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PubMed1999

Drug-induced hypoglycemic coma in 102 diabetic patients.

BACKGROUND: Hypoglycemic coma is a continuous threat for diabetic patients treated with insulin and/or oral hypoglycemic agents; it may be associated with substantial morbidity and mortality. METHODS: We retrospectively reviewed our clinical experience with drug-induced hypoglycemic coma during a 7-year period. RESULTS: The study consisted of 102 patients and included 61 females and 41 males. The median age was 72 years. Ninety-two patients suffered from type 2 diabetes mellitus; 10 patients had type 1 diabetes mellitus. The median lowest blood glucose level was 1.77 mmol/L (32 mg/dL). Drug-induced hypoglycemic coma occurred in 99 patients out of the hospital, while 3 patients developed it during hospitalization. Drug-induced hypoglycemic coma occurred in patients undergoing treatment with insulin, glyburide, and combined therapy with insulin and glyburide, insulin and metformin, or glyburide and metformin. Ninety-three patients had at least 1 of the following risk factors: age older than 60 years, renal dysfunction, decreased intake of energy, and infection. Fourteen patients concomitantly received drugs that potentiated hypoglycemia. Forty patients responded to treatment within the first 12 hours, while 62 patients had protracted hypoglycemia of 12 to 72 hours' duration. Morbidity included physical injuries in 7 patients, myocardial ischemia in 2 patients, and stroke in 1 patient. Death occurred in 5 patients. CONCLUSIONS: Hypoglycemic coma is a serious and not an uncommon problem among elderly patients with diabetes mellitus and treated with insulin and/or oral hypoglycemic drugs. Risk factors contribute substantially to the morbidity and mortality of patients with drug-induced hypoglycemic coma. Enhanced therapeutic monitoring may be warranted when hypoglycemic drugs are administered to an elderly patient with the above predisposing factors and potentiating drugs for hypoglycemia.

Adolescent↗

PubMed1997

Oral sulfonylurea hypoglycemic agents prevent ischemic preconditioning in human myocardium. Two paradoxes revisited.

BACKGROUND: Patients receiving oral hypoglycemic agents for diabetes mellitus are at increased risk of cardiovascular mortality. Oral hypoglycemic agents are inhibitors of the ATP-sensitive potassium (KATP) channel. Ischemic preconditioning is mediated by KATP channel activation. We therefore hypothesized that myocardium from patients taking long-term oral hypoglycemic agents would be resistant to the protection by ischemic preconditioning. METHODS AND RESULTS: Isolated human right atrial trabeculae were suspended in an organ bath at 37 degrees C, with field stimulation at 1 Hz. Control trabeculae were then subjected to 45 minutes of simulated ischemia (hypoxic, glucose-free buffer with pacing at 3 Hz) and 120 minutes of reperfusion. Ischemic preconditioned (IPC) trabeculae from patients without oral hypoglycemic therapy and from patients taking insulin (Ins+IPC) were given 5 minutes of simulated ischemia before this injury. Trabeculae (Oral Hypo+IPC) were obtained from patients taking long-term oral hypoglycemic agents and were also exposed to 5 minutes of simulated ischemia before this injury. Developed force (DF) was recorded. Recovery of DF relative to preischemic values was 28 +/- 4% in control trabeculae, whereas IPC trabeculae showed 52 +/- 5% recovery (P < .05 versus control). In patients receiving long-term oral hypoglycemic agents (Oral Hypo+IPC), recovery of DF was 27 +/- 3%, but in trabeculae from insulin-treated patients (Ins+IPC), it was 45 +/- 6%. CONCLUSIONS: Human myocardium from patients without long-term exposure to oral hypoglycemic agents is functionally protected by preconditioning. Long-term oral hypoglycemic intake blocks the protection by preconditioning. These data suggest that ischemic preconditioning in human myocardium relies on KATP channels, and long-term inhibition of KATP channels with oral hypoglycemic agents may explain the excess cardiovascular mortality in these patients.

Administration, Oral↗

PubMed1998

Influence of hypoglycemic coma on brain water and osmolality.

To study the effects of pronounced hypoglycemia on brain osmolality and brain edema formation, fasted rats were rendered hypoglycemic by injection of insulin, and subjected to 30 min of hypoglycemic coma. Recovery was accomplished by glucose administration. The change in water content in different brain regions was measured as a change in specific gravity after 30 min of hypoglycemic coma, or 30, 60, and 180 min after glucose administration. Plasma and brain tissue osmolality were measured in separate animals. The results show a significant decrease in specific gravity (increase in water content) in all structures measured (caudoputamen, neocortex, hippocampus, and cerebellum) at the end of the period of coma, as well as after 30 min and 60 min of recovery. At 180 min of recovery, brain water was normalized. The edema affected all structures to the same degree regardless of their vulnerability to hypoglycemic damage. Brain tissue osmolality showed a tendency to decrease with decreasing tissue glucose content. The decrease was significant (P<0.01) at 30 min of isoelectric coma. In the recovery phase, normal brain osmolality was restored within 30 min. Measurements of blood-brain barrier (BBB) permeability after 30 min of hypoglycemic coma showed no extravasation of Evan's blue, though a small but significant increase in the permeability for aminoisobutyric acid (AIB) in caudoputamen and in cerebellum was found. To analyze the importance of tissue acidosis for formation of edema, hypoglycemic animals were made acidotic by increasing the CO2 concentration in inspired air to produce an arterial plasma pH of 6.8-6.9. In these animals the edema was of a similar degree to the normocapnic animals, and the permeability for AIB was normal. We conclude that osmolytic mechanisms are not the primary cause of the selective neuronal vulnerability in hypoglycemic coma. Furthermore, the BBB is largely intact during a hypoglycemic insult.

Acidosis↗

PubMed2005

Involvement of serotonin in the hypoglycemic response to 2 Hz electroacupuncture of zusanli acupoint (ST36) in rats.

In our previous studies, an insulin-dependent hypoglycemic effect produced by electroacupuncture (EA) was shown to be mediated by endogenous opioid peptides (EOP). In the present study, we applied 2 Hz EA to both zusanli acupoints (ST36) in the test group for 30 min, and to a nonacupoint area in the control group for 30 min to compare the acupoint specific character in the hypoglycemic effect of EA. Assays of plasma beta-endorphin and insulin levels were performed by ELISA kits. The insulin-dependent mechanism of the hypoglycemic effect was also investigated in streptozotocin (STZ)-induced diabetic rats. The mediation of EOP and the role of mu-opioid receptor were examined by naloxone and mu-opioid receptor knockout mice (MOR-KOM). The serotonin depletion was carried out by injecting (i.p.) p-chlorophenylalanine (PCPA); two low doses of serotonin were also injected (i.v.) to analyze the direct effect on plasma glucose levels. The hypoglycemic effect of EA was much greater in rats stimulated at ST36 than in rats receiving the same stimulation at the nonacupoint area. The plasma levels of insulin and beta-endorphin were also significantly elevated after stimulation of both zusanli acupoints, but remained unchanged following stimulation at the nonacupoint area. There was no sharp hypoglycemic response to 2 Hz EA at zusanli acupoint of STZ-induced diabetic rats. However, the hypoglycemic effect of this EA was not totally blocked by the sufficient dose of naloxone (1 mg/kg, i.v.). Additionally, 2 Hz EA at ST36 also showed a sharp decrease in plasma glucose levels of MOR-KOM. Pretreatment with PCPA did not reproduce hypoglycemic response to 2 Hz EA in naloxone-treated rats and MOR-KOM mice. Furthermore, injection of serotonin decreased the plasma glucose levels significantly. Therefore, we suggest that serotonin also involved in the hypoglycemic action of 2 Hz EA at both zusanli acupoints of normal rats.

Acupuncture Points↗

PubMed2003

Laboratory evaluation of the hypoglycemic effect of Anacardium occidentale Linn (Anacardiaceae) stem-bark extracts in rats.

This study evaluated the hypoglycemic effect of stem-bark extracts of Anacardium occidentale Linn., of the Anacardiaceae family, in normal (normoglycemic) and in streptozotocin-treated diabetic rats. Young adult, male Wistar rats weighing 250-300 g were used. Diabetes mellitus was induced in the test rats by intraperitoneal injections of streptozotocin (STZ, 90 mg/kg). In one set of experiments, graded doses of the aqueous and methanolic stem-bark extracts of A. occidentale (100-800 mg/kg p.o.) were separately administered to groups of fasted normal and fasted diabetic rats. In another set of experiments, 800 mg/kg p.o. of the aqueous or methanolic extract of the plant, a dose which produced maximal hypoglycemic effects in both fasted normal and diabetic rats in the previous set of experiments, were used. The hypoglycemic effects of single doses (i.e., 800 mg/kg p.o.) of A. occidentale stem-bark aqueous and methanolic extracts were compared with those of insulin (5 microU/kg s.c.) and glibenclamide (0.2 mg/kg p.o.) in both fasted normal and fasted diabetic rats. Following acute treatment, relatively moderate-to-high doses of A. occidentale stem-bark extracts (100-800 mg/kg p.o.) produced dose-dependent, significant reductions (p< 0.05-0.001) in the blood glucose concentrations of both fasted normal and fasted diabetic rats. On their own, both insulin (5 microU/kg s.c.) and glibenclamide (0.2 mg/kg p.o.) produced significant reductions (p< 0.01-0.001) in the blood glucose concentrations of the fasted normal and fasted diabetic rats. At single doses of 800 mg/kg p.o., A. occidentale stem-bark aqueous and methanolic extracts significantly reduced (p< 0.001) the mean basal blood glucose concentrations of fasted normal and fasted diabetic rats. The hypoglycemic effect of the methanolic plant extract was found to be slightly more pronounced than that of the aqueous plant extract in both the normal and diabetic rats examined. A. occidentale contains a diverse group of chemical compounds. Since methanol extractives of plants usually contain many chemical compounds, each of which is capable of producing definite biological activities via different mechanisms, it is difficult to draw any logical conclusion on the mechanism of the hypoglycemic effect of such a diverse mixture of chemical compounds contained in the plant extracts used in this study. While it is possible that the hypoglycemic effects of the plant extracts may be due, at least in part, to their terpenoid and/or coumarin contents, the mechanism of their hypoglycemic action remains largely speculative. However, this is unlikely to be due to the stimulation of pancreatic beta-cells and subsequent secretion of insulin. Although A. occidentale stem-bark aqueous or methanolic extract is less potent than insulin as an antidiabetic agent, the results of this experimental animal study indicate that it possesses hypoglycemic activity, and thus lends credence to the folkloric use of the plant in the management and/or control of adult-onset, type-2 diabetes mellitus among the Yoruba-speaking people of Western Nigeria.

Anacardium↗

PubMed1991

Increasing incidence of hypoglycemic coma in children with IDDM.

OBJECTIVE: To examine the incidence of hypoglycemic coma in children with insulin-dependent diabetes mellitus (IDDM) over 8 yr from 1981 to 1988 and to investigate the importance of residual beta-cell function of HbA1 levels and other variables as risk factors for hypoglycemic coma. RESEARCH DESIGN AND METHODS: The study consisted of 155 children with IDDM aged less than 16 yr at study entry. Mean age at onset of diabetes was 7.9 yr (range 1.1-15.6 yr). We made a prospective assessment of hypoglycemic coma episodes, with a standardized questionnaire, over a total observation time of 816.6 person-yr. Three monthly clinical and laboratory examinations, which included determinations of C-peptide and HbA1 levels, were conducted. We compared children with hypoglycemic coma (cases) with children without hypoglycemic coma (controls) in a case-control analysis matched for diabetes duration. Yearly incidence of hypoglycemic coma, calculated as the number of subjects having an attack in 1 yr divided by the cumulative number of person-years for that year, was measured. Univariate and multivariate odds ratios were calculated from logistic regression. RESULTS: Over the first 4 yr, the average yearly incidence was 4.4/100 person-yr compared with 7.4/100 person-yr during the later 4 yr (P less than 0.0001). This tendency was accompanied by intensification of insulin treatment with an increase in the mean number of daily injections and a decrease in mean HbA1 levels. In the case-control analysis, absent residual beta-cell function was the most important risk factor for hypoglycemic coma (adjusted odds ratio 7.8, 95% confidence intervals 2.0-31.2), followed by near-normal HbA1 levels (adjusted odds ratio 4.5, 95% confidence intervals 1.9-10.5). CONCLUSIONS: In this group of children, improvement of glycemic control apparently led to an increase in the incidence of severe hypoglycemia. In children with recurrent hypoglycemic coma and undetectable C-peptide levels, it may be safer to aim for somewhat less tight glycemic control.

Adolescent↗

PubMed1998

Previous episodes of hypoglycemic coma are not associated with permanent cognitive brain dysfunction in IDDM patients on intensive insulin treatment.

Intensive insulin treatment of IDDM is associated with increased frequency of hypoglycemic coma. The extent of possible cerebral sequelae after recovery is still unknown. We studied the impact of previous hypoglycemic coma on neurophysiological measures of cognitive brain function in 108 patients with adult-onset IDDM receiving intensive insulin treatment. In the study, 55 IDDM patients (age 38 +/- 14 years, mean +/- SD) who had a history of > or =1 (median 3, range 1-35) comatose hypoglycemic event were compared with 53 IDDM patients (age 34 +/- 12 years) with no history of hypoglycemic events using P300 event-related potentials and psychometric tests (the Mini-Mental State Exam and trailmaking test, part A). Findings on these patients were compared with those from 108 matched healthy control subjects. No difference was observed in P300 latencies and psychometric tests between patients with and without a history of hypoglycemic coma (P300 latency, 346 vs. 342 ms; trailmaking test, 31 vs. 30 s; Mini-Mental State Exam, 29.5 vs. 29.6; NS). In diabetic patients, however, P300 latencies were delayed compared with those of healthy control subjects (344 vs. 332 ms; P < 0.001) and were correlated to diabetes duration but not to total hypoglycemic episodes. Scores on the Mini-Mental State Exam (29.5 vs. 29.6; P = 0.59) and trailmaking test (31 vs. 28 s; P = 0.10) were not different between patients and control subjects. In conclusion, previous episodes of hypoglycemic coma are not associated with permanent impairment of cognitive brain function in patients with adult-onset IDDM receiving intensive insulin treatment compared with patients without such episodes. Cognitive brain function, however, is subclinically impaired in relation to duration of diabetes.

Adult↗

PubMed1986

Effects of new hypoglycemic agent 2-piperazinyl-4-methyl-amino-5-methylthieno [2,3-d]pyrimidine dihydrochloride hydrate.

The antidiabetic effects of 2-piperazinyl-4-methylamino-5-methylthieno [2,3-d]pyrimidine dihydrochloride hydrate (Compound-(I] were investigated in various animals and in various conditions. Compound-(I) is a new hypoglycemic agent structurally unrelated to sulfonylurea and biguanide. It produced dose dependent hypoglycemic effects (10-100 mg/kg) in rats and mice under fed, fasted and glucose tolerated states. However, it was ineffective in fasted guinea pigs even when given at 100 mg/kg. In normal fed rats and mice, hypoglycemic effects of Compound-(I) were estimated to be 3-19 times and 12-70 times more potent than tolbutamide and phenformin, respectively. Compound-(I) also produced hypoglycemic action in streptozocin diabetic rats and genetically diabetic KK mice. Especially, its hypoglycemic effect was observed at the dose as low as 3 mg/kg p.o. in KK mice. However, elevation of blood lactate was accompanied by lowering of blood glucose after oral administration of Compound-(I) in normal rats and mice and in streptozocin diabetic rats, while these effects were not observed in guinea pigs. In addition, plasma insulin significantly increased after administration of Compound-(I) in both normal and KK mice, while this increase in plasma insulin was not so prominent in fed rats. This elevation in plasma insulin might be produced by alpha 2-adrenergic antagonism at pancreatic B cell as Compound-(I) suppressed epinephrine induced hyperglycemia by elevating plasma insulin. In conclusion, Compound-(I) seems mainly to produce hypoglycemic action through extrapancreatic mechanism which increases blood lactate associated with anaerobic glycolysis or inhibition of gluconeogenesis. In addition, elevation of plasma insulin also might be responsible for hypoglycemic effects.

Adrenergic alpha-Antagonists↗

PubMed1995

Characterization of the hypoglycemic effects of Trigonella foenum graecum seed.

The whole powder of Trigonella foenum graecum seeds and its extracts were tested for their hypoglycemic effect on normal and diabetic model rats. The powder, its methanol extract, and the residue remaining after methanol extraction had significant hypoglycemic effects when fed simultaneously with glucose. The water extract of the methanol extractive-free residue of the seed powder showed significant hypoglycemic activity at different prandial states. The Soluble Dietary Fibre (SDF) fraction showed no effect on the fasting blood glucose levels of nondiabetic or NIDDM model rats. However, when fed simultaneously with glucose, it showed a significant hypoglycemic effect (p < 0.05) in NIDDM model rats. Chemical analysis showed that the major constituent of the SDF is a galactomannan. The results confirm the involvement of SDF in the hypoglycemic effect of T. foenum graecum seeds. However, compound(s) other than SDF is (are) also involved in the hypoglycemic activity.

Animals↗

PubMed2006

Hypoglycemic effects of multiflorine derivatives in normal mice.

(-)-Multiflorine isolated from leguminous plants produces a hypoglycemic effect when administered to mice with streptozotocin-induced diabetes. (-)-Multiflorine has an enaminone-type conjugation on the A ring, which is unusual in lupine alkaloids. Proceeding on the assumption that the A-B ring is responsible for the hypoglycemic effect, several compounds bearing the quinolizidin-2-one ring system were synthesized, and their hypoglycemic effects were examined. In addition, tricyclic compounds bearing 4-pyridone were synthesized, and their hypoglycemic effects were examined. The hypoglycemic effect of a 4-pyridone-type compound was similar to that of (-)-multiflorine as measured by oral glucose tolerance testing in normal mice. No hypoglycemic effect of a 4-piperidone-type compound was observed. These results indicate that compounds possessing double bond(s) in the A ring of multiflorine may be lead compounds for a new type of diabetes drug.

Alkaloids↗

PubMed2003

Hypoglycemic effect of Hypoxis hemerocallidea corm (African potato) aqueous extract in rats.

Diabetes mellitus has been recognized as a clinical syndrome since ancient times, and remains a crippling global health problem today. It is a group of heterogeneous, autoimmune, hormonal and metabolic disorders, often accompanied by hypertension, hyperlipidemia and obesity. Current estimates suggest that approximately 150 million people worldwide suffer from diabetes mellitus. The present study was undertaken to examine the hypoglycemic effect of aqueous extract of Hypoxis hemerocallidea (family: Hypoxidaceae) corm (locally known as "African Potato") in normal (normoglycemic) and in streptozotocin (STZ)-treated, diabetic rats. Young adult, male Wistar rats weighing 250-300 g were used. Diabetes mellitus was induced in the group of diabetic test rats by intraperitoneal injections of STZ (90 mg/kg). In one set of experiments, graded doses of the aqueous extract of African Potato (100-800 mg/kg p.o.) were administered to 12-h fasted normal and diabetic rats. In another set of experiments, 800 mg/kg of African potato extract, a dose of the plant extract that produced maximal hypoglycemic effects in fasted normal and diabetic rats in our pilot experiments, was used. The hypoglycemic effect of this single dose was compared with those of insulin (5 micro U/kg s.c.) and glibenclamide (5 mg/kg p.o.) in 12-h fasted normal and diabetic rats. Following acute treatment, relatively moderate to high doses of African potato extract (100-800 mg/kg p.o.) produced dose-dependent, significant reductions (p < 0.05-0.001) in the blood glucose concentrations of fasted normal and diabetic rats. Similarly, insulin (5 micro U/kg s. c.) and glibenclamide (5 mg/kg p.o.) produced significant reductions (p < 0.01-0.001) in the blood glucose concentrations of the fasted normal and diabetic rats. At a dose of 800 mg/kg, the plant extract caused 30.20% and 48.54% reductions in the blood glucose concentrations of fasted normal and STZ-treated diabetic rats, respectively. While it is likely that the hypoglycemic effect of the plant extract is largely due to its phytosterols and/or sterolin content, the exact mechanism of its hypoglycemic action is still obscure and will have to await further studies. However, the results of this experimental animal study indicate that African potato possesses hypoglycemic activity; and thus lends credence to the suggested folkloric use of the herb in the control and/or management of adult-onset, type 2 diabetes mellitus in some communities of South Africa.

Administration, Oral↗

PubMed2006

Hypoglycemic events and glycosylated hemoglobin values in patients with type 2 diabetes mellitus newly initiated on insulin glargine or premixed insulin combination products.

PURPOSE: Rates of hypoglycemic events and their associated costs were compared among patients with type 2 diabetes mellitus newly initiated on insulin glargine or a premixed insulin fixed-combination product. METHODS: Patients newly initiated on insulin glargine or premixed insulin fixed-combination products (including pen delivery systems) between June 1, 2001, and February 29, 2004, were identified using an administrative claims database. Hypoglycemic events were identified from International Classification of Diseases, 9th Revision, Clinical Modification codes. Multivariate analyses were performed. RESULTS: A total of 2315 patients met the inclusion criteria. Of those, 1212 received insulin glargine and 1103 received a premixed fixed-combination insulin product. The mean +/- S.D. treatment duration was 13.7 +/- 8.1 months. Patients treated with premixed insulin had a higher hypoglycemic event rate than glargine patients (13.8 versus 7.0/100 patients/year; p = 0.027), which yielded a number needed to treat of 15 patients. The mean cost per hypoglycemic event was $1049 (95% confidence interval, $426-1672). The mean annual cost of all insulin use was $46 more for the insulin glargine cohort than for those who received premixed insulin ($534 versus $488, respectively) (p < 0.05). Mean postindex insulin use was higher in patients receiving premixed insulin than in those treated with insulin glargine (48.1 versus 43.8 units per day) (p < 0.05). CONCLUSION: Patients with type 2 diabetes mellitus who were newly initiated on insulin glargine had a lower rate of hypoglycemic events compared with patients newly initiated on a premixed fixed-combination insulin product. Treatment of 15 patients with insulin glargine instead of premixed insulin for one year would avoid one hypoglycemic event per year.

Adult↗

PubMed1989

Symptomatic hypoglycemia in NIDDM patients treated with oral hypoglycemic agents.

We assessed the prevalence of hypoglycemic symptoms in patients (aged 40-65 yr) treated with oral hypoglycemic agents (OHAs) attending routine diabetes clinics at our hospital. Symptoms were experienced during the previous 6 mo in 41 of 203 (20.2%) patients treated with sulfonylureas but in none of the 16 patients treated with metformin alone. Hypoglycemic symptoms were experienced at least monthly in 5.9% and less frequently in 14.3% of patients. The prevalence of symptoms decreased with increasing duration of sulfonylurea administration (P less than .01). Mean glycosylated hemoglobin and postprandial plasma glucose were significantly lower in patients reporting hypoglycemic symptoms than in those without symptoms (P less than .001). The prevalence of hypoglycemic symptoms was significantly higher in patients treated with glyburide than in patients treated with gliclazide (P less than .01) or chlorpropamide (P less than .05). The prevalence of symptoms was higher in patients taking medications in addition to OHAs (P less than .01). Ten (24%) of the patients who experienced hypoglycemic symptoms were taking drugs that may potentiate sulfonylureas.

Adult↗

PubMed2005

Adherence to oral hypoglycemic agents in Hawaii.

INTRODUCTION: Adherence to oral hypoglycemic agents is essential to reducing the poor health outcomes of populations at high risk for developing diabetes and its chronic complications. The goal of this study was to identify characteristics of patients in Hawaii least likely to adhere to oral hypoglycemic agents. METHODS: This retrospective administrative data analysis included prescription refill claims for oral hypoglycemic agents from January 1, 1999, through June 30, 2003 (n = 20,685). Multivariate logistic regression analysis was used to examine the relationship between adherence and patient characteristics. RESULTS: Adherence was found to be strongly associated with age and ethnicity. Relative to the age subset 55 to 64 years, adherence increased as age increased, reaching a peak at age 74 (odds ratio [OR] 1.1; 95% confidence interval [CI], 1.0-1.20). Past the age of 85, adherence declined (OR 0.90; 95% CI, 0.82-0.98). Relative to white patients, the odds ratio of adherence was highest for Japanese patients (OR 1.20; 95% CI, 1.0-1.30) and lowest for Filipino patients (OR 0.78; 95% CI, 0.68-0.90). Gender was not associated with adherence. CONCLUSION: Differences in adherence to oral hypoglycemic agents were found to be related to ethnicity and age. Adherence was found to be lowest in younger patients and Filipino patients. This is a significant finding considering that younger diabetic patients have been shown to have the poorest glycemic control and worst health outcomes. Although the literature on adherence to oral hypoglycemic agents and health outcomes in Filipino patients is limited, studies support an increased risk for developing diabetes in this group. This information can be used to target younger patients and Filipino patients to improve their adherence to oral hypoglycemic agents.

Age Factors↗

PubMedDate not supplied

The Continuous Glucose Monitoring System (CGMS) in type 1 diabetic children is the way to reduce hypoglycemic risk.

BACKGROUND: Diabetic children treated with intensive insulin therapy are showing a dangerous increase in severe hypoglycemic episodes. The Continuous Glucose Monitoring System (CGMS) allows glycemic profiles to be monitored over a 72-h period. The aim of the present study was to evaluate whether this system is sufficiently sensitive to detect asymptomatic hypoglycemia, and to determine if its periodic application would help to minimize the hypoglycemic risk in children with type 1 diabetes mellitus (T1DM). METHODS: Twenty-seven T1DM children (age range 6-13.1 years) were enrolled in the study. The sensor was inserted subcutaneously in each patient and the standard four or five registrations of capillary glycemia per day were performed. Eighteen patients continued in the study and the glucose sensor was again inserted after a 6-week interval. At the beginning and end of the study, fructosamine, glycosylated hemoglobin (HbA(1c)), median glycemia, number and duration of hypoglycemic events and insulin requirement were evaluated. RESULTS: A significantly higher number of asymptomatic hypoglycemic events was revealed by CGMS in comparison with the standard system (3.6 +/- 2.3 vs 0.7 +/- 0.9; p < 0.0001). In patients who continued in the study, insulin therapy adjustments reduced the incidence of hypoglycemic events (2.5 +/- 1.7 vs 3.9 +/- 2.2; p < 0.05). At the 6-week point, the fructosamine level was reduced (330 +/- 30 vs 349 +/- 24 micro mol/l; p < 0.05). CONCLUSIONS: The CGMS is a useful device not only for detecting unrecognized hypoglycemia, but also for modifying insulin therapy in order to reduce hypoglycemic events. The system appears to be useful in avoiding long exposure to hypoglycemia.

Adolescent↗

PubMed2001

MK801 decreases glutamate release and oxidative metabolism during hypoglycemic coma in piglets.

Hypoglycemic coma increases extracellular excitatory amino acids, which mediate hypoglycemic neuronal degeneration. Cerebral oxygen consumption increases during hypoglycemic coma in piglets. We tested the hypothesis that the NMDA-receptor antagonist dizocilpine (MK801) attenuates the increase in cerebral oxygen consumption during hypoglycemia. We measured EEG, cerebral blood flow (CBF), cerebral oxygen consumption (CMRO(2)) and cortical microdialysate levels of glutamate, aspartate and glycine in pentobarbital-anesthetized piglets during 60 min of insulin-induced hypoglycemic coma. NMDA-receptor distribution was measured by autoradiography. MK801 (0.75 mg/kg i.v.) was given within 5 min after onset of isoelectric EEG. Saline- and MK801-treated normoglycemic control animals were also studied. Brain temperature was maintained at 38.5+/-0.5 degrees C. MK801 prevented the 5--10-fold increase in glutamate and aspartate occurring in saline-treated hypoglycemic animals, and attenuated the increase in CMRO(2). Increases in CBF of 200--400% during hypoglycemic coma were not affected by MK801. MK801 did not alter CBF, CMRO(2) or microdialysate amino acid levels in normoglycemic control animals. Parietal cortex corresponding to microdialysis sites was highly enriched in NMDA receptors, and the density and distribution overall of NMDA receptor binding sites were comparable to that reported in other species. We conclude that NMDA receptor activation plays a central role in hypoglycemia-induced glutamate release, and contributes to increased cerebral oxygen consumption. Neuroprotective effects of MK801 during hypoglycemia in piglets may involve inhibitory effects on glutamate release and oxidative metabolism.

Animals↗

PubMed1993

Brain calcium metabolism in hypoglycemic coma.

The present experiments were designed to provide information on brain calcium metabolism during hypoglycemic coma. We specifically wished to evaluate changes in extracellular calcium concentration (Ca2+e) during prolonged hypoglycemic coma and recovery and to assess whether Ca2+e falls to similar values during hypoglycemia and ischemia. To that end, Ca2+e and K+e in neocortical tissue were recorded by ion-sensitive microelectrodes during hypoglycemic coma of 30 min duration and during 15 min of recovery. Cardiac arrest ischemia was induced either at the end of the period of hypoglycemia or after 15 min of recovery. Hypoglycemic coma, as reflected by a DC potential shift and by cellular release of K+, was accompanied by a sustained decrease in Ca2+e from approximately 1.2 to approximately 0.02 mM, i.e., to approximately 1% of control. Infusion of glucose was followed by a biphasic recovery of Ca2+e, starting within 2 min of infusion. During the first phase, completed within the initial 3-4 min, Ca2+e rose to about 25% of control. During the second phase, Ca2+e slowly increased toward normal within 25-30 min. Ischemia, when induced at the end of the period of hypoglycemia, was accompanied by a rise in Ca2+e to about 0.1 mM, i.e., about 10% of control. A similar value was recorded when ischemia was induced after 15 min of recovery following a 30-min hypoglycemic coma. Although the present results do not give information on Ca2+i during hypoglycemic coma, it is tempting to conclude that partial preservation of the nucleoside triphosphate stores, and absence of acidosis, allow some binding and sequestration of the calcium entering the cell.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

Hypoglycemic brain injury: potentiation from respiratory depression and injury aggravation from hyperglycemic treatment overshoots.

Hypoglycemia can cause brain dysfunction, brain injury, and death. The present study seeks to broaden current information regarding mechanisms of hypoglycemic brain injury by investigating a novel etiology. The cat's high resistance to brain injury from hypoglycemia suggested that additional influences such as respiratory depression might play a facilitating role. Three groups of cats were exposed to fasting and insulin-induced hypoglycemia (HG; n = 6), euglycemic respiratory depression (RD; n = 5), and combined hypoglycemic respiratory depression (HG/RD; n = 10). The HG animals were maintained at <1.5 mmol (mean 1 mmol) serum glucose concentration for 2 to 6.6 hours. The respiratory depression was associated with PaO2 and PaCO2 values of approximately 50 mm Hg for 1 hour and of approximately 35 and approximately 75 mm Hg, respectively, for the second hour. Magnetic resonance diffusion-weighted imaging estimated brain energy state before, during, and after hypoglycemia. The hypoglycemic respiratory depression exposures were terminated either to euglycemia (n = 4) or to hyperglycemia (n = 6). Brain injury was assessed after 5 to 7 days of survival. Cats exposed to hypoglycemia alone maintained unchanged diffusion coefficients; that is, they lacked evidence of brain energy failure and all six remained brain-intact. Only 1 of 5 euglycemic RD but 10 of 10 HG/RD cats developed brain damage (HG and RD vs. HG/RD, P < 0.01). This difference in brain injury rates suggests injury potentiation by hypoglycemia and respiratory depression acting together. Three injury patterns emerged, including activation of microglia, selective neuronal necrosis, and laminar cortical necrosis. Widespread activation of microglia suggesting damage to neuronal cell processes affected all damaged brains. Selective neuronal necrosis affecting the cerebral cortex, hippocampus, and basal ganglia was observed in all but one case. Instances of laminar cortical necrosis were limited to cats exposed to hypoglycemic respiratory depression treated with hyperglycemia. Thus, treatment with hyperglycemia compared with euglycemia after hypoglycemic respiratory depression exposures significantly increased the brain injury scores (24 +/- 6 vs. 13 +/- 2 points; P < 0.05). This new experimental hypoglycemia model's contribution lies in recognizing additional factors that critically define the occurrence of hypoglycemic brain injury.

Animals↗