Dr. Long Zheng

The Role of Complement Factor H Abnormality in Pathogenesis of Thrombotic Thrombocytopenic Purpura
Dr. Long Zheng, Associate Professor of Pathology and Laboratory Medicine, The University of Pennsylvania, Perelman School of Medicine.
Director of Hematology & Coagulation Laboratories, The Children's Hospital of Philadelphia.
Research Aims of this Study:
"The aim of the current study is to determine the role of complement activation in pathogenesis of acquired TTP with inhibitors."
How Dr. Zheng became interested in TTP research:
"During the first day of my residency in Laboratory Medicine, Washington University School of Medicine in St. Louis, Missouri, I saw a 42-year old African American woman with TTP. The mechanism of her disease was not known. I became interested in studying her and identified autoantibody against ADAMTS13 was the cause."
How Dr. Zheng believes this research will impact individuals living with or impacted by TTP:
"The results of the proposed study may shed new light on the mechanisms of TTP and provide scientific basis for designing novel therapeutics for TTP."
Comments from Dr. Zheng to donors:
"My colleagues and I appreciate your generous gift to support our research, which may lead to cure for TTP. "


December 15, 2014

On December 15, 2014 the Answering TTP Foundation received an exciting update from Dr. Zheng in regards to the above-mentioned research he is conducting with funding from the Foundation. Below is an excerpt from the letter he sent the Foundation along with a link to additional information. Congratulations to Dr. Zheng and his team, this is a very exciting developement for the TTP community!  

"As we reported on December 8 at the Annual Meeting of American Society of Hematology, an inhibition of complement factor H with antibody resulted in excessive complement activation, which triggers the onset of TTP in mice with severe deficiency of ADAMTS13. Complement activation is also prevalent in patients with autoimmune TTP. These results suggest the synergistic effect of complement activation and ADAMTS13 deficiency in pathogenesis of TTP. Therefore, we propose that anti-complement treatment such as the use of eculizumab may be indicated in patients refractory to plasma exchange therapy. More studies in the mouse models and in patients will be necessary for such a recommendation." - Dr. Long Zheng

CLICK HERE for additional information.