对氧磷酯酶1与2型糖尿病肾病的关系

目的　探讨血清对氧磷酯酶 1(PON1)活性与 2型糖尿病 (DM)并发肾病 (DN)的关系。方法　血清PON1活性用酚乙酸酯为底物测定 ,血浆氧化型低密度脂蛋白 (ox LDL)用ELISA法测定 ,尿 2 4小时微量白蛋白用放免法测定。结果　 91例 2型DM患者的PON1活性比 5 4例正常对照显著降低〔(138.2± 31.4 )kU/Lvs (184 .1± 2 9.5 )kU/L ,P <0 .0 0 1〕 ,且 2型DM的Ⅰ组 (UAER <30mg/ 2 4h)、Ⅱ组 (UAER 30～ 30 0mg/ 2 4h)和Ⅲ组 (UAER >30 0mg/ 2 4h)相比 ,PON1活性依次显著下降〔(15 1.8± 2 4 .5 )kU/L ,(12 4 .5± 32 .8)kU/L ,(10 1.1± 36 .6 )kU/L ,P <0 .0 1〕 ,而ox LDL的浓度却依次显著升高〔(6 16 .2± 135 .7) μg/L ,(75 3.9± 132 .5 ) μg/L ,(875 .1± 15 3.2 ) μg/L ,P <0 .0 1〕。PON1活性与ox LDL的浓度呈高度负相关 (r =- 0 .83,P <0 .0 0 1) ,也与UAER呈负相关 (r =- 0 .2 8,P<0 .0 5 ) ,多元回归分析表明PON1活性是 2型DM并发DN的高度危险因素 (P <0 .0 1)。结论　PON1活性在 2型DM显著下降 ,且在并发DN的 2型DM患者下降更显著。PON1活性与ox LDL呈负相关。PON1活性降低是 2型DM并发DN的高度危险因素     

对氧磷酯酶-1与老年人2型糖尿病关系的研究

目的 探讨血清对氧磷酯酶-1(PON-1)活性、基因Glu-Arg192位多态性与老年人2型糖尿病(DM)及并发症的关系。方法 用酚乙酸酯为底物测定血清PON-1活性;用多聚酶链限制片段多态件反应技术对老年2型DM各组及健康老年人的PON-1基因192位进行基因分型。结果 老年单纯2型DM组PON-1活性为(98.32±21.68)kU/L,比健康对照组显著降低〔(13.29±19.74)kU/L,P<0.01〕,老年2型DM合并大、微血管病变组PON-1活性分别为(73.18±13.00)和(74.02±15.13)kU/L,比老年单纯2型DM组显著降低对(P<0.01)。重庆市老年居民PON-1基因192位A、B等位基因频率在健康对照组为0.44、0.56,老年人单纯2型DM组及大、微血管病变组为0.43、0.57,0.33、0.67和0.38、0.62,老年人2型DM各组与健康对照组比较PON-1、AA、AB、BB基因到分布差异无显著性。结论 PON-1活性在老年2型DM及共发血管病变患者中均显著降低,提示PON-1活性的降低参与了DM血管并发症的发生。重庆市老年居民PON-1基因192位B等位基因与老年人2型DM及2型DM并发血管病变无明显关系。     

对氧磷酯酶-1与老年人2型糖尿病合并高血压的研究

目的探讨血清对氧磷酯酶-1(PON-1)活性与老年人2型糖尿病(DM)合并高血压(EH)的关系。方法设健康对照组、单纯2型DM组和2型DM合并EH组,分别测定PON-1、NO水平。结果老年单纯2型DM组PON-1活性为(94.81±28.50)kU/L,比健康对照组显著降低犤(132.93±19.45)kU/L,P<0.01犦,老年2型DM合并EH组PON-1活性(66.02±14.60)kU/L,比老年单纯2型DM组显著降低(P<0.01)。NO水平在老年2型DM合并EH组比健康对照组和老年单纯2型DM组显著降低(P<0.01)。PON-1活性与NO水平呈高度正相关(r=0.63,P<0.001),Logistic回归分析表明PON-1活性是2型DM合并EH的高度危险因素(P<0.01)。结论PON-1活性在2型DM显著下降,且在2型DM合并EH患者下降更显著。PON-1活性与NO呈正相关。PON-1活性降低是2型DM合并EH的高度危险因素。     

糖尿病及其合并冠心病C反应蛋白的改变

目的在不同类型糖尿病探讨糖代谢异常的炎性机制,观察其合并冠心病时高敏C反应蛋白(hsCRP)的变化,比较是否具有不同的发病基础。方法选择经临床确诊的符合入选标准的1型糖尿病(T1DM)和2型糖尿病(T2DM)患者,后者部分合并冠心病,用ELISA方法分别测定它们的血清hsCRP值,健康者为对照。结果在两种类型糖尿病中,单纯T2DM组hsCRP水平较T1DM组明显升高(1.57±1.24mg/Lvs1.08±0.87mg/L,P=0.04),T1DM组与对照组hsCRP未见显著差异;合并冠心病的T2DM组比单纯T2DM组升高更明显(1.78±1.49mg/Lvs1.57±1.24mg/L,P=0.02)。结论糖代谢异常与冠脉疾病可能有共同的慢性亚临床炎症起源,T2DM与T1DM有不同的发病学机制,前者与炎症状态有关,炎症的水平对预测T2DM合并大血管病变有重要临床价值。     

老年2型糖尿病视网膜病变患者骨密度变化的研究

目的探讨老年2型糖尿病(T2DM)合并视网膜病变患者骨密度(BMD)变化的特点。方法测定56例老年T2DM合并糖尿病视网膜病变患者(DR组)、60例无糖尿病视网膜病变T2DM患者(NDR组)和58例健康老年人(健康对照组)股骨颈、大转子、Ward's三角区(ward's)及前后位腰椎BMD,并检测血清骨钙素(BGP)、血钙(Ca)、血磷(P)、甲状旁腺激素(PTH)及Ⅰ型胶原降解产物(Crosslaps)/尿肌酐(Cr)水平。结果DR组的股骨颈的BMD低于健康对照组及NDR组〔分别为(0.66±0.15)、(0.76±0.15)、(0.81±0.18)g/cm2〕,差异有统计学意义(P<0.05及P<0.01);前后位腰椎各部位BMD在DR组BMD均高于健康对照组及NDR组(P<0.05)。DR组血清BGP显著低于健康对照组(P<0.01),与NDR组比较,差异无统计学意义(P>0.05);DR组血清PTH、P显著高于NDR组及健康对照组(P<0.05及P<0.01)。结论老年T2DM合并视网膜病变者的股骨近端BMD显著低于无视网膜病变糖尿病患者和健康人群,而腰椎各部位BMD水平则与之相反。     

同型半胱氨酸与2型糖尿病肾病的相关性研究

目的研究血清同型半胱氨酸(Hcy)与2型糖尿病(T2DM)伴发糖尿病肾病(DN)的关系。方法对60名T2DM患者进行24h尿蛋白,肾小球滤过率测定,并根据其结果分为单纯糖尿病组(DM)和DN组,另选择健康对照组20名。取空腹静脉血测定血糖(BG)、甘油三酯(TG)、糖化血红蛋白(HbAlc)、Hcy。结果DM患者血浆Hcy水平〔(15.01±5.99)μmol/L〕较健康对照组〔(12.00±1.96)μmol/L〕有明显升高(P<0.001)。将Hcy≥15.80μmol/L作为高Hcy血症的诊断标准,将T2DM分为高Hcy组和无高Hcy组,高Hcy组DN发生率比无高Hcy组明显升高(50%vs26.8%)(P<0.05)。各危险因素与DN多元回归分析表明,Hcy与DN的发生有关。结论Hcy血症是T2DM、DN的一个独立危险因素,Hcy为DN早期发现和临床诊断提供了有力的指标。     

老年糖尿病患者高同型半胱氨酸血症与肾病及胰岛素抵抗的关系

目的探讨老年2型糖尿病患者血清总同型半胱氨酸(tHcy)水平与不同程度肾病和胰岛素抵抗的关系。方法测定98例老年2型糖尿病患者和36例健康对照者血清tHcy及血糖、血脂、肾功能、胰岛素等指标。结果(1)糖尿病组血清tHcy显著高于对照组[(172±76)μmol/L对(94±35)μmol/L,P<001],糖尿病组tHcy水平随着肾病程度的加重而升高,其中肾功能受损组显著高于无肾病组[(286±79)μmol/L对(157±63)μmol/L,P<0001];(2)与正常tHcy组比较,高tHcy组的年龄、尿酸、肌酐、胰岛素抵抗指数(HomaIR)均显著升高(P<005),肌酐清除率(Ccr)显著降低(P<001);(3)相关分析显示,糖尿病患者血清tHcy水平与肌酐、尿酸、HomaIR、年龄均呈显著正相关,与Ccr呈显著负相关。结论老年糖尿病患者高tHcy血症是肾功能减退及胰岛素抵抗的两个重要相关因素。     

冠心病并发糖尿病患者血同型半胱氨酸以及铜水平的相关性研究

目的探讨冠心病(CHD)并发糖尿病(DM)患者血清同型半胱氨酸(Hcy)、铜(Cu)的水平及二者的相关性。方法以31例CHD并发2型DM患者(DM组)为研究对象,以同期不并发DM的CHD患者36例为对照组(非DM组),另选择健康对照组30例,测定外周血Hcy、Cu浓度、体质指数和血脂。结果DM组血Hcy、Cu[分别为(18.8±3.5)、(21.1±3.8)μmol/L]高于健康对照组[分别为(10.7±2.3)、(16.8±2.7)μmol/L](P<0.01)和非DM组[分别为(15.6±1.9)、(14.8±2.2)μmol/L],均P<0.05;非DM组Hcy高于健康对照组(P<0.01),而Cu水平与对照组比较差异无统计学意义(P>0.05)。CHD并发DM组患者血Hcy与Cu呈正相关(P<0.01)。结论高Hcy致DM患者发生冠状动脉硬化可能与Cu的协同作用有关。     

老年2型糖尿病合并非酒精性脂肪肝患者血清蛋白激酶Cε活性和胰岛素抵抗的关系研究

目的探讨老年2型糖尿病(T2DM)合并非酒精性脂肪肝(NAFLD)患者血清蛋白激酶Cε(PKCε)活性与胰岛素抵抗的相关性。方法回顾性分析2017年10月至2018年10月西安交通大学医学院第二附属医院住院的T2DM患者229例,根据病情分为T2DM组112例,T2DM+NAFLD组117例,另选同期健康对照组110例。比较3组入选者临床资料和实验室检查结果,计算稳态模型的胰岛素抵抗指数(HOMA-IR),采用酶联免疫吸附法测定血清PKCε活性,并分析其与胰岛素抵抗的相关性。结果T2DM+NAFLD组患者血清PKCε活性和HOMA-IR均高于单纯T2DM组和健康对照组[(195.5±62.1)μg/L比(188.7±61.2)μg/L和(89.1±20.2)μg/L、(12.5±7.9比14.1±5.7和5.8±4.1),F值分别为9.76、10.21,均P=0.010]。Pearson相关分析,T2DM+NAFLD组患者血清PKCε活性、HOMA-IR及三酰甘油呈正相关(r值分别为0.339、0.305、0.329,均P<0.015)。Logistic回归分析,血清PKCε活性、HOMA-IR和三酰甘油是T2DM+NAFLD组的危险因素(β值分别为0.849、0.022和0.710,均P<0.05)。血清PKCε活性升高是T2DM合并NAFLD的独立影响因素。结论老年T2DM合并NAFLD患者血清PKCε活性升高与胰岛素抵抗呈正相关,降低血清PKCε活性和改善胰岛素抵抗有助于延缓或改善T2DM及NAFLD。     

他汀类对2型糖尿病合并骨质疏松骨密度的影响

目的探讨他汀类药物对2型糖尿病(T2DM)合并骨质疏松(OP)患者骨密度的影响。方法86例T2DM合并OP患者随机分为两组,T2DM1组46例,男性30例,女性16例;T2DM2组40例,男性26例,女性14例,均给予标准治疗控制血糖、血压等,T2DM2组另外加服他汀类药物,疗程12个月,比较两组治疗前后在骨密度(BMD),空腹血糖(FBG)、餐后2h血糖(2h-PBG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)和甘油三酯(TG),糖化血红蛋白(HbA1c)方面的变化。结果治疗后T2DM2组TC和LDL-C水平均有所下降,分别为(3.98±1.21/4.68±1.29)mmol/L,(2.29±0.42/2.58±0.52)mmol/L,BMD增加(-2.26±0.27/-2.69±0.17)g/cm2,与治疗前比较有显著性差异(P<0.05);治疗后T2DM2组TC、LDL-C和BMD与T2DM1组比较分别为(3.98±1.21/5.02±1.19)mmol/L,(2.29±0.42/3.52±0.47)mmol/L,(-2.26±0.27/-3.53±0.43)g/cm2(P<0.05)。结论他汀类药物在发挥其积极有效调脂作用的同时,能够使糖尿病患者的骨密度得到提高,可能为糖尿病合并骨质疏松的治疗提供新的手段。     

The incidence of Type 1 (insulin-dependent) diabetes mellitus in subjects aged 0–19 years in Luxembourg: a retrospective study from 1977 to 1986

Summary A decrease in the incidence of Type 1 (insulin-dependent) diabetes mellitus in the age group 0–14 years has been observed from north to south over north-western Europe. To evaluate whether this trend could be found in Luxembourg (a small country between the Netherlands and France) we performed a retrospective study over a period of 10 years. Information concerning all Type 1 diabetic patients (aged 0–19 years at diagnosis), diagnosed between January 1, 1977 and December 31, 1986 was obtained through paediatricians, internists, general practitioners and the Luxembourg Diabetes Association (LDA). The LDA was used as the ascertainment group (to estimate the real number and incidence of Type 1 diabetes mellitus). During the study period 91 Type 1 diabetic patients aged between 0–19 years were diagnosed. An incidence of 11.2 was found in boys (0–19 years). Girls in the same age group showed a considerably lower incidence of 8.8. Standardised incidence (using as standard the world population) revealed an almost similar incidence in the Netherlands and Luxembourg (respectively 10.3 and 10.2) for the age group aged 0–14 years. In France a considerably lower incidence is found (3.6). To what extent different methodology contributes to the differences remains to be clarified. Further prospective studies are necessary to investigate the role of environmental and genetic factors.     

Apolipoprotein (a) levels in type 1 and type 2 diabetes mellitus

Type 1 and type 2 diabetes mellitus are both characterized by increased cardiovascular mortality and morbidity. Since several reports have indicated that apolipoprotein (a) [apo (a)] levels are positively associated with an increased risk of macrovascular disease, we investigated whether apo (a) levels are elevated in both types of diabetes mellitus and may thus represent an independent risk factor for atherosclerotic disease. Apo(a) concentrations in type 1 diabetic patients were not significantly different from matched controls (276±78 vs 149±46 units/l). Type 2 diabetic patients had considerably higher levels of apo (a) than matched controls (471±89 vs 221±61 units/l,P=0.06), though the difference was not statistically significant. However, concentrations of apo (a) were above 300 units/l in 36% of type 1 and 67% of type 2 diabetic patients, but in only 14% and 25% respectively of matched control subjects. Plasma triglycerides were positively and independently correlated with apo (a) levels in both diabetic and non-diabetic subjects. On the other hand, no significant correlation was found between apo (a) levels and glycosylated haemoglobin, total cholesterol or high density lipoprotein cholesterol in any of the groups studied. In conclusion, apo (a) levels are not significantly elevated either in type 1 or type 2 diabetic patients without proteinuria and in moderate metabolic control; however, levels above 300 units/l were 2.6 times more frequent in both types of diabetes mellitus than in carefully age-, sex-, and weight-matched control subjects.     

Circulating endothelin-1 levels in type 2 diabetic patients with ischaemic heart disease

To investigate whether circulating endothelin-1 (Et-1) may be related to the increased incidence and severity of ischaemic heart disease in type 2 diabetes mellitus, we compared the concentrations in type 2 diabetic patients and in non-diabetic patients with coronary artery disease (CAD) angiographically documented. Plasma levels of Et-1 were determined in 34 type 2 diabetic patients with CAD (16 with stable angina, 6 with unstable angina, 12 with previous myocardial infarction) and in 19 non-diabetic patients with CAD (4 with stable angina, 5 with unstable angina, 10 with previous myocardial infarction). Fifteen diabetic patients without CAD and 9 healthy volunteers served as control subjects. In the type 2 diabetic patients, the mean Et-1 levels were 3.19±1.61 pmol/l in those with stable angina, 3.58±1.92 pmol/l in those with unstable angina, 4.24±2.53 pmol/l in those with myocardial infarction. These values were not significantly different one another, nor from the values obtained from type 2 diabetic controls (3.64±2.13 pmol/l). In the non-diabetic patients, the mean Et-1 levels were 3.92±0.73 pmol/l in those with stable angina, 4.35±1.67 pmol/l in those with unstable angina, 4.33±1.66 pmol/l in those with myocardial infarction. These values were not significantly different one another, but significantly higher than those obtained from healthy controls (2.07±0.67 pmol/l;P<0.001). No significant differences were found in Et-1 levels between diabetic and non-diabetic patients with stable, unstable angina and previous myocardial infarction. In contrast, a statistically significant difference was found in Et-1 levels between diabetic and non-diabetic control subjects (P<0.05). In conclusion, similar raised concentrations of Et-1 in diabetic and non-diabetic patients with stable, unstable angina and previous myocardial infarction do not support the hypothesis that higher levels of Et-1 in diabetic patients are responsible for the increased incidence of CAD in diabetes mellitus. However, the raised Et-1 levels found in diabetic patients in the absence of CAD strongly suggest that a generalised endothelial dysfunction, documented in our study by increased levels of Et-1, most probably precedes subsequent cardiovascular diseases.     

2011年第2期英文目录

糖尿病（DM）常并发血管及血栓性疾病,而DM发生血管病变的机制复杂。血栓前状态分子标志物之一的纤溶活性指标——纤溶酶原激活物抑制物-1（PAI-1）在DM及其血管病变的发生发展中起到重要作用。本文拟对DM血管病变与PAI-1关系的研究进展作一综述。     

糖化血红蛋白的临床应用进展

美国糖尿病协会(ADA)和世界卫生组织(WHO)正式推荐糖化血红蛋白(HbA1c)作为糖尿病的诊断标准之一,国内关于HbA1c检测方法的标准化及其筛查、诊断糖尿病前期和糖尿病切点等问题仍存在争议。该文就HbA1c的检测方法标准化及其临床应用等作一综述。     

葡萄糖转运蛋白基因多态性与糖尿病和糖尿病肾病的关系

目的：探讨葡萄糖转运蛋白（ＧＬＵＴ１）基因多态性与糖尿病及糖尿病肾病（ＤＮ）的关系。 方法：应用ＰＣＲ方法对１３１例Ⅱ型糖尿病（ＮＩＤＤＭ）患者ＧＬＵＴ１基因多态性与ＮＩＤＤＭ及ＤＮ发生之间的关系进行了观察，并结合患者体重指数（ＢＭＩ）和胰岛素敏感指数（ＩＳＩ）进行分析。 结果：①ＮＩＤＤＭ组患者Ｘｂａ Ｉ（＋／－）基因型的发生频率明显高于正常人群（６２％ｖｓ３３％，Ｐ〈０．０１），而Ｘｂａ Ｉ（     

Long-term bone loss in insulin-dependent diabetes mellitus

The bone mineral content (BMC) in patients with insulin-dependent diabetes is reduced by 10% early in the disease, but due to a lack of long-term longitudinal studies it is unknown whether this diabetic osteopenia develops further through life. Over a time period of 11 years we examined the BMC in a group of seven adult insulin-dependent diabetics, in whom physiological and pathological factors affecting bone metabolism had been excluded; the patients were well regulated without diabetic complications. The BMC was not significantly decreased at the initial examination. The longitudinal study revealed a small but statistically significant fall in BMC, mainly in trabecular bone. The narrow (95%) confidence interval of median end value (93.3-99.0% of initial BMC) indicates that the annual decrease in BMC in such patients is of the order of 0.5%, a reduction that is probably clinically insignificant.     

Subclinical diabetic neuropathy: similarities between electrophysiological results of patients with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus

Summary Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients share many clinical and biochemical characteristics. However, sural nerve biopsies from patients with advanced and chronic neuropathy show ultrastructural differences between these two groups. We investigated whether at a subclinical stage of the illness, when Type 1 and Type 2 diabetic patients are clinically uniform and the histopathological nerve alterations are not advanced, comparison between the two diabetes groups might show differences in nerve fibre involvement related to the different pathogeneses of the neuropathies. A total of 88 diabetic patients (52 Type 1 and 36 Type 2), with a subclinical form of polyneuropathy were selected. The clinical neurophysiological examination consisted of motor and sensory nerve conduction studies, Hoffmann (H)-reflex, single fibre electromyography and static as well as dynamic pupillometry. With regard to clinical neurophysiological abnormalities, the severity of the polyneuropathy appeared to be equal in both groups. Despite the absence of clinical symptoms the neurophysiological abnormalities were pronounced and it was impossible to differentiate Type 1 diabetic patients from Type 2 diabetic patients on a clinical neurophysiology basis when correcting for differences in age, height, and duration of illness. In the Type 1 diabetic group as well as in the Type 2 diabetic group the autonomic nerve fibres and nerves in the legs were more frequently affected than the thick myelinated nerves in the arms. These findings do not support the assumption that there is a difference in the manifestation of polyneuropathy between Type 1 and Type 2 diabetic patients.     

Shared genetic susceptibility of Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus: contributions of HLA and haptoglobin

Summary Epidemiologic data suggest that having a parent with Type 2 (non-insulin-dependent) diabetes mellitus increases the risk for Type 1 (insulin-dependent) diabetes in siblings of a Type 1 diabetes proband. This increase in risk is consistent with a shared genetic susceptibility between Type 1 diabetes and Type 2 diabetes. We contrast genetic risk factors in three sets of families, consisting of (1) a single Type 1 diabetic child (proband) and non-diabetic parents, (2) multiple Type 1 diabetic siblings and non-diabetic parents, and (3) at least one Type 1 diabetic child and at least one Type 2 diabetic parent. Previous studies have demonstrated that HLA region genes, which elevate the risk in Type 1 diabetes, have no significant effect with respect to the risk for developing Type 2 diabetes. An earlier report cited a contribution by the haptoglobin locus to genetic susceptibility for Type 2 diabetes. We provide evidence that a high risk HLA antigen (HLA-DR3) is decreased to a greater extent in Type 1 patients with a Type 2 parent than in Type 1 patients in which the parents are not diabetic. The role of HLA-DR4 is maintained in these families, with an unexpectedly significant increased rate of transmission of the HLA-DR4 allele from Type 2 parent to Type 1 offspring. The role of haptoglobin in these families does not appear to be important, either with respect to association with diabetes or with respect to linkage with a secondary susceptibility locus. These results indicate that families with a Type 2 parent and Type 1 child, heavily determined by HLA-DR4 linked factors, may represent a homogeneous subset of diabetes susceptibility.     

Raised serum apolipoprotein (a) in active diabetic retinopathy

Summary Progressive capillary occlusion often leads to severe retinopathy within 15–20 years of the onset of Type 1 (insulin-dependent) diabetes mellitus. Lipoprotein (a), a complex formed by apolipoprotein (a), apo B-100 and lipids, is considered an independent, genetically determined, predictor of cardiovascular disease. It may have antifibrinolytic properties in view of its similarity to plasminogen. To test the hypothesis that circulating lipoprotein (a) is associated with the process that leads to clinically active diabetic retinopathy, we measured the circulating levels of apolipoprotein (a) (which are strictly correlated with those of lipoprotein (a)) in two groups of patients with Type 1 diabetes of at least 15 years duration: 25 with active retinopathy and 27 without clinically detectable retinal lesions. Thirty-eight healthy subjects of the same age and sex served as controls. Serum apolipoprotein (a) was higher in the patients with active retinopathy (36(2-193) U/dl, geometric mean and range) than in those without clinically detectable retinal lesion (17(1–160)) and the control subjects (14(0–115)), p < 0.01 in both cases. The distribution of apolipoprotein (a) levels was skewed to the left, as expected, in the patients without clinically evident retinal lesions and the control groups, but there was a bimodal trend of distribution among those with active retinopathy. The levels of glycated haemoglobin were similar in the two groups of diabetic patients, and no significant differences were found for total and HDL cholesterol, triglycerides or apolipoproteins A1 and B between them and the control subjects. These preliminary results suggest that serum apolipoprotein (a) is elevated in patients with active retinopathy. The role of this lipoprotein as a predictor or a pathogenic effector of diabetic retinopathy, or both deserves further investigation.