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Diabetes mellitus and hypoglycaemia: an overview


Essentials

  • 1

    Type I diabetes is characterized by pancreatic beta cell destruction with an absolute insulin deficiency, usually but not exclusively associated with autoimmune damage.

  • 2

    Type II diabetes results from a progressive insulin secretory deficiency on the background of insulin resistance.

  • 3

    Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS) are both life-threatening acute complications of diabetes mellitus.

  • 4

    The aim of excellent long-term blood sugar control is an HbA1c (glycated haemoglobin) level of less than 7.5% without frequent disabling hypoglycaemia for the prevention of microvascular disease, and 6.5% in those at increased risk of arterial disease.

  • 5

    Oral antidiabetic drug groups include the sulphonylureas, biguanide metformin, alpha-glucosidase inhibitor acarbose, the thiazolidinediones pioglitazone and rosiglitazone, and dipeptidyl peptidase 4 (DDP-4) inhibitors, such as sitagliptin.

  • 6

    Optimal blood sugar control aids in reducing the incidence of multisystem diabetic complications.

  • 7

    Hypoglycaemic coma requires immediate treatment with intravenous glucose. Intramuscular glucagon 0.5 to 2.0 mg may be used if liver glycogen stores are adequate, and can be given pre-hospital.

Diabetes Mellitus

Classification system and diagnostic criteria

The diagnosis and management guidelines for diabetes were revised in 2016 by the American Diabetes Association. The classification of type I and type II diabetes mellitus was retained, with the recommended criteria for the diagnosis of diabetes as a fasting plasma glucose of 7 mmol/L or greater (fasting is defined as no calorie intake for ≥8 hours), a random plasma glucose of over 11 mmol/L associated with polyuria, polydipsia and weight loss, or an HbA1 C (glycated haemoglobin) level of ≥6.5%. The oral glucose tolerance test is no longer routinely recommended.

Aetiology

The exact aetiology of diabetes is unclear. Type I diabetes is characterized by pancreatic beta cell destruction with an absolute insulin deficiency usually, but not exclusively, associated with autoimmune damage from a range of antibodies including islet cells (ICA), glutamic acid decarboxylase, insulin, tyrosine phosphatases and zinc transporter (ZnT8). Genetic and environmental factors are implicated, such as some human leucocyte antigen (HLA) types (most Caucasian patients are HLA-DR3 or DR4 or both), and abnormal immune responses, such as following viral infection. Certain genes are also implicated as co-contributors, particularly sites on chromosomes 6, 7, 11, 12, 14 and 18.

Type II diabetes is far more common, and results from a progressive insulin secretory deficiency on the background of insulin resistance. Genetic factors are implicated by strong familial aggregation of cases, and environmental factors in the context of genetic susceptibility, including obesity and diet. Populations with an increasing predisposition to type II diabetes encompass East Asians including China and the Western Pacific.

Although type I diabetes occurs most frequently among Caucasians throughout the world, diabetes in Australia is three times more common in the Aboriginal community. Other groups with a high prevalence include Pacific Islanders and Native Americans.

Diabetes secondary to other conditions

Diabetes mellitus may be secondary to conditions that damage the exocrine pancreas including chronic pancreatitis, carcinoma of the pancreas and pancreatectomy, haemochromatosis, cystic fibrosis, pregnancy (gestational) and endocrinopathies, such as Cushing syndrome, acromegaly, phaeochromocytoma and glucagonoma.

Drug-induced diabetic state

Certain drugs can impair glucose tolerance or cause overt diabetes mellitus. These include glucocorticoids, the oral contraceptive pill, thiazide diuretics at higher doses, clozapine, tacrolimus, sirolimus and ciclosporin, pentamadine (which may also cause severe hypoglycaemia) and HIV protease inhibitors.

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