Acquired resistance to infliximab against uveitis due to Behçet’s disease after one year of administration

2010 ◽  
Vol 54 (5) ◽  
pp. 502-504 ◽  
Author(s):  
Takako Ito ◽  
Koh-Hei Sonoda ◽  
Kuniaki Hijioka ◽  
Takeshi Fujimoto ◽  
Tatsuro Ishibashi
Author(s):  
Jaejoon Lee ◽  
Eun-Mi Koh ◽  
Chin-Sang Chung ◽  
Seung-Chul Hong ◽  
Yong-Bum Kim ◽  
...  

Background:Perimesencephalic subarachnoid hemorrhage (PSH) is a relatively benign clinical entity with a low risk of recurrent bleeding. The precise etiology of PSH has not yet been determined. We report here three cases of PSH with clinical and radiological features that support a venous system as a cause.Case Presentation:The first patient, a 72-year-old woman, had PSH and venous hemorrhagic infarct in the left thalamus on non-contrast CT. Subsequent cerebral angiography revealed widespread thrombosis in the cerebral venous system, a potential cause for reflux overflow hemorrhage. The second patient, a 55-year-old man with an established diagnosis of neuro-Behçet's disease, a well-known cause for cerebral venulitis, presented with PSH one year later. The third patient, a 39-year-old female, with incomplete Behçet's disease was admitted with PSH.Discussion:Current concepts on the anatomic origin and the possible pathophysiologic mechanism leading to PSH are discussed. The underlying pathological conditions in the venous system in our cases provide theoretical clues to the anatomic origin of PSH in general.


1991 ◽  
Vol 66 (03) ◽  
pp. 292-294 ◽  
Author(s):  
K K Hampton ◽  
M A Chamberlain ◽  
D K Menon ◽  
J A Davies

SummaryCoagulation and fibrinolytic activities were studied in 18 subjects with Behçet's disease and compared with results from 14 matched control patients suffering from sero-negative arthritis. Significantly higher plasma concentrations (median and range) were found in Behçet's patients for the following variables: fibrinogen 3.7 (1.7-6.9) vs 3.0 (2.0-5.1) g/1, p <0.05; von Willebrand factor antigen, 115 (72-344) vs 74 (60-119)%, p <0.002; plasminogen activator activity (106/ECLT2) 219 (94-329) vs 137 (78-197) units, p <0.002; tissue plasminogen activator inhibitor (t-PA-I) activity, 9.1 (5.5-19.3) vs 5.1 (1.8-12.0) IU/ml, p <0.002; and PAI-1 antigen, 13.9 (4.5-20.9) vs 6.4 (2.4-11.1) ng/ml, p <0.002. Protein C antigen was significantly lower: 97 (70-183) vs 126 (96-220)%, p <0.02. No differences were observed in antithrombin III activity or antigen, factor VIII coagulant activity, fibrinopeptides A and Bβ15-42, plasminogen, α-2-antiplasmin, functional and immunological tissue-plasminogen activator, thrombin-antithrombin complexes and D-dimer. Levels of tissue plasminogen activator inhibitor (activity and antigen) correlated with disease activity while fibrinogen and von Willebrand factor concentrations did not. Seven of the 18 subjects with Behçet's disease had suffered thrombotic events but it was not possible to distinguish these from the 11 patients without thrombosis using the assays performed. The results suggest the abnormal fibrinolytic activity in Behçet's disease is due to increased inhibition of tissue plasminogen activator. No abnormality of coagulation or fibrinolytic activity specific to Behçet's disease was detected.


1996 ◽  
Vol 75 (06) ◽  
pp. 974-975 ◽  
Author(s):  
İbrahim C Haznedaroğlu ◽  
Oktay Özdemir ◽  
Osman Özcebe ◽  
Semra V Dündar ◽  
Şerafettin Kirazli

1993 ◽  
Vol 29 (1) ◽  
pp. 62 ◽  
Author(s):  
Kyung Hwan Lee ◽  
Jae Hyung Park ◽  
Joon Ku Han ◽  
Hyun Ae Park ◽  
Jin Wook Chung ◽  
...  

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