7 :3

MANAGEMENT OF JAUNDICE IN PREGNANCY

ABSTRACT
Abnormal liver tests occur in 3%-5% of pregnancies, with many
potential causes, including coincidental liver disease (most
commonly viral hepatitis or gallstones) and underlying chronic
liver disease. However, most liver dysfunction in pregnancy is
pregnancy-related and caused by 1 of the 5 liver diseases unique to
the pregnant state: these fall into 2 main categories depending on
their association with or without preeclampsia.The preeclampsiaassociated liver diseases are preeclampsia itself, the hemolysis
(H), elevated liver tests (EL), and low platelet count (LP) (HELLP)
syndrome, and acute fatty liver of pregnancy. Hyperemesis
gravidarum and intrahepatic cholestasis of pregnancy have no
relationship to preeclampsia. Although still enigmatic, there have
Table 1 : Features of pregnancy-associated liver
diseases
Disease

Timing of
occurrence
First trimester

Clinical
features
Nausea, vomiting,
weight loss,
nutritional
deficiency

Second/third
trimester

Syndrome
Third trimester
of hemolysis,
elevated liver
tests, and low
platelets (HELLP)

Hypertension,
edema,
proteinuria,
neurological
deficits
(headaches,
seizures, coma)
Abdominal
pain, nausea,
vomiting, edema,
hypertension,
proteinuria

Acute fatty liver

of pregnancy
(AFLP)
Intrahepatic
cholestasis of
pregnancy (ICP)

Nausea, vomiting,
abdominal pain,
fatigue, jaundice
Pruritus, jaundice,
fatigue, abdominal
pain, steatorrhea

Hyperemesis
gravidarum

Preeclampsia/
eclampsia

Third trimester

Second/third
trimester

Histology
No distinct
histopathology,
may see
normal tissue
or hepatocyte
necrosis, bile
plugs, steatosis
Periportal
hemorrhage,
necrosis, fibrin
deposits, may see
microvesicular fat

Necrosis,
periportal
hemorrhage,
fibrin deposits

Microvesicular fat

Centrilobular
cholestasis, no
inflammation

Rajendra Kumar Jain, Bhopal

been recent interesting advances in understanding of these unique
pregnancy-related liver diseases. Hyperemesis gravidarum is
intractable,dehydrating vomiting in the first trimester of pregnancy;
50% of patients with this condition have liver dysfunction.
Intrahepatic cholestasis of pregnancy is pruritus and elevated bile
acids in the second half of pregnancy, accompanied by high levels
of aminotransferases and mild jaundice. Maternal management is
symptomatic with ursodeoxycholic acid; for the fetus, however,
this is a high-risk pregnancy requiring close fetal monitoring and
early delivery. Severe preeclampsia itself is the commonest cause
of hepatic tenderness and liver dysfunction in pregnancy, and 2%12% of cases are further complicated by hemolysis (H), elevated
liver tests (EL), and low platelet count (LP)-the HELLP syndrome.
Immediate delivery is the only definitive therapy,but many maternal
complications can occur, including abruptio placentae, renal failure,
subcapsular hematomas, and hepatic rupture. Acute fatty liver
of pregnancy is a sudden catastrophic illness occurring almost
exclusively in the third trimester; microvesicular fatty infiltration
of hepatocytes causes acute liver failure with coagulopathy and
encephalopathy. Early diagnosis and immediate delivery are
essential for maternal and fetal survival.

HYPEREMESIS GRAVIDARUM
Hyperemesis gravidarum (HG) is defined as intractable nausea and
vomiting during pregnancy that often leads to fluid and electrolyte
imbalance, weight loss of 5% or greater, and nutritional deficiency
requiring hospital admission 1. The incidence of HG varies from
0.3%-2% of all live births 2. HG often occurs between the 4th
and 10th wk of gestation and usually resolves by the 20th wk.
However, in approximately 10% of HG patients, symptoms
continue through pregnancy and resolve only with delivery of the
fetus 3. Liver involvement is seen in about 50%-60% of patients with
HG 4. Most commonly seen are mild serum aminotransferases
elevations, but there are reported cases of severe transaminase
elevations (alanine aminotransferase (ALT) levels 400 to over
1000 U/L) 5. Mild hyperbilirubinemia with mild jaundice can be seen
as well. Other complications include disturbances in electrolytes
and in water and acid-base balance that can usually be treated
adequately with hydration.

Management of Jaundice in Pregnancy

Table 2 : Safety of drugs used in pregnancy-associated liver diseases
Drug
FDA pregnancy category
Comments
Antiemetics Promethazine
C
Possible respiratory depression if drug is administered near time of delivery
Metoclopramide
B
Available evidence suggests safe use during pregnancy
Ondansetron

Prochlorperazine

Antihypertensives
ACE inhibitors

C/D

Beta blockers

C/D

Calcium channel blockers

Enoxaparin

Heparin

Teratogenic and embryotoxic effects have been demonstrated in small animals. There are no
adequate and well-controlled studies in pregnant women
Adverse effects in the fetus include intrauterine growth retardation, salicylate intoxication,
bleeding abnormalities, and neonatal acidosis. Use of aspirin close to delivery may cause
premature closure of the ductus arteriosus. Data have shown low-dose aspirin (60-150 mg/ day)
may be safe in pregnancy
No adequate and well-controlled studies using enoxaparin. Postmarketing reports include
congenital abnormalities and also fetal death
Does not cross the placenta

Intrahepatic cholestasis
Ursodeoxycholic acid
S-adenosyl-L-methionine
Cholestyramine

Relatively low risk

Anticoagulation Aspirin

Additional studies are needed to determine safety to the fetus, particularly during the first
trimester
There are isolated reports of congenital anomalies; however, some included exposures to other
drugs. Jaundice, extrapyramidal signs, hyper-/hyporeflexes have been noted in newborns
First trimester exposure to ACE inhibitors may cause major congenital malformations Second
and third trimester use of an ACE inhibitor is associated with oligohydramnios and anuria,
hypotension, renal failure, skull hypoplasia, and death in the fetus/neonate
Fetal bradycardia, hypotension, risk of intrauterine growth retardation

C (1st/2nd trimesters)
D (3rd trimester)

Not evaluated by FDA

C

Relatively low risk

Cholestyramine is not absorbed systemically, but may interfere with vitamin absorption

While maternal morbidity is well documented,the effects of HG on

the fetus are less clear. Some data suggest no differences between
fetuses born to mothers with HG and non-HG mothers 6. In one
large cohort study, infants of HG mothers were found to have
lower birth weights and higher rates of being small for gestational
age 7. Treatment of HG is primarily supportive. Patients should
avoid triggers that aggravate nausea, and eat small, frequent, lowfat meals. Intravenous fluids, thiamine and folate supplementation,
and antiemetic therapy may be administered. Promethazine is a
first-line agent, but other medications such as metoclopramide,
ondansetron, and steroids have also been used.

PREECLAMPSIA/ECLAMPSIA
Preeclampsia defined by the triad of hypertension, edema, and
proteinuria. It affects about 5%-10% of all pregnant women
and usually occurs late in the second trimester or in the third
trimester. In preeclampsia, hypertension is defined as having a
systolic pressure greater than 140 mmHg and a diastolic pressure
greater than 90 mmHg on at least two occasions that are at least 4
to 6 h apart in a previously normotensive patient, and proteinuria is
defined as equal to or greater than 300 mg of protein in a 24 h urine
collection or 1+ protein or greater on urine dipstick testing of two
random urine samples collected at least 4 to 6 h apart 8. Eclampsia
involves all features of preeclampsia and includes neurologic
symptoms such as headaches, visual disturbances, and seizures
or coma. Risk factors for preeclampsia and eclampsia include
nulliparity, extremes of maternal age, insulin resistance, obesity,
and infection 8, 9.The pathophysiology of preeclampsia/ eclampsia is

471

thought to involve procoagulant and proinf lammatory states that

create glomerular endotheliosis, increased vascular permeability,
and a systemic inflammatory response that results in end organ
damage and hypoperfusion.
Abnormal laboratory values include a 10- to 20-fold elevation
in aminotransferases, elevations in alkaline phosphatase levels
that exceed those normally observed in pregnancy, and bilirubin
elevations of less than 5 mg/dL. Liver histology generally shows
hepatic sinusoidal deposition of fibrin along with periportal
hemorrhage,liver cell necrosis,and in severe cases,infarction;these
changes are likely due to vasoconstriction of hepatic vasculature10.
Microvesicular fatty infiltration has also been observed in some
cases of preeclampsia, suggesting a possible overlap with acute
fatty liver of pregnancy 11. Maternal mortality from preeclampsia/
eclampsia is rare in developed countries, but may approach 15%20% in developed countries 8. Likewise, the fetal mortality rate is
rare, occurring in 1%-2% of births.The only effective treatment for
preeclampsia is delivery of the fetus and placenta. Pharmacological
agents used in preeclampsia include antihypertensives such as
calcium channel blockers and low-dose aspirin. Magnesium sulfate
may be administered if eclampsia develops.

HEMOLYSIS, ELEVATED LIVER TESTS AND LOW

PLATELETS (HELLP)
HELLP syndrome is a multisystemic disorder of pregnancy
involving hemolysis, elevated liver tests, and low platelets. About
70% of cases occur antenatally, during the last trimester of
pregnancy 12. The pathogenesis of HELLP is thought to involve

Medicine Update 2010 Vol. 20

alterations in platelet activation, increases in proinflammatory

cytokines, and segmental vasospasm with vascular endothelial
damage.An association with a defect in long-chain 3-hydroxyacylcoenzyme A dehydrogenase (LCHAD) has also been described,
suggesting a possible overlap of HELLP syndrome and acute fatty
liver of pregnancy.
Most patients present with right upper quadrant abdominal pain,
nausea, vomiting, malaise, and edema with significant weight gain.
Less commonly associated conditions include renal failure (with
increased uric acid), diabetes insipidus, and antiphospholipid
syndrome. Other late findings of HELLP include disseminated
intravascular coagulopathy (DIC), pulmonary edema, placental
abruption, and retinal detachment. Laboratory findings include
hemolysis with increased bilirubin levels (usually less than 5 mg/
dL) and lactate dehydrogenase (LDH) levels greater than 600 IU/L,
moderately elevated aspartate aminotransferase (AST) and ALT
levels (200 IU/L to 700 IU/L), and thrombocytopenia (less than 100
000/mL). In early stages, prothrombin time and activated partial
thromboplastin time are normal, but in later phases, DIC may be
present with increased levels of fibrin degradation products and
D-dimer, and thrombin- antithrombin complexes.

Histology of Hemolysis, elevated liver enzymes, low platelet

count syndrome
Pathogenesis involve intravascular fibrin deposition and sinusoidal
obstruction that can lead to hepatic hemorrhage and infarction.
Histologically, one may see focal hepatocyte necrosis, periportal
hemorrhage, and fibrin deposits.The reported maternal mortality
from HELLP is 1%, and the perinatal mortality rate ranges from
7%-22% and may be due to premature detachment of placenta,
intrauterine asphyxia, and prematurity 4. Other complications of
HELLP syndrome include acute renal failure, adult respiratory
distress syndrome, pulmonary edema, stroke, liver failure, and
hepatic infarction. The only definitive treatment for HELLP
syndrome is delivery. If the pregnant woman is greater than 34
wk gestation, immediate induction is recommended. If gestational
age is between 24 wk and 34 wk, corticosteroids are administered
to accelerate fetal lung maturity in preparation for delivery 48
h later. After delivery, close monitoring of the mother should
continue, as data have shown worsening thrombocytopenia and
increasing LDH levels up to 48 h postpartum 13. However, most
laboratory values (transaminases, bilirubin, LDH) normalize in
48 h. For patients with ongoing or newly developing postpartum
symptoms of HELLP, modalities such as antithrombotic agents,
plasmapheresis, and dialysis may be employed.

472

ACUTE FATTY LIVER OF PREGNANCY

Acute fatty liver of pregnancy (AFLP) is a rare but serious maternal
illness that occurs in the third trimester of pregnancy. With an
incidence of 1 in 10 000 to 1 in 15 000 pregnancies, it has a
maternal mortality rate of 18% and a fetal mortality rate of 23%
10,14
. AFLP is more commonly seen in nulliparous women and
with multiple gestation. The pathophysiology of AFLP involves
defects in mitochondrial fatty acid beta-oxidation. Under normal
circumstances, an individual that is heterozygous for enzymatic
mutations in fatty acid oxidation will not have abnormal fatty
oxidation. However, when a heterozygous woman has a fetus that
is homozygous for such mutations, fetal fatty acids accumulate
and return to the mothers circulation. The extra load of longchain fatty acids and subsequent triglyceride accumulation lead to
hepatic fat deposition and impaired hepatic function in the mother.
A deficiency in longchain 3-hydroxyacyl-CoA dehydrogenase
(LCHAD) is thought to be associated with the development of
AFLP. LCHAD is a component of an enzyme complex known
as the mitochondrial trifunctional protein (MTP), and it is
believed that the G1528C and E474Q mutations of the MTP are
responsible for causing LCHAD deficiency that subsequently leads
to AFLP 15. Patients with AFLP typically present with a 1 to 2 wk
history of nausea, vomiting, abdominal pain, and fatigue. Jaundice
occurs frequently, and some women experience moderate to
severe hypoglycemia, hepatic encephalopathy, and coagulopathy.
Approximately 50% of these patients will also have signs of
preeclampsia, although hypertension is generally not severe 16.
Laboratory findings include elevations in aminotransferase levels,
which may range from being mildly elevated to approaching 1000
IU/L.
Since AFLP can lead to significant maternal and fetal morbidity
and mortality, prompt diagnosis must be made.The most definitive
test is liver biopsy. Histopathologic findings reveal swollen, pale
hepatocytes in the central zones with microvesicular fatty
infiltration that can be identified on frozen section with oil red O
staining. Electron microscopy may also show megamitochondria
and paracrystalline mitochondrial inclusions. Although liver
biopsy may be helpful, it is often not done due to the presence
of coagulopathy. Therefore, the diagnosis of AFLP is usually made
on clinical and laboratory findings.

Histology of acute fatty liver of pregnancy

Management of Jaundice in Pregnancy

As with most pregnancy-associated liver diseases, the treatment
of AFLP involves delivery of the fetus. In rare cases, patients
will progress to fulminant hepatic failure with need for liver
transplantation 17. careful attention should also be paid to the infant
given the increased risk of cardiomyopathy, neuropathy, myopathy,
nonketotic hypoglycemia, hepatic failure, and death associated
with fatty acid oxidation defects in newborns.

INTRAHEPATIC CHOLESTASIS OF PREGNANCY

Intrahepatic cholestasis of pregnancy (ICP),also known as obstetric
cholestasis, is a rare pregnancyspecific liver condition that occurs
in the late second or third trimester and has a prevalence of about
1/1000 to 1/10 000. It is significantly more common in South
Asia, South America (especially Chile), and Scandinavian countries.
ICP is also more common in women of advanced maternal age,
multiparous women, and in women with a personal history of
cholestasis with oral contraceptive use 18. The prognosis for
women with ICP is usually good, but it is associated with increased
fetal morbidity and mortality, particularly from chronic placental
insufficiency, preterm labor, fetal distress, and intrauterine death
19
. The etiology of ICP is likely multifactorial and variations.
Mutations in the phospholipid translocator known as the ATPcassette transporter B4 (ABCB4) or multidrug resistant protein-3
(MDR3) are associated with the development of ICP 20. Changes
induced by these genetic mutations lead to increased sensitivity
to estrogen, which impairs the sulfation and transportation of bile
acids. Estrogens are thought to act on hepatocytes by decreasing
membrane permeability and bile acid uptake by the liver. The
maternal-tofetal transfer of bile acids across the placenta becomes
impaired, leading to potentially toxic bile acid levels in the fetus
21
. The elevation in bile acid levels is also thought possibly to
affect myometrial contractility and to cause vasoconstriction of
chorionic veins in the placenta, which may contribute to preterm
deliveries and fetal distress seen in ICP 22, 23.
The classic symptom is pruritus that usually begins in the second
or third trimester. It usually occurs in the palms and soles and may
progress to the rest of the body, and the pruritus is often worse
at night. Pruritus may be severe but is usually relieved within 48
h after delivery of the fetus. Jaundice occurs in approximately
10%-25% of patients and may appear within the first four weeks
of the onset of pruritus 24. Cholelithiasis and cholecystitis have
been observed to occur with greater frequency in women with
ICP 25. Abnormal laboratory findings include elevated total bile
acid levels up to 10- to 25-fold, with an increase in cholic acid
and a decrease in chenodeoxycholic acid leading to a marked
elevation in the cholic/ chenodeoxycholic acid ratio. The glycine/
taurine ratio is also reduced. AST and ALT levels rarely exceed
two times the upper limits of normal, but may approach 10- to
20-fold elevations in rare cases. Bilirubin levels may be elevated,
but are usually less than 6 mg/dL. Serum alkaline phosphatase
levels may also be elevated, but this is usually less helpful to follow
given typical alkaline phosphatase elevations seen in pregnancy.
Liver biopsy is usually not required to make the diagnosis of ICP.

473

The treatment of choice for ICP is ursodeoxycholic acid (UDCA),

which helps to relieve pruritus and improve liver test abnormalities.
It is unclear how UDCA works, but it is felt that UDCA conjugates
help target and insert key transporter proteins, such as MRP2
(ABCC2) or bile salt export pumps (ABCB11) into the canalicular
membranes 26. Other medications, such as cholestyramine and
S-adenosyl-L-methionine, have been associated with improving
pruritus and normalizing biochemical profiles, but studies have
found UCDA to be superior over cholestyramine and S-adenosylL-methionine 27, 28. Dexamethasone has also been used, but has
shown to be much less effective in reducing bile acids and bilirubin
and ineffective in relieving pruritus 29.Antihistamines are frequently
used to alleviate pruritus, and vitamin K and other fat-soluble
vitamin supplementation should also be administered if fat
malabsorption is suspected.

COMMON LIVER DISEASES AND PREGNANCY

Viral Hepatitis
Viral hepatitis is the most common form of liver disease
worldwide and it frequently affects women of childbearing age,
either as an acute infection or as a chronic disease. Hepatitis A
does not appear to alter the normal course of pregnancy nor
does pregnancy appear to influence the natural history of hepatitis
A. Acute and chronic viral hepatitis of other types however may
have implications for maternal well-being as well as the outcome
of gestation.

HEPATITIS E
Hepatitis E virus infection occurs in non-industrialized nations,
usually as an epidemic disease during the monsoon season in
central and south Asia and India; it is rare in the West. Acute
hepatitis E during the third trimester of pregnancy is a cause of
fulminant hepatic failure and has a mortality rate of up to 20%
30
. Maternal Hepatitis E virus infection also has been associated
with intrauterine fetal death 31, 32. The risks of intrauterine death
and abortion in any trimester are greater in pregnant women
with hepatitis E than they are in their uninfected counterparts.
Maternal-fetal transmission of hepatitis E resulting in symptomatic
neonatal hepatitis has occurred 33; no known therapy will prevent
vertical transmission of this virus.

HEPATITIS B
As a rule maternal hepatitis B virus infection does not influence
the course of pregnancy nor does pregnancy alter the natural
history of maternal hepatitis B. Most women of childbearing age
with chronic hepatitis B are healthy virus carriers with a very low
risk of developing complications of their disease during gestation.
The importance of hepatitis B during pregnancy is related to its
role in the perpetuation of chronic infection through vertical
transmission: Maternal-fetal transmission of hepatitis B virus is
responsible for most cases of chronic hepatitis B worldwide
especially in Southeast Asia and Africa 34. Mothers with a reactive
serum test for hepatitis B e antigen (HBeAg) have more circulating

Medicine Update 2010 Vol. 20

virus and higher rates of perinatal transmission than do mothers

without detectable serum HBeAg and a reactive serum test for
anti-HBeAg 35 although the latter individuals are still a source
of neonatal infection 36. Without treatment 90% of infants born
to HBeAg positive mothers and 10% of infant born to HBeAgnegative mothers develop hepatitis B virus infection. The infants
of mothers with a reactive serum test for hepatitis B surface
antigen should receive hepatits B immunoglobulin at birth and also
hepatitis B vaccine during the first day of life and at ages 1 and 6
months 37. Women with chronic hepatitis B are not treated with
interferon during pregnancy. Therapy with the nucleoside analog,
lamivudine is probably safe in pregnant patients and has been
reported to reduce the incidence of neonatal vaccination failure 38.
Data concerning the toxicity and efficacy in this setting of adefovir
dipivoxil a newer nucleotide analog of adenosine monophosphate
and of entecavir a guanosine nucleoside analog are insufficient to
allow any conculsion.
HEPATITIS C
HCV infection in pregnancy has a presentation that is similar to
that of HCV infection in non-pregnant patients. HCV-infected
women do not need to be advised against pregnancy, but
they should be counseled on the risks of mother-to-infant
transmission of HCV. The risk for vertical transmission of
HCV is about 5%-10%.The risk of perinatal transmission of HCV
is associated with the presence of HCV RNA in maternal blood at
the time of birth and coinfection with human immunodeficiency
virus (HIV) 39. HIV coinfection in pregnant women increases
the risk of perinatal HCV transmission by 2-fold, and in more
than 25% of cases, both HCV and HIV are transmitted together.
Prolonged rupture of membranes (greater than 6 h) has also
been associated with an increased risk of perinatal HCV
transmission; thus, it is advised that the second stage of labor be
kept short in HCV-infected pregnant women 40. Data on the effects
of the mode of delivery on HCV transmission are conflicting;
therefore, there are no recommendations regarding the
method of delivery that should be used in HCV-infected pregnant
women. Although HCV is detectable in breast milk, there is little
documented evidence of transmission of HCV via breastfeeding.
However, the Centers for Disease Control and Prevention (CDC)
recommend that HCV-infected women with cracked or bleeding
nipples should abstain from breastfeeding 41.
Combination antiviral therapy with pegylated interferon
and ribavirin is generally recommended for HCV-infected
patients. Ribavirin has a category X designation by the
FDA. Interferon has a designation as category C, as it has
been shown to have abortifacient effects in animal models.
Therefore, combination antiviral therapy is not recommended
for HCV-infected pregnant women. There are a few reports of
women becoming pregnant while on interferon monotherapy for
HCV, and in these cases, healthy babies were delivered and were
found to have normal growth and development at follow up 42-44.

474

CHRONIC LIVER DISEASE & PORTAL

HYPERTENSION
Fertility is decreased in women with significant hepatic
dysfunction due to hypothalamic-pituitary dysfunction. However,
cirrhosis is not a contraindication, as pregnancy may be tolerated if
cirrhosis is well-compensated and without features of portal
hypertension 45. Portal hypertension leads to increased maternal
complications, including variceal hemorrhage , hepatic failure,
encephalopathy, jaundice, malnutrition , and splenic artery
aneurysm 46. Bleeding from esophageal varices has been reported
in 20%-25% of pregnant women with cirrhosis 47. All pregnant
women with cirrhosis should be screened for varices starting in
the second trimester and started on beta-blockers if indicated.
The treatment of variceal bleeding consists of both endoscopic
and pharmacologic treatment. However, vasopressin has been
shown to cause placental ischemia, necrosis, and amputation of
fetal digits and is contraindicated in pregnancy; there is a paucity
of information about the use of octreotide in pregnancy 48. Finally,
though there are no good studies evaluating the impact of vaginal
delivery of the risk of variceal bleeding, it is recommended
that patients have cesarean section to avoid increased straining 49.

WILSON DISEASE
Wilson disease in women of childbearing age is associated with
amenorrhea and infertility. Treatment of affected individuals to
remove excess copper may result in resumption of ovulatory
cycles and subsequent pregnancy. Pregnant patients must remain
on medication to treat Wilson disease because discontinuation
of therapy can cause sudden copper release hemolysis, acute liver
failure and death 50. D-penicillamine is potentially teratogenic in
humans 51 but has beeen used safely during pregnancy at doses
necessary for copper chelation 52. Similarly trientine is teratogenic
in animals but appears to be saafe in humans as treatment for
copper overload. Zinc is not teratogenic and some experts favor
its use during pregnancy as therapy for Wilson disease for this
reason 53.

AUTOIMMUNE LIVER DISEASE

Autoimmune diseases of all types including autoimmune hepatitis
are more common in women then in men. In women, classic
(type 1) autoimmune hepatitis typically presents around the
expected time of menarche but is associated with amenorrhea.
Immunosuppressive therapy is highly effective in controlling the
disease in most patients;treated women who subsequently conceive
a child should continue taking immunosuppressive medications
during pregnancy.The doses of azathioprine prescribed as part of
standard treatment regimens are belived not to be teratogenic.
Occasionally autoimmune liver disease will worsen during the
postpartum period when the physiologic immunosuppression
of pregnancy resolves. For this reason affected patients should
have frequent measurements of serum aminotransferase levels
for approximately 6 months after delivery.

Management of Jaundice in Pregnancy

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