As a senior consultant on the prenatal ward at a women’s clinic, Stefan Hansson is often witness on a daily basis to the suffering caused by pre-eclampsia. He considers it a fantastic privilege to be involved in investigating the mysterious mechanisms behind “the disease of theories”, and perhaps also identifying a future therapeutic product and developing the world’s first pharmacological treatment.
Stefan Hansson
Stefan Hansson, a senior consultant on the prenatal ward at Skåne University Hospital in Malmö and a professor in obstetrics and gynaecology at Lund University.

How did pre-eclampsia become your preferred research subject?

“In 1998 I defended my thesis on the subject of neuroscience, where I had studied the function and distribution of so-called monoamine transporters (MAT) in the central nervous system during fetal development. When we studied rat fetuses, we always included a piece of the placenta, which also appeared to express different types of MAT.

“When I began my clinical specialist training in Obstetrics and Gynaecology in 1999, I became curious about the function of MAT in the placenta and their significance in complex pregnancies. As MAT regulate the levels of stress hormone, it led me towards the condition pre-eclampsia – a condition that is characterised by, among other features, high stress hormone levels and high blood pressure.

“The causes of pre-eclampsia have always been an unanswered riddle, something that I saw as an exciting challenge; it is even called “the disease of theories” because so many different explanatory models have been put forward. Having the opportunity to be involved in discovering and describing a new mechanism is fantastic. There is a lot to suggest that there is a central disease mechanism, which means that I am cautiously optimistic about our potential treatment.”

Can you explain how your partnership with Bo Åkerström began?

“After having identified free fetal hemoglobin in pre-eclampsia-affected placentas with the aid of proteomics and genomics technology, the idea arose that free fetal hemoglobin is harmful and that it can leak into the mother’s blood circulation where it continues to damage the surrounding tissue. The concept became more widely known when our findings were published in Dagens Nyheter.

“My good friend and colleague Martin Olsson, a professor in transfusion medicine, introduced me to Bo Åkerström. Martin and Bo had previously worked on free hemoglobin and A1M. That proved to be the beginning of a fruitful and very exciting partnership.”

Can you describe how A1M-based diagnosis and treatment of a patient with pre-eclampsia may work in the future?

“There are two potential treatment strategies:


  1. Because we can measure the levels of free fetal hemoglobin as early as the 10th to 14th week of pregnancy in women who will develop pre-eclampsia (i.e. at least 10 weeks before the condition manifests), early treatment could prevent it appearing. So-called prophylactic treatment could begin at an early stage. By knowing the levels of the harmful substance – free fetal hemoglobin, the A1M dose can also be adjusted for each individual patient.
  2. The second treatment scenario involves an established condition. By administering the right dose in relation to the levels of free fetal hemoglobin, the progress of the disease can be halted and the symptoms alleviated – perhaps even eliminated. If A1M works as efficiently in-vivo as ex-vivo, the prophylactic treatment could be so effective that nobody need develop pre-eclampsia!”

What questions are you looking for research to answer in the next few years?

“We intend to evaluate the mechanisms behind A1M’s neutralising and healing effects as demonstrated in ex-vivo models. Methods of administration and effective doses must also be tested on various animal models. In parallel with this, we are planning for Phase 1 trials.”.
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