The impact of nutrition intervention on glycemic control in a pediatric type 1 diabetes mellitus population

Aim: The goal of this study was to evaluate the change in hemoglobin A1C and glycemic control after nutrition intervention among a population of type 1 diabetic pediatric patients. Methods: Data was collected from all type 1 diabetic patients who were scheduled for a consultation with the diabetes/endocrine RD from January 2006 through December 2006. Two groups were compared, those who kept their RD appointment and those who did not keep their appointment. The main outcome measure was HgbA1C. An independent samples t-test compared the two groups with respect to change in HbgA1C before and after the most recent scheduled appointment with the RD. Baseline characteristics were used as covariates and analyzed and controlled for using analysis of covariance (ANCOVA). Results: There was no difference in HgbA1c after either attending an RD appointment or not having attended an RD appointment. Those who arrived for and attended their RD appointment and those who did not arrive for and attend their RD appointment, had statistically different HgbA1C's before their scheduled appointment as well as after the RD appointment. However, the two groups were not equal at the beginning of the study period. Discussion: A study design with inclusion criteria of a specified range of HgbA1C values within which the study subjects needed to fall, would have potentially eliminated the difference between the two groups at the beginning of the study period. Conducting either another retrospective study that controlled for the initial HgbA1C value or conducting a prospective study that designated a range of HgbA1C values would be worth investigating to evaluate the impact of medical nutrition therapy intervention and the role of the RD in diabetes management. It is an interesting finding that there was a significant difference in the initial HgbA1c for those who came to the RD appointment compared to those who did not come. The fact that in this study those who did not arrive for their RD appointment had worse control of their diabetes suggests that this is a high-risk group. Targeting diabetes education toward this group of patients may prove to be beneficial. ^

Does diabetes mellitus contribute to the disease burden of vascular dementia?

Background. Vascular dementia (VaD) is the second most common of dementia. Multiple risk factors are associated with VaD, but the individual contribution of each to disease onset and progression is unclear. We examined the relationship between diabetes mellitus type 2 (DM) and the clinical variables of VaD.^ Methods. Data from 593 patients evaluated between June, 2003 and June, 2008 for cognitive impairment were prospectively entered into a database. We retrospectively reviewed the charts of 63 patients who fit the NINDS-AIREN criteria of VaD. The patients were divided into those with DM (VaD-DM, n=29) and those without DM (VaD, n=34). The groups were compared with regard to multiple variables.^ Results. Patients with DM had a significantly earlier onset of VaD (71.9±6.54 vs. 77.2±6.03, p<0.001), a faster rate of decline per year on the mini mental state examination (MMSE; 3.60±1.82 vs. 2.54±1.60 points, p=0.02), and a greater prevalence of neuropsychiatric symptoms (62% vs. 21%, p=0.02) at the time of diagnosis.^ Conclusions. This study shows that a history of pre-morbid DM is associated with an early onset and faster cognitive deterioration in VaD. Moreover, the presence of DM predicts the presence of neuropsychiatric symptoms in patients with VaD. A larger study is needed to verify these associations. It will be important to investigate whether better glycemic control will mitigate the potential effects of DM on VaD.^

Macular edema in Hispanics with non-insulin dependent diabetes mellitus in Starr County, Texas: Prevalence, incidence and risk factors

This project is based on secondary analyses of data collected in Starr County, Texas from 1981 till 1991 to determine the prevalence, incidence and risk factors for macular edema in Hispanics with non-insulin-dependent diabetes in Starr County, Texas. Two studies were conducted. The first study examined the prevalence of macular edema in this population. Of the 310 diabetics that were included in the study 22 had macular edema. Of these 22 individuals 9 had clinically significant macular edema. Fasting blood glucose was found to be significantly associated with macular edema. For each 10 mg/dl increase in fasting blood glucose there was a 1.07 probability of an increase in the risk of having macular edema. Individuals with fasting blood glucose $\ge$200 mg/dl were found to be more than three times at risk of having macular edema compared to those with fasting blood glucose $<$200 mg/dl.^ In the second study the incidence and the risk factors that could cause macular edema in this Hispanic population were examined. 240 Hispanics with non-insulin-dependent diabetes mellitus and without macular edema were followed for 1223 person-years. During the follow-up period 27 individuals developed macular edema (2.21/100 person-years). High fasting blood glucose and glycosylated hemoglobin were found to be strong and independent risk factors for macular edema. Participants taking insulin were 3.9 times more at risk of developing macular edema compared to those not taking insulin. Systolic blood pressure was significantly related to macular edema, where each 10 mmHg increase in systolic blood pressure was associated with a 1.3 increase in the risk of macular edema.^ In summary, this study suggests that hyperglycemia is the main underlying factor for retinal pathological changes in this diabetic population, and that macular edema probably is not the result of sudden change in the blood glucose level. It also determined that changes in blood pressure, particularly systolic blood pressure, could trigger the development of macular edema.^ Based on the prevalence reported in this study, it is estimated that 35,500 Hispanic diabetics in the US have macular edema. This imposes a major public health challenge particularly in areas with high concentration of Mexican Americans. It also highlights the importance of public health measures directed to Mexican Americans such as health education, improved access to medical care, and periodic and careful ophthalmologic examination by ophthalmologists knowledgeable and experienced in the management of diabetic macular edema. ^

DIABETIC RETINOPATHY IN NON-INSULIN-DEPENDENT DIABETES MELLITUS IN BLACK WOMEN: A DESCRIPTIVE STUDY OF RISK FACTORS

This cross-sectional study examines the prevalence of selected potential risk factors by stage of diabetic retinopathy (DR) among Black American women with non-insulin-dependent diabetes mellitus (NIDDM) followed at a university diabetes clinic. DR was assessed by ophthalmoscopy and five-field retinography, and graded on counts of microaneurysms, hemorrhages and/or exudates, and presence of proliferative DR. Prevalence of other vascular diseases was assessed from medical records. Potential risk factors included age, known duration of diabetes, type of hypoglycemic treatment, concentrations of random capillary blood glucose, glycosylated hemoglobin, urine protein and fibrinogen, body mass index, and blood pressure. Prevalence of these risk factors is reported for three categories: No DR, mild background DR, severe background or proliferative DR (including surgically treated DR). Duration, age at diagnosis and treatment of diabetes, concentration of urine protein and average blood glucose, hypertension and cardiovascular disease were significantly associated with DR in univariate analysis. The covariance analysis employed stratification on duration, age at diagnosis and therapy of diabetes. The highest DR scores were calculated for those diagnosed before age 45, regardless of duration, therapy, or average blood glucose. Only individuals diagnosed before age 45 had high blood glucose concentrations in all categories of duration. These findings suggest that in this clinic population of Black women, those diagnosed with NIDDm before age 45 who eventually required insulin treatment were at the greatest risk of developing DR and that longterm poor glucose control is a contributing factor. These results suggest that greater emphasis be placed on this subgroup in allocating the limited resources available to improve the quality of glucose regulation, particularly through measures affecting compliance behavior.^ Findings concerning the association of DR with concentration of blood glucose and urine protein, blood pressure/hypertension and weight were compared with those reported from American Indian and Mexican American populations of the Southwestern United States where prevalence of NIDDM, hypertension and obesity is also high. Additional comparative analyses are outlined to substantiate the preliminary finding that there are systematic differences between these ethnic populations. ^

A Mobile Feedback System for Integrated E-health Platforms to improve Self-Care and Compliance of Diabetes Mellitus Patients

Exploiting the full potential of telemedical systems means using platform based solutions: data are recovered from biomedical sensors, hospital information systems, care-givers, as well as patients themselves, and are processed and redistributed in an either centralized or, more probably, decentralized way. The integration of all these different devices, and interfaces, as well as the automated analysis and representation of all the pieces of information are current key challenges in telemedicine. Mobile phone technology has just begun to offer great opportunities of using this diverse information for guiding, warning, and educating patients, thus increasing their autonomy and adherence to their prescriptions. However, most of these existing mobile solutions are not based on platform systems and therefore represent limited, isolated applications. This article depicts how telemedical systems, based on integrated health data platforms, can maximize prescription adherence in chronic patients through mobile feedback. The application described here has been developed in an EU-funded R&D project called METABO, dedicated to patients with type 1 or type 2 Diabetes Mellitus

Parallel workflows to personalize clinical guidelines recommendations: application to gestational diabetes mellitus

The MobiGuide system provides patients with personalized decision support tools, based on computerized clinical guidelines, in a mobile environment. The generic capabilities of the system will be demonstrated applied to the clinical domain of Gestational Diabetes (GD). This paper presents a methodology to identify personalized recommendations, obtained from the analysis of the GD guideline. We added a conceptual parallel part to the formalization of the GD guideline called "parallel workflow" that allows considering patient?s personal context and preferences. As a result of analysing the GD guideline and eliciting medical knowledge, we identified three different types of personalized advices (therapy, measurements and upcoming events) that will be implemented to perform patients? guiding at home, supported by the MobiGuide system. These results will be essential to determine the distribution of functionalities between mobile and server decision support capabilities.

Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus: United Kingdom prospective diabetes study (UKPDS: 23)

Objective: To evaluate baseline risk factors for coronary artery disease in patients with type 2 diabetes mellitus.

Will new diagnostic criteria for diabetes mellitus change phenotype of patients with diabetes? Reanalysis of European epidemiological data

Objective: To evaluate the impact of the revised diagnostic criteria for diabetes mellitus adopted by the American Diabetes Association on prevalence of diabetes and on classification of patients. For epidemiological purposes the American criteria use a fasting plasma glucose concentration ⩾7.0 mmol/l in contrast with the current World Health Organisation criteria of 2 hour glucose concentration ⩾11.1 mmol/l.

Spontaneous diabetes mellitus in transgenic mice expressing human islet amyloid polypeptide.

The islet in non-insulin-dependent diabetes mellitus (NIDDM) is characterized by loss of beta cells and large local deposits of amyloid derived from the 37-amino acid protein, islet amyloid polypeptide (IAPP). We have hypothesized that IAPP amyloid forms intracellularly causing beta-cell destruction under conditions of high rates of expression. To test this we developed a homozygous transgenic mouse model with high rates of expression of human IAPP. Male transgenic mice spontaneously developed diabetes mellitus by 8 weeks of age, which was associated with selective beta-cell death and impaired insulin secretion. Small intra- and extracellular amorphous IAPP aggregates were present in islets of transgenic mice during the development of diabetes mellitus. However, IAPP derived amyloid deposits were found in only a minority of islets at approximately 20 weeks of age, notably after development of diabetes mellitus in male transgenic mice. Approximately 20% of female transgenic mice spontaneously developed diabetes mellitus at 30+ weeks of age, when beta-cell degeneration and both amorphous and amyloid deposits of IAPP were present. We conclude that overexpression of human IAPP causes beta-cell death, impaired insulin secretion, and diabetes mellitus. Large deposits of IAPP derived amyloid do not appear to be important in this cytotoxicity, but early, small amorphous intra- and extracellular aggregates of human IAPP were consistently present at the time of beta-cell death and therefore may be the most cytotoxic form of IAPP.

IA-2, a transmembrane protein of the protein tyrosine phosphatase family, is a major autoantigen in insulin-dependent diabetes mellitus.

IA-2 is a 105,847 Da transmembrane protein that belongs to the protein tyrosine phosphatase family. Immunoperoxidase staining with antibody raised against IA-2 showed that this protein is expressed in human pancreatic islet cells. In this study, we expressed the full-length cDNA clone of IA-2 in a rabbit reticulocyte transcription/translation system and used the recombinant radiolabeled IA-2 protein to detect autoantibodies by immunoprecipitation. Coded sera (100) were tested: 50 from patients with newly diagnosed insulin-dependent diabetes mellitus (IDDM) and 50 from age-matched normal controls. Sixty-six percent of the sera from patients, but none of the sera from controls, reacted with IA-2. The same diabetic sera tested for autoantibodies to islet cells (ICA) by indirect immunofluorescence and glutamic acid decarboxylase (GAD65Ab) by depletion ELISA showed 68% and 52% positivity, respectively. Up to 86% of the IDDM patients had autoantibodies to IA-2 and/or GAD65. Moreover, greater than 90% (14 of 15) of the ICA-positive but GAD65Ab-negative sera had autoantibodies to IA-2. Absorption experiments showed that the immunofluorescence reactivity of ICA-positive sera was greatly reduced by prior incubation with recombinant IA-2 or GAD65 when the respective antibody was present. A little over one-half (9 of 16) of the IDDM sera that were negative for ICA were found to be positive for autoantibodies to IA-2 and/or GAD65, arguing that the immunofluorescence test for ICA is less sensitive than the recombinant tests for autoantibodies to IA-2 and GAD65. It is concluded that IA-2 is a major islet cell autoantigen in IDDM, and, together with GAD65, is responsible for much of the reactivity of ICA with pancreatic islets. Tests for the detection of autoantibodies to recombinant IA-2 and GAD65 may eventually replace ICA immunofluorescence for IDDM population screening.

NMR studies of muscle glycogen synthesis in insulin-resistant offspring of parents with non-insulin-dependent diabetes mellitus immediately after glycogen-depleting exercise.

To examine the impact of insulin resistance on the insulin-dependent and insulin-independent portions of muscle glycogen synthesis during recovery from exercise, we studied eight young, lean, normoglycemic insulin-resistant (IR) offspring of individuals with non-insulin-dependent diabetes mellitus and eight age-weight matched control (CON) subjects after plantar flexion exercise that lowered muscle glycogen to approximately 25% of resting concentration. After approximately 20 min of exercise, intramuscular glucose 6-phosphate and glycogen were simultaneously monitored with 31P and 13C NMR spectroscopies. The postexercise rate of glycogen resynthesis was nonlinear. Glycogen synthesis rates during the initial insulin independent portion (0-1 hr of recovery) were similar in the two groups (IR, 15.5 +/- 1.3 mM/hr and CON, 15.8 +/- 1.7 mM/hr); however, over the next 4 hr, insulin-dependent glycogen synthesis was significantly reduced in the IR group [IR, 0.1 +/- 0.5 mM/hr and CON, 2.9 +/- 0.2 mM/hr; (P < or = 0.001)]. After exercise there was an initial rise in glucose 6-phosphate concentrations that returned to baseline after the first hour of recovery in both groups. In summary, we found that following muscle glycogen-depleting exercise, IR offspring of parents with non-insulin-dependent diabetes mellitus had (i) normal rates of muscle glycogen synthesis during the insulin-independent phase of recovery from exercise and (ii) severely diminished rates of muscle glycogen synthesis during the subsequent recovery period (2-5 hr), which has previously been shown to be insulin-dependent in normal CON subjects. These data provide evidence that exercise and insulin stimulate muscle glycogen synthesis in humans by different mechanisms and that in the IR subjects the early response to stimulation by exercise is normal.