A case report of abnormally high AFP
OPTIONAL
LOGO HERE
OPTIONAL
LOGO HERE
N Aedla, A Duncan
Princess Royal Maternity Hospital, Glasgow, UK
Case
Introduction
AFP is an effective screening tool in identifying
women with pregnancies at risk of neural tube
defects. The levels are measured as multiples of
normal median rather than percentiles as they are
stable and easy to derive. AFP levels of 2-5 MoM give
a 1 in 20 chance of a fetus with open spina bifida
and 1 in 10 chance of any neural tube defect.1
Alpha-fetoprotein (AFP) is a major fetal protein
weighing 65KD and has similar properties to albumin.
AFP is formed initially from the yolk scan, then the
fetal liver and smaller concentrations from the
gastrointestinal tract.2 AFP can be raised due to
abnormality of any of these structures. In the fetus,
AFP levels peak at the end of the first trimester and
decline from 14 weeks onwards. Maternal serum AFP
levels are 50,000 times lower and rise from 10-32
weeks, declining thereafter. Only 9% of fetuses with
>4 MoM AFP levels have a normal outcome. We
present one such case.
•Antenatal:
Case
A 34- year old lady booked with us at 11+3 gestation
in her first pregnancy. Her BMI measured 24. She
smoked 10 cigarettes a day and was keen for
smoking cessation referral. Her booking ultrasound
scan was reassuring. Her booking bloods returned as
normal. She opted for second trimester serum
screening and fetal anomaly scan at 20 weeks. Her
maternal serum AFP returned as abnormally high at
80 MoM. This result was discussed with the Prenatal
screening specialist and repeated as it was thought
to be spurious. The repeat result returned as 40
MoM. The lab had not encountered a result as high
as this before and did not have facilities to subtype
the AFP result. She was promptly counselled and
offered amniocentesis, which she declined.
TEMPLATE DESIGN © 2008
www.PosterPresentations.com
•Investigations:
•In the form of investigations, she had a
transvaginal ultrasound scan to rule out ovarian
pathology, chest X-ray, liver functions tests, CEA &
Ca125 levels, AFP levels, bone profile and MRI
abdomen. Of all these tests, the only positive test
was the AFP level which measured 40KU/L. There
were few simple cysts noted in the liver which
were not suspicious. Fetal MRI showed an intact
abdominal wall and no gross neural tube defects.
Her case was discussed at the high risk meeting
and she was offered serial growth scans and
planned delivery by her due date. She was made
aware of the association of congenital nephrosis by
the paediatricians and they planned to organise
abdomen ultrasound scan, blood urea &
electrolytes once the baby was born.
Discussion
Raised AFP is associated with adverse perinatal
outcomes.3
•Causes of raised AFP:
Maternal
Gastrointestin
al disorders
Gastrointestin
al
abnormalities
Endodermal
sinus tumours
Germ cell
tumours
Neural tube
defects
Placental
previa
Smoking
Congenital
Nephrosis
•She was induced at 39 weeks with 3 doses of 3mg
Prostaglandin tablets, artificial rupture of
membranes and syntocinon infusion. She had a
mid-cavity forceps delivery due to a non-reassuring
CTG in active 2nd stage of labour. She had blood
cultures and had IV Co-Amoxiclav for intrapartum
pyrexia. The cultures were negative. She delivered
a live girl weighing 2.64kgs with apgars of 9 at 1
and 9 at 5 minutes. She had 1 litre blood loss due
to atonic PPH which was managed with uterotonic
agents. The cord gases and placenta were normal.
Flu vaccine
for contraception.
Placental
Yolk sac
tumours
Nephrosis
•She bottle fed the baby and both recovered well.
She was reviewed postnatally by the Obstetric
team and Gastroenterologists. Her AFP levels were
<3KU/L at 6 weeks postnatally. She had no signs of
chronic liver inflammation. She uses Microgynon
Fetal
Liver disorders Liver
abnormalities
•Intrapartum:
•Postnatal:
Summary
Placental permeability and villous space influence
serum AFP levels. This response is due presence of
intra-uterine adverse conditions.
In our case, there were a few factors which could
have contributed to abnormally high AFP levels.
These include smoking, flu vaccination, low lying
placenta in the 2nd trimester (resolved in the 3rd
trimester) and simple liver cysts. The possibility of
nephrosis was discussed and this has not been
proven thus far. None of these have proven to be
confirmatory.
AFP itself is not harmful, but is a marker of
adverse outcomes. A multi-disciplinary team
approach involving prenatal screening specialists,
gastroenterologists and paediatricians is
important. Investigations should involve blood
tests, imaging and placental pathology.
References
•Effects of raised AFP:
Maternal
Fetal
Miscarriage
Oligohydramnios
Pre-ecclampsia
Stillbirth
Placental abruption
Low birth-weight
Neonatal death
1. Wald, N.J., H. Cuckle, J.H. Brock et al. 1977.
Maternal serum alpha-fetoprotein measurement in
antenatal screening for anencephaly and spina bifida in
early pregnancy. Report of the U.K. collaborative study
in alpha-fetoprotein in relation to neural-tube defects.
Lancet 1:1323-1332.
2. Boyd P A. Why might maternal serum AFP be high in
pregnancies in which the fetus is normally formed. BJOG
Feb 1992, Vol.99, pp. 93-95
3. Gagnon A, Wilson RD, Audibert F et al. Society of
Obstetricians and Gynaecologists of Canada Genetics
Committee. Obstetric complications with abnormal
maternal serum markers analytes. J Obstet Gynaecol
Can.2008 Oct;30(10):918-49