The Somogyi Phenomenon The Concept Of Rebound Hyperglycaemia

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In the late 1930s, a Hungarian biochemist, Michael Somogyi, working in St Louis, USA, suggested that nocturnal hypoglycaemia might provoke rebound hyperglycaemia on the following morning, and he supported his hypothesis with a demonstration that reducing evening doses of insulin led to a reduction in fasting urinary glycosuria (Somogyi, 1959). He proposed that nocturnal hypoglycaemia provokes a counterregulatory response with rises in plasma epinephrine, cortisol and growth hormone resulting in the release of glucose from the liver and inhibition of the effects of insulin over the next few hours. The logical conclusion from his hypothesis was that this 'rebound' elevated fasting blood glucose in the morning should be treated, not by an increase in the evening dose of insulin, but paradoxically by a reduction. The idea of 'rebound hyperglycaemia' following nocturnal hypoglycaemia, (also known as the Somogyi phenomenon) as an explanation for a high fasting blood glucose in insulin-treated patients, has proved to be very attractive to many diabetes healthcare professionals who firmly believe in its existence. The consequences are important as patients are often advised to reduce their evening insulin dose, particularly if they complain of nocturnal hypoglycaemia. However, its clinical relevance was challenged over 20 years ago and repeated studies have established that fasting hyperglycaemia is largely a result of falling plasma insulin concentrations during the night, as the subcutaneous depot of insulin that was injected the day before is dissipated.

Gale et al. (1980) demonstrated that periods of hypoglycaemia during the night were often prolonged and were not accompanied by a large rise in counterregulatory hormones.

Rebound Hyperglycaemia

7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 Morning blood glucose (mmol/I)

Figure 4.3 Risk of nocturnal hypoglycaemia according to fasting morning blood glucose (95% Cl) in 594 nights. Black bars = hypoglycaemic nights; shaded bars = possibly hypoglycaemic nights. Reproduced from Hoi-Hansen et al. (2005). With kind permission from Springer Science and Business Media

7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 Morning blood glucose (mmol/I)

Figure 4.3 Risk of nocturnal hypoglycaemia according to fasting morning blood glucose (95% Cl) in 594 nights. Black bars = hypoglycaemic nights; shaded bars = possibly hypoglycaemic nights. Reproduced from Hoi-Hansen et al. (2005). With kind permission from Springer Science and Business Media

Although fasting glucose concentrations were frequently high in the patients they studied, this was related directly to a waning of circulating plasma insulin concentrations. Some investigators have demonstrated that when hypoglycaemia is experimentally-induced during the night, this can raise blood glucose on the following morning, even if circulating plasma insulin concentrations are maintained (Perriello et al., 1988). However, the additional increase in the fasting blood glucose concentration is modest (around 2.0mmol/l) and its clinical relevance is questionable. Other researchers have found no effect on daytime concentrations of 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 blood glucose (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 hypoglycaemia does not provoke rebound fasting hyperglycaemia.

Many insulin-treated diabetic patients experience high fasting blood glucose levels but this common clinical problem is essentially a consequence of inadequate basal insulin replacement overnight. The important mechanisms that contribute to fasting hyperglycaemia appear to be a combination of waning plasma insulin levels and glucose release from the liver secondary to nocturnal spikes of growth hormone secretion (Campbell et al., 1985), a physiological process termed the 'dawn phenomenon'. High blood glucose levels following symptomatic nocturnal hypoglycaemia may also result from excessive intake of oral carbohydrate, ingested as treatment of the hypoglycaemia, rather than a powerful counterregulatory response, which is usually suppressed at night. The clinical message is therefore clear: fasting hyperglycaemia indicates a need for adjusting basal insulin in terms of type or timing rather than reducing the dose. Some useful clinical steps to be undertaken in patients presenting with this problem are listed in Box 4.2.

Box 4.2 Clinical approach to high fasting blood glucose complicated by nocturnal hypoglycaemia

1. Measure blood glucose at 2-3 a.m. over a few days.

2. If nocturnal hypoglycaemia is present, ensure that basal insulin is taken at bedtime (i.e., split pre-mixed evening insulin).

3. Progressively increase bedtime long-acting insulin in doses of 2-4 units while checking with 3 a.m. blood glucose measurements that this is not precipitating nocturnal hypoglycaemia

4. Use a long-acting insulin analogue, either glargine or detemir.

5. Teach patients to take an appropriate (but not excessive) quantity of a high energy glucose drink, orange juice or glucose as sweets or tablets to treat nocturnal hypo-glycaemic episodes.

6. When available, consider obtaining a continuous glucose monitoring profile.

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