Daria Martin, Schering Stiftung Projektraum

 

Friedmund Neumann Prize 2012

PD Dr. Sylvia Mechsner

Department of Gynecology at the Charité University Hospital in Berlin

for her outstanding work on the pathogenesis of endometriosis

Friedmund Neumann Preis 2012

Sylvia Mechsner

Born in Reinbek in 1972, Sylvia Mechsner grew up near Hamburg. After her Abitur in 1991 and a Voluntary Social Year in Berlin, she started to study medicine at the Free University of Berlin in 1992. Following her prelims, she wrote her dissertation at the Institute of Biochemistry at the FU Berlin. Completing her residency in 2001, Mechsner is currently a senior physician in the Department of Gynecology with Outpatient Clinic at the Charité’s Benjamin Franklin Campus, where the focus of her work is at the Endometriosis Research Center. Since 2002, she has treated both in- and outpatients and since 2005 has directed the Endometriosis Research Lab. In 2010 she habilitated with a thesis on “Endometriose, das verkannte Frauenleiden – Untersuchungen zur Pathogenese und Schmerzentstehung“ (Endometriosis – Investigation of the Pathogenesis and Pain Conduction). Sylvia Mechsner is married and has three children.

Endometriosis

Endometriosis is a health problem that affects women during their childbearing years and whose symptoms such as lower abdominal (pelvic) pain, bleeding disorders, and fertility problems can severely compromise patients’ quality of life while also having major social, clinical, and economic relevance.

Two to twenty percent of all women of reproductive age are said to suffer from endometriosis. An estimated 2 million women are affected in Germany and up to 40,000 new cases are diagnosed every year. About 50 percent of these women need to have ongoing therapy. In addition to the physical pain, the relapse rate of 50-80 percent, even following surgical and endocrinal treatment, is a huge problem.

Another big problem is the fact that the average time interval between the appearance of the first symptoms and the diagnosis is 6 to 8 years. This is, among other things, due to the ignorance about the genesis and development of endometriosis and the mechanisms of pain generation underlying the disorder. What also makes the diagnosis difficult is that medical tests frequently yield “normal” results. The clinical picture of endometriosis-associated symptoms is very well defined, however, so that a detailed patient history in most cases would enable early diagnosis and the initiation of treatment.

Since most patients suffer from pain that significantly impairs their quality of life, knowledge in this area is crucial for both diagnosis and therapy. There are still no causal therapy approaches, which means that doctors continue to be confronted with the problem of chronic disease and a high relapse rate. In the past few years, there has been little change in the established treatments (surgical and hormonal therapies, pain therapy), even though treatment in many cases is insufficient and unsatisfactory or has severe side effects. There are no new, innovative approaches.

Sylvia Mechsner’s Research

Sylvia Mechsner’s working group deals with the mechanisms of endometriosis generation and development and with possible mechanisms of pain generation through endometriotic lesions. Aiming to establish new therapeutic approaches, the studies were done with a focus on their clinical relevance.

Mechsner and her team for the first time were able to show the lymphatic spread of endometriosis cells and study its clinical importance. Given the occurrence of endometriosis in lymph nodes, it was possible to show mechanisms of lymphangiogenesis in endometriotic lesions – a new aspect in the genesis and development of endometriosis, which deserves special attention.

Another focus of Mechsner’s work is on demonstrating and characterizing endometriosis-associated muscle cells that express estrogen, progesterone as well as oxytocin receptors. Supporting the evidence that endometriosis always involves smooth muscle cells in addition to epithelial and stromal cells, these findings are important for understanding the generation and development of the disease and may offer new therapeutic approaches.

Sylvia Mechsner has successfully begun to shed light on the connection between inflammation and pain in endometriosis. The question is not just how inflammation causes pain, but how the nervous system controls the inflammation. Mechsner and her team managed to demonstrate the density of nerve fibers in peritoneal endometriotic lesions, which most frequently occur with patients with severe pelvic pain/dysmenorrhea. This suggests that, in addition to inflammatory pain, neuropathic pain is also involved in pain generation. Of importance is also her most recent work on the neuromodulatory processes of endometriosis where she was able to show that endometriosis is involved in neurotrophic events and induces neurite outgrowth, but reduces the density of sympathetic nerve fibers. What is interesting is that the inflammatory response is most probably leading to neuromodulation.

Award Ceremony

September 10, 2012, 5:00 p.m.

Berlin-Brandenburg Academy of Sciences and Humanities
Leibniz Hall
Markgrafenstr. 38 | 10117 Berlin

The prize will be awarded in conjunction with the Ernst Schering Foundation’s Ernst Schering Prize.
Please register at This e-mail address is being protected from spambots. You need JavaScript enabled to view it

For more information, please contact Andrea Bölling, Project Manager Science of the Ernst Schering Foundation, at This e-mail address is being protected from spambots. You need JavaScript enabled to view it or by phone at +49 (0)30-20 62 29 60.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Abb. A

A: Depiction of an endometriosis-associated nerve in a peritoneal endometriotic lesion

 

 

Abb. B

B: Trichrome staining to depict nerve fibers (green) co-localized with immature vessels (red) (L: lumen, E: epithelial cells; S: stromal cells)

 

 

Abb. C

C: Peritoneal fluids from an endometriosis patient induce neurite outgrowth from chicken dorsal root ganglia.