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An Urban Experience
WSVA7-0464
INTERNAL MEDICINE II
THE MYTH OF THE SOMOGYI & HOW I ADJUST INSULIN
J. Rand1,2, K. Roomp3,
L.C.f.S.B.E. University of Luxembourg3
1School of Veterinary Science, University of Queensland, Queensland, Australia
2Australian Pet Welfare Foundation, Brisbane, Australia
The Myth of the Somogyi & How I Adjust Insulin Authors: Jacquie Rand and Kirsten Roomp
Many clinicians believe that the Somogyi effect or rebound hyperglycemia following hypoglycaemia commonly occurs in diabetic cats treated with insulin, but there is only one study of 6 cats from 1986 purportedly documenting this. In contrast, numerous studies in human diabetic patients over the last quarter century have rejected the common occurrence of the Somogyi phenomenon. Most such cases in humans are now thought to be associated with inadequate duration of insulin action in the early morning. In some patients, an early morning surge of growth hormone, termed the “dawn phenomena”, resulting in insulin resistance was thought to exacerbate the hyperglycaemia. However, human patients with apparent rebound hyperglycemia were found not to have higher levels of growth hormone, cortisol, or glucagon than those who had little or no rebound hyperglycemia. A close inverse correlation
was found between blood glucose and free insulin concentrations. Therefore, it was concluded that hyperglycemia, when present, was more likely to be due to relative insulin de ciency in the latter part of the night than a response to antagonist hormones. Similarly, a study in human diabetic patients using continuous blood glucose measurements found that mean morning blood glucose concentrations after hypoglycemic nights were lower than after nights without hypoglycemia, indicating that nocturnal hypoglycemia did not subsequently
cause hyperglycemia. Another study investigating the association between preceding nocturnal hypoglycemia and daytime hyperglycemia, found that nocturnal hypoglycemia did not appear to cause clinically important daytime hyperglycemia. Daytime plasma glucose concentrations were unrelated to peak nocturnal plasma glucagon, epinephrine, norepinephrine, growth hormone, or cortisol concentrations. Therefore, most apparent cases of rebound hyperglycemia in humans are now thought to be associated with inadequate duration of insulin action in the early morning, unrelated to any preceding nocturnal hypoglycemia.
Despite these  ndings in humans, many clinicians
treating diabetic cats make insulin dose adjustments believing that the Somogyi effect is contributing to hyperglycaemia. They subsequently reduce insulin
dose even when there is no evidence of preceding hypoglycaemia. In the case series of cats reported to have the Somogyi effect, all cats were treated with
once daily with NPH or PZI (Protamine zinc insulin). These cats has insulin-induced hypoglycemia (<70 mg/dL (<3.9 mmol/L) within 4 to 8 hours, followed
by hyperglycemia for up to 24 hours after injection. However, a number of other explanations other than
the Somogyi effect account for this blood glucose pattern and the observed improvement following changes to the cats’ management. NPH typically has
its nadir four hours after insulin injection, and after 7-8 hours there is little exogenous insulin action, and blood glucose concentrations are often at pre-insulin injection values. Resolution of the rebound pattern in 5/6 cats is consistent with  ndings in humans that hyperglycemia after resolution of hypoglycemia re ects inadequate insulin concentration to adequately control blood glucose concentration. Cats improved after they were changed to insulin dosing protocols expected to give more sustained glucose lowering effect. Use of intermediate-acting insulin and/or once daily insulin dosing likely resulted in inadequate duration of insulin action to control blood glucose concentrations after the hypoglycemic nadir.
Supporting the  ndings in humans that the Somogyi effect is rare, a study of 55 cats under intensive blood glucose control with glargine found that blood glucose curves which were consistent with insulin-induced rebound hyperglycemia were very rare, despite the frequent occurrence of biochemical hypoglycemia. Rebound hyperglycemia associated with persistent marked insulin resistance was extremely rare in glargine- treated cats, with less than 4 events in 10,000 daily blood glucose curves. Rebound hyperglycemia without persistent insulin resistance was more common, occurring in 25% of cats, albeit infrequently, and in affected cats is evident in less than one in 50 daily
blood glucose curves. Overall, rebound hyperglycemia without insulin resistance occurred in less than one in 200 daily curves. Further investigation of the cause of marked morning hyperglycemia in diabetic cats treated with glargine is indicated to determine if inadequate duration of insulin and/or a growth hormone surge is the underlying cause.
Clinicians managing diabetic cats treated with lente
and exhibiting marked morning hyperglycemia or insulin resistance should either swap to a longer-acting insulin or increase frequency of insulin dosing. Continuous glucose monitoring is one method of determining if hypoglycemia is preceding hyperglycemia. However, continuous glucose
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42ND WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND FECAVA 23RD EUROCONGRESS


































































































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