The effect of paternal and maternal history of diabetes mellitus on the development of gestational diabetes mellitus.

BACKGROUND: There is an ongoing debate whether maternal diabetes is a more important risk factor for gestational diabetes (GDM) development than paternal diabetes. AIM: To describe the risk of GDM associated with paternal and maternal diabetes, and to further characterise GDM women with maternal diabetes. SUBJECTS AND METHODS: Case-control study within a population-based GDM screening program in an urban area of Hungary in 2002-2003. All GDM women (no.=133) and an age-matched control group (no.=135) with a mean age of 31 years was evaluated. Blood pressure, anthropometric data, and blood glucose values from a 75 g Oral Glucose Tolerance Test (OGTT) were recorded at 24-28 weeks of gestation. Family history data were by self-report. RESULTS: Known paternal diabetes was not related to GDM risk [odds ratio (OR) 0.83, 95% confidence interval (CI) 0.35-2.00]. Known maternal diabetes (OR 2.90, 95% CI 0.99-8.49) and diabetes in the maternal line (OR 2.83, 95% CI 1.16-6.89) were both related to GDM after adjustment for body mass index (BMI). GDM women with known maternal diabetes had a higher BMI, 31.6 [9.1] kg/m2 median [interquartile range], than GDM women with or without diabetes in the maternal line, 26.1 [4.9] and 26.3 [6.1] kg/m2, respectively, while figures for fasting glucose during OGTT were 5.2 [0.7] vs 4.4 [1.1] vs 4.9 [0.8] mmol/l respectively (all p<0.05). CONCLUSIONS: Maternal history of diabetes and history of diabetes in the maternal line seems to be a stronger predictor of GDM than paternal history.

Deficient leucocyte antisedimentation is related to post-stroke infections and outcome.

BACKGROUND: Patients with stroke are more susceptible to infections, suggesting possible deficiencies of early immune responses, particularly of leucocytes. AIMS: To serially examine leucocyte antisedimentation rate (LAR), a simple test to detect activation of leucocytes, and correlate it with S100beta, procalcitonin and outcome in patients with acute ischaemic events. METHODS: Venous blood samples were taken from 61 healthy volunteers and 49 patients with acute ischaemic events (acute ischaemic stroke (AIS), n = 38; transient ischaemic attack (TIA), n = 11) within 6 hours, at 24 and 72 hours after onset of symptoms. RESULTS: LAR was significantly higher in acute ischaemic events compared to controls within 6 hours after onset of stroke regardless of post-stroke infections. In addition, the increase of LAR was delayed and attenuated in TIA in contrast to AIS. A deficiency in early increase of LAR was associated with post-stroke infections and a poor outcome, measured by the Glasgow Outcome Scale in AIS. There was a positive correlation between LAR and S100beta at 72 hours after the onset of ischaemic stroke. Increased levels of S100beta at 24 and 72 hours after stroke were associated with poor outcome. CONCLUSIONS: An early activation of leucocytes indicated by an increase of LAR is characteristic of acute ischaemic cerebrovascular events. A delayed and ameliorated leucocyte activation represented by LAR is characteristic of TIA in contrast to stroke. Deficient early activation predisposes to post-stroke infections related to poor outcome. In addition, the extent of tissue injury correlates with the magnitude of innate immune responses.