Background:

CF patients with exocrine pancreatic insufficiency (PI) have less alpha, beta and pancreatic polypeptide cell function than sufficient patients.

Prevalence of non-diabetic hypoglycaemia (hypo) in adults with cystic fibrosis (CF), have been observed as 7-15%. No significant association between hypo and development of CF-related diabetes has been found to date.

Aim:

Review prevalence and characteristics of hypoglycaemia, in non-diabetic adults with cystic fibrosis.

Method:

A retrospective audit was performed (2013) including pre transplant CF adults >18 years (n=275), excluding diabetic / impaired glucose tolerant patients (n=84). Audit group n=191.

Hypoglycaemic patients (plasma glucose < 3.9mmol/l), were compared with normal glucose tolerant (NGT) controls.

Additional characteristics were summarised.

Results:

Results indicate prevalence of non-diabetic hypoglycaemia: 28/275 patients (10.2 %). No differences were identified between hypo and NGT control groups for age, gender, genotype, liver disease and lung function.

Mean BMI was significantly less in hypo group (21.96 kg/m2 sd3.01) compared to controls (24.04 sd 4.63) (p=0.023). The hypo group had significantly higher pancreatic insufficiency (p<0.001).

Characteristics of the hypo group: mean onset 21.75years (sd7.09), mean length of diagnosis 5.46years (sd4.56), 89% symptomatic adrenergic reactions, 11% asymptomatic.

Most common hypo triggers: fasting/insufficient carbohydrates or delayed meal (61%).

The majority of prevention strategies received by patients was inclusion of regular low glycaemic index (GI) carbohydrates and higher protein items (75%).

Conclusion:

This audit identified 10.2 % prevalence of non-diabetic hypoglycaemia.

The hypo group had significantly lower mean BMI and higher rate of pancreatic insufficiency. This may be due to lack of gluconeogenic reserves (lower BMI) and/or pancreatic dysfunction in hypoglycaemic pathophysiology. The majority of hypo patients reported symptomatic adrenergic reactions, the biggest trigger was fasting /insufficient carbohydrate or meal delay. The major prevention strategy in patient education was inclusion of regular low GI carbohydrate/high protein meals and snacks. Further studies are required.