Unusually rapid b-cell failure in a patient newly diagnosed with type 2 diabetes presenting acutely with unprovoked severe hyperglycaemic hyperosmolar state: a case report

Pancreatic b-cell failure on a background of insulin resistance results in the inability to compensate for fasting hyperglycaemia and eventually produces type 2 diabetes mellitus. We describe an interesting case of a patient who presented acutely with unprovoked severe hyperglycaemic hyperosmolar state and was subsequently diagnosed with type 2 diabetes mellitus on a background of only impaired first phase insulin secretion 4 months prior. Glucagon stimulation test detected significant b-cell failure necessitating long term exogenous insulin therapy which is highly unusual by virtue of the rapid apparent deterioration. Introduction Type 2 Diabetes Mellitus (T2DM) is undoubtedly the scourge of the developed world and a source of considerable socioeconomic burden [1]. It accounts for 90-95% of diabetes cases worldwide [2]. Although the exact aetiology of T2DM remains unknown, it involves a combination of insulin resistance and some degree of pre-existing b-cell secretory dysfunction conferring a state of relative rather than absolute insulin deficiency which progressively deteriorates with time irrespective of treatment [2-5]. Individuals at risk of developing overt T2DM, including the pre-diabetic states of impaired glucose tolerance (IGT) and impaired fasting glycaemia (IFG) already exhibit b-cell dysfunction and the weight of evidence suggests that this occurred long before the onset of pre-diabetes, when normal fasting glucose was still present [5,6]. Pancreatic b-cell compensation initially keeps glycaemia near normal despite underlying insulin resistance by increasing insulin secretion during the normoglycaemic and pre-diabetes stages [3-5]. The failure of b-cells to compensate at some point leads to development of overt T2DM [5,6]. This b-cell failure develops in a progressive fashion and continues after diagnosis, frequently resulting in secondary failure and exogenous insulin requirement [5,6]. It has not been reported <6 months from detection