張 凌,崔光淑,郭啟煜,黃金華
臨床較少見的真性糖尿病性白內障一例報告
張 凌,崔光淑,郭啟煜,黃金華
目的探討真性糖尿病性白內障的臨床特點。方法對我院收治的1例真性糖尿病性白內障的臨床資料進行回顧性分析,并復習相關文獻。結果本例因視物模糊1個月,尿酮陽性1 d入院。初步診斷為雙眼白內障,后發現血糖升高,遂到我院就診。查隨機血糖29.87 mmol/L;尿糖(++++),尿酮(++);糖化血紅蛋白13.0%;空腹、口服葡萄糖后1 h、2 h及3 h C肽分別為0.19 nmol/L、0.26 nmol/L、0.32 nmol/L、0.45 nmol/L。診斷為雙眼真性糖尿病性白內障,予降糖、補液等治療,后于外院行雙眼白內障摘除術+人工晶狀體植入術,術后視力恢復良好。隨訪1年,患者血糖控制良好,視力恢復正常。結論接診年輕且病情進展較快的白內障患者,要考慮到真性糖尿病性白內障的可能,常規監測血糖,早期明確診斷,盡早予有效治療,以改善預后。
白內障;糖尿病,2型;糖尿病視網膜病變
女,28歲。因視物模糊1個月,尿酮陽性1 d入院。1個月前無明顯誘因出現視物模糊,并逐漸加重,曾就診外院,診斷為雙眼白內障,擬行手術治療,術前常規檢查發現空腹血糖20.69 mmol/L,同時伴口干癥狀,無多飲、多尿,近期體重無明顯下降,為進一步診治到我院就診。查隨機血糖>33.3 mmol/L,尿酮(+),遂以糖尿病酮癥收入院。既往體健,近2年有大量進食含糖飲料史,1年前常規體檢排除糖尿病及白內障,有糖尿病家族史。查體:體溫36.5℃,脈搏88/min,呼吸19/min,血壓120/80 mmHg。身高162 cm,體重75 kg,體重指數28.6 kg/m2。意識清楚,心肺腹檢查未見異常,雙側足背動脈搏動正常,10 g彈力絲試驗陰性。視力粗測:左眼4.3,右眼4.5。查隨機血糖29.87 mmol/L;尿糖(++++),尿酮(++);血鈉133 mmol/L,鉀4.3 mmol/L;糖化血紅蛋白13.0%;總膽固醇7.83 mmol/L,低密度脂蛋白膽固醇5.55 mmol/L,高密度脂蛋白膽固醇及甘油三酯正常;肝腎功能、血尿酸、血常規、便常規及24 h尿微量白蛋白定量均正常;C肽釋放試驗示:空腹、口服葡萄糖后1 h、2 h及3 h C肽分別為0.19 nmol/L、0.26 nmol/L、0.32 nmol/L、0.45 nmol/L;胰島素抗體、胰島細胞抗體及谷氨酸脫羧酶抗體均陰性;血氣分析未見異常。頸椎動脈彩色多普勒超聲(彩超)示:左側頸總動脈分叉處可見軟斑塊,右側頸內動脈起始段內、中膜局部增厚;雙側椎動脈未見明顯異常。請眼科會診,行裂隙燈檢查示:雙眼白內障(成熟期),建議控制血糖后予手術治療。雙下肢動脈彩超示:左側股總動脈局部內、中膜增厚。心電圖、X線胸片均未見異常。
診斷:①2型糖尿病;②糖尿病酮癥;③雙眼真性糖尿病性白內障;④高膽固醇血癥。明確診斷后經積極補液、小劑量胰島素抑酮治療,酮體轉陰后予胰島素強化聯合二甲雙胍、吡格列酮降糖治療,待血糖控制良好,到外院行雙眼白內障摘除術+人工晶狀體植入術。術后視力恢復良好,繼續予二甲雙胍聯合吡格列酮控制血糖。隨訪1年,患者血糖控制良好,視力恢復正常,復查C肽釋放試驗示:空腹、口服葡萄糖后1 h、2 h及3 h C肽分別為0.6 nmol/L、3.1 nmol/L、3.5 nmol/L、1.7 nmol/L。
2.1疾病概況 糖尿病性白內障已成為僅次于糖尿病視網膜病變的第二大糖尿病眼部疾病,是致盲的主要原因[1]。糖尿病性白內障分為真性糖尿病性白內障和與糖尿病患者年齡相關性白內障,前者極為罕見。自1998年以來,國內僅報道5例真性糖尿病性白內障,視物模糊3個月~3年,均為1型糖尿病,其中4例為青年女性,1例為兒童[2-6]。本例為2型糖尿病患者,從輕微視物模糊到白內障成熟僅1個月。真性糖尿病性白內障晶狀體呈雪花狀改變,多見于30歲以下、病情嚴重的1型糖尿病患者,常雙眼同時發病,病情進展迅速,晶狀體可在數天、數周或數月內完全渾濁,視力明顯下降,且病情進展與血糖水平明顯相關,隨著血糖的控制,病情得以延緩或停止,甚至逆轉。與糖尿病患者年齡相關性白內障為老年性白內障與真性糖尿病性白內障并存,可單眼發病,較無糖尿病的老年性白內障患者平均年齡小、病情進展快,發病率為非糖尿病患者的3~10倍。
2.2發病機制 目前糖尿病性白內障的發病機制尚未完全清楚,可能與多元醇代謝異常、非酶糖基化、氧化應激等有關。醛糖還原酶(aldose reductase, AR)路徑是葡萄糖的補充代謝通路,機體處于高糖狀態下可激活AR,導致山梨醇大量積聚[7-9],形成細胞內高滲狀態,引發細胞內滲透壓升高,大量水分通過滲透梯度進入細胞內,引起晶狀體水腫、混濁。Oishi等[10]發現,部分1型糖尿病患者急性白內障形成和發展的基礎是AR受體介導的多元醇積聚導致廣泛晶狀體纖維腫脹。非酶糖基化學說主要指在高糖環境中游離氨基與糖分子的醛基經復雜的分子重排,形成不可逆的晚期糖基化終末產物(AGEs),干擾細胞代謝,使水通過滲透壓作用進入細胞內,致晶狀體內水分增多[11],同時還可引發炎癥反應及血管舒縮功能障礙,導致血管管腔狹窄。有研究表明,氧化自由基損傷能使晶狀體蛋白的結構發生改變,是白內障發病的觸發因素[12]。
2.3藥物治療 ①醛糖還原酶抑制劑(ARIs):AR作為多元醇通路的限速酶,通過抑制其活性阻止糖尿病性白內障的發生、發展。依帕司他、托瑞司他、索比尼爾、GP-1447、Zopolrestant等均曾應用于糖尿病性白內障的治療,因多種藥物有效性差或有嚴重的不良反應,目前臨床常應用依帕司他[13]。②抗氧化劑:在正常的人類晶狀體中,牛磺酸占游離氨基酸的50%以上。隨白內障病程的發展,晶狀體中牛磺酸含量逐漸降低。補充牛磺酸不僅可使白內障的發生時間推遲,還可減輕晶狀體混濁程度,抑制上皮細胞凋亡,可能成為臨床防治糖尿病性白內障的一種理想藥物[14]。此外,大量實驗證實[15-17],阿司匹林、氨基胍、賴氨酸及必需氨基酸、丙酮酸等在治療糖尿病性白內障方面亦有廣闊前景。
2.4手術治療 藥物治療主要維持晶狀體營養狀態、延緩晶狀體衰老及糾正代謝障礙,但單純藥物治療不能使晶狀體恢復透明,只有手術才是重見光明的有效方法[18]。目前小切口微創白內障囊外摘除術具有切口小、手術費用低、成本小等特點,在發展中國家和經濟較落后地區廣泛應用,特別是對Ⅳ級以上硬核、老年人角膜內皮功能欠佳患者較超聲乳化手術更為安全[19]。超聲乳化手術是發達國家治療糖尿病性白內障的標準術式,特別適用于軟核(Ⅳ級核及以下)糖尿病性白內障。飛秒激光輔助白內障手術是最新的白內障微創術式,但費用高。然而,任何手術均需術前有效地控制血糖,術后定期檢查,減少糖尿病視網膜病變的發生、發展。
真性糖尿病性白內障因早期極易漏診而錯過最佳治療時機。本例以視物模糊為首發癥狀,在白內障診斷明確考慮手術治療前進行常規檢查才明確糖尿病診斷。提示接診年輕白內障且病情進展較快的患者時,除考慮眼科常見病外,要想到糖尿病性白內障的可能,常規監測血糖,早期明確診斷,盡早予有效治療,以改善預后。
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RareTrueDiabeticCataractaCaseReport
ZHANG Ling1, CUI Guang-shu1, GUO Qi-yu2, HUANG Jin-hua1
(1. Department of Endocrinolog, Zhongguancun Hospital of Beijing, Beijing 100190, China; 2. Department of Endocrinology, General Hospital of PLA Navy, Beijing 100048, China)
ObjectiveTo investigate clinical characteristics of true diabetic cataract.MethodsClinical data of 1 patient with true diabetic cataract was retrospectively analyzed, and the related literature was reviewed.ResultsThe patient was admitted for blurred vision for 1 month and positive urine acetone body for 1 d. The patien's result was normal by medical examination 1 year ago, and primary diagnosis was binocular cataract, and then elevated blood sugar was found, so the patient was transferred to our hospital. Examinations showed that random blood sugar was 29.87 mmol/L, urine sugar (++++),urine acetone body (++) and 13% glycosylated hemoglobin. Values of C peptides in fasting, 1 h, 2 h and 3 h after taking glucose orally were 0.19 nmol/L, 0.26 nmol/L, 0.32 nmol/L and 0.45 nmol/L respectively. The true diabetic cataract was confirmed. After treatments such as hypoglycemic and fluid replacement, binocular cataract extraction and intraocular lens implantation were performed in other hospital, and postoperative visual acuity recovered well. With follow-up for 1 year, the patient's blood sugar was controlled well, and vision returned to normal.ConclusionYoung cataract patients have rapid conditions development, clinicians should take into account the possibility of true diabetic cataracts, and routine monitoring of blood sugar should be given to confirm the diagnosis early in order to give effective treatment as early as possible and improve prognosis.
Cataract; Diabetes mellitus, type 2; Diabetic retinopathy
100190 北京,北京市中關村醫院內分泌科(張凌、崔光淑、黃金華);100048 北京,解放軍海軍總醫院內分泌科(郭啟煜)
R776.1
A
1002-3429(2017)12-0034-03
10.3969/j.issn.1002-3429.2017.12.015
2017-08-22 修回時間:2017-09-30)