Reversal of renal failure in Wegener??s granulomatosis by heparin

Whitaker, A N; Emmerson, B. T.; Bunce, Ian; Nicoll, Peter; Sands, John M.

doi:10.1097/00000441-197305000-00007

Cited by 10 publications

(3 citation statements)

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“…In addition, one should consider the likely participation of the in situ microvascular thrombosis in WG-related stroke, cutaneous necrosis, deep vein thrombosis (DVT), and glomerulonephritis, corroborated by the description of renal failure that is reversed by heparin in WG. (19) The high prevalence of in situ pulmonary microvascular thrombosis and the elevated incidence of DVT/pulmonary embolism (PE) in WG might be a consequence of endothelial damage. Such endothelial damage might correlate with various alterations detected in the serum of patients with this kind of vasculitis, such as those seen in the levels/concentrations of ANCA, proteinase 3 (PR3), apoptotic endothelial cells, and thrombomodulin.…”

Section: Discussionmentioning

confidence: 99%

Trombose em artérias pulmonares pequenas e médias em granulomatose de Wegener: um estudo com microscopia confocal por varredura a laser

et al. 2010

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Objective: Wegener's granulomatosis (WG) can cause endothelial cell damage and thromboembolic events. Nevertheless, there have been few studies on the pulmonary microcirculation-small and medium-sized pulmonary arteries (SMSPA)-in patients with WG. The objective of this study was to quantify fibrin thrombi in the SMSPA of patients with WG. Methods: We analyzed 24 SMSPA samples collected from six patients with WG and 16 SMSPA samples collected from four patients without WG. In all samples, we used the endothelial cell marker CD34 and confocal laser scanning microscopy in order to detect intravascular fibrin thrombi. We calculated the total vessel area, the free lumen area, and the thrombotic area. Results: The mean total vessel area was similar in the WG and control groups (32,604 µm 2 vs. 32,970 µm 2 , p = 0.8793). Thrombi were present in 22 (91.67%) of the 24 WG group samples and in none of the control group samples (p < 0.0001; OR = 297; 95% CI: 13.34-6,612). The mean thrombotic area was greater in the WG group samples than in the control group samples (10,068 µm 2 vs. 0.000 µm 2 ; p < 0.0001). In contrast, the mean free lumen area was smaller in the WG group samples than in the control group samples (6,116 µm 2 vs. 24,707 µm 2 ; p < 0.0001). Conclusions: Confocal laser scanning microscopy revealed a significant association between pulmonary microvascular thrombosis and WG. This suggests a possible role of microvascular thrombosis in the pathophysiology of pulmonary WG, evoking the potential benefits of anticoagulation therapy in pulmonary WG. However, further studies are needed in order to confirm our findings, and randomized clinical trials should be conducted in order to test the role of anticoagulation therapy in the treatment of patients with pulmonary WG. Keywords:Vasculitis; Antibodies, antineutrophil cytoplasmic; Wegener granulomatosis; Thrombosis; Lung; Microscopy, confocal. ResumoObjetivo: A granulomatose de Wegener (GW) pode causar dano nas células endoteliais e fenômenos tromboembólicos. Entretanto, poucos estudos analisaram a microcirculação pulmonar -artérias pulmonares de pequeno/médio calibre (APPMC) -em pacientes com GW. O objetivo deste estudo foi quantificar trombos de fibrina em amostras de APPMC de pacientes com GW. Métodos: Analisamos 24 APPMC de seis pacientes com GW e 16 APPMC de quatro pacientes controles sem WG. Utilizamos CD34 para a marcação do endotélio em todas as amostras e microscopia confocal a laser para detectar trombos de fibrina intravasculares. Calculamos a área total do vaso, a área livre do lúmen e a área trombótica. Resultados: A média da área total do vaso foi similar no grupo GW e no grupo controle (32.604 µm 2 vs. 32.970 µm 2 , p = 0,8793). Trombos foram identificados em 22 das 24 APPMC (91,67%) no grupo GW, e em nenhuma do grupo controle (p < 0,0001; OR = 297 (IC95%: 13,. A média da área trombótica foi maior no grupo GW do que no grupo controle (10.068 µm 2 vs. 0.000 µm 2 , p < 0,0001). Em contraste, a média da área livre do lúmen foi menor no grupo GW que n...

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Section: Discussionmentioning

confidence: 99%

Trombose em artérias pulmonares pequenas e médias em granulomatose de Wegener: um estudo com microscopia confocal por varredura a laser

et al. 2010

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“…(13)(14)(15)(16)(17)(18)(19)(20) of anticoagulation therapy. (10) A finding of acute tubular necrosis is also quite common.…”

Section: Historymentioning

confidence: 99%

Atualização do tratamento das vasculites associadas a anticorpo anticitoplasma de neutrófilos

et al. 2011

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As vasculites antineutrophil cytoplasmic antibody (ANCA, anticorpo anticitoplasma de neutrófilos) associadas (VAAs) são caracterizadas por uma inflamação sistêmica das artérias de pequeno e médio calibre (especialmente no trato respiratório superior e inferior, e nos rins). As VAAs compreendem a granulomatose de Wegener (agora chamada de granulomatose com poliangeíte), poliangeíte microscópica, VAA limitada ao rim e a síndrome de Churg-Strauss. Neste artigo, discutiremos as fases de tratamento dessas vasculites, como fase de indução (com ciclofosfamida ou rituximab) e fase de manutenção (com azatioprina, metotrexato ou rituximab). Além disso, discutiremos como manusear os casos refratários à ciclofosfamida.

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“…366 Studies have confirmed the role of microvascular thrombosis in the development of renal failure. 368 Active hem orrhage, a common complication of pleuropulmonary involvement with Wegener's granuloma tosis, may, unfortunately, limit the utilization of anticoagulation therapy. 366…”

Section: Wegener's Granulomatosismentioning

confidence: 99%

Clinical Aspects of Disseminated Intravascular Coagulation: A Clinician's Point of View

Baker¹

1989

Semin Thromb Hemost

151

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DIC is a disorder of coagulation that is demonstrated to occur in many settings. In view of the fulminant nature of the disorder once it is fully activated, the potential for considerable morbidity and mortality, and the difficulty in treating this syndrome, the necessity for a thorough understanding of the disorder is clear. A high index of suspicion is absolutely essential; however, this requires a thorough knowledge of the medical and surgical disorders in which DIC is likely to occur. The presenting manifestations of DIC, the time course of development of the fulminant syndrome, and the specific complications of the disorder may be intrinsically related to the specific clinical characteristics of the underlying disease. Clinical evaluation of the patient must be comprehensive and consider not only the laboratory and clinical manifestations of DIC but the triggering illness. Without the ability to treat the underlying primary illness, controlling or abating the DIC may be difficult or impossible. This comprehensive review of the disease entities in which DIC is likely to occur and the associated clinical manifestations will, it is hoped, guide a more precise definition of the overall clinical picture that confronts the clinician when evaluating a patient with possible DIC.

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Reversal of renal failure in Wegener??s granulomatosis by heparin

Cited by 10 publications

References 0 publications

Trombose em artérias pulmonares pequenas e médias em granulomatose de Wegener: um estudo com microscopia confocal por varredura a laser

Trombose em artérias pulmonares pequenas e médias em granulomatose de Wegener: um estudo com microscopia confocal por varredura a laser

Atualização do tratamento das vasculites associadas a anticorpo anticitoplasma de neutrófilos

Clinical Aspects of Disseminated Intravascular Coagulation: A Clinician's Point of View

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