The aim of the article was to use prospectively collected data on people with type 1 diabetes to assess which routinely collected clinical measures predict the development of macrovascular disease in people with type 1 diabetes. Data have been collected in a structured format at an annual review since 1985. For this study, all people with type 1 diabetes in the database in both 1992 and 2001 were ascertained. Data were extracted for a diagnosis of coronary artery disease, stroke, and peripheral vascular disease (macrovascular complications). Presence of other microvascular complications was also ascertained. Forty-one of 404 (10.1%) people had macrovascular disease at the index visit in 1992 and 61 others developed macrovascular complications during follow-up. People who developed macrovascular complications were older (48 +/- 12 versus 36 +/- 11 [SD] years; P = 0.000), had longer duration of diabetes (28 +/- 12 versus 18 +/- 11 years; P = 0.000), higher BMI (26.7 +/- 4.6 versus 25.4 +/- 3.6 kg/m2; P = 0.041), higher base line serum cholesterol (5.9 +/- 1.7 versus 5.2 +/- 1.1 mmol/L, P = 0.007), higher median base line triglyceride levels (1.5 [IQ range 0.9-2.6] versus 1.1 [0.8-1.7] mmol/L; P = 0.002), higher systolic BP (145 +/- 21 versus 129 +/- 20 mmHg; P = 0.000), and higher serum creatinine (102 +/- 57 versus 86 +/- 17 micromol/L; P = 0.038) than those who did not. We found no significant difference in the base line glycated hemoglobin in the two groups. The multivariate model showed that age, duration of diabetes, systolic BP, and serum cholesterol and creatinine levels predicted the development of macrovascular complications, which were also associated with the later development of microalbuminuria. Macrovascular complications developed in 16.8% of people with type 1 diabetes over a 9-year follow-up, and were predicted by potentially modifiable factors including higher BP, BMI, and serum triglyceride and cholesterol levels.
"Likewise it is important to evaluate the effect of lipids and renal dysfunction on mortality and IHD. This has only been done in a few other studies with conflicting results (Klein et al. 2004; Soedamah-Muthu et al. 2004; Sibal et al. 2006). However, as with studies evaluating glycaemic control as a risk factor of mortality and IHD, most studies this far were based on data obtained at a single baseline examination. "
[Show abstract][Hide abstract] ABSTRACT: The incidence of type 1 diabetes is increasing in Denmark as well as the rest of the world. Due to diabetes-related micro- and macrovascular complications, the morbidity and the mortality is higher among type 1 diabetic patients.
The aim of this thesis was to examine a population-based cohort of 727 type 1 diabetic patients from Fyn County, Denmark, with an onset of diabetes before 1 July 1973 in order to:
In the years 1973–2006 an overall MR of 22.3 per 1000 person-years was found. Furthermore a relative mortality of 3.4 was found as compared to the general population in Denmark. The relative mortality was especially high for patients aged 30–39 (SMR 9.8). There was a tendency towards a better survival for patients diagnosed after 1964. This was especially seen for men. Diabetes was the most common cause of death for those who died in the group.
In 1993–1996 blood samples were drawn and glycaemic regulation, lipids and renal markers were subsequently used as predictors of all-cause mortality, cardiovascular mortality and ischaemic heart disease. Glycaemic regulation, dyslipidaemia and creatinine were all significantly associated with all three endpoints. Furthermore, variations in glycaemic control were also identified as a risk factor for overall mortality.
Two hundred and one patients were examined for diabetic retinopathy in 1981–1982 and 2007–2008. At follow-up, 97.0% had DR and 42.9% of all patients without PDR at baseline developed this during the follow-up period. Patients who had had a poor glycaemic regulation as well as those who had NPDR at baseline were more likely to develop PDR than the remaining patients. On the other hand, other risk factors such as high blood pressure and proteinuria did not predict PDR.
In the comparative study between ETDRS seven standard field 30° stereoscopic colour films and nine field 45° monoscopic digital colour images, 43 eyes of 43 patients were examined in 2008. A poor correlation was found between the two methods: only 29.3% were graded alike. In the remaining, the level of DR was graded higher in the digital photos. Among these, PDR was detected in three eyes using digital photos but remained undetected on all films. This suggests that digital photos with wide fields are the best way to detect DR in long-term type 1 diabetic patients.
Overall, it is concluded that mortality is still higher among type 1 diabetic patients. This depends, among other things, on glycaemic regulation, lipid status and, partly, renal dysfunction. Diabetic retinopathy is almost universal in long-term type 1 diabetic patients, and almost half of all patients will develop PDR in 25 years. Nine field digital photos provide the best grading of retinopathy in long-term type 1 diabetic patients.
[Show abstract][Hide abstract] ABSTRACT: Aims/hypothesis
Type 1 diabetes is associated with premature arterial disease. Bone-marrow derived, circulating endothelial progenitor cells (EPCs) are believed to contribute to endothelial repair. The hypothesis tested was that circulating EPCs are reduced in young people with type 1 diabetes without vascular injury and that this is associated with impaired endothelial function and increased carotid intima–media thickness (CIMT).
We compared 74 people with type 1 diabetes with 80 healthy controls. CD34, CD133, vascular endothelial (VE) growth factor receptor-2 (VEGFR-2) and VE-cadherin antibodies were used to quantify EPCs and progenitor cell subtypes using flow-cytometry. Ultrasound assessment of endothelial function by brachial artery flow-mediated dilatation (FMD) and CIMT was made. Circulating endothelial markers, inflammatory markers and plasma plasminogen activator inhibitor-1 (PAI-1) levels were measured.
CD34+VE-cadherin+, CD133+VE-cadherin+ and CD133+VEGFR-2+ EPC counts were significantly lower in people with diabetes (46–69%; p = 0.004–0.043). In people with type 1 diabetes, FMD was reduced by 45% (p
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study is to evaluate the effect of glycemic regulation, dyslipidemia, and renal dysfunction on mortality (all-cause and cardiovascular) and ischemic heart disease (IHD) in a long-term follow-up of a population-based cohort of Danish type 1 diabetic patients with at least 20 years of diabetes.
A population-based cohort of type 1 diabetic patients was identified as of July 1, 1973 (n=727). In 1993 to 1996, the cohort was reassessed and baseline data were collected from blood and urine samples in 389 patients. Mean (glycemic regulation and lipids) and highest values (creatinine and albuminuria) of the baseline period were used to predict mortality and IHD between baseline and 2006. Data of mortality and morbidity were provided by the Danish Civil Registration System, the Danish Causes of Death Registry, and the Danish National Patient Registry.
At the follow-up in 2006, 256 patients (65.8%) were still alive. In a statistical model adjusted for age, sex and duration of diabetes, the following parameters were related to all-cause mortality and cardiovascular mortality: glycemic regulation, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (inversely), total cholesterol, creatinine, and macroalbuminuria. Furthermore, all markers except macroalbuminuria were associated with IHD. Microalbuminuria at baseline was not related to any of the endpoints.
Glycemic regulation, dyslipidemia, and renal dysfunction were all related to mortality and IHD in a 13-year follow-up of long-term Danish type 1 diabetic patients. These results underscore the better outcome for tightly regulated type 1 diabetic patients, even in long-term survivors.
Journal of diabetes and its complications 08/2009; 24(4):223-8. DOI:10.1016/j.jdiacomp.2009.05.003 · 3.01 Impact Factor
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