Excess risk of hospitalisation for heart failure among people with type 2 diabetes

Aims/hypothesis

Type 2 diabetes is an established risk factor for heart failure, but age-specific data are sparse. We aimed to determine excess risk of heart failure, based on age, glycaemic control and kidney function in comparison with age- and sex-matched control individuals from the general population.

Methods

Individuals with type 2 diabetes registered in the Swedish National Diabetes Registry 1998–2012 (n?=?266,305) were compared with age-, sex- and county-matched control individuals without diabetes (n?=?1,323,504), and followed over a median of 5.6 years until 31 December 2013.

Results

We identified 266,305 individuals with type 2 diabetes (mean age 62.0 years, 45.3% women) and 1,323,504 control individuals. Of the individuals with type 2 diabetes and control individuals, 18,715 (7.0%) and 50,157 (3.8%) were hospitalised with a diagnosis of heart failure, respectively. Comparing individuals with diabetes with those in the control group, men and women with type 2 diabetes who were younger than 55 years of age had HRs for hospitalisation for heart failure of 2.07 (95% CI 1.73, 2.48) and 4.59 (95% CI 3.50, 6.02), respectively, using analyses adjusted for socioeconomic variables and associated conditions. Younger age, poorer glycaemic control and deteriorating renal function were all associated with increased excess risk of heart failure in those with type 2 diabetes compared with the control group. However, people with diabetes who were ≥75 years and without albuminuria or with good glycaemic control (HbA_1c ≤52 mmol/mol [≤6.9%]) had a similar risk of hospitalisation for heart failure as control individuals in the same age group.

Conclusions/interpretation

Men and women aged <55 years with type 2 diabetes are at markedly elevated excess risk of heart failure. The excess risk declined with age, but persisted even with good glycaemic control. However, among those who were 75 years and older, diabetic individuals with well controlled glucose levels or without albuminuria had a risk of heart failure that was on a par with individuals without diabetes.

     

Angiotensin converting enzyme gene polymorphism and glomerular filtration rate changes in type 2 diabetic patients

It has been suggested that an insertion/deletion (I/D) polymorphism in intron 16 of the angiotensin-converting enzyme (ACE) gene may be associated with diabetic nephropathy The aim of this study was to investigate whether an association exists between ACE I/D polymorphism and glomerular filtration rate (GFR) in type 2 diabetes mellitus. A total of 128 type 2 diabetic patients were included in the study with the following ACE genotype distribution: DD 40, ID 58,11 30. I/D polymorphism was determined by polymerase chain reaction (PCR). Mean GFR was not statistically different according to ACE genotype (DD: 89.9 +/- 28.1 ml/min, ID: 99.5 +/- 25.1 ml/min, II: 96.6 +/- 19.6 ml/min). There was no significant difference in genotype distribution in normo-, micro- and macroalbuminuric patients (DD:ID:II [%], normo- 35:46:19, micro-28:55:17, macro- 31:55:14). ACE I/D polymorphism does not seem to be associated with GFR in type 2 diabetic patients.     

Vitamin D deficiency might pose a greater risk for ApoEɛ4 non-carrier Alzheimer’s disease patients

Vitamin D is a secosteroid hormone that shares a synthetic pathway with cholesterol. ApoE, which is involved in the transport of cholesterol, is the most significant genetic risk factor for sporadic Alzheimer’s disease (AD). Surprisingly, recent studies have indicated the presence of an evolutionary juncture between these two molecules. To demonstrate this possible relationship, we investigated serum levels of 25-hydroxyvitamin-D₃ (25OHD) in patients with early onset-AD (EOAD; n:22), late onset-AD (LOAD; n:72), mild cognitive impairment (MCI; n:32) and in healthy subjects (n:70). We then analyzed the correlation between 25OHD and cytokines, BDNF and Hsp90 with respect to ApoE alleles, as these molecules were investigated in our previous studies. The LOAD patients had low levels of 25OHD, but these low levels originated only from ApoE?4 non-carrier patients. Negative correlations were observed between serum 25OHD and TNFα, IL-1β or IL-6 levels in healthy subjects or MCI patients, but these same correlations were positive in LOAD patients. ApoE alleles indicated that these positive correlations exist only in ?4 carrier LOAD patients. Consequently, our results indicate that vitamin D deficiency presents a greater risk for ApoE?4 non-carrier AD patients than for ?4 carriers. Therefore, it might be beneficial to monitor the vitamin D status of ApoE?4 allele non-carrier AD patients.     

Frequency of neonatal hypoglycemia in large for gestational age infants of non-diabetic mothers in a community maternity hospital

Large for gestational age (LGA) infants are at increased risk for hypoglycemia. The aim of the study was to determine the frequency of neonatal hypoglycemia in LGA infants of non-diabetic mothers in a Community Maternity Hospital in Gaziantep, Turkey. Hospital records of 5229 infants of non-diabetic mothers were examined retrospectively. Newborns with birth weight more than 4000 g were defined as LGA. The control group consisted of 100 appropriate for gestational age (AGA) newborns. Capillary blood glucose was measured at the second hour of life. Glucose values lower than 40 mg/dL (2.2 mmol/L) were defined as hypoglycemia. Ninety-six (1.8%) of the 5229 infants were found to be LGA. The mean capillary glucose levels of the LGA newborns were significantly lower than those of the AGA newborns (54 mg/dL (3.0 mmol/L) vs. 95 mg/dL (5.2 mmol/L), p < 0.0001). Neonatal hypoglycemia was established in 16 of 96 LGA infants (16.7%). In the control group hypoglycemia was absent. The rate of hypoglycemia in LGA infants was significantly higher than the rate in the AGA infants (p = 0.0000). As hypoglycemia is not rare in LGA infants and can have serious consequences, blood glucose levels should be screened routinely in LGA infants.     

Transient hypogonadotrophic hypogonadism in males with acute toxoplasmosis: suppressive effect of interleukin-1 beta on the secretion of GnRH

BACKGROUND: In September 2002, an outbreak of toxoplasmosis was noted in a male boarding high school on the Aegean coast of Turkey. We have focused our efforts to investigate the sex hormones in this population. METHODS: Blood samples were collected from 40 male patients, 17-18 years old, who also had positive titres of antibody to Toxoplasma gondii. Serum FSH, LH, free testosterone (FT), total testosterone (TT), interferon-gamma (IFN-gamma), interleukin-1beta (IL-1beta) and macrophage-inflammatory protein-1alpha (MIP-1alpha) concentrations were measured in all patients and 20 control subjects. Initially, the patients were divided on the basis of the levels of sex hormones into the following groups: patients who had normal sex hormone levels (n = 31) as group A and patients with low sex hormone levels (n = 9) as group B. RESULTS: IL-1beta levels were found to be higher in group B patients than group A. The levels of IL-1beta correlated significantly in a negative manner with FSH, LH, FT and TT in all patients with acute toxoplasmosis (n = 40). CONCLUSIONS: Acute toxoplasma infection may cause temporary hypogonadotrophic gonadal insufficiency regardless of the course of the disease.     

Share of Mass Transit Miles Traveled and Reduced Motor Vehicle Fatalities in Major Cities of the United States

The USA leads the developed world in motor vehicle fatalities, presenting a critical public health threat. We examined whether an increasing share of mass transit use, relative to vehicle miles traveled on public roads, was associated with reduced motor vehicle fatalities. We used annual city-level data for the USA from 1982–2010 provided by the Fatality Accident Reporting System, the Texas A&M Transportation Institute, the Census Bureau, and the National Oceanic and Atmospheric Administration to estimate a structural equation model of the factors associated with mass transit miles and motor vehicle fatalities. The final analytic data included 2,900 observations from 100 cities over 29 years. After accounting for climate, year, and the economic costs of driving, an increasing share of mass transit miles traveled per capita was associated with reduced motor vehicle fatalities. The costs of congestion to the average commuter and gas prices were positively associated with increasing the share of mass transit miles traveled. The economic costs of driving increased over time, while both the fatality rate and the share of mass transit miles traveled decreased over time. Increasing the share of mass transit miles traveled may be associated with fewer motor vehicle miles traveled. Increasing mass transit uptake may be an effective public health intervention to reduce motor vehicle fatalities in cities.