Factors increasing risk of ectopic pregnancy

We believe that pregnancies implant in the fallopian tube because of a combination of factors: A failure of the mechanisms which move the pregnancy along the fallopian tube into the womb and a change in the environment in the fallopian tube that allows early implantation to occur.

We also know that some things make a patient more at risk of having an ectopic pregnancy. For example, where a patient has had previous abdominal surgery, the risk is said to be increased up to 4 times. If a patient had a sexually transmitted infection like Chlamydia, then the risk is increased up to 2 and 3 times. If the patient is a smoker, again, the risk is increased between 2 and 3 times. The risk is even increased by fertility treatment, such as IVF.

How the risk factors cause ectopic pregnancy is something that is not yet fully understood and studies are ongoing. To find out more about each of these individual risks and associated research, please click on the titles below and they will expand into more detail.

Chlamydia

The following paper in Fertility and Sterility offers a review of the literature examining the mechanism of action of Chlamydia on the Fallopian tube. It summarises what we know and where the gaps are in our knowledge.

Shao R, Wang X, Wang W, Stener-Victorin E, Mallard C, Brännström M, Billig H. From mice to women and back again: casualties and clues for Chlamydia-induced tubal ectopic pregnancy. Fertility and Sterility 2012 Nov; 98(5):1175-1185.

The paper outlines how complex the mechanisms are that can lead to tubal infertility. It suggests biological and epidemiological evidence that progression of Chlamydia Trachomatis infection causes intense and persistent inflammation, injury, and scarring in the fallopian tube, leading to a substantially increased risk of ectopic pregnancy and infertility. The main targets of Chlamydia infection are epithelial cells lining the mucosal surface, which play a central role in host immune responses and pathophysiology.

The paper also describes how knockout mouse models can be used to study tubal function in the hope of better understanding how Chlamydia impacts on tubal motility and implantation. Tubal phenotypes at the cellular level in mutant mice appear to reflect alterations in the balance between inflammatory mediator and factor deficiency. While studies in mice infected with Chlamydia muridarum have provided insight into potential inflammatory mediators linked to fallopian tube pathology, it is unclear how inflammation induced by Chlamydia infection prevents or retards normal tubal transport and causes embryo implantation in the fallopian tube.

It is also worth noting that studies at the University of Edinburgh’s Centre for Reproductive Biology led by Dr Andrew Horne, Trustee and Medical Advisor to the EPT, have revealed that Chlamydia can also increase production of a protein that can encourage eggs to implant ectopically in the fallopian tubes.

Shaw JL, Wills GS, Lee KF, Horner PJ, McClure MO, Abrahams VM, Wheelhouse N, Jabbour HN, Critchley HO, Entrican G, Horne AW. Chlamydia trachomatis infections increases fallobian tube PROKR2 via TLR2 and NFkB activiation resulting in a microenvironment predisposed to ectopic pregnancy. American Journal of Pathology 2011 Jan; 178(1):253-260. PubMed link

Smoking

A study at the University of Edinburgh’s Centre for Reproductive Biology led by Dr Andrew Horne, Trustee and Medical Advisor to the EPT, identified that women who smoke could be as much as four times more likely to suffer an ectopic Pregnancy.

The research shows that smokers have an increased level of the protein PROKR1 in their fallopian tubes. The protein is instrumental in helping pregnancies implant in the womb, but when present in the fallopian tubes can hinder the progress of a fertilised egg, increasing the chances of a pregnancy being ectopic.

Shaw JL, Wills GS, Lee KF, Horner PJ, McClure MO, Abrahams VM, Wheelhouse N, Jabbour HN, Critchley HO, Entrican G, Horne AW. Chlamydia trachomatis infections increases fallobian tube PROKR2 via TLR2 and NFkB activiation resulting in a microenvironment predisposed to ectopic pregnancy. American Journal of Pathology 2011 Jan; 178(1):253-260. PubMed link