Jae Hyo Park, Jeong Eun Kim, Seung Hun Sheen, Cheol Kyu Jung, Bae Ju Kwon, O-Ki Kwon, Chang Wan Oh, Moon Hee Han and Dae Hee Han
Experience with intraarterial abciximab for the treatment of thromboembolism during endovascular coil embolization is limited. The authors report the outcome of intraarterial abciximab use, with an emphasis on fatal hemorrhagic complications.
Between March 2003 and May 2006, the authors treated 606 aneurysms by using endovascular coil embolization, and in 32 (5.3%) of these aneurysms (31 patients) an intraarterial thrombus developed. Sixteen of these aneurysms were ruptured and the other 16 were unruptured. Arterial thrombi were totally occlusive in 3 and partially occlusive in the remaining 29 cases. Intraarterial abciximab was administered at a concentration of 0.2 mg/ml as a bolus of 4–15 mg over a period of 15–30 minutes.
Complete thrombolysis was achieved in 17 (53%) and partial thrombolysis in 15 (47%) of 32 lesions. Twenty-eight patients (90.3%) were asymptomatic after abciximab thrombolysis, but 3 had postprocedural rebleeding that occurred after abciximab treatment; all of these patients had recently experienced an aneurysm rupture. Of these patients, 1 displayed severe thrombocytopenia and the other 2 showed a > 25% reduction in platelet count after abciximab treatment.
Intraarterial abciximab is effective for the treatment of thromboembolic complications that occur during intracranial aneurysm coil insertion. Nevertheless, attention should be paid to prevent potentially fatal complications such as thrombocytopenia and hemorrhage, especially in patients with a ruptured aneurysm.
Ji Hoon Phi, Jung Won Choi, Moon-Woo Seong, Tackeun Kim, Youn Joo Moon, Joongyub Lee, Eun Jung Koh, Seul Ki Ryu, Tae Hee Kang, Jae Seung Bang, Chang Wan Oh, Sung Sup Park, Ji Yeoun Lee, Kyu-Chang Wang and Seung-Ki Kim
In a minority of patients with neurofibromatosis Type 1 (NF-1), cerebral vasculopathy reminiscent of moyamoya disease develops. This phenomenon is called moyamoya syndrome (MMS), but there are no known risk factors for the prediction of MMS in NF-1 patients. Polymorphism of the RNF213 gene has exhibited strong associations with familial and sporadic moyamoya disease and other cerebral vasculopathies. The aim of this study is to find whether the RNF213 c.14576G>A variant is associated with MMS development in the NF-1 population or not.
The MMS group included 16 NF-1 patients with documented MMS. The control group consisted of 97 NF-1 patients without MMS. Genomic DNA samples were obtained from the saliva or blood of both groups, and the presence of the RNF213 c.14576G>A variant was assessed by Sanger sequencing.
In the MMS group, 3 patients had the RNF213 c.14576G>A variant (18.7%), whereas no patients with this genetic variation were observed in the control group (0%). There was a meaningful association between the RNF213 c.14576G>A variant and MMS development (p = 0.0024). The crude odds ratio was calculated as 50.57 (95% CI 1.57–1624.41). All 3 patients with MMS and the c.14576G>A variant were diagnosed with MMS at an early age and had bilateral involvement.
The RNF213 c.14576G>A variant is more common in NF-1 patients who develop MMS than in NF-1 patients without MMS. This variant might be a susceptibility gene for the NF-1–moyamoya connection.