Unleashed platelets in aHUS.
نویسنده
چکیده
bridge, Cambridge University Press, 2000:1457-1465. 6. Lalezari JP, Aberg JA, Wang LH, et al. Phase I dose escalation trial evaluating the pharmacokinetics, antihuman cytomegalovirus (HCMV) activity, and safety of 1263W94 in human immunodeficiency virus-infected men with asymptomatic HCMV shedding. Antimicrob Agents Chemother. 2002;46:2969-2976. 7. Peggs KS, Verfuerth S, Pizzey A, et al. Adoptive cellular therapy for early cytomegalovirus infection after allogeneic stem-cell transplantation with virus-specific T-cell lines. Lancet. 2003;362:1375-1377.
منابع مشابه
Factor H dysfunction in patients with atypical hemolytic uremic syndrome contributes to complement deposition on platelets and their activation.
Atypical hemolytic uremic syndrome (aHUS) may be associated with mutations in the C-terminal of factor H (FH). FH binds to platelets via the C-terminal as previously shown using a construct consisting of short consensus repeats (SCRs) 15 to 20. A total of 4 FH mutations, in SCR15 (C870R) and SCR20 (V1168E, E1198K, and E1198Stop) in patients with aHUS, were studied regarding their ability to all...
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Atypical hemolytic uremic syndrome (aHUS), a thrombotic microangiopathy (TMA), is a rare, life-threatening, systemic disease. When unrecognized or inappropriately treated, aHUS has a high degree of morbidity and mortality. aHUS results from chronic, uncontrolled activity of the alternative complement pathway, which activates platelets and damages the endothelium. Two-thirds of aHUS cases are as...
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Platelet/granulocyte aggregates (PGAs) increase thromboinflammation in the vasculature, and PGA formation is tightly controlled by the complement alternative pathway (AP) negative regulator, Factor H (FH). Mutations in FH are associated with the prothrombotic disease atypical hemolytic uremic syndrome (aHUS), yet it is unknown whether increased PGA formation contributes to the thrombosis seen i...
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Introduction Atypical hemolytic uremic syndrome is a thrombotic microangiopathy, which is linked to hereditary or autoimmune defects in complement activators or regulators present in blood and on vascular endothelial cells. Acute thrombotic microangiopathy episodes are typically preceded by infections, which by themselves would not be expected to manifest HUS. Thus, it is possible that the host...
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Background: Atypical HUS (aHUS) occurs due to endothelial damage following abnormal complement regulation, with some cases being deficient in complement regulating factors H, I and Membrane Cofactor P. Case presentation: We present a case of a 28 year old female presenting with flu like illness, mild renal impairment, haematoproteiunurea and anaemia. Renal biopsy showed widespread endothelial s...
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عنوان ژورنال:
- Blood
دوره 111 11 شماره
صفحات -
تاریخ انتشار 2008