Abstract：
:Thrombotic thrombocytopenic purpura (TTP) is a severe, occlusive, thrombotic microangiopathy characterized by a systemic platelet aggregation, organ ischemia, profound thrombocytopenia and erythrocyte fragmentation. Recent observations have documented that a deficiency of a von Willebrand factor (VWF)-cleaving protease, termed ADAMTS13, that normally cleaves hyper-reactive unusually large VWF multimers into smaller and less adhesive VWF forms, may be responsible for many cases of TTP. Multiple mutations of the ADAMTS13 gene can result in ADAMTS13 deficiency and cause congenital TTP, while autoantibodies neutralizing ADAMTS13 protease activity have been associated with acquired TTP. However, in spite of the recent progresses in the pathophysiology of TTP, many aspects of this disease remain still controversial. In this study, basing on the laboratory results of a group of eight patients with an acquired form of TTP, an alternative pathogenic mechanism for TTP involving Helicobacter pylori infection is proposed. In fact, Helicobacter pylori, which has been recently implied in the pathogenesis of idiopathic thrombocytopenic purpura (ITP), could function as a triggering factor in TTP by inducing platelet aggregation through an interaction with VWF.
journal_name
Med Hypothesesjournal_title
Medical hypothesesauthors
Franchini Mdoi
10.1016/j.mehy.2005.06.015keywords:
subject
Has Abstractpub_date
2005-01-01 00:00:00pages
1128-31issue
6eissn
0306-9877issn
1532-2777pii
S0306-9877(05)00327-0journal_volume
65pub_type
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