9 research outputs found
硝子体手術後に網膜静脈分枝閉塞症を来したタモキシフェン内服患者の1例
タモキシフェンは主に乳癌治療薬として使用されているが,眼副作用の報告は非常に少ない.今回,タモキシフェン内服患者における,硝子体手術後に発症した網膜静脈分岐閉塞症(branch retinal vein occlusion,以下BRVO)の1例を経験したので報告する.症例は51歳女性,乳癌の術後1日量20mgのタモキシフェンによるアジュバント療法を受けていた.2年後に左眼の黄斑円孔が発見され硝子体手術を行った.後部硝子体剥離を起こしている際にアーケード血管から出血を認めたため出血部位の圧迫及び眼内灌流圧を上げることで止血を行った.術翌日には黄斑円孔の閉鎖が確認されたが,術後15日目に出血部位を閉塞起点とするBRVOを認めた.視力は左矯正0.7pと術前と比べほぼ変わりはなかったが,光干渉断層計で黄斑浮腫を認めたためベバシズマブ硝子体内投与を行った.同時にタモキシフェンによる副作用を疑い,内服を中止した.タモキシフェンの眼副作用として,BRVOも念頭におく必要がある.Tamoxifen is often used for treating breast cancer. However, tamoxifen-induced ocular complications are very rare. We will report on a case of branch retinal vein occlusion (BRVO) associated with tamoxifen use. A fifty-one year old female was receiving peroral tamoxifen with daily doses of 20 mg following surgery for breast cancer. A macular hole was detected in her left eye two years later and vitreous surgery was performed. It was observed that there was bleeding from the inferior arcade vessels after inducing the posterior vitreous detachment. Hemostasis of the vein was performed by raising the intraocular perfusion pressure and by compression of the bleeding site. The macular hole was closed on a postoperative day. A fundus examination revealed that the left branch retinal vein occlusion started bleeding fifteen days after the surgery. There was almost no change compared with preoperative visual acuity, but optical coherence tomography (OCT) showed a macular edema. Therefore, intravitreal injections of bevacizumab and tamoxifen therapy were discontinued. Although BRVO is rare, ophthalmologists should be alerted to this type of ocular side effect
A Pair-Feeding Study Reveals That a Y5 Antagonist Causes Weight Loss in Diet-Induced Obese Mice by Modulating Food Intake and Energy Expenditure
ABSTRACT Neuropeptide Y (NPY) is thought to have a significant role in the physiological control of energy homeostasis. We recently reported that an NPY Y5 antagonist inhibits body weight gain in diet-induced obese (DIO) mice, with a moderate reduction in food intake. To clarify the mechanism of the antiobesity effects of the Y5 antagonist, we conducted a pair-feeding study in DIO mice. The Y5 antagonist at 100 mg/kg produced a moderate feeding suppression leading to an 18% decrease in body weight, without altering body temperature. In contrast, the pairfed group showed only a transient weight reduction and a reduced body temperature, thus indicating that the Y5 antagonist stimulates thermogenesis. The Y5 antagonist-treated mice showed an up-regulation of uncoupling protein mRNA in brown adipose tissue (BAT) and white adipose tissue (WAT), suggesting that both BAT and WAT contribute to energy expenditure. Thus, the Y5 antagonist induces its antiobesity effects by acting on both energy intake and expenditure
A Pair-Feeding Study Reveals That a Y5 Antagonist Causes Weight Loss in Diet-Induced Obese Mice by Modulating Food Intake and Energy Expenditure
Discovery of Tetrasubstituted Imidazolines as Potent and Selective Neuropeptide Y Y5 Receptor Antagonists: Reduced Human Ether-a-go-go Related Gene Potassium Channel Binding Affinity and Potent Antiobesity Effect
Discovery of Tetrasubstituted Imidazolines as Potent and Selective Neuropeptide Y Y5 Receptor Antagonists: Reduced Human Ether-a-go-go Related Gene Potassium Channel Binding Affinity and Potent Antiobesity Effect
A series of novel imidazoline derivatives was synthesized and evaluated as neuropeptide Y (NPY) Y5 receptor antagonists. Optimization of previously reported imidazoline leads, <b>1a</b> and <b>1b</b>, was attempted by introduction of substituents at the 5-position on the imidazoline ring and modification of the bis(4-fluorphenyl) moiety. A number of potent derivatives without human ether-a-go-go related gene potassium channel (hERG) activity were identified. Selected compounds, including <b>2a</b>, were shown to have excellent brain and CSF permeability. Compound <b>2a</b> displayed a suitable pharmacokinetic profile for chronic in vivo studies and potently inhibited d-Trp<sup>34</sup>NPY-induced acute food intake in rats. Oral administration of <b>2a</b> resulted in a potent reduction of body weight in a diet-induced obese mouse model