心电图同期CT脑血管造影诊断动脉瘤小泡样突起

目的了解心电图同期CT脑血管造影(CTA)技术对于未破裂动脉瘤的小泡样突起诊断的准确性。方法2004年间对15例患者进行了心电图同期CTA检查。结果其中10例患者在心电图同期CTA图像上发现有搏动部位存在,提示动脉瘤上有小泡样突起,手术中也有同样发现。切除的15例动脉瘤标本组织学检查均发现肌层和内弹力层部分或完全缺失,而有小泡的10例动脉瘤中发现胶原层减少,这与小泡样突起的存在相吻合。结论心电图同期CTA可用于未破裂动脉瘤的小泡样突起的诊断,其准确性可用标本的组织学检查加以证明。     

Identification of Ki23819, a highly potent inhibitor of kinase activity of mutant FLT3 receptor tyrosine kinase.

Constitutively active internal tandem duplication (ITD) in the juxtamembrane domain of Fms-like tyrosine kinase 3 (FLT3), a type III receptor tyrosine kinase, is the most common molecular defect associated with acute myeloid leukemia. Its presence confers a poor outcome in patients with acute myeloid leukemia who receive conventional chemotherapy. FLT3-ITD has therefore been considered to be an attractive molecular target for a novel therapeutic modality. We describe here the identification and characterization of Ki23819 as a novel FLT3 inhibitor. Ki23819 suppressed proliferation and induced apoptosis of FLT3-ITD-expressing human leukemia cell lines. The growth-inhibitory effect of Ki23819 on MV4-11 cells was superior to that of SU11248, another FLT3 inhibitor (IC(50)<1 vs 3-10 nM). Ki23819 inhibited the autophosphorylation of FLT3-ITD more efficiently than that of wild-type FLT3. FLT3-ITD-dependent activation of the downstream signaling proteins ERK and STAT5 was also inhibited within similar concentration ranges. Thus, Ki23819 is a potent in vitro inhibitor of FLT3.     

A Clinicopathologic Case Report of Inflammatory Pseudotumors Involving the Conjunctiva and Lung

Background Inflammatory pseudotumors are characterized histopathologically by aggregates of inflammatory lymphocytes, plasma cells, neutrophils, and fibroblasts. We report a rare case of inflammatory pseudotumor involving both the conjunctiva and lung.Case A 58-year-old man with a 6-year history of pulmonary inflammatory pseudotumor was referred to our hospital for evaluation of conjunctival swelling in the left eye and bilateral iritis.Observations The subconjunctival tumor enlarged slowly, but regressed spontaneously. After partial resection of the subconjunctival and lung tumors, the presence was confirmed of aggregates of chronic inflammatory cells (lymphocytes, plasma cells, neutrophils, fibroblasts) without noncaseating epithelioid granuloma formation. Gene rearrangement testing ruled out malignancy. The patient was treated with oral corticosteroids for fever and primary biliary hepatic cirrhosis. Iritis signs subsided slightly in response to corticosteroids, but persisted. The temporal subconjunctival pseudotumor resolved without recurrence.Conclusions This case was compatible histopathologically with inflammatory pseudotumor, and is a rare case of simultaneous occurrence in the lung and conjunctiva. Jpn J Ophthalmol 2004;48:573–577 © Japanese Ophthalmological Society 2004     

Rhabdomyolysis Caused by Gefitinib Overdose

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are common therapeutic agents for EGFR mutation-positive advanced non-small-cell lung cancer. There has been no report of rhabdomyolysis caused by an overdose of EGFR-TKIs. We herein review the existing literature on the subject and report a rare case of rhabdomyolysis due to an overdose of gefitinib, an EGFR-TKI.     

Necrotizing Bacillus cereus infection of the meninges without inflammatory reaction in a patient with acute myelogenous leukemia: a case report

A 64-year-old man in a severely immunocompromised state due to acute myelogenous leukemia died, respirator-unaided, about 10 h after the abrupt onset of coma. An earlier blood culture had yielded Bacillus cereus. The autopsy, performed 2 h after death, demonstrated diffuse subarachnoid hemorrhage without berry aneurysms, and the formalin-fixed brain was tinged with gray-brownish discoloration. The sections of the brain presented a whitish tint of the surface layer of all portion of the cerebral cortices, even those in the sulci. Histological examination of the brain revealed leptomeningeal B. cereus dissemination, and widespread necrosis of the leptomeninges and arachnoid vessels without inflammatory cell reaction. The grossly recognizable whitish surface layer of the cerebral cortex showed overt hyperchromatism, and contained neurons more degenerative than those located in the deeper cortical layer. The total absence of inflammatory reaction may be explained by a combination of the immunocompromised state of the patient and the character of B. cereus infection, which in itself induces little inflammatory reaction. The prominent lesions were confined to the cerebral surface layer and leptomeningeal tissue including the arachnoid vessels, which were all bathed in the cerebrospinal fluid, suggesting that some necrotizing toxins had been secreted into the fluid by the B. cereus. The necrosis of arachnoid vessels is thought to have in turn caused diffuse subarachnoid hemorrhage and marked disturbance of the cerebral blood flow, resulting in the terminal coma. Received: 4 April 1996 / Revised, accepted: 8 September 1996