利拉鲁肽长期单药治疗对1例家族性部分脂肪营养不良的日本女性糖尿病患者血糖控制和糖尿病微血管病变的有益影响

M. Iwanishi, C. Azuma, Y. Tezuka, Yuji Yamamoto, J. Ito-Kobayashi, M. Washiyama, A. Shimatsu, A. Mizuno, Y. Osafune
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摘要

我们经历了一位日本女性糖尿病部分脂肪营养不良患者长期坚持利拉鲁肽单药治疗的病例。首次检查时,患者血糖控制不佳,体重下降,脂肪量减少是由糖尿病未控制引起的。她有严重的非增殖性糖尿病视网膜病变和肾病伴微量白蛋白尿。血糖控制改善后体重增加,下肢脂肪减少,腹部脂肪过多。她有胰岛素缺乏和相对严重的胰岛素抵抗。根据临床表现和基因分析,她可能符合家族性部分脂肪营养不良(FPLD)的范畴1。我们给予利拉鲁肽治疗她的糖尿病,正如之前的报道所显示的利拉鲁肽对FPLD1患者的有效性约为3个月。我们使用双能x线吸收仪(DEXA)和口服葡萄糖耐量试验(OGTT)评估利拉鲁肽治疗期间脂肪分布和胰岛素抵抗的变化。利拉鲁肽长期有效地达到良好的血糖和体重控制。DEXA显示上肢和躯干脂肪量增加,但由于体重稳定,我们推测没有进一步增加。OGTT显示胰岛素抵抗和胰岛素分泌能力的改善。我们认为这可能是由于利拉鲁肽的降血糖作用和通过增加脂肪细胞的脂肪储存能力对肥胖的预防作用引起的。利拉鲁肽、抗高血压药物和他汀类药物加强多因素干预可减轻糖尿病微血管病变。本病例提示利拉鲁肽可能是一种有效的治疗选择,因为它具有多效性作用。
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Beneficial effects of long-term liraglutide monotherapy on glycemic control and diabetic microangiopathies in a female Japanese diabetic patient with familial partial lipodystrophy 1
We experienced the case that a Japanese female diabetic patient with partial lipodystrophy continued liraglutide monotherapy for a long period on her will. At first examination, she had poor glycemic control and body weight reduction with decreased fat mass had been caused by uncontrolled diabetes. She had severe non-proliferative diabetic retinopathy and nephropathy with microalbuminuria. When she had weight gain after her glycemic control was improved, she still had fat loss in the lower limbs with abdominal fat excess. She had insulin deficiency and relatively severe insulin resistance. According to the clinical findings and genetic analysis, she might fit the category of familial partial lipodystrophy (FPLD)1. We administered liraglutide for her diabetes care, as previous report suggested the effectiveness of liraglutide in patients with FPLD1 for about three months. We assessed changes in fat distribution and insulin resistance during liraglutide therapy using dual energy X-ray absorptiometry (DEXA) and the oral glucose tolerance test (OGTT). Liraglutide effectively has achieved favorable glycemic and body weight control for a long period. The DEXA showed that fat mass in the upper limbs and trunk was increased, but we could speculate no further increase as her body weight was stable. The OGTT showed the amelioration of insulin resistance and insulin secretory capacity adjusted for insulin sensitivity. We thought that this might be caused by the blood-glucose-reducing effects of liraglutide and preventive effects on obesity through increasing the fat storage capacity of adipocytes. The intensified multifactorial intervention with liraglutide, anti-hypertensive drugs, and statin attenuated diabetic microangiopathies. The present case suggests that liraglutide might be as an efficient therapeutic option through its pleiotropic effects in diabetic patients with FPLD1.
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