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To test the hypothesis that nocturnal hypoglycemia causes fasting hyperglycemia (the Somogyi phenomenon) in patients with insulin-dependent diabetes mellitus, we studied 10 patients, who were on their usual therapeutic regimens, from 10 p.m. through 8 a.m. on three nights. On the first night, only a control procedure was performed (blood sampling only); on the second night, hypoglycemia was prevented (by intravenous glucose infusion, if necessary, to keep plasma glucose levels above 100 mg per deciliter [5.6 mmol per liter]); and on the third night, hypoglycemia was induced (by stepped intravenous insulin infusions between midnight and 4 a.m. to keep plasma glucose levels below 50 mg per deciliter [2.8 mmol per liter]). After nocturnal hypoglycemia was induced (36 +/- 2 mg per deciliter [2.0 +/- 0.1 mmol per liter] [mean +/- SE] from 2 to 4:30 a.m.), 8 a.m. plasma glucose concentrations (113 +/- 18 mg per deciliter [6.3 +/- 1.0 mmol per liter]) were not higher than values obtained after hypoglycemia was prevented (182 +/- 14 mg per deciliter [10.1 +/- 0.8 mmol per liter]) or those obtained after blood sampling only (149 +/- 20 mg per deciliter [8.3 +/- 1.1 mmol per liter]). Indeed, regression analysis of data obtained on the control night indicated that the 8 a.m. plasma glucose concentration was directly related to the nocturnal glucose nadir (r = 0.761, P = 0.011). None of the patients was awakened by hypoglycemia. Scores for symptoms of hypoglycemia, which were determined at 8 a.m., did not differ significantly among the three studies. We conclude that asymptomatic nocturnal hypoglycemia does not appear to cause clinically important fasting hyperglycemia in patients with insulin-dependent diabetes mellitus on their usual therapeutic regimens.
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PMID:Failure of nocturnal hypoglycemia to cause fasting hyperglycemia in patients with insulin-dependent diabetes mellitus. 331 53

We analyzed 216 overnight blood glucose profiles (samples at 2100, 0300, and 0700 h) in 75 consecutive patients with diabetes mellitus primarily to assess the impact of nocturnal hypoglycemia on morning hyperglycemia and secondarily to assess the frequency and magnitude of a night-to-morning increase in glucose levels in a clinical context. A dawn phenomenon (an 0300 to 0700 h increment in blood glucose) was rather uncommon in our patients (about one-third of profiles), was readily demonstrable in groups of patients only when nocturnal glucose levels were low (less than or equal to 50 mg/dl) or normal (51-100 mg/dl), and was generally not of great magnitude (mean 0700 h glucose levels of 114 mg/dl after 0300 h values of less than or equal to 100 mg/dl). Nocturnal hypoglycemia (0300 h blood glucose of less than or equal to 50 mg/dl, 7% of profiles) was followed by significant increments in blood glucose. However, the 0700 h glucose values averaged only 113 mg/dl and ranged up to only 172 mg/dl. Clearly, the magnitude of this Somogyi phenomenon was not great. Mean glucose levels were not higher at 1100, 1600, or 2100 h the day after nocturnal hypoglycemia than those at the same times the day before hypoglycemia. Thus, nocturnal hypoglycemia does not commonly result in major morning, or daytime, hyperglycemia in patients with diabetes mellitus sampled while using their usual therapeutic regimens.
Diabetes Care
PMID:Nocturnal hypoglycemia does not commonly result in major morning hyperglycemia in patients with diabetes mellitus. 358 75

Posthypoglycemic hyperglycemia (Somogyi phenomenon) occurs infrequently in insulin-treated diabetic patients. When it occurs it is often in children and adolescents, or patients with a short duration of diabetes. Marked hyperglycemia (greater than 220 mg/dL) after hypoglycemia results from a large meal to relieve the symptoms of hypoglycemia. Posthypoglycemic hyperglycemia correlates with falling plasma insulin levels, rather than increasing concentrations of counterregulatory hormones, whose secretion may be defective. Asymptomatic nocturnal hypoglycemia is common but subsequent fasting hyperglycemia is not necessarily the result of "rebound." More likely, fasting hyperglycemia is due to a falling predawn insulin level. Nocturnal hypoglycemia is dealt with by a readjustment in the timing and dose of insulin. The failure of the Somogyi phenomenon to occur puts insulin-dependent diabetic patients at increased risk to potential lethal consequences of nocturnal hypoglycemia.
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PMID:The Somogyi phenomenon. Sacred cow or bull? 637 Jan 62

To determine the roles of glucose counterregulation and the waning of insulin action in the development of posthypoglycemic hyperglycemia (the Somogyi phenomenon), we studied changes in plasma glucose and glucose turnover in five patients with insulin-dependent diabetes mellitus (IDDM) after subcutaneous injection of insulin under conditions in which hypoglycemic glucose counterregulation and the waning of insulin action were allowed to occur or were prevented. In control experiments, in which both glucose counterregulation and insulin waning were allowed to occur, plasma glucose levels decreased from 94 +/- 3 to 47 +/- 7 mg per deciliter and then increased to 289 +/- 20 mg per deciliter at 12 hours because of a marked increase in glucose production. When the waning of insulin action was prevented by insulin infusion, glucose production increased less (P less than 0.01), but marked rebound hyperglycemia still occurred (188 +/- 26 mg per deciliter at 12 hours). When both insulin waning and glucose counterregulation were prevented by infusion of both glucose and insulin, glucose production did not increase, and rebound hyperglycemia did not occur. We conclude that hypoglycemia can cause rebound hyperglycemia in the absence of insulin waning in patients with IDDM, and that this results primarily from an excessive increase in glucose production due to activation of glucose counterregulatory systems.
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PMID:Glucose counterregulation and waning of insulin in the Somogyi phenomenon (posthypoglycemic hyperglycemia). 638 83

Level of knowledge was tested in 137 volunteer registered nurses in three hospitals in the Midwest. A 34-item multiple choice Diabetes Knowledge Test (DKT) was developed by the first author (S.D.S.) working with a panel of expert nurse diabetes educators. Reliability using coefficient alpha was 0.61. Staff nurses obtained a mean score of 25.3, or 74% correct. Thirty-four nurses (25%) scored above 80% correct; 62 (45%) scored between 70% and 79% correct; and 41 (30%) scored below 70% correct. Higher-scoring nurses did well on items requiring use of exchange lists, but they missed items on physiologic actions of insulin, side effects of sulfonylureas, where insulin should be stored, and areas of the body suitable for injections of insulin. Nurses who scored below 60% on the test consistently missed items requiring use of exchange lists, effects of regular exercise and illness on blood glucose, and symptoms and causes of hypoglycemia and hyperglycemia. A strong trend (P = 0.055) was found for surgical nurses to score lower than medical unit nurses, and significant differences (P less than 0.05) were found among scores between hospitals. Staff nurses employed in a hospital where clinical specialists also were employed to teach diabetic patients had the lowest scores of the three hospitals. Test content subareas should be developed in the future to test knowledge reliably about urine testing, use of oral medications, home blood glucose monitoring, effects of exercise, and Somogyi phenomenon. A curriculum for regular inservice should be developed for nurses to assure a high level of knowledge for patient teaching with diabetes patients.
Diabetes Care
PMID:Registered nurses' knowledge about diabetes mellitus. 683 22

A major problem in replacing insulin in type I diabetes mellitus is that currently no depot preparation exists that is capable of mimicking the background insulin secretion of the healthy pancreas. Because all of the currently available intermediate- or long-acting insulin preparations have a peaked-action profile, excess insulin action at midnight and insulin waning at dawn occur whenever such an insulin preparation is given at supper time. If the target fasting plasma glucose is the ambitious near-normoglycemia of intensive insulin therapy, intermediate-acting insulin at suppertime easily results in hypoglycemia in the early evening hours and hyperglycemia in the fasting state. The problems of overnight glycemia in type I diabetes are further complicated by the dawn phenomenon and the Somogyi phenomenon. The dawn phenomenon is the combination of an initial decrease in insulin requirements between approximately 2400 and approximately 0300, followed by an increase in the insulin needs between approximately 0500 and approximately 0800. The dawn phenomenon is the result of changes in hepatic (and extrahepatic) insulin sensitivity, which are best attributed to nocturnal growth hormone secretion. The dawn phenomenon is a day-to-day reproducible event that occurs in nearly all diabetic patients. Its contribution to fasting hyperglycemia correlates with diabetes duration (inversely) and the HbA1c percentage (directly). Overall, it is estimated that the specific contribution of the dawn phenomenon to fasting hyperglycemia is approximately 2 mM (approximately 35 mg/dl), but it may be much greater because of the warning of the depot-insulin preparation injected the previous evening. The Somogyi phenomenon, strictly speaking, refers to fasting hyperglycemia that occurs after inducement of nocturnal hypoglycemia by regular insulin. Because the present therapeutic regimens of NPH/Lente insulin given at suppertime cause overnight hyperinsulinemia, excessive fasting hyperglycemia rarely follows nocturnal hypoglycemia, except when excessive glucose is ingested to correct hypoglycemia. However, nocturnal hypoglycemia may easily deteriorate glycemic control later in the day, because it induces prolonged posthypoglycemic insulin resistance, which results in postbreakfast and late-morning hyperglycemia. With nocturnal insulin therapy, it is important to consider the problems of insulin pharmacokinetics, the dawn phenomenon, and the Somogyi phenomenon to prevent both nocturnal hypoglycemia and excessive fasting hyperglycemia.(ABSTRACT TRUNCATED AT 400 WORDS)
Diabetes Care 1993 Dec
PMID:Nocturnal blood glucose control in type I diabetes mellitus. 829 80

The differential diagnosis of fasting hyperglycemia in type I diabetes includes the Somogyi effect, the dawn phenomenon, and insufficient insulin administration. To determine the causes of fasting hyperglycemia and their effect on subsequent daytime blood glucose control, the authors retrospectively reviewed blood glucose profiles of 126 patients with type I diabetes. The Somogyi effect accounted for 12.6% of all instances of fasting hyperglycemia, the dawn phenomenon, 24.1%, and poor control, 63.3%. Measurement of 3 AM and 5 AM blood glucose values is the key to making a correct diagnosis. Once a patient's fasting hyperglycemia is placed in one of these groups, appropriate treatment can be started.
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PMID:Fasting hyperglycemia in type I diabetes mellitus. 836 23

Suboptimal glycemic control in individuals with type 1 and type 2 diabetes mellitus is associated with an increased risk of microvascular and macrovascular complications. Even brief periods of hyperglycemia increase the risk of complications. Fasting hyperglycemia is a phenomenon that has been observed in essentially all individuals with diabetes and may be due to dysregulation of the normal circadian hormonal patterns resulting in increased hepatic glucose output. Controlling hepatic glucose output and disposal is essential for effectively managing fasting hyperglycemia. Fasting hyperglycemia generally can be attributed to inadequate or inappropriate hepatic insulinization or the dawn phenomenon (fasting hyperglycemia occurring in the absence of antecedent hypoglycemia). Less commonly, the Somogyi effect (marked fasting hyperglycemia following antecedent hypoglycemia) can cause fasting hyperglycemia. Accurate diagnosis with overnight home blood glucose monitoring is important in developing an appropriate treatment strategy. Manipulation of the individual's diet or oral agent therapy may be all that is required in some individuals to reduce fasting hyperglycemia. Hepatic glucose output and disposal in the fasting state may be controlled via bedtime administration of either an intermediate-acting insulin such as NPH or a long-acting true basal insulin such as insulin glargine. Attention to fasting hyperglycemia coupled with appropriate individualization of treatment should improve the long-term outcome of individuals with type 1 and type 2 diabetes by reducing the risk of complications. Normalization of the fasting blood glucose, through whatever strategy, minimizes glucotoxicity and insulin resistance, profoundly influences daytime glycemic control, and profoundly reduces the risk of the complications of diabetes.
Diabetes Technol Ther 2004 Aug
PMID:Fasting hyperglycemia: etiology, diagnosis, and treatment. 1532 Oct 11

Morning hyperglycaemia in diabetic subjects may be caused by the dawn phenomenon, or the Somogyi effect, or poor glycaemic control. The dawn phenomenon occurs when endogenous insulin secretion decreases or when the effect of the exogenous insulin administered to the patient the day before disappears, together with a physiological increase in insulin-antagonistic hormones. The Somogyi effect is present in the case of excessive amounts of exogenous insulin. The dawn phenomenon is more common than the Somogyi effect. To diagnose these phenomena, it is useful to measure plasma glucose levels for several nights between 3 a.m. and 5 a.m. or use a continuous glucose monitoring system. Although their treatment differs, the best way of preventing both the dawn phenomenon and the Somogyi effect is an optimal diabetes control with insulin therapy.
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PMID:The dawn phenomenon and the Somogyi effect - two phenomena of morning hyperglycaemia. 2171 14

In patients with diabetes receiving chronic haemodialysis, both very high and low glucose levels are associated with poor outcomes, including mortality. Conditions that are associated with an increased risk of hypoglycaemia in these patients include decreased gluconeogenesis in the remnant kidneys, deranged metabolic pathways, inadequate nutrition, decreased insulin clearance, glucose loss to the dialysate and diffusion of glucose into erythrocytes during haemodialysis. Haemodialysis-induced hypoglycaemia is common during treatments with glucose-free dialysate, which engenders a catabolic status similar to fasting; this state can also occur with 5.55 mmol/l glucose-containing dialysate. Haemodialysis-induced hypoglycaemia occurs more frequently in patients with diabetes than in those without. Insulin therapy and oral hypoglycaemic agents should, therefore, be used with caution in patients on dialysis. Several hours after completion of haemodialysis treatment a paradoxical rebound hyperglycaemia may occur via a similar mechanism as the Somogyi effect, together with insulin resistance. Appropriate glycaemic control tailored for patients on haemodialysis is needed to avoid haemodialysis-induced hypoglycaemia and other glycaemic disarrays. In this Review we summarize the pathophysiology and current management of glycaemic disarrays in patients on haemodialysis.
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PMID:Haemodialysis-induced hypoglycaemia and glycaemic disarrays. 2584 81


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