Hypoglycaemia in Clinical Diabetes

THE SOMOGYI PHENOMENON 91Probability of hypoglycaemic episodes in the night1.00.80.60.40.22 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21Morning blood glucose (mmol/I)Figure 4.3 Risk of nocturnal hypoglycaemia according to fasting morning blood glucose (95% Cl) in594 nights. Black bars = hypoglycaemic nights; shaded bars = possibly hypoglycaemic nights. Reproducedfrom Hoi-Hansen et al. (2005). With kind permission from Springer Science and Business MediaAlthough fasting glucose concentrations were frequently high in the patients they studied,this was related directly to a waning of circulating plasma insulin concentrations. Someinvestigators have demonstrated that when hypoglycaemia is experimentally-induced duringthe night, this can raise blood glucose on the following morning, even if circulating plasmainsulin concentrations are maintained (Perriello et al., 1988). However, the additional increasein the fasting blood glucose concentration is modest (around 2.0 mmol/l) and its clinicalrelevance is questionable. Other researchers have found no effect on daytime concentrationsof blood glucose after lowering blood glucose to hypoglycaemic levels during the night(Hirsch et al., 1990). Careful analysis of data collected both by self-monitoring of bloodglucose (Havlin and Cryer, 1987) and by continuous glucose monitoring (Hoi-Hansen et al.,2005) (Figure 4.3) during everyday activities, has also shown that nocturnal hypoglycaemiadoes not provoke rebound fasting hyperglycaemia.Many insulin-treated diabetic patients experience high fasting blood glucose levels butthis common clinical problem is essentially a consequence of inadequate basal insulinreplacement overnight. The important mechanisms that contribute to fasting hyperglycaemiaappear to be a combination of waning plasma insulin levels and glucose release fromthe liver secondary to nocturnal spikes of growth hormone secretion (Campbell et al.,1985), a physiological process termed the ‘dawn phenomenon’. High blood glucose levelsfollowing symptomatic nocturnal hypoglycaemia may also result from excessive intakeof oral carbohydrate, ingested as treatment of the hypoglycaemia, rather than a powerfulcounterregulatory response, which is usually suppressed at night. The clinical message istherefore clear: fasting hyperglycaemia indicates a need for adjusting basal insulin in termsof type or timing rather than reducing the dose. Some useful clinical steps to be undertakenin patients presenting with this problem are listed in Box 4.2.