Management of diabetes in pregnancy: comparison of guidelines with current practice at Austrian and Australian obstetric center

Aim

To compare Austrian and Australian national guidelines for gestational and pre-gestational diabetes and estimate the level to which physicians comply with their country’s guidelines.

Methods

Austrian (ÖDG, Austrian Diabetes Society) and Australian guidelines (ADIPS, Australasian Diabetes in Pregnancy Society) for the treatment of gestational diabetes and pre-gestational diabetes were systematically reviewed. Current practices in two obstetric centers in Austria and Australia were assessed by interviewing key stakeholders through questionnaires assessing different components of diabetes care. For gestational diabetes, these components were screening, abnormal oral glucose tolerance test values (mmol/L), abnormal values for diagnosis, further management when abnormal values are detected, monitoring/glucose targets (mmol/L), further management and indications for insulin therapy, route and timing of delivery, and postpartum management and counseling. For pre-gestational diabetes, the components were management during the preconceptional period, glucose target values, medical surveillance, obstetric surveillance, medication used, route and timing of delivery, and postpartum management and counseling.

Results

More variation was found in the management of gestational than pre-gestational diabetes. There were differences in oral glucose tolerance test and cut-off levels for diagnosing gestational diabetes in both centers and guidelines. Australian guidelines recommended two-stage screening for gestational diabetes, while Austrian guidelines recommended one-stage screening. At the Austrian obstetric center, amniocentesis was recommended for determining the start of insulin treatment in pregnant women with gestational diabetes. This approach was neither used at the Australian obstetric center nor recommended by any of the two guidelines.

Conclusion

Our study showed that it was difficult to standardize screening criteria and diagnostic methods for gestational and pre-gestational diabetes. National and international consensus has yet to be achieved in the management of diabetes in pregnancy.The number of cases of diabetes worldwide has significantly increased in the last decade and it is expected to double by 2030 (1). This “diabetic epidemic” also considerably affects pregnant women (2). However, the management of pre-gestational and gestational diabetes, the latter being defined as glucose intolerance first detected in pregnancy, remains controversial (3). Gestational and pre-gestational diabetes are associated with increased feto-maternal morbidity, including stillbirth, macrosomia, and fetal malformations, as well as long-term complications in the mother and offspring (4-6). However, treatment and/or monitoring reduce perinatal mortality to the rate in the healthy population. There is no internationally agreed approach and there are neither up-to-date World Health Organization (WHO) recommendations nor fact sheets designed especially for diabetes in pregnancy. The complexity of gestational and pre-gestational diabetes, its underlying pathogenetic mechanism, and recent insights into potential and far-ranging complications have justified the establishment of a considerable number of recent national guidelines (7). Variation in treatment strategies has originated from different views, approaches, and traditional management in obstetric clinics around the globe.As a novelty, this study does not only compare national guidelines of Austria and Australia, two developed high-income countries situated on different continents, but also estimates the level to which physicians comply with their country’s guidelines. Since currently no international standardized approach to screening criteria and diagnostic methods for gestational diabetes and pre-gestational diabetes exists and opinions differ even on the national level, we hypothesized that there were major differences in screening, diagnosing, and treating diabetes in pregnancy. An additional aim of this study was to produce a table of requirements that should be incorporated into future guidelines.     

Antiphospholipid antibodies in serum and follicular fluid: is there a correlation with IVF implantation failure?

Sir, We have read the paper of Buckingham et al. (2006) with considerableinterest because we have recently published a related study(Matsubayashi et al., 2006). Buckingham et al. (2006) reportedthat antiphospholipid antibodies (aPLs) do not appear selectivelyconcentrated in follicular fluids and, when present, do notadversely affect the reproductive outcome     

The spectrum of spontaneous mutations caused by deficiency in proteasome maturase Ump1 in Saccharomyces cerevisiae

Ump1 is responsible for maturation of the catalytic core of the 26S proteasome. Dysfunction of Ump1 causes an increase in the frequency of spontaneous mutations in Saccharomyces cerevisiae. In this study we analyze the spectrum of mutations occurring spontaneously in yeast deficient in Ump1 by use of the SUP4-o system. Single base substitutions predominate among the mutations analyzed (73 of the 91 alterations examined). Two major classes are GC to TA transversions and GC to AT transitions ( approximately 50 and approximately 30% of base substitutions, respectively). Besides base substitutions, almost all the major types of sequence alterations are represented. The specificity and distribution of mutations occurring in the ump1 strain are unique compared to the spectra previously established for other yeast mutators. However, the profile of mutations arising in this strain is similar to that observed in wild type. The same similarity has previously been reported for yeast deficient in Mms2, a protein involved in Rad6-dependent postreplication DNA repair (PRR). The specificity of the mutator effect caused by ump1 is discussed in light of the proposed role of the proteasome activity in the regulation of the PRR mechanisms.     

Nociceptive flexion reflex thresholds and pain during rest and computer game play in patients with hypertension and individuals at risk for hypertension

Supraspinal pain modulation may explain hypertensive hypoalgesia. We compared nociceptive flexion reflex (NFR) thresholds and pain during rest and computer game play in hypertensives and normotensives (Experiment 1) and normotensives with and without hypertensive parents (Experiment 2). The game was selected to modulate activity in pain pathways. NFR thresholds did not differ between groups during rest or game play. Pain ratings never differed between hypertensives and normotensives, whereas individuals with hypertensive parents reported less pain during the first two NFR assessments, compared to those without. NFR thresholds and pain were reduced by game play compared to rest. The failure of game play to differentially modulate NFR thresholds or associated pain reports between groups argues against enhanced supraspinal modulation of nociception and pain in hypertensives and those at increased risk for hypertension.     

Platelet-activating factor, a pleiotrophic mediator of physiological and pathological processes

Platelet-activating factor (PAF) is a potent proinflammatory phospholipid with diverse pathological and physiological effects. This bioactive phospholipid mediates processes as diverse as wound healing, physiological inflammation, apoptosis, angiogenesis, reproduction and long-term potentiation. Recent progress has demonstrated the participation of MAP kinase signaling pathways as modulators of the two critical enzymes, phospholipase A2 and acetyltransferase, involved in the remodeling pathway of PAF biosynthesis. The unregulated production of structural analogs of PAF by non-specific oxidative reactions has expanded this superfamily of signaling molecules to include "PAF-like" lipids whose mode of action is identical to that of authentic PAF. The action of members of this family is mediated by the PAF receptor, a G protein-coupled membrane-spanning molecule that can engage multiple signaling pathways in various cell types. Inappropriate activation of this signaling pathway is associated with many diseases in which inflammation is thought to be one of the underlying features. Inactivation of all members of the PAF superfamily occurs by a unique class of enzymes, the PAF acetylhydrolases, that have been characterized at the molecular level and that terminate signals initiated by both regulated and unregulated PAF production.     

Modulation of human upper intestinal nutrient transit by a beta adrenoreceptor mediated pathway.

To explore the role played by beta adrenoreceptor mediated pathways on human upper gut function a series of studies were conducted into the effects of beta adrenoreceptor agonists and antagonists on orocaecal and duodenocaecal transit and on antral and duodenal motor activity. Under control conditions orocaecal transit was consistent within individuals (mean coefficient of variation (18.0%) but varied widely between individuals (median transit 63 minutes, range 33-164). Prior administration of the non-selective beta adrenergic antagonist propranolol consistently hastened orocaecal transit (median transit 51:25-93, v control p < 0.005). The selective beta-1 antagonist, atenolol, also hastened transit (median transit 50:35-93 minutes, v control p < 0.01). The magnitude of an individual's response to beta blockade correlated closely with the orocaecal transit (Tau = 0.54, p < 0.01). Duodenocaecal transit was also hastened by propranolol from control values of 66:45-107 minutes to 50:16-62 minutes, p < 0.025). In contrast neither duodenal nor antral motility were consistently altered by beta blockade. The beta adrenoreceptor agonist, isoprenaline, delayed both orocaecal transient (97:55-178 minutes, v control p < 0.005) and also duodenocaecal transit (160:45-215 minutes, v 73:40-133) (p < 0.025). Isoprenaline also reduced antral motility by an effect which appeared to occur predominantly through a reduction in contraction amplitude (from a median amplitude of 27:5.39 mm Hg to 14:3-24 mm Hg, p < 0.03) rather than an effect on the interval between contractions. No effect on either amplitude or frequency of duodenal motor activity was observed. A beta adrenoreceptor mediated pathway thus appears to exert a biologically relevant effect on gut function not only under conditions of sympathetic stimulation, but also at rest when a basal beta adrenergic tone appears to influence the speed of nutrient transit through the human upper gut.