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As non-communicable or chronic diseases are a growing threat to human health and economic growth, political stakeholders are aiming to identify options for improved response to the challenges of prevention and management of non-communicable diseases. This paper is intended to contribute ideas on personalized chronic disease management which are based on experience with one major chronic disease, namely diabetes mellitus. Diabetes provides a pertinent case of chronic disease management with a particular focus on patient self-management. Despite advances in diabetes therapy, many people with diabetes still fail to achieve treatment targets thus remaining at risk of complications. Personalizing the management of diabetes according to the patient's individual profile can help in improving therapy adherence and treatment outcomes. This paper suggests using a six-step cycle for personalized diabetes (self-)management and collaborative use of structured blood glucose data. E-health solutions can be used to improve process efficiencies and allow remote access. Decision support tools and algorithms can help doctors in making therapeutic decisions based on individual patient profiles. Available evidence about the effectiveness of the cycle's constituting elements justifies expectations that the diabetes management cycle as a whole can generate medical and economic benefit., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Objectives: Primary aim: to determine the degree of control of HbA(1c) at the time of treatment intensification (TI) in T2DM patients. Secondary aims: fasting plasma glucose levels; estimation of the elapsed time between HbA(1c) exceeding 7% and TI; antidiabetic combinations used, % patients with good cardiometabolic control (LDL-c<100mg/dL; SBP<130 and DPB<80mmHg and HbA(1c)<7%)., Research Design and Methods: one-cohort, multicenter, retrospective, observational study conducted in Spain. Patients diagnosed with T2DM that had switched from monotherapy to combination antidiabetic therapy were evaluated at baseline and after one year of follow-up., Results: a total of 1202 T2DM patients were analyzed. At the time of TI: mean HbA(1c) 8.1%; median time of uncontrolled disease: 2.0 years. After one-year of TI: significant reduction in mean HbA(1c) (8.1% vs.7.0%, p<0.001) and a mean fasting plasma glucose levels reduction (181.1mg/dL vs.144.1mg/dL, p<0.001) was also observed. The percentage of patients under glycemic control (HbA(1c)<7%) increased from 12.2% to 51.6% (p<0.001). Most common antidiabetic combinations: metformin+sulfonylurea (44.1%) and metformin+thiazolidindione (15.9%)., Conclusions: in the population of T2DM patients analyzed, TI was carried out when HbA(1c) values were above those recommended in clinical guidelines (≤ 7%), with a delay of two years to address the second step of therapy, despite the consensus recommendation of the ADA/EASD of 3 months. TI was shown to be effective since addition of a second antidiabetic drug led to an average reduction of HbA(1c) of approximately 1%. Metformin was the drug most commonly used as monotherapy being the most frequent combination metformin+sulfonylurea., (2010 Elsevier Ireland Ltd. All rights reserved.)

The AT.LANTUS trial recently demonstrated the efficacy and safety of insulin glargine initiation and maintenance using two different treatment algorithms in poorly controlled type 2 diabetes mellitus (T2DM). This sub-analysis investigated glycemic control and safety in 686 patients switching from premixed insulin (premix) with or without (+/-OADs) to once-daily glargine (+/-OADs/prandial insulin). A 24-week, multinational (n=59), multicenter (n=611), randomized study comparing two algorithms (Algorithm 1: clinic-driven titration; Algorithm 2: patient-driven titration) in four glargine+/-OADs treatment groups: alone, once- (OD), twice- (BD) or >twice- (>BD) daily prandial insulin. After switching to the glargine regimen, HbA(1c) levels significantly improved in the overall group (9.0+/-1.3 to 8.0+/-1.2%; p<0.001) and in all subgroups; fasting blood glucose levels also improved in all subgroups (overall: 167.1+/-50.0 to 106.9+/-27.2 mg/dL [9.3+/-2.8 to 5.9+/-1.5 mmol/L]; p<0.001). The incidence of severe hypoglycemia was also low in all four subgroups (< or =1.7%). Patients with T2DM switching from premix+/-OADs to glargine+/-OADs had significant reductions in glycemic control with a low incidence of severe hypoglycemia. The addition of prandial (OD, BD or >BD) insulin was associated with further improvements in glycemic control. These data provide support for the stepwise introduction of prandial insulin to a more physiologic basal-bolus regimen, which is under investigation.

This study assessed the incidence of severe hypoglycaemia with two insulin glargine titration algorithms: Algorithm 1 (increments of at least 10%, but not exceeding 4U) versus Algorithm 2 (1-6U increments). In this multicenter (n=409), multinational (n=54), open-label, 24-week randomized trial in 2442 subjects with sub-optimally controlled Type 1 diabetes (T1DM), mean prior insulin therapy duration was 14.6+/-10.3 years. The incidence of severe hypoglycaemia was similar with Algorithms 1 and 2 (16.6events/100 patient-years versus 14.4events/100 patient-years). There were similar rates of both symptomatic and nocturnal hypoglycaemia. HbA(1c) and fasting blood glucose (FBG) decreased significantly (baseline to endpoint; p<0.001), and comparably with Algorithms 1 and 2 (HbA(1c): -0.64% versus -0.72%; FBG: -57mg/dL versus -59mg/dL). Mean basal insulin dose increased with both algorithms (+5.7U versus +5.9U). In a diverse population with longstanding T1DM, transfer from any insulin regimen, including basal-bolus or premixed insulin to an insulin glargine-based regimen resulted in significant improvements in glycaemic control, with low rates of severe hypoglycaemia, irrespective of the titration algorithm used.

The aim of the study was to examine the effects of intensive insulin therapy using lispro on metabolic control, immunogenicity and beta-cell function of newly diagnosed type 1 diabetic subjects in comparison with intensive insulin therapy using regular insulin. An open study was conducted in 45 newly diagnosed type 1 diabetic subjects. Patients were randomly assigned to intensive insulin therapy using insulin lispro (lispro) (lispro, n=22; 22.8 years) or intensive insulin therapy using regular insulin (regular) (regular, n=23; 24.4 years): three to five injections of subcutaneous rapid-acting insulin before meals and Neutral Protamine Hagedorn (NPH) before dinner/bed-time. GAD, IA2, insulin antibodies, basal and stimulated plasma C-peptide and HbA(1c) were measured initially and at months 1, 4, 8 and 12. Daily blood glucose profiles tended to be lower in the lispro group, particularly values after breakfast, without reaching statistical significance. There were no differences in terms of HbA(1c) throughout the study. The proportion of subjects achieving an HbA(1c)<6% at the end of the study was similar in both groups (regular 73.9%, lispro 68.0%). The number of mild hypoglycemic episodes tended to be lower with lispro, but not significantly. beta-Cell function was not significantly different in both groups. During follow-up there were no differences in antibodies, including IAAb. In summary, insulin lispro used in intensive insulin therapy is as effective as regular insulin in optimizing metabolic control and preserving beta-cell function at diagnosis of type 1 diabetes.

The aim of our study was to evaluate the efficiency of an individual intensive educational control program on improving the metabolic control of insulin-dependent diabetic patients at short- and long-term follow-up. Fifteen insulin-dependent diabetic subjects with poor metabolic control (hemoglobin A1c > 9%) were included. At entry, their knowledge of diabetes (DKQ2 test), total energy intake and its distribution, insulin schedule, technical skill for insulin administration and self monitoring of blood glucose were evaluated. According to the initial evaluation, individual goals were stipulated and monitored in weekly visits. Individual life-style was particularly kept in mind. Thereafter, patients were switched to our ambulatory clinic for outpatients. At 1, 6, 12 and 24 months of follow-up, the items analyzed at the beginning were reevaluated. After 1 month, the program produced a significant decrease in hemoglobin A1c and an increase in knowledge of diabetes. The same beneficial effects were present at 6, 12 and 24 months evaluation compared to those values recorded at entry. There were neither major changes in dietary intake nor insulin schedule nor any increase in the frequency of hypoglycemic episodes. In conclusion, our program (5.2 +/- 0.8 weekly visits) significantly reduced and sustained hemoglobin A1c values close to those levels recommended by multicenter controlled trials. We consider that our program produced two major changes: a long-lasting improvement in knowledge of diabetes and an increase in self-monitoring blood glucose which provided the key for optimal self-regulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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 beta-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.

Unlabelled: 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, HbA1), 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 micrograms/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 HbA1: 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.

The effect of corticosteroids on beta cell function and humoral immune response in type 1 diabetes was tested in a 2-month trial conducted on 32 newly diagnosed patients (age 22.8 +/- 1.4 years, mean +/- S.E.M.). Prednisone was administered at immunosuppressive dosage (1 mg.kg-1.day-1) during the initial 10 days and at a maintenance dosage (0.3 mg.kg-1.day-1) for 50 days. Patients (n = 32) were enrolled within 6 weeks after diagnosis and matched in pairs for age, sex, presence of islet cell antibodies (ICA) and glucagon stimulated C-peptide levels. Insulin discontinuation was not contemplated. All the patients who received prednisone became ICA during treatment but in some (4 out of 10) this effect was only transient. Insulin antibodies (IA) were significantly lower in the prednisone group at second and third month (P < 0.05). No patient experienced complete remission but in 10 prednisone and 4 control patients the insulin requirements were below 0.3 IU/kg (P < 0.05). With similar glycemia the fasting C-peptide levels were higher in the treated patients. The profile of the insulin requirements during the follow-up was different in the two groups and at 9 months the prednisone group needed less insulin than the control (P < 0.05). Interestingly, within the prednisone-treated group and after 6 months, the levels of stimulated C-peptide improved significantly among the ICA+ patients while they were steady or declined in ICA- (P < 0.01). The analysis of variance covariance confirmed a positive interaction between ICA and the administration of prednisone on the outcome of beta cell function.(ABSTRACT TRUNCATED AT 250 WORDS)

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 250-8,000 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, HbA1c 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.

Although restoration of normoglycemia in non-insulin-dependent diabetic subjects improves insulin release evoked by several secretagogues, conflicting data were reported concerning the effect of intensive insulin therapy on the first-phase response of the B-cell to an intravenous glucose challenge. In the present study, 14 non-insulin-dependent diabetics underwent an intravenous glucose test performed before and after 20 h of glycemic normalization. Before insulin treatment, glucose failed, as a rule, to provoke an early positive secretory response. On the contrary, a paradoxical inhibition of insulin release was observed in most patients. This phenomenon was reproducible when a second test was performed 120 min after the first one. The paradoxical inhibition was not observed any more after glycemic normalization. As judged from the paired difference (delta) between the early increment in insulin release before and after insulin treatment, normoglycemia resulted in an improved secretory response (delta greater than 5.0 microU/ml) in seven patients, whilst the first-phase response remained little affected (delta less than 3.0 microU/ml) in the other seven subjects. These findings suggest that an impaired first-phase response to glucose does not always represent an irreversible primary defect of the pancreatic B-cell in diabetic subjects.