Modeling patients’ choice between a primary care physician or a diabetes specialist for the management of type-2 diabetes using a bivariate probit analysis

AimsTo determine the prevalence of type-2 diabetes patients that were initially and currently being treated by primary care physicians (PCPs) or diabetes specialists and assess predictors influencing their choice.MethodsThis cross-sectional study was conducted in nine Greek primary healthcare units. Patients’ choices were modeled using a bivariate probit analysis.ResultsA total of 225 patients participated (84% response rate). Only 15.9% and 11.9% of the respondents acknowledged having chosen a diabetes specialist for their initial or current treatment, respectively. The family history of diabetes in siblings and the screening for diabetic retinopathy during the past year were significantly positively associated with choosing a diabetes specialist (initially p = 0.033 or currently p = 0.007), and resulted in a statistically significant reduction of the joint probabilities of choosing a PCP by 15.6% and 13.6%, respectively. Younger age (p = 0.040), female sex (p = 0.017), higher HbA1c (p = 0.004), experience of hypoglycemia (p = 0.029) and low cardiovascular morbidity index (p = 0.016) emerged as important predictors for choosing a diabetes specialist for their treatment.ConclusionsOur findings provide a better insight in diabetes patients’ choices regarding the category of their treating physicians and their predictors. More studies are required to replicate them and identify patient subpopulations that may favor diabetes specialists’ guidance.     

Who should benefit from diabetes cell therapy?

Type 1 diabetes are intrinsically unstable conditions because of the loss of both insulin secretion and glucose sensing. Guidelines to treat type 1 diabetes have become stricter since the Diabetes Control and Complications Trial (DCCT) results demonstrated the close relationship between microangiopathy and HbA1c levels, whereas the deleterious role of glucose variability on macroangiopathy has been more recently suspected. Therapeutic strategies first require the treatment of underlying organic causes of the brittleness whenever possible and, secondly, the optimization of insulin therapy using analogues, multiple injections and consideration of continuous subcutaneous insulin infusion. Alternative approaches may still be needed for the most severely affected patients, including islet transplantation. We propose islet after kidney transplantation in diabetic patients with end-stage kidney disease ineligible for double kidney-pancreas transplantation (i.e C peptide negative patients over 45 years of age or with severe macroangiopathy) if creatinine blood levels are stable below 20 mg/l at least six months after kidney transplantation and steroid discontinuation. Islet transplantation alone is proposed to (1) C peptide negative diabetic patients, (2) aged 18–65 with a duration of diabetes of at least five years, (3) treated with intensive subcutaneous insulin therapy, but unable to obtain a glycated hemoglobin level below 7% without hypoglycemia and / or with brittleness and unpredictable hyper- and hypoglycemia altering quality of life, (4) with normal body weight (< 80 kg) and / or low daily insulin needs (the lower, the better), (5) with renal function close to normal (creatinine clearance above 60 ml/min with albuminuria lower than 300 mg/24 h), (6) with no desire for pregnancy in women. Currently and until more complete assessment of the 5-year overall benefit–risk ratio, islet transplantation remains a clinical research procedure. As already provided for other types of transplantation, and once recognized as a “routine” procedure, prioritization of enlisted patients for islet transplantation could be aided by the calculation of a score that should be determined by a multidisciplinary team.     

Who needs an RVAD in addition to an LVAD?

Mechanical circulatory support using left ventricular assist devices (LVAD) has become an accepted mode of therapy for both bridging patients with end-stage heart failure to transplant and as a destination therapy. Right ventricular (RV) dysfunction is common after LVAD insertion and is a significant source of morbidity and mortality in patients undergoing LVAD placement. Several studies have identified clinical, laboratory, hemodynamic, and echocardiographic parameters that may serve as risk factors for RV dysfunction after LVAD placement. Furthermore, scoring systems have been established to help quantitatively predict the potential need for RV support after LVAD placement.     

Diabetic nephropathy--what are the unmet needs?

In this pandemic of diabetes and obesity, Asia will have the highest number of affected people with the greatest increase in the young-to-middle aged group. Asian patients have increased risk for diabetic kidney disease which may be compounded by low grade infection, obesity and genetic factors. In these subjects, the onset of albuminuria and diabetic kidney disease causes further perturbation of metabolic milieu with increased oxidative stress, anaemia and vascular calcification which interact to markedly increase the risk of cardiovascular disease. Despite receiving optimal care to control blood pressure and metabolic risk factors as well as inhibition of the renin-angiotensin system in a clinical trial setting, there is a considerable residual risk for cardio-renal complications in patients with diabetic kidney disease. Control of obesity and low grade inflammation as well as correction of anaemia may represent areas where novel strategies can be developed and tested to curb this rising global burden of cardio-renal complications.     

Who should have genetic testing for maturity‐onset diabetes of the young?

Maturity-onset diabetes of the young (MODY) is a clinically heterogeneous group of monogenic disorders characterized by autosomal dominant inheritance of young-onset, non-insulin-dependent diabetes. The genes involved are important in beta cell development, function and regulation and lead to disorders in glucose sensing and insulin secretion. Heterozygous GCK mutations cause impaired glucokinase activity resulting in stable, mild hyperglycaemia that rarely requires treatment. HNF1A mutations cause a progressive insulin secretory defect that is sensitive to sulphonylureas, most often resulting in improved glycaemic control compared with other diabetes treatment. MODY owing to mutations in the HNF4A gene results in a similar phenotype, including sensitivity to sulphonylurea treatment. HNF1B mutations most frequently cause developmental renal disease (particularly renal cysts) but may also cause MODY in isolation or may cause the renal cysts and diabetes syndrome (RCAD syndrome). Mutations in NEUROD1, PDX1 (IPF1), CEL and INS are rare causes of MODY. MODY is often misdiagnosed as type 1 or type 2 diabetes. However, a correct genetic diagnosis impacts treatment and identifies at-risk family members. Thus, it is important to consider a diagnosis of MODY in appropriate individuals and to pursue genetic testing to establish a molecular diagnosis.