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Evaluate the relationship between high and low exposure continuous glucose monitoring (CGM)-derived glucometrics and micro- and macrovascular complications in type 1 diabetes (T1D).Cross-sectional study in T1D without cardiovascular disease (CVD) and with ≥ 1 of the following: ≥40 years, diabetic nephropathy, or ≥ 10 years of diabetes duration with CVD risk factors. Glucometrics were obtained over 14 consecutive days: glucose management indicator (GMI) and proportion of time 54 (TBR 54),70, 70-180 (TIR),180 (TAR). Carotid plaque was evaluated by ultrasonography. Logistic regression models adjusted for age, sex, and other risk factors were constructed to test the independent associations with chronic complications.We included 152 patients (54.6% men, 48.7 ± 10.0 years-old). Sixty-seven patients had plaque and n = 71 microvascular complications. TAR (OR 1.28 [1.09-1.51]) and GMI (OR 3.05 [1.46-6.36]) were directly associated with the presence of microvascular complications, while TIR had an inverse relationship (OR 0.79 [0.66-0.93]). TBR 54 was directly associated with the presence of plaque, even after adjusting for 5-year mean HbA1c (OR 1.51 [1.07-2.13]).High-glucose glucometrics were independently associated with microvascular complications. Only low-glucose exposure glucometrics was significantly associated with preclinical atherosclerosis. Our data support the role of hypoglycemia in the development of CVD in this population.

Evaluate the weight trajectories after pancreas transplantation (PT) and their relationships with pancreas graft outcomes in type 1 diabetes (T1D).Retrospective cohort study. T1D individuals who underwent PT were recruited (T1D-PT; n = 194) and divided into three groups according to transplantation date: 1999-2004 (n = 57), 2005-2009 (n = 79), 2010-2015 (n = 58). For weight comparisons, a random sample of T1D without renal impairment was also recruited during 2015 (n = 61; T1D-control).The median follow-up for the T1D-PT group was 11.1 years. Despite significant weight loss at 6 months (65.7 ± 12.4 vs. 64.1 ± 11.4 Kg; p 0.001), a stepped increase was seen thereafter (60 months: 68.0 ± 14.0 Kg; p 0.001). Participants from the 2010-2015 period showed higher weight gain (p 0.001), outweighing that observed in the T1D-control (60 months: +4.69 ± 8.49 vs. -0.97 ± 4.59 Kg; p = 0.003). Weight gain between 6 and 36 months was directly associated with fasting glucose and HbA1c at 36 months, and with HbA1c at 60 months (p 0.05). However, in Cox-regression models adjusted for age, sex, and several recipient and PT-related variables, the third tertile of weight gain between 6 and 36 months showed a non-significant increase in the graft failure/dysfunction (HR 2.33 [0.75-7.27]).Weight gain post-PT was associated with glucose-related biochemical markers of graft dysfunction, which needs confirmation in further studies.

Aims Information on the impact of insulin therapy before pancreas donation on pancreas outcomes is scarce. We aim to explore the influence of insulin therapy before donation on recipient and pancreas graft survival. Methods Registry study including 12,841 pancreas recipients from the OPTN/UNOS registry performed between 2000 and 2017. Inverse probability of treatment weighting (IPTW) was used to account for covariate imbalance between recipients from a donor with and without insulin requirements. Results A total of 7765 (60%) patients received a pancreas from a donor with insulin before donation (IBD). Pancreas graft survival (death-censored) was similar between recipients from IBD and non-IBD donors at 1, 5 and 10 years (89% vs 89%, 78% vs 79 and 69% vs 70%, respectively, P = 0.35). Recipients from IBD donors presented a similar 90-days pancreas graft survival. After IPTW weighting, IBD donors were neither associated with any post-transplant surgical complication (HR 1.11 [95% CI 0.98–1.24], P = 0.06), nor with risk for recipient death (HR 0.94 [95% CI 0.85–1.04], P = 0.26), nor pancreas graft failure (HR 1.06 [95% CI 0.98–1.16], P = 0.15). Conclusions Insulin therapy before donation in accepted pancreas donors was not associated, per se, with an impaired pancreas graft and patient survival.

To evaluate the changes in cardiovascular risk factors (CVRFs) and cardiovascular disease (CVD) in patients with type 1 diabetes (T1D) and end-stage renal disease (ESRD) who were candidates for kidney-pancreas transplantation (KPTx) from 1999 to 2017.Patients with T1D referred for KPTx evaluation were included. The cohort was divided into five groups according to the year of evaluation (1999-2002, 2003-2006, 2007-2010, 2011-2014 and 2015-2017). The control of CVRFs and the prevalence of prior CVD were evaluated.We evaluated 360 patients (64.4% men, age 38.9 ± 7.1 years). LDL-cholesterol100 mg/dl increased from 22.7% to 76.9% (1999-2002 vs. 2015-2017; p 0.001), as did the use of statins (from 24.7% to 74.5%; p 0.001). Systolic blood pressure decreased from 138.8 ± 27.6 to 125.1 ± 27.9 mmHg (p = 0.001) and current smokers from 48% to 25% (p = 0.018). Intensive insulin treatment increased from 34.4% to 93.6% (p 0.001). Diabetes duration before the initiation of renal replacement therapy increased from 23 ± 5.5 to 26.9 ± 8.9 years (p = 0.001). Overall, 30.3% had previous CVD, without significant changes over time (p = 0.699), albeit patients were older and had longer diabetes duration.Patients with T1D and ESRD referred for KPTx have better control of CVRFs over time, which might lead to a decrease in cardiovascular events.

Objective To assess the effects of telecare on the results of intensive follow-up in T1D patients with poor metabolic control. Methods After initial evaluation, 40 T1D were randomised to either a Telecare (TG) or Conventional Group (CG). Patients had an intensive 6-month follow-up and helped to make decisions concerning treatment self-management. The TG had 12 appointments: 9 telematic with the GlucoBeep system + 3 ambulatory. The CG had 12 outpatient appointments. At 0, 6 (end of study) and 12 months, metabolic control, self-management and quality of life were evaluated. Cost analysis was made at study end. Results Thirty patients completed the study (16 TG, 14 CG). Intention to treat analysis included 19 TG and 16 CG. Improvement in HbA1c was similar in both groups TG: 8.4 ± 1.2%; 7.5 ± 1.4%; 7.6 ± 0.9%, p = 0.008; CG: 8.9 ± 1.3%; 7.7 ± 0.9%; 7.6 ± 0.7%, p = 0.001; with a decrease in hypoglycaemic events and improvement in self-management and quality of life. Patient costs were lower in the TG versus CG in appointment length (0.25 h versus 0.5 h). However, 30% of the diabetes team and patient appointments were longer than expected due to technical difficulties: (0.25 h versus 1 h). Conclusions Intensive telematic follow-up achieves similar results to those of intensive face-to-face follow-up with lower patient costs. However, communication technology must be improved.

Objective: To evaluate the possible effect of short- and long-term insulin treatment on arterial blood pressure (BP) and endothelin-1 (ET-1) plasma levels in type 2 diabetic patients. Research design and methods: Seven type 2 diabetic patients with secondary failure to oral hypoglycemic drugs (SFOH) were studied. Twenty-four-hour arterial BP monitorization (Spacelabs 90207) was performed before initiation of insulin treatment (time 0), 6 days after (time 1) and 1 year later (time 2). Moreover, ET-1 plasma levels were measured. Results: Insulin treatment did not produce any variation in systolic (124.3±11.6; 120.7±7.9; 127.0±13.4 mmHg) and diastolic (72.8±5.9; 71.5±3.4; 71.8±5.2 mmHg) 24-h BP monitorization at times 0, 1 and 2, respectively. The systolic and diastolic day/night differences did not change in the three times studied. Neither were significant differences observed in ET-1 plasma levels. Conclusions: In patients with SFOH, insulin treatment did not induce any short- or long-term increase in BP or any variation in plasma ET-1 levels.

The aim of this cross-sectional study was to establish the prevalence of renal involvement and to identify associations with its most important possible risk factors in a group of patients with Type II diabetes mellitus, representative of the population living in Catalonia. One thousand two hundred and three patients (47% males, mean age: 61 ± 6 years, diabetes duration 9 ± 6 years) were studied. Overnight urine samples were collected to determine urinary albumin excretion (UAE). If UAE was > 15 μg/min, a new 24-h urine collection for UAE measurement to establish the existence of microalbuminuria (20–200 μg/min) or macroalbuminuria (> 200 μg/min) was obtained. Clinic and metabolic evaluations were also performed. The prevalence (%) of microalbuminuria, macroalbuminuria and hypertension were, respectively, 23, 1, 5.4 and 42. In comparison with normoalbuminurics, patients with microalbuminuria were predominately male (P

Despite the high prevalence of white coat hypertension (WCH) in diabetes mellitus and the evidence that hypertension is a clear risk factor for the development of microalbuminuria (MA) in these patients, there is no information on the long-term prognostic significance of this condition in the diabetic population. We studied the evolution of 40 patients with type 1 diabetes mellitus (Type 1 DM). Twenty patients with WCH (office blood pressureor =140/90mmHg associated with mean daytime blood pressure135/85mmHg) classified as the WCH group and 20 patients with type 1 DM with a similar age and disease evolution, but who were normotensive, (office blood pressure140/90mmHg associated with mean daytime blood pressure135/85mmHg) classified as the normotensive control group. After 5 years of follow-up, MA appeared in four subjects and sustained hypertension in another, with a total of 31% of events in the WCH group, with none in the normotensive group. Kaplan-Meier analysis showed that the relative risk of developing these hypertensive events was 25% higher in the WCH group. At baseline, the night time systolic and diastolic blood pressure levels were significantly higher in patients who further developed MA and sustained hypertension. The findings in this study highlight the clinical importance of careful follow-up of type 1 diabetic patients with WCH.

Aims: To determine the prevalence and the incidence of diabetic nephropathy in Type 1 diabetes mellitus in Spain and to investigate the risk factors for the development of microalbuminuria. Methods: One thousand five hundred and two patients with Type 1 diabetes mellitus were prospectively followed in 15 hospital diabetes outpatient clinics in Spain. Blood pressure, body weight, HbA 1c , total cholesterol, HDL-cholesterol, triglycerides, plasma creatinine and urinary albumin excretion (UAE) were determined every 3–5 months. Results: A total of 1225 patients (624 males and 601 females), age 30.7±9.3 years with diabetes duration of 14.1±9.1 years completed 4.3 (4.0–5.1) years of follow-up. At baseline 14.2 (95% CI 12.3–16.3)% of patients had microalbuminuria, 5.1 (3.9–6.4)% macroalbuminuria and 3.4 (2.5–4.6)% kidney failure. During follow-up the annual incidence of microalbuminuria was 2.7 (2.2–3.2)%. In a multiple logistic regression analysis the predictors of progression to microalbuminuria were initial UAE, HbA 1c , diabetes duration, smoking, and HDL-cholesterol Conclusions: The prevalence and incidence of diabetic nephropathy in Spain are comparable to data obtained in similar studies carried out in other countries. The development of microalbuminuria is associated not only with glycaemic control and hypertension, but also to the control of other risk factors such as dyslipaemia and smoking.

In spite of the high prevalence of diabetes mellitus (DM) in patients with liver cirrhosis (LC) few studies have focused on the clinical implications of this association. We investigated the clinical and pancreatic-endocrine features of 34 patients who developed DM after LC (Group I). Results were compared with 34 carefully matched patients with only Type II DM (Group II). A standard meal test was performed in 26 patients with normal renal function from each group to assess β-cell function. Group I patients, less frequently had retinopathy (14.7% vs. 45.5%, P < 0.05) and a family history of diabetes (23.5% vs. 58.8%, P < 0.01). Group I patients also showed signs of enhanced insulin resistance, reflected by higher insulin dose requirements in insulin-treated patients (0.87 ± 0.10 vs. 0.62 ± 0.05 IU/kg/day, P < 0.01) and increased basal C-peptide values (0.88 ± 0.06 vs. 0.68 ± 0.07 pmol/l, P < 0.05, respectively) than those in Group II. These results suggest that several clinical features, probably related to the hepatopathy, define DM occurring in patients with LC.

To assess risk factors associated with microalbuminuria development in short-term evolution insulin-dependent diabetes mellitus (IDDM) we undertake a cross-sectional study with retrospective examination of the 34 patients diagnosed with IDDM between 1982 and 1983 and followed up for at least 7 years in an outpatient endocrinology clinic. Main measures: (1) At IDDM diagnosis: age, sex, parameters of metabolic control (fasting glycemia, HbA 1 ), islet-cell antibodies, insulin autoantibodies, endogenous insulin secretion (EIS) and HLA type. (2) At 1 year evolution: EIS re-evaluation. (3) From IDDM diagnosis (every 3–4 month): body mass index, insulin schedule and dose, and parameters of metabolic control. (4) At 7-year evolution: 24-h urinary albumin excretion (UAE) and arterial blood pressure measurements on two consecutive outpatient controls. Microalbuminuria was defined as UAE above 30 μg/min on the two consecutive measurements. After 7-year follow-up, 8 (23.5%; 95% Cl: 9.3 to 37.7%) patients developed microalbuminuria. Their metabolic control was worse (7 years mean HbA 1 : 10.7 vs. 9.7%; P = 0.04) and 1 year EIS lower (1.9 vs. 7.6 ng/ml.10 min; P = 0.03) than in normoalbuminuric patients. They also had higher prevalence of ‘high-normal’ arterial blood pressure ( P = 0.03) and diabetic retinopathy ( P = 0.01) than normoalbuminuric patients did. Stepwise logistic regression analysis showed that diabetic retinopathy was the only independent and significant risk factor related to microalbuminuria development ( P = 0.01). We conclude that in subjects with short-term evolution IDDM, microalbuminuria development was associated with glycemic control, EIS and arterial blood pressure levels, however the strongest association was found with diabetic retinopathy occurrence.

Comprehension of the effect of diabetes mellitus on auditory function has been hindered by the fact that previous studies have evaluated hearing function in heterogeneous groups of patients with diabetes mellitus, thus giving conflicting results. We have performed audiometric studies in 46 consecutive patients, 13 with newly diagnosed type 1 diabetes mellitus (group 1) and 33 with type 1 diabetes mellitus of more than 3 years of duration (group 2), of 14 to 40 years of age. The results were compared to an age-matched control group. Pure-tone auditory thresholds were significantly higher in all frequencies 250–8000 Hz in both groups when compared to the control subjects. Ten patients, all of which belonged to group 2, had auditory thresholds above 30 dB in at least one frequency, showing a conversational hearing loss that ranged between 11 and 44%. However, none of them referred subjective hypoacusia. Univariate analysis revealed significant associations between auditory thresholds and age, duration of disease as well as retinopathy, but not with neuropathy, HbA 1c or hypoglycaemic episodes. Only age and duration of disease independently correlated with an auditory threshold using multiple regression. We conclude that type 1 diabetes mellitus can cause mild sensorineural hearing impairment which correlates with age and duration of disease.

The total insulin dosage and its distribution throughout the day were evaluated in newly diagnosed Spanish IDDM patients treated with semisynthetic human insulin. We assessed the insulin dosage and its distribution modifications related to an inpatient versus outpatient setting. We compared our results with classical theoretical algorithms based on patients treated with animal insulin and with alimentary habits which differ from our geographical area. The initial total daily dose (0.68 +/- 0.27 U/kg per day) did not substantially differ from the usual recommended dose (0.70-0.80 U/kg per day). A substantial decrease in total insulin dose was observed in ambulatory patients (0.55 U/kg per day). The reduction in dosage when we substituted regular insulin for intermediate acting insulin was smaller than what is commonly advised. A very low proportion of patients needed to add extra regular insulin to the pre-dinner intermediate insulin dose to achieve acceptable glucose control. Moreover, in these cases regular insulin comprised only 10% of total daily dosage, a proportion clearly inferior to that recommended. The majority of this group of patients needing regular insulin plus intermediate insulin at pre-dinner were treated with human zinc insulin. Most of our patients were acceptably controlled with a regular insulin dose before breakfast and lunch and an intermediate dose before dinner. Finally, human insulin pharmacokinetics plus our Mediterranean alimentary habits might be the explanation to our findings.

Ophthalmic evolution was studied for 2 years in 17 patients with insulin-dependent diabetes mellitus and background diabetic retinopathy. Nine patients were treated with triflusal, a new platelet antiaggregant drug, and the eight remaining patients, with similar clinical and biological characteristics, were considered the control group. At the end of the study the ophthalmic evolution was different in the two groups. In the control group the degree of fluorescein leakage and the number of microaneurysms increased, while in the triflusal-treated group both parameters were reduced. There were no differences in visual acuity and computerised perimetry between the groups. Our results suggest that platelet antiaggregant therapy can be useful in the treatment of background diabetic retinopathy.