Masatoshi Muramatsu

Intracranial Heme Metabolism and Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Background and Purpose— The goal of this prospective study was to clarify the potential role of an inducible heme-metabolizing enzyme, heme oxygenase (HO)-1, and an inducible iron-detoxifying protein, ferritin, in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). Methods— The authors measured the levels of bilirubin and iron, which are by-products of HO-1, and the ferritin levels in the cerebrospinal fluid in 39 consecutive patients with aneurysmal SAH of Fisher computed tomography group III, and determined the relationship between these by-products of HO-1 or ferritin and vasospasm. Results— Fourteen of 39 patients (35.9%) developed asymptomatic vasospasm, while 6 patients (15.4%) developed symptomatic vasospasm. The levels of ferritin, bilirubin, and iron were all significantly elevated after SAH. The levels of ferritin and bilirubin were significantly higher in patients with no vasospasm than in patients with asymptomatic and symptomatic vasospasm on days 5 through 7 (P <0.05, respectively) and on days 11 through 14 (P <0.025 in bilirubin) after SAH. However, no significant difference was observed in the iron levels between these patient groups. Conclusions— This is the first study to show that higher levels of bilirubin and ferritin in the cerebrospinal fluid after SAH were associated with no vasospasm in clinical settings. These findings support the concept that the induction of HO-1 and ferritin may be an intrinsic regulatory mechanism that acts against cerebral vasospasm.

Cerebrospinal fluid ferritin in chronic hydrocephalus after aneurysmal subarachnoid hemorrhage

ObjectivesSubarachnoid hemorrhage (SAH) is a common cause of chronic hydrocephalus. Blood in the subarachnoid space is intracranially metabolized to bilirubin and iron, and free iron is thereafter detoxified by ferritin. However, no studies have reported the relationship between intracranial heme metabolism and chronic hydrocephalus after SAH. The goal of this prospective study was to clarify the relationship between intracranial heme metabolism and chronic hydrocephalus after SAH.MethodsThe authors measured the levels of bilirubin, iron and ferritin in the cerebrospinal fluid (CSF) of 70 consecutive patients with aneurysmal SAH of Fisher computed tomography Group III, and determined the relationship between these substances’ levels and hydrocephalus requiring ventriculoperitoneal shunting.ResultsThe CSF concentrations of ferritin and inflammatory cells were significantly higher in shunted patients (n = 27) than in non-shunted patients (n = 43) on Days 3 and 4 (p<0.05 in ferritin and p<0.01 in inflammatory cells) and 11 to 14 (p<0.005 in ferritin) post-SAH. These results were independent of other clinical factors. The occurrence of chronic hydrocephalus was not affected by the extent of the intracranial heme metabolism in terms of the bilirubin and iron levels.ConclusionsThis is the first study to show that patients who subsequently had chronic hydrocephalus requiring CSF shunting were associated with higher CSF levels of ferritin in the acute stage of SAH. Higher CSF ferritin levels may not reflect the amount of blood in the subarachnoid space that was intracranially metabolized, but rather more intense subarachnoid inflammatory reactions which may cause chronic hydrocephalus after SAH.

Pituitary Apoplexy Caused by Ruptured Internal Carotid Artery Aneurysm

Background and Purpose — We report the first case of pituitary apoplexy caused by the rupture of an intracavernous carotid artery aneurysm embedded in a pituitary adenoma. Case Description — A 46-year-old man presented with clinical and CT findings typical of pituitary apoplexy. MRI showed an unusual flow-void protrusion into the intratumoral hematoma, which, however, was not diagnosed as a ruptured aneurysm until severe intraoperative bleeding occurred. Angiography after surgery revealed an intracavernous carotid artery aneurysm. Conclusions — The possible association of adenoma and aneurysmal rupture should be kept in mind when assessing any case of pituitary apoplexy.

Severe QT interval prolongation associated with moxifloxacin: a case report

IntroductionThe QT interval prolongation is an adverse effect associated with moxifloxacin. This adverse effect can lead to potentially life-threatening arrhythmias such as Torsades de pointes. We describe a case of severe QT interval prolongation associated with moxifloxacin which may cause the development of Torsades de pointes. There have been no reported case of severe corrected QT interval prolongation caused by moxifloxacin in the patient of normal heart rate.Case presentationIn an 85-year-old Japanese woman, oral moxifloxacin 400 mg daily was initiated for the forearm cellulitis. On the sixth day of oral moxifloxacin administration, monitor electrocardiogram showed prolongation of the corrected QT interval to 523 ms at a rate of 40 beats/min. Electrocardiogram before moxifloxacin therapy showed the corrected QT interval to 460 ms at a rate of 72 beats/min. On the sixth day after moxifloxacin discontinuance, monitor electrocardiogram showed the corrected QT interval to 432 ms at a rate of 70 beats/min.ConclusionThis case suggests that electrocardiogram monitoring during moxifloxacin therapy may be necessary in the patients even if they do not have high risk factors for QT interval prolongation.