血浆chemerin水平与增殖型糖尿病视网膜病变相关

目的 探讨2型糖尿病患者血浆chemerin水平与糖尿病视网膜病变的相关性.方法 2型糖尿病患者200例,根据眼底镜或眼底荧光造影结果将其分为糖尿病对照组98例,非增殖型糖尿病视网膜病变组83例,增殖型糖尿病视网膜病变组19例.采用酶联免疫吸附测定法检测患者血chemerin水平,并采用Pearson相关分析法,分析患者血chemerin水平与患者年龄、体质量指数(BMI)、病程、血压、血脂、尿蛋白、超敏C 反应蛋白(hsCRP)等临床指标的相关性.结果 Chemerin在增殖型糖尿病视网膜病变组显著升高,并且chemerin水平与患者的糖尿病病程、胰岛素抵抗指数(HOMA-IR)、血hsCRP、尿白蛋白排泄量呈显著正相关.结论 Chemerin水平与增殖型视网膜病变相关,对糖尿病增殖型视网膜病变可能具有监测价值.     

An evaluation of factors associated with proliferative diabetic retinopathy

Many individual factors have been related to development of proliferative diabetic retinopathy. To evaluate possible interactions among these, a constellation of variables were studied in 22 patients with long duration of insulin-dependent diabetes mellitus for greater than 25 years, with minimal background diabetic retinopathy, and compared to 27 patients with insulin-dependent diabetes mellitus for a variable duration, but with bilateral proliferative retinopathy. The patients were compatible in age at onset of diabetes (12 +/- 2 in proliferative retinopathy group vs 12 +/- 1 yr in the background retinopathy group). Following initial standard statistical analyses, data were further analysed using Logistic Regression Analysis. In the proliferative retinopathy group males were more prevalent (2.9:1), and patients were treated with larger insulin doses (0.86 +/- 0.07 vs 0.59 +/- 0.04 U/Kg B.W., p less than 0.001). Systemic hypertension and neuropathy were more prevalent (p less than 0.02 and less than 0.004 respectively), and diastolic blood pressure was higher (87 +/- 3 vs 75 +/- 2, p less than 0.01). In the same group diet was higher in carbohydrate and the ratio of polyunsaturated to saturated fats was lower (p less than 0.03, less than 0.05 respectively). HbA1 was higher (0.127 +/- 0.004 vs 0.110 +/- 0.004%, p less than 0.004), but the mean of all available plasma glucose values was not different. Impaired renal function expressed by higher BUN, serum creatinine, and urinary protein and lower creatinine clearance was observed. Nerve conduction parameters were more significantly impaired and plasma triglycerides were higher (1.74 +/- 0.2 vs 0.85 +/- 0.1 mmol/l, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Epidemiology of proliferative diabetic retinopathy.

OBJECTIVE--This review examines recent epidemiological data about the prevalence and incidence of and risk factors for proliferative diabetic retinopathy. In addition, the relation of proliferative retinopathy to other systemic complications associated with diabetes is reviewed. RESEARCH DESIGN AND METHODS--The data come mostly from the baseline and 4-yr follow-up examinations of a large population-based study, the WESDR, which involved 996 younger-onset insulin-dependent people whose diabetes was diagnosed at < 30 yr of age and 1370 older-onset people whose diabetes was diagnosed at > or = 30 yr of age, and who were taking or not taking insulin. RESULTS--The major finding is that proliferative retinopathy is a prevalent complication (23% in the WESDR younger-onset group, 10% in the WESDR older-onset group that takes insulin, and 3% in the group that does not take insulin). Hyperglycemia, longer duration of diabetes, and more severe retinopathy at baseline were associated with an increased 4-yr risk of developing proliferative retinopathy. However, higher blood pressure at baseline was associated only with the development of proliferative retinopathy in the younger-onset group. The presence of proliferative diabetic retinopathy was associated with an increased 4-yr risk of loss of vision, cardiovascular disease, diabetic nephropathy, and mortality. In the WESDR, a significant number of diabetic people with proliferative retinopathy at risk for vision loss were not under the care of an ophthalmologist or had not undergone panretinal photocoagulation. CONCLUSIONS--These data suggest that hyperglycemia and, possibly, high blood pressure are related to proliferative retinopathy. They also suggest that once proliferative diabetic retinopathy is detected, people should have a medical evaluation, because it is a strong indicator for the presence and development of systemic disease. These data also indicate that diabetic patients and their physicians should be aware of the need for routine ophthalmological examinations to detect and treat proliferative retinopathy.     

Severe retinopathy in type 1 diabetic patients is not related to the level of plasma homocysteine

The vascular-injuring amino acid homocysteine was previously shown to be increased in plasma in type 1 diabetic patients with clinical signs of nephropathy. Previous studies have also shown an inconsistent relationship between the development of diabetic nephropathy and retinopathy, indicating different pathogenetic mechanisms. In this study, plasma homocysteine was measured in 25 type 1 diabetic patients with a well-characterized form of severe retinopathy. Furthermore, a group of 24 type 1 diabetic patients with similar age at onset of diabetes and diabetes duration with no or minimal background retinopathy were investigated, in order to determine whether plasma homocysteine levels are different from those in patients with severe retinopathy. Patients with severe retinopathy did not have higher plasma levels of homocysteine (13.9 micromol/L; 5.9-30.7, median and range) than those without retinopathy (10.4 micromol/L; 5.7-18.9). Within the group of patients with severe retinopathy, increased homocysteine levels were confined to the patients (19.9 micromol/L; 10.0-30.7, n=9) with serum creatinine levels > 100 micromol/L, compared to those patients (9.6; 5.9-14.3 micromol/L, n=15) with a serum creatinine below 100 micromol/L. None of the patients without or with minimal background retinopathy had serum creatinine levels > 100 micromol/L. We conclude that diabetic retinopathy is not associated with increased plasma homocysteine levels, but plasma homocysteine accumulates, probably owing to reduced glomerular filtration, in diabetic patients with signs of nephropathy. In these patients, the promoting effect of nephropathy on the development of retinopathy does not seem to be mediated through homocysteine.     

ACE gene polymorphism and proliferative retinopathy in type 1 diabetes: results of a case-control study.

OBJECTIVE: To evaluate the relationship between the ACE insertion/deletion polymorphism and proliferative diabetic retinopathy in patients with type 1 diabetes of long duration. Based on epidemiological and pathophysiological findings, risk factors apart from glycemic control and duration of disease are likely to be involved in the development of proliferative retinopathy. RESEARCH DESIGN AND METHODS: In this case-control study, we compared 81 patients with longstanding (> or =20 years) type 1 diabetes who had nonproliferative (mild or moderate background) retinopathy with 95 patients with diabetes of similar duration and HbA1c who had proliferative retinopathy. To avoid the confounding effect of nephropathy, patients with overt nephropathy were excluded, and microalbuminuria was introduced into the multiple logistical regression model. The polymorphic region in intron 16 of the ACE gene (17q23) was analyzed using the polymerase chain reaction. RESULTS: The ACE genotype distribution in patients with proliferative retinopathy (DD 39.4%, ID 48.9%, II 11.7%) was significantly different (P < 0.001) from that of patients with nonproliferative retinopathy (DD 17.3%, ID 54.3%, II 28.4%). In a multiple logistical regression analysis, the adjusted relative risk for proliferative retinopathy in a patient with a DD genotype compared with a patient with an II genotype was 6.6 (95% CI 2.2-19.5), P = 0.0026. In addition to genotype, systolic blood pressure (odds ratio 1.027 [95% CI 1.0-1.1], P = 0.0093) but not microalbuminuria (< or =20 vs. > or =20 microg/min) reached statistical significance in the multiple regression model. Because subjects were matched regarding diabetes duration and HbA1c, we did not interpret the respective parameter estimates. CONCLUSIONS: These data provide evidence that deletion in the ACE gene is associated with the prevalence of proliferative retinopathy in type 1 diabetes and suggest that the DD genotype confers susceptibility to proliferative retinopathy independent of diabetic nephropathy     

Increased plasma urotensin-II levels are associated with diabetic retinopathy and carotid atherosclerosis in Type 2 diabetes

Human U-II (urotensin-II), the most potent vasoconstrictor peptide identified to date, is associated with cardiovascular disease. A single nucleotide polymorphism (S89N) in the gene encoding U-II (UTS2) is associated with the onset of Type 2 diabetes and insulin resistance in the Japanese population. In the present study, we have demonstrated a relationship between plasma U-II levels and the progression of diabetic retinopathy and vascular complications in patients with Type 2 diabetes. Eye fundus, IMT (intima-media thickness) and plaque score in the carotid artery, BP (blood pressure), FPG (fasting plasma glucose), HbA(1c) (glycated haemoglobin), U-II, angiogenesis-stimulating factors, such as VEGF (vascular endothelial growth factor) and heregulin-beta(1), and lipid profiles were determined in 64 patients with Type 2 diabetes and 24 non-diabetic controls. FPG, HbA(1c) and VEGF levels were significantly higher in patients with Type 2 diabetes than in non-diabetic controls. Diabetes duration, insufficient glycaemic and BP control, plasma U-II levels, IMT, plaque score and nephropathy grade increased significantly across the subjects as follows: non-diabetic controls, patients with Type 2 diabetes without retinopathy (group N), patients with Type 2 diabetes with simple (background) retinopathy (group A) and patients with Type 2 diabetes with pre-proliferative and proliferative retinopathy (group B). The prevalence of obesity and smoking, age, low-density lipoprotein, triacylglycerols (triglycerides) and heregulin-beta(1) were not significantly different among the four groups. In all subjects, U-II levels were significantly positively correlated with IMT, FPG, and systolic and diastolic BP. Multiple logistic regression analysis revealed that, of the above parameters, U-II levels alone had a significantly independent association with diabetic retinopathy. In conclusion, the results of the present study provide the first evidence that increased plasma U-II levels may be associated with the progression of diabetic retinopathy and carotid atherosclerosis in patients with Type 2 diabetes.     

Increased levels of plasma homocysteine are associated with nephropathy, but not severe retinopathy in type 1 diabetes mellitus

The reactive vascular-injuring amino acid homocysteine was measured in plasma samples from 79 well-characterized type 1 diabetic patients and 46 control subjects. Patients with proliferative retinopathy had higher homocysteine levels (15.0 +/- 6.3 mumols l-1; mean +/- SD, p less than 0.001; n = 42) than those with progressive retinopathy during a two-year period (10.4 +/- 1.6 mumols l-1; n = 12), no or minimal retinopathy (10.7 +/- 4.3 mumols l-1; n = 25), and the control subjects (11.0 +/- 3.4 mumols l-1). Within the group of patients with proliferative retinopathy increased homocysteine levels were confined to those patients that had serum creatinine levels greater than 115 mumols l-1 and/or an albumin:creatinine clearance ratio greater than or equal to 0.02 x 10(-3) (17.0 +/- 5.9 mumols l-1; n = 23), whereas those with no or only minimal nephropathy had levels (12.1 +/- 5.5 mumols l-1; n = 18) that were not different from the control group. We conclude that neither type 1 diabetes mellitus nor diabetic retinopathy per se is associated with increased plasma homocysteine levels. In contrast, homocysteine accumulates, probably owing to reduced glomerular filtration, in diabetic patients with advanced nephropathy. This suggests that homocysteine might contribute to the accelerated development of macroangiopathy seen especially in this subgroup of diabetic patients.     

Is leptin associated with diabetic retinopathy?

OBJECTIVE: In advanced stages of diabetic retinopathy, new blood vessels are formed based on undefined mechanisms. Recently, leptin was shown to possess an angiogenic action in vitro and to induce neovascularization in vivo. The aim of the present study was to investigate the relationship between plasma leptin levels and the severity of diabetic retinopathy. RESEARCH DESIGN AND METHODS: There were 70 patients with type 2 diabetes (age 47.9 +/- 9.7 years, BMI 26.4 +/- 3.3 kg/m2) who were seen in a retina outpatient clinic recruited and assigned to subgroups according to the stage of their diabetic retinopathy. There were 66 healthy volunteer subjects matched with the diabetic patients for age, BMI, and sex who served as control subjects (age 46.0 +/- 8.8 years, BMI 27.1 +/- 2.3 kg/m2). Fasting plasma leptin levels were measured. RESULTS: Plasma leptin level of the diabetic patients was not significantly different from the control subjects. In patients with proliferative diabetic retinopathy (n = 17), the mean plasma level of leptin (16.1 +/- 9.2 ng/ml) was significantly higher than that in patients with nonproliferative retinopathy (n = 20) (11.5 +/- 3.5 ng/ml, P = 0.039) or patients without retinopathy (n = 33) (5.8 +/- 3.7 ng/ml, P = 0.001). The mean leptin level in patients with nonproliferative diabetic retinopathy was also significantly higher than that in patients without retinopathy (P = 0.002). CONCLUSIONS: Our results show that the more advanced the diabetic retinopathy, the higher the plasma leptin levels, even after adjusting the leptin levels for BMI. The presence of such a positive correlation need not imply a causal relationship. Nevertheless, previously observed leptin-induced promotion of angiogenesis and neovascularization lends support to the possibility that leptin may play a role in the progression of human diabetic retinopathy to a proliferative phase. This possibility deserves further investigation.     

Relationship of muscle capillary basement membrane thickness and diabetic retinopathy

We examined the relationship between the thickness of the quadriceps muscle capillary basement membrane and diabetic retinopathy. Basement membrane thickness was measured in two groups of patients with long-standing type II diabetes mellitus. One group of patients (N = 13) had no evidence of diabetic retinopathy on fluorescein angiography, whereas the other (N = 12) had proliferative microvascular disease. All the patients were male, and both groups were of similar ages, duration of diabetes, serum creatinines, and glycemic control as reflected by HbA1 levels. Mean muscle capillary basement membrane width (+/- SE) of the patients with proliferative retinopathy (3346 +/- 262) was significantly greater (P less than .05) than that observed in the patients without retinopathy (2660 +/- 177). The results of this study suggest that there is a relationship between capillary basement membrane thickness in skeletal muscle and the severity of microangiopathy in the eye. However, there was a substantial overlap between the two groups, indicating that for any individual patient the measurement of muscle capillary basement width will probably not be useful in identifying the presence or absence of retinopathy.     

Different patterns of insulin resistance in relatives of type 1 diabetic patients with retinopathy or nephropathy: the Genesis France-Belgium Study

OBJECTIVE: Insulin resistance may be a risk factor for diabetic microangiopathy, which may have a familial component. We carried out a family-based study to determine which components of the insulin resistance syndrome are associated with diabetic retinopathy and nephropathy in type 1 diabetes. RESEARCH DESIGN AND METHODS: The Genesis France-Belgium Study is a multicenter binational study designed to investigate the genetic factors involved in the microvascular complications of type 1 diabetes using a family-based design. Probands were type 1 diabetic patients with diabetic retinopathy (classified as background, preproliferative, or proliferative) and possibly diabetic nephropathy (absent, incipient, established, or advanced). The insulin resistance score of their first-degree relatives was calculated according to their BMI and history of arterial hypertension, lipid disorders, and type 2 diabetes. RESULTS: The insulin resistance score of relatives was positively correlated with the albumin excretion rate (P = 0.0009) and fasting plasma glucose (P = 0.0003) and HbA(1c) (P < 0.0001) concentrations. This score was higher in the relatives of probands with than in those without diabetic nephropathy (P = 0.0370). Similarly, it was higher in relatives of subjects with proliferative diabetic retinopathy than in those of probands without, even after controlling for subjects with versus without diabetic nephropathy (P = 0.0379). However, the components of the insulin resistance score in relatives differed according to the severity of diabetic retinopathy or nephropathy in the probands. Obesity and history of arterial hypertension were most common in relatives of probands with proliferative diabetic retinopathy, whereas obesity and history of lipid disorders were most common in the relatives of probands with diabetic nephropathy. CONCLUSIONS: Familial insulin resistance segregates with diabetic complications: lipid disorders and obesity segregate with diabetic nephropathy, whereas arterial hypertension and obesity segregate with diabetic retinopathy.     

Beta-hexosaminidase activities in tears and plasma,diphosphoglycerate in blood of diabetic patients

In a study on 10 normal controls, 7 pregnant women and 16 diabetic patients, β-hexosaminidase in tears and 2,3-diphosphoglycerate in blood were investigated for possible use as index for diabetic retinopathy during pregnancy. Tears were used as source for β-hexosaminidase because the concentration in plasma and the isoenzyme pattern are affected by the occurrence of a placentar isoenzyme in pregnancy. It has been found that in diabetes the concentration of β-hexosaminidase in plasma may be elevated, but that it remains unchanged in tears and that there is no correlation between the plasma and tear values in all individuals. Neither β-hexosaminidase in tears nor 2,3-diphosphoglycerate in blood appears as indicator for the onset or development of diabetic retinopathy.     

2型糖尿病视网膜病变患者糖化血红蛋白测定的临床意义

目的 探讨糖化血红蛋白对糖尿病视网膜病变的临床意义.方法 对307例2型糖尿病患者做眼底检查和荧光眼底血管造影检查,分为糖尿病正常眼底（NDR）98例,糖尿病视网膜病变（DR）组209例,其中单纯型视网膜病变（SDR）157例,增殖型视网膜病变（PDR）52例,进行糖化血红蛋白（HbAlc）、空腹血浆葡萄糖（FPG）检测.结果 HbAlc水平越高,视网膜病变发生率越高（P〈0.01）.SDR组HbA1c明显高于NDR组（P〈0.05）,PDR组高于SDR组,差异有统计学意义（P〈0.05）;而FPG水平在SDR组与NDR组无统计学意义（P〉0.05）.结论 控制血浆葡萄糖,降低糖化血红蛋白水平,有助于降低糖尿病视网膜病变发生的危险.     

Rapid deterioration of diabetic retinopathy during treatment with continuous subcutaneous insulin infusion

The effect of continuous subcutaneous insulin infusion (CSII) on diabetic retinopathy was studied in 19 patients with insulin-dependent diabetes mellitus (IDDM). All had diabetes before age 30. Three patients had no retinal abnormalities at the start of the study, 12 had minimal or mild background retinopathy, and 4 had a preproliferative retinopathy. The follow-up period was 12-14 mo. Fundus photography and fluorescein angiography was performed every 2-6 mo. Despite marked improvement of metabolic control, none of the patients with retinopathy showed reversal of the fundal abnormalities. In seven patients with background retinopathy the abnormalities remained unchanged; in five patients a slight worsening was noted. Four patients with moderate-to-severe background retinopathy showed a rapid and severe progression of the fundal abnormalities into a florid proliferative diabetic retinopathy 3-6 mo after initiation of CSII. A higher incidence of hypoglycemic episodes could not be demonstrated in this group. Two of these patients showed a marked reduction in glomerular filtration rate (GFR), 34% and 38%, respectively, during the course of their follow-up. This is compared with a decrease in GFR by only 5.6% for the group as a whole. The four patients with rapidly progressive retinopathy all had long-standing poorly controlled diabetes with preproliferative retinal changes, diabetic neuropathy, and, with the exception of one patient, signs of nephropathy at the start of CSII. The incidence of these features was nil or very low in the remaining 15 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Four-Year Screening Interval and Vision-Threatening Retinopathy in Type 2 Diabetes Patients With Good Glycemic Control

ObjectiveTo assess whether vision-threatening retinopathy developed after 4 years in patients with type 2 diabetes with good glycemic control during follow-up.Patients and MethodsUsing data from the Action to Control Cardiovascular Risk in Diabetes and Action to Control Cardiovascular Risk in Diabetes Follow-on studies (conducted from January 1, 2001, to October 14, 2014), we investigated the incidence of vision-threatening retinopathy after 4 years in patients with type 2 diabetes with good or poor glycemic control. Patients with proliferative diabetic retinopathy at baseline were excluded. Vision-threatening retinopathy was defined as severe nonproliferative diabetic retinopathy, proliferative diabetic retinopathy, laser photocoagulation, or vitrectomy. Good and poor glycemic control was defined as mean glycated hemoglobin level less than 7% and 7% or greater during follow-up, respectively.ResultsThis study included 2285 patients. Among patients with no retinopathy at baseline, the 4-year incidence of vision-threatening retinopathy was 0% (0 of 386) and 0.8% (6 of 721) in those with good and poor glycemic control, respectively (P=.54). Similarly, severe retinopathy was not observed at 8 years in patients who did not have retinopathy at 4 years. Among patients with mild to moderate nonproliferative diabetic retinopathy at baseline, the 4-year incidence of vision-threatening retinopathy was significantly higher in those with poor glycemic control than in those with good glycemic control (9.7% [77 of 790] vs 4.4% [13 of 297]; P=.004). Additionally, the remission rate of diabetic retinopathy was low in patients with a long duration of diabetes. Four-year incidences of vision-threatening retinopathy were higher in patients with retinopathy at baseline who had poorer glycemic control and longer durations of diabetes.ConclusionIt may be safe to extend screening intervals for diabetic retinopathy to 4 years or longer in patients with type 2 diabetes with no retinopathy.     

The metabolism of fibrinogen and plasminogen related to diabetic retinopathy in man

Abstract. Metabolic turnover of fibrinogen and plasminogen were studied in thirty insulin-treated diabetics and ten non-diabetic controls. 131-iodine labelled fibrinogen and 125-iodine labelled plasminogen were injected intravenously and the plasma clearance of the two proteins measured simultaneously over a period of 8 days. The diabetics were selected to represent three grades of severity of diabetic retinopathy assessed by ophthalmoscopy and fiuorescein angiography; ten patients had no significant retinopathy, ten background and ten proliferative retinopathy. Subjects were matched as closely as possible for body weight, age and duration of diabetes.
Plasma fibrinogen concentrations were higher in diabetics (3–24 g/1) than controls (2–65 g/1; P <0.025); the patients with the severest retinopathy had the highest fibrinogen concentrations (3.75 g/1). As a direct consequence of the elevation of plasma fibrinogen the catabolic rate was higher in diabetics (20.9 mg kg^-1 day^-1) than controls (140 mg kg^-1 day^-1; P < 0.025) and higher in patients with background retinopathy (24.1 mg kg^-1 day^-1) and proliferative retinopathy (22.4 mg kg^-1 day^-1) than diabetics without retinopathy (16.3 mg kg^-1 day^-1; P = 0.05). Fibrin(ogen) degradation products were detectable in all diabetics but in only one-third of controls.
Plasminogen metabolism was normal in all groups of diabetics.
It is concluded that fibrinogen metabolism is increased in diabetes and bears a relationship to diabetic retinopathy but is not accompanied by significant alterations of plasminogen metabolism.     

23G+、25G+微创玻璃体切割术治疗增殖性糖尿病性视网膜病变的效果比较

目的 比较23G+、25G+微创玻璃体切割术治疗增殖性糖尿病性视网膜病变的效果.方法 选取2018年1月至2020年12月我院收治的152例增殖性糖尿病性视网膜病变患者作为研究对象,遵循随机数字表法将其分为参照组和研究组,各76例.参照组开展23G+微创玻璃体切割术,研究组开展25G+微创玻璃体切割术.比较两组的临床效...     

Association between diabetic microangiopathy and vascular endothelial function evaluated by flow-mediated vasodilatation in patients with type 2 diabetes

The main purpose of the study was to investigate the association between vascular endothelial function and diabetic microangiopathy (nephropathy, retinopathy and neuropathy) in patients with type 2 diabetes. In addition, the association between endothelial function and macroangiopathy evaluated by intimal-medial complex thickness (IMT) was also investigated. Endothelial function was evaluated non-invasively by the measurement of flow-mediated vasodilatation (FMD) of the brachial artery. Diabetic nephropathy and neuropathy were assessed by urinary albumin excretion (UAE) and motor or sensory nerve conduction velocity (MCV, SCV), respectively, and retinopathy was evaluated by an ophthalmologist using the Davis classification. FMD was measured in 102 patients with type 2 diabetes and in 20 control subjects, and showed a tendency to be lower in the diabetic patients. There was a significant decrease in FMD in patients with proliferative diabetic retinopathy, compared with those in patients with no diabetic retinopathy. FMD showed significant positive correlations with MCV and SCV, and significant negative correlations with log UAE, systolic blood pressure and diabetic duration, but no correlation was obtained between FMD and IMT. In stepwise regression analysis, MCV alone showed a significant association with FMD. In conclusion, our results show that in patients with type 2 diabetes FMD is closely associated with all types of microangiopathy, with neuropathy being most strongly associated with FMD; however, FMD is not associated with macroangiopathy evaluated by IMT.     

RBP4、Hcy与糖尿病视网膜病变的关系研究

目的探讨糖尿病视网膜病变(DR)患者视黄醇结合蛋白4(RBP4)与同型半胱氨酸(Hcy)水平变化及相关性。方法自内分泌科接诊2型糖尿病患者中选取124例,将其分为糖尿病伴非增值型视网膜病变(NPDR)组40例,糖尿病伴增值型视网膜病变(PDR)组41例,糖尿病无视网膜病变(NDR)组43例,另选取健康志愿者组(NC组)40例进行比较,取空腹静脉血,测定各项指标并行相关性与多元回归分析。结果 PDR组RBP4、Hcy水平均高于NPDR组、NDR组,差异有统计学意义(P0.05);NPDR组RBP4、Hcy均高于NDR组,差异有统计学意义(P0.05);RBP4与空腹血糖(FBG)、糖化血红蛋白(HbA1c)、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-c)、Hcy均呈正相关(P0.05),与高密度脂蛋白胆固醇(HDL-C)呈负相关(P0.05);Hcy与FPG、HbA1c、TC、TG、LDL-C、RBP4均呈正相关(P0.05),与HDL-C呈负相关(P0.05);多因素回归分析,DR与Hcy、RBP4、HbA1c均呈正相关(P0.05)。结论 DR患者Hcy、RBP4水平呈现为高表达,且随着病情进展表现为逐步升高,即与DR发生、发展呈正相关,可作为重要危险因素。     

细胞因子VEGF、IGF-1与2型糖尿病视网膜病变的相关性研究

目的探讨血浆VEGF、IGF-1水平与2型糖尿病视网膜病变的相关性。方法选择2型糖尿病患者60例,分为2型糖尿病不伴有视网膜病变组(NDR)20例;2型糖尿病伴视网膜病变(非增值期)组(BDR)20例;糖尿病伴视网膜病变(增值期)组(PDR)20例;健康对照组20例,经口服葡萄糖耐量试验证实排除糖尿病。分别检测空腹血糖、糖化血红蛋白、甘油三脂、总胆固醇、低密度脂蛋白胆固醇及细胞因子VEGF、IGF-1等各项指标。结果①VEGF水平:2型糖尿病各组均高于正常对照组;BDR组明显高于NDR组,但PDR组VEGF含量下降;②IGF-1水平:呈正常对照组相似文献   

糖尿病视网膜病变患者尿微量清蛋白与血清C-反应蛋白水平的变化及意义

目的探讨糖尿病视网膜病变(DR)患者尿微量清蛋白(UMA)和血清C-反应蛋白(CRP)水平的变化及意义。方法选取2型糖尿病(T2DM)患者152例,分为无糖尿病视网膜病变组(NDR组)65例、非增生性糖尿病视网膜病变组(NPDR组)53例、增生性糖尿病视网膜病变组(PDR组)34例;另选取40例健康体检者为健康对照组(NC组),检测UMA和血清CRP水平及相关临床参数。结果 UMA及血清CRP水平在NC组、NDR组、NPDR组及PDR中依次升高,差异均有统计学意义(P0.05);Spearman相关分析显示,T2DM患者UMA与CRP呈显著正相关(r=0.311,P0.05);UMA与病程、空腹血糖(FBG)、低密度脂蛋白胆固醇(LDL-C)、糖化血红蛋白A1c(HbA1c)及胰岛素抵抗指数(HOMA-IR)呈正相关(P0.05),CRP与病程、FBG、HbA1c及HOMA-IR呈正相关(P0.05)。结论 DR的发展与肾损害联系密切,慢性炎症与高糖血症及胰岛素抵抗可能通过影响T2DM患者的肾功能参与DR的发生与发展。