Intra‐amniotic inflammation in human gastroschisis: possible aetiology of postnatal bowel dysfunction

Objective To assess amniotic fluid for evidence of an inflammatory exudate in association with fetal gastroschisis. Setting University College Hospital, London and Institute of Child Health, London. Sample Samples of amniotic fluid in the third trimester from pregnant women with a diagnosis of fetal gastroschisis (n = 10) and from a control group (n= 10) with a normal fetus. Methods Cytological analysis of the fluid was performed. Flow cytometry was performed on the amniotic fluid using antibodies for the myeloid cell antigen CD 15, the leucocyte beta integrin CDI1b/CD18 and CD3, CD19, CD56 and CD25. Tumour necrosis factor alpha and interleukin‐8 levels were assayed in the amniotic fluid. Results An acute inflammatory exudate, composed predominantly of neutrophil polymorphs and mononuclear cells, was found in the amniotic fluid in fetal gastroschisis but not in control cases. When amniotic fluid samples from cases of fetal gastroschisis were stained with CD 15, analysis by flow cytometry showed a clear positive population. This CD 15 population showed markedly elevated levels of CD 11b. No distinct population of CD 15 positive cells was seen in amniotic fluid samples examined from the control group. No staining was seen with antibodies to CD3, CD 19, CD56 or CD25 in amniotic fluid obtained from either group. There was no significant difference between tumour necrosis factor alpha levels measured in the amniotic fluid of cases of fetal gastroschisis (median 102 pg/mL; range 20–340) and those of the control group (140 pg/mL; range 20–548) (P= 0.1). The levels of interleukin‐8 were markedly elevated in the amniotic fluid of cases of fetal gastroschisis (median 6320 pg/mL; range 4732–13,800) compared with the control group (median 1738 pg/mL; range 623–2861;) (P < 0.01). Conclusion Human fetal gastroschisis is associated with an inflammatory exudate in the amniotic fluid which may have implications for postnatal bowel function.