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A case report of abnormally high AFPN Aedla, A Duncan

Princess Royal Maternity Hospital, Glasgow, UK

Introduction Discussion Summary

References

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

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.

Case

•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.

•Intrapartum:

•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.

•Postnatal:

•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 for

contraception.

Raised AFP is associated with adverse perinatal outcomes.3

•Causes of raised AFP:

OPTIONALLOGO HERE

OPTIONALLOGO HERE

Maternal Fetal Placental

Liver disorders

Liver abnormalities

Yolk sac tumours

Gastrointestinal disorders

Gastrointestinal abnormalities

Endodermal sinus tumours

Germ cell tumours

Neural tube defects

Placental previa

Smoking Congenital Nephrosis

Nephrosis

Flu vaccine

•Effects of raised AFP:

Maternal Fetal

Miscarriage Oligohydramnios

Pre-ecclampsia Low birth-weight

Stillbirth Neonatal death

Placental abruption

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:

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.

Case