3 should be
performed.
Liver disorders in pregnancy generally present in a non-specic
way and box 1 highlights some of the symptoms and signs that
should alert one to the possibility of a hepatic disorder. Women
presenting in the second or third trimester with abdominal pain,
nausea and vomiting or jaundice in the context of abnormal liver
function should be admitted and a rapid assessment made. If
HELLP or AFLP is suspected, the woman should be nursed on
a high dependency unit with rapid assessment of hepatocyte
damage, synthetic function, metabolic function, renal function
and uid status and fetal well-being. Delivery will need to be
Key learning points
<
Liver function tests in pregnancy have a different normal
reference range (table 1).
<
Liver disease in pregnancy can mimic common symptoms of
pregnancy (box 1).
< Several of the most serious and common pregnancy specic
disorders affect the liver, therefore it is important to know and
be able to manage these conditions.
< Acute fatty liver of pregnancy and HELLP have a signicant
maternal and fetal morbidity and mortality, and multidisci-
plinary care in a centre with expertise in high risk pregnancy
and hepatology is required.
Current research questions
< When is the appropriate time to deliver women with obstetric
cholestasis who have responded to ursodeoxycholic acid and
have normal bile acids?
< Does treatment with corticosteroids affect maternal and fetal
morbidity in the HELLP syndrome?
<
What is the inuence of fetal metabolism or genes on the
aetiology of maternal liver disease in pregnancy?
Postgrad Med J 2010;86:160e164. doi:10.1136/pgmj.2009.089631 163
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expedited, but medical management is mandatory before delivery
to correct clotting, stabilise blood pressure, optimise uid
balance, maintain plasma glucose values, and, if the clinical
picture allows, give steroids for fetal lung maturity.
CONCLUSION
Abnormal liver function tests are commonly detected in preg-
nancy, not least because this is a time when women will be
accessing medical services often and blood tests will be done
more readily. Thus previously asymptomatic liver disease may
be picked up in pregnancy. Differentiating between pregnancy
specic disorders and disorders coincident to pregnancy is
important as it will inuence management and, in particular,
timing of delivery. Liver disease complicating pregnancy may
lead to serious maternal and fetal morbidity and needs to be
managed in a centre specialising in high risk pregnancy.
MULTIPLE CHOICE QUESTIONS (TRUE (T)/FALSE (F); ANSWERS
AFTER THE REFERENCES)
1. Normal pregnancy:
A. Normal ranges for liver function tests in pregnancy are
unaltered
B. Albumin is a better marker of hepatic synthetic function that
prothrombin time in pregnancy
C. Blood ow to the liver is increased in pregnancy
D. The nding of mildly raised transaminases is common
postnatally
2. Haemolysis, elevated liver enzymes and low platelets (HELLP):
A. The diagnosis of HELLP is made only when all elements of the
syndrome are present
B. HELLP is a severe form of pre-eclampsia syndrome
C. Renal impairment is more common in HELLP compared to
pre-eclampsia
D. HELLP improves rapidly post-delivery
E. Delivery is the cure for HELLP
3. Obstetric cholestasis (OC):
A. Commonly presents with painless jaundice
B. Itch not affecting soles and palms rules out a diagnosis of OC
C. OC may be diagnosed on clinical grounds only
D. The development of OC may uncover previously undiag-
nosed liver disease
E. OC is associated with an increased risk of perinatal morbidity
and mortality
4. Viral hepatitis:
A. The viral hepatidides are more common in pregnancy
B. Hepatitis E confers a particularly poor prognosis in pregnancy
C. The maternal hepatitis E antigen level predicts neonatal
transmission
D. Breast feeding should always be avoided with hepatitis B and
C
E. Co-infection with HIV does not alter prognosis for mother or
baby
5. Acute fatty liver of pregnancy:
A. Is more common in women carrying a male fetus
B. May lead to liver failure
C. Is less likely to cause coagulation abnormalities than HELLP
D. May be associated with pre-eclampsia
E. Should be managed in a high dependency facility
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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ANSWERS
1. A (F); B (F); C (F); D (T); 2. A (F); B (T); C (T); D (F); E (T); 3. A (F); B (F); C (F); D (T);
E (T); 4. A (F); B (T); C (T); D (F); E (F); 5. A (T); B (T); C (F); D (T); E (T)
Key references
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164 Postgrad Med J 2010;86:160e164. doi:10.1136/pgmj.2009.089631
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2010 86: 160-164 Postgrad Med J

Lucy Mackillop and Catherine Williamson

Liver disease in pregnancy

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