Lower treatment targets for gestational diabetes: is lower really better?

Proposed lower diagnostic thresholds and lower treatment targets for gestational diabetes have been controversial internationally. Intervention trials for the recently revised lower Australian treatment targets are currently lacking. While there may be benefits, lowering treatment targets may cause a number of harms including increased risk of hypoglycaemia in pregnant women, greater medicolegal risk for health practitioners, and heavier economic costs for the health system. Regional and remote care providers in particular will have greater costs, and may be overwhelmed in attempts to implement new treatment targets. An excessively glucose-centric focus may divert attention and resources from identifying and addressing other important and growing contributors to adverse pregnancy outcomes, such as obesity. Important groups such as Aboriginal and Torres Strait Islander Australians may not gain overall benefit from lowering treatment targets for gestational diabetes because of current low birthweights and the effect of social costs. It has not yet been established whether implementing lower treatment targets for gestational diabetes will create more benefit than harm. Implementation at this stage is premature.

Extreme diabetic lipaemia associated with a novel lipoprotein lipase gene mutation.

Diabetic lipaemia, severe hypertriglyceridaemia associated with diabetic ketoacidosis, is a well recognised, but rare condition. Why this occurs in some patients and not others is unknown. We report a case of extreme lipaemia in a 20-year-old woman with type 1 diabetes who presented to hospital with diabetic ketoacidosis (DKA). At admission the patient's blood was grossly lipaemic and plasma lipid analyses showed triglyceride and cholesterol concentrations of 379 mmol/L and 52 mmol/L, respectively. She had no peripheral stigmata of chronic hyperlipidaemia and 1 year previously her plasma triglyceride and total cholesterol concentrations were 2.5 mmol/L and 4.4 mmol/L respectively. She was treated with insulin and the hypertriglyceridaemia resolved over several days. Because of the marked hypertriglyceridaemia, lipoprotein lipase (LPL) genetic testing was performed. Sequencing of the LPL gene revealed that she was heterozygous for the common S447X LPL variant and heterozygous for a novel missense mutation in exon five (I225N). Ile(225) is highly conserved among species and this mutation is predicted to impair function of the mature LPL protein. We conclude that heterozygosity for LPL mutations may predispose to transient severe hypertriglyceridaemia, when combined with insulin deficiency.