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PubMed2004

Multiple sources of endogenous opioid peptide involved in the hypoglycemic response to 15 Hz electroacupuncture at the Zhongwan acupoint in rats.

A decrease in plasma glucose levels was observed in rats which received electroacupuncture (EA) stimulation at the Zhongwan acupoint. In the present study, the role of the adrenal gland in this hypoglycemic response to EA at high frequency (15 Hz) was investigated on adrenalectomized (ADX) normal rats. There was a sharper decrease in plasma glucose by EA stimulation in the fasting ADX group than in the fasting sham-operated group. Naloxone blocked this hypoglycemic response to EA stimulation in rats which received ADX. Stimulation of EA failed to elicit an increase in plasma beta-endorphin and insulin levels in ADX rats. Similar results were observed in sham and ADX mice. EA stimulation of ADX mice can reduce plasma glucose levels. Furthermore, naloxone abolished the hypoglycemic response to EA stimulation in mice. Such a hypoglycemic response to EA stimulation was also observed in micro-opioid receptor knockout mice (MOR-KOM). Mediation by another opioid peptide should also be considered in future experiments. We conclude that multiple sources of endogenous opioid peptide participated in the lowering of plasma glucose in rats induced by EA stimulation at higher frequency (15 Hz) at the Zhongwan acupoint. Increase in beta-endorphin levels from the adrenal gland enhances the secretion of insulin, there by reducing plasma glucose levels, and is partially involved in this EA stimulation.

Acupuncture Points↗
PubMed1985

Relationship between hypoglycemic symptoms and blood glucose levels due to self-monitoring in summer camp for diabetic children in Japan.

In a summer camp for 47 diabetic children in Kinki district, Japan, in 1984, the relationship between hypoglycemic symptoms and blood glucose levels by self-monitoring was analyzed. During the 7-day camp, self-monitoring of blood glucose (SMBG) was carried out 599 times in total, 12.7 times per camper. SMBG due to hypoglycemic complaints amounted to 371. 154 measurements out of 371 indicated blood glucose levels under 80 mg/dl, but 78 monitorings were found to be over 200 mg/dl. Fatigue or weakness were the most frequent hypoglycemic symptoms, as was hunger sensation, each reaching approximately 40% in frequency. In most complaints of tremor, the blood glucose level was critically low. Prompt measurement of blood glucose is indeed necessary to properly treat diabetic children with 'hypoglycemic' symptoms.

Adolescent↗
PubMed2000

Hypoglycemic effect of cibenzoline in patients with abnormal glucose tolerance and frequent ventricular arrhythmias.

While some antiarrhythmic agents have potential hypoglycemic effects and indeed some reports of hypoglycemic adverse effect of those drugs, no systematic reports have been issued. We studied the hypoglycemic effects of cibenzoline, a class I antiarrhythmic agent. Cibenzoline succinate (150-300 mg/day) was given orally for 12 weeks to 10 patients who had ventricular premature complexes (VPCs) of >1000 per 24 hours and abnormal glucose tolerance before treatment with cibenzoline. Abnormal glucose tolerance, judged by a 75-g oral glucose tolerance test (OGTT), was defined as the response designated as "diabetic" or "borderline" type according to the criteria specified by the Japan Diabetes Society. In OGTT, the insulinogenic index (defined as the ratio of the increment of IRI [immunoreactive insulin] to that of plasma glucose at 30 minutes after a glucose load) and the sum of IRI (sigma IRI) were also determined. Holter ECG recordings, OGTT, and measurements of fasting plasma glucose IRI, and HbA(1c) were performed before and during cibenzoline treatment. Cibenzoline caused VPC reduction of >70% in 6 of the 10 patients. The drug significantly decreased fasting plasma glucose and HbA(1c) (mean +/- SD) 12 weeks after treatment, from 6.18 +/-0.92 mM/L to 5.54 +/- 1.08 mM/L and from 6.17 +/- 1.03% to 5.83 +/- 0.96%, respectively (P < 0.05). While it significantly increased fasting IRI from 4.99 +/- 1.50 to 6.51 +/- 1.47 microU/mL (P < 0.01), the insulinogenic index from 0.33 +/- 0.26 to 0.65 +/- 0.38 (P < 0.05), and sigma IRI from 168 +/- 67 microU/mL to 199 +/-46 (P < 0.05). Cibenzoline exerted a hypoglycemic effect, facilitating insulin secretion in patients with abnormal glucose tolerance and ventricular arrhythmias.

Aged↗
PubMed1986

Changes in extra- and intracellular pH in the brain during and following ischemia in hyperglycemic and in moderately hypoglycemic rats.

Incomplete forebrain ischemia of 15-min duration was induced in rats made hyperglycemic or moderately hypoglycemic prior to ischemia. Tissue CO2 tension, CO2 content, labile tissue metabolites, and extracellular pH (pHe) were measured, and intracellular pH (pHi) was derived by calculation on the assumption that cerebral intracellular fluids can be lumped into one space. In hypoglycemic animals, mean tissue lactate content increased from 2 to 10 mumol g-1. Tissue CO2 content was virtually unchanged and the CO2 tension increased from approximately 50 to approximately 145 mm Hg. In hyperglycemic animals, tissue lactate content rose to 20 mumol g-1, and the CO2 content decreased by 25%, demonstrating that some CO2 was lost to the blood supplied by the remaining perfusion. Accordingly, tissue CO2 tension did not rise above 200 mm Hg. pHe was reduced in proportion to the amount of lactate accumulated, the values obtained in hypo- and hyperglycemic animals showing relatively little scatter (6.76 +/- 0.03 and 6.25 +/- 0.04, respectively). In hypoglycemic animals the extracellular HCO-3 concentration was virtually unchanged, demonstrating that any influx of lactic acid from the cells must have been accompanied by H+ efflux and/or HCO-3 influx via independent routes. In hyperglycemic animals [HCO-3]e fell by greater than 10 mumol ml-1. In both groups [HCO-3]e was reduced during the first 5 min of recovery. Recovery of pHe was slower in hyper- than in hypoglycemic animals. During ischemia calculated pHi fell to 6.37 +/- 0.04 and 5.95 +/- 0.06 in hypo- and hyperglycemic animals, respectively. Differences in pHi were maintained for the first 15 min of recovery, but in both hypo- and hyperglycemic animals pHi had normalized after 30 min. It is concluded that preischemic hyperglycemia leads to a more pronounced intra- and extracellular acidosis than normo- and hypoglycemia, an acidosis that also resolves more slowly during recirculation.

Acidosis↗
PubMed1990

Extracellular pH in the rat brain during hypoglycemic coma and recovery.

It has previously been shown that hypoglycemic coma is accompanied by marked energy failure and by loss of cellular ionic homeostasis. The general proposal is that shortage of carbohydrate substrate prevents lactic acid formation and thereby acidosis during hypoglycemic coma. The objective of the present study was to explore whether rapid downhill ion fluxes, known to occur during coma, are accompanied by changes in extra- and/or intracellular pH (pHe and/or pHi), and how these relate to the de- and repolarization of cellular membranes. Cortical pHe was recorded by microelectrodes in insulin-injected rats subjected to 30 min of hypoglycemic coma, with cellular membrane depolarization. Some rats were allowed up to 180 min of recovery after glucose infusion and membrane repolarization. Arterial blood gases and physiological parameters were monitored to maintain normotension, normoxia, normocapnia, and normal plasma pH. Following depolarization during hypoglycemia, a prompt, rapidly reversible alkaline pHe shift of about 0.1 units was observed in 37/43 rats. Immediately thereafter, all rats showed an acid pH shift of about 0.2 units. This shift developed during the first minute, and pHe remained at that level until repolarization was induced. Following repolarization, there was an additional, rapid, further lowering of pHe by about 0.05 units, followed by a more prolonged decrease in pHe that was maximal at 90 min of recovery (delta pHe of approximately -0.4 units). The pHe then slowly normalized but was still decreased (-0.18 pH units) after 180 min when the experiment was terminated. The calculated pHi showed no major alterations during hypoglycemic coma or after membrane repolarization following glucose administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1995

The influence of acidosis on hypoglycemic brain damage.

The objective of the study was to explore whether hypoglycemic brain damage is affected by super-imposed acidosis. To that end, animals with insulin-induced hypoglycemic coma, defined in terms of a negative DC potential shift, massive release of K+, or cellular uptake of Ca2+, were exposed to excessive hypercapnia (PaCO2 approximately 200 or approximately 300 mm Hg) during the last 25 min of the 30-min coma period. Animals were allowed to survive for 7 days before their brains were fixed by perfusion, and the cell damage was assessed by light microscopy. Other animals were analyzed with respect to changes in extracellular pH (pHe) or extracellular K+ or Ca2+ concentrations (K+e and Ca2+e, respectively). The total CO2 content (TCO2) was also measured to allow derivation of intracellular pH (pHi). The increase in PaCO2 to 190 +/- 15 and 312 +/- 23 mm Hg (means +/- SD) reduced the pHe from a predepolarization value of approximately 7.4 and a postdepolarization value (after the first 5 min of coma) of approximately 7.3 to 6.8 and 6.7, respectively. The corresponding mean pHi values were 6.7 and 6.5. The hypercapnia did not alter the K+e, which rose to 50-60 mM at the onset of hypoglycemic coma, but it increased the Ca2+e from approximately 0.05 to 0.10-0.16 mM. Normocapnic animals with induced hypoglycemic coma of 30-min duration showed the expected neuronal lesions in the neocortex, hippocampus, and caudoputamen. Hypercapnia clearly aggravated this damage, particularly in the caudoputamen, subiculum, and CA1 region of the hippocampus, and caused additional damage to cells in the CA3 region and piriform cortex. A rise in CO2 tension from approximately 200 to 300 mm Hg did not further aggravate the damage. The results thus demonstrate that relative moderate acidosis aggravates damage that is believed to be mostly neuronal, sparing glia cells and vascular tissue.

Acidosis↗
PubMed2003

Can paramedics safely treat and discharge hypoglycemic patients in the field?

To determine whether paramedics can safely treat and discharge insulin-dependent diabetic patients experiencing uncomplicated hypoglycemic events, we conducted a prospective, observational study with a convenience sample of diabetic patients whose hypoglycemia resolved after intravenous administration of dextrose and before they were transported by paramedics. On-line medical control was contacted to obtain approval and informed consent for participation from interested patients who met all eligibility criteria for the study. Participating patients were given instructions upon discharge from the study and were contacted by telephone 24 hours later to ascertain their medical outcomes and their opinions of the study protocol. We enrolled a total of 36 patients with 38 incidents of hypoglycemia. Of these, 91% reported no complications after discharge. Two patients developed recurrent hypoglycemia but treated themselves and did not require further emergency care. One further patient was found unresponsive on the morning following discharge and was subsequently admitted to a long-term care facility with hypoglycemic encephalopathy. Of the study participants, 85% were very satisfied with not being transported to an emergency department (ED) and 91% were very satisfied with the care they had received. All (100%) of the patients surveyed favored a permanent protocol allowing discharge of hypoglycemic patients without admission to an ED. We conclude that paramedics successfully treated, without complication, most of the patients with uncomplicated hypoglycemic events who were examined in our study. These patients generally preferred discharge without transportation to an ED.

Brain Diseases↗
PubMed1982

Epidural triamcinolone and adrenal response to hypoglycemic stress in dogs.

The effect of an epidural steroid injection (triamcinolone) on plasma cortisol levels was studied in twelve beagle dogs following an insulin-induced hypoglycemic stress. The control group (n = 6) received epidural bupivacaine only. This group consistently increases their plasma cortisol values in response to the hypoglycemic stress induced by 0.6 units of insulin/kg administered intravenously. Dogs in the study group (n = 6) received epidural bupivacaine plus 2 mg/kg of triamcinolone. This group was unable to increase their plasma cortisol values in response to similar insulin-induced hypoglycemic stress for four weeks. Return to normal function occurred five weeks following epidural triamcinolone. The authors hypothesize that the inability of the dogs to respond to hypoglycemic stress by increasing their plasma cortisol may interfere with homeostasis and decrease their tolerance to other types of stress up to 4 weeks following epidural triamcinolone administration.

Animals↗
PubMed1976

Regional levels of glucose, amino acids, high energy phosphates, and cyclic nucleotides in the central nervous system during hypoglycemic stupor and behavioral recovery.

The effects of insulin-induced hypoglycemic stupor and subsequent treatment with glucose on mouse cerebral cortical, cerebellar and brain stem levels of glucose, glycogen, ATP, phosphocreatine, glutamate, aspartate and GABA and on cerebral cortical and cerebellar levels of cyclic AMP and cyclic GMP have been measured. Hypoglycemia decreased glucose, glycogen and glutamate levels and had no effect on ATP levels in all three regions of brain. GABA levels were decreased only in cerebellum. Aspartate levels rose in cerebral cortex and brain stem, and creatine phosphate increased in cerebral cortex and cerebellum. In the hypoglycemic stuporous animals, cyclic GMP levels were elevated in cerebral cortex and depressed in cerebellum whereas cyclic AMP levels were unchanged from control values. Intravenous administration of 2.5-3.5 mmol/kg of glucose to the hypoglycemic stuporous animals produced recovery of near normal neurological function within 45 s. Only brain glucose and aspartate levels returned to normal prior to behavioral recovery. These results suggest that of the several substances examined in this study, only glucose and perhaps aspartate have important roles in the biochemical mechanisms producing neurological abnormalities in hypoglycemic animals.

Adenosine Monophosphate↗
PubMed1998

The short-term outcome of hypoglycemic diabetic patients who refuse ambulance transport after out-of-hospital therapy.

OBJECTIVE: To determine the short-term medical outcome of hypoglycemic insulin-dependent diabetic patients who refuse transport after out-of-hospital therapy and return to baseline mental status. METHODS: Prospective, descriptive, short-term medical outcome data for adult patients were collected between May 1996 and December 1996. Paramedics responding to the aid of hypoglycemic insulin-dependent diabetic patients who refused transport after administration of dextrose solution (D50W) contacted a medical command physician at the University of Pennsylvania. The patients' medical histories, names, addresses, and telephone numbers were recorded. Three days after their hypoglycemic episodes, these patients were contacted by telephone by a registered nurse to determine their medical conditions. RESULTS: Of 132 patients enrolled in the study, 103 (78%) could be contacted by telephone follow-up. Ninety-four (91%) of these patients had no recurrence of symptoms. Nine patients (9%) had recurrence of hypoglycemia and recontacted 911. Eight of these (8%) were transported to a hospital via ambulance and 3 (3%) were admitted, 1 (1%) for a cancer-related illness and 2 (2%) for hypoglycemia, 1 of whom died (1%). The remaining patient refused transport a second time after being treated, despite having the risks of refusal explained to him by a medical command physician. CONCLUSIONS: The practice of treating and releasing most hypoglycemic insulin-dependent diabetic patients who return to normal mental status after D50W administration appears in general to be safe. Patients should be advised of the risks of recurrent hypoglycemia.

Adult↗
PubMed1997

Interaction of exercise, insulin, and hypoglycemia studied using euglycemic and hypoglycemic insulin clamps.

Hyperinsulinemic euglycemic and hypoglycemic clamps were used to study the interaction of exercise, insulin, and hypoglycemia at rest and during exercise in the dog. Sampling (artery and portal, hepatic, and iliac veins) and infusion (vena cava) catheters and a flow probe (external iliac artery) were implanted surgically >16 days before study. After an 18-h fast and an 80-min tracer equilibration period, dogs were studied in the basal state (t = -40 to 0 min) and during a moderate treadmill exercise (t = 0-150 min) period or an equivalent duration sedentary period. Insulin was infused at 1 mU x kg(-1) x min(-1) from t = 0-150 min. In one group of sedentary (n = 7) and one group of exercised (n = 6) dogs, glucose was clamped at basal during the insulin infusion. In another group of sedentary (n = 6) and another group of exercised (n = 6) dogs, arterial glucose was clamped at hypoglycemic levels (approximately 65 mg/dl) during the insulin infusion. Arteriovenous difference and isotopic ([3-(3)H]glucose, [U-(14)C]glucose) techniques were used to assess glucose metabolism. Insulin levels were approximately 40 microU/ml in all groups. Data show that 1) counterregulatory hormone (glucagon, catecholamines, and cortisol) responses to exercise and hypoglycemia combined are synergistically higher than the response to either stimulus alone; 2) exercise-induced increases in insulin action are negated during hypoglycemia by the counterregulatory response; 3) decreased need for exogenous glucose during hypoglycemic compared with euglycemic exercise is due to stimulation of endogenous glucose production, which accounts for approximately 30% of the decrease, and reduction of glucose utilization, which accounts for approximately 70%; and 4) insulin-stimulated nonoxidative glucose metabolism is unaffected by exercise or hypoglycemia, whereas insulin-stimulated oxidative glucose metabolism is selectively increased by exercise and decreased by hypoglycemia. In conclusion, the marked rise in insulin action during exercise is matched, under insulin-induced hypoglycemic conditions, by an equally profound increase in counterregulation. The effectiveness of the potent insulin counterregulatory response may be important in decreasing the magnitude and frequency of exercise-induced hypoglycemia.

Animals↗
PubMed1999

Brain O2 consumption and glutamate release during hypoglycemic coma in piglets are temperature sensitive.

Hypoglycemic injury in the mature brain is mediated by excitotoxicity, which is worsened by disordered cellular energy metabolism. The role of excitotoxicity in relation to brain energy metabolism during hypoglycemia has not been studied in the immature brain. Brain oxygen consumption (CMRO2) increases during hypoglycemia in piglets, whereas CMRO2 decreases in adult pig models. We tested the hypothesis that increased CMRO2 during hypoglycemic coma is temperature dependent and coincides with increased excitatory amino acids (EAA). We measured cerebral blood flow (CBF), CMRO2, and cortical microdiaysate EAA in pentobarbital-anesthetized piglets during hypoglycemic coma and during 2 h of recovery and in normoglycemic controls. In warmed animals brain temperature was kept normothermic (38.5 degrees C). In unwarmed animals brain temperature was allowed to fall (37.6 degrees C). During hypoglycemia CBF increased similarly in warmed animals and unwarmed animals; CMRO2 increased in warmed animals but not unwarmed animals. Glutamate increased during coma and increased more in warmed animals than unwarmed animals but normalized quickly during recovery. EEG recovered earlier in unwarmed animals. We conclude that during a hypoglycemic coma in the immature brain, CMRO2 and glutamate are increased in a temperature-dependent manner.

Animals↗
PubMed1994

Plasma chromium levels in hypoglycemic preterm, full-term and in intrauterine-growth-retarded babies.

Serum chromium levels of hypoglycemic preterm and full-term babies were investigated. Normoglycemic preterm and full-term babies were selected as the control group. There was no statistically significant difference in serum Cr levels between preterm and full-term, hypoglycemic and normoglycemic, preterm hypoglycemic and preterm normoglycemic, full-term hypoglycemic and full-term normoglycemic babies. Serum Cr levels of intrauterine-growth-retarded babies were relatively low compared to infants appropriate for gestational age. Serum Cr levels of babies with mothers younger than 35 years of age had significantly lower levels than older mothers' babies.

Chromium↗
PubMed1996

23Na nuclear magnetic resonance spectral changes during and after forebrain ischemia in hypoglycemic, normoglycemic, and hyperglycemic rats.

BACKGROUND AND PURPOSE: The severity of brain injury in animal models of forebrain ischemia increases with blood glucose level. During ischemia, energy failure is slower and maintenance of ion gradients is prolonged as the level of glycemia increases. It is not clear how the level of glycemia influences recovery of ion homeostasis on reperfusion. It has been shown that changes in the intensity of the multiple-quantum 23Na nuclear magnetic resonance (NMR) signals reflect changes in intracellular Na+ levels. We have used 23Na NMR spectroscopy to evaluate the influence of the level of glycemia on changes in Na+ concentration during and after forebrain ischemia in rats. METHODS: Single-quantum (SQ) and double-quantum (DQ) 23Na NMR spectra were measured before and during 10-minute forebrain ischemia and during reperfusion in hypoglycemic, normoglycemic, and hyperglycemic rats. RESULTS: The DQ 23Na NMR signal increased to 210% of preischemia intensity in all rats, but a delay in this increase was observed in normoglycemic and hyperglycemic animals. The rate of the DQ 23Na NMR signal increase was fastest in hypoglycemic (apparent first-order rate constant 0.673 +/- 0.046 min-1, P < .002 compared with normoglycemic animals) and slowest in hyperglycemic (0.285 +/- 0.024 min-1, P < .03) rats. During reperfusion, the signal intensity recovered rapidly in hypoglycemic (0.385 +/- 0.050 min-1) and normoglycemic (0.464 +/- 0.047 min-1) rats, whereas in hyperglycemic animals recovery was slow (0.108 +/- 0.044 min-1, P < .0001 compared with normoglycemic animals). The SQ 23Na NMR signal intensity increased to 117% of preischemia level in hypoglycemic (P < .05 compared with normoglycemic animals) and to 107% in normoglycemic and hyperglycemic animals during reperfusion. CONCLUSIONS: The slower increase in the 23Na DQ NMR signal intensity during forebrain ischemia in rats with higher blood glucose levels suggests that Na+ homeostasis is maintained longer in these animals. On reperfusion, the slower recovery of the DQ 23Na NMR signal intensity in hyperglycemic animals likely indicates a slower recovery of Na+ homeostasis, perhaps contributing to the increased neuronal injury after cerebral ischemia in hyperglycemic animals.

Animals↗
PubMed1988

Modest decrements in plasma glucose concentration cause early impairment in cognitive function and later activation of glucose counterregulation in the absence of hypoglycemic symptoms in normal man.

To establish the glycemic threshold for onset of neuroglycopenia (impaired cognitive function, measured by the latency of the P300 wave), activation of hormonal counterregulation and hypoglycemic symptoms, 12 normal subjects were studied either under conditions of insulin-induced, glucose-controlled plasma glucose decrements, or during maintenance of euglycemia. A decrement in plasma glucose concentration from 88 +/- 3 to 80 +/- 1 mg/dl for 150 min did not result in changes in the latency of the P300 wave nor in an activation of counterregulatory hormonal response. In contrast, a greater decrement in plasma glucose concentration from 87 +/- 3 to 72 +/- 1 mg/dl for 120 min caused an increase in the latency of the P300 wave (from 301 +/- 12 to 348 +/- 20 ms, P less than 0.01), a subsequent increase in all counterregulatory hormones but no hypoglycemic symptoms. Finally, when plasma glucose concentration was decreased in a stepwise manner from 88 +/- 2 to 50 +/- 1 mg/dl within 75 min, the increase in the latency of the P300 wave was correlated with the corresponding plasma glucose concentration (r = -0.76, P less than 0.001). The glycemic threshold for hypoglycemic symptoms was 49 +/- 2 mg/dl. Thus, in normal man the glycemic threshold for neuroglycopenia (72 +/- 1 mg/dl) is greater than currently thought; the hormonal counterregulation follows the onset of neuroglycopenia; the hypoglycemic symptoms are a late indicator of advanced neuroglycopenia.

3-Hydroxybutyric Acid↗
PubMed1995

Preserved counterregulatory hormone release and symptoms after short term hypoglycemic episodes in normal men.

To test the hypothesis that subsequent neuroendocrine and symptomatic responses are sustained after short term hypoglycemic episodes of less than 1-h duration, we studied hypoglycemia on 4 consecutive days and after an 8-day pause in 10 nondiabetic men. Highly reproducible decreases in plasma glucose (< 2.8 mmol/L) occurred on study days 1, 2, 3, 4, and 12 after iv insulin boluses (0.04 U/kg). Levels of the counterregulatory hormones rose during the hypoglycemic episodes in all instances, but maximal concentrations on study day 4 were not attenuated: glucagon (peaks on day 1 vs. day 4), 150 +/- 10 vs. 180 +/- 20 ng/L; cortisol, 400 +/- 30 vs. 420 +/- 40 nmol/L; ACTH, 12 +/- 2 vs. 13 +/- 2 pmol/L; GH, 11.1 +/- 1.8 vs. 12.5 +/- 2.2 micrograms/L; norepinephrine, 1.68 +/- 0.17 vs. 1.65 +/- 0.13 nmol/L; and epinephrine, 1370 +/- 440 vs. 1520 +/- 480 pmol. On each study day, symptoms of hypoglycemia were produced after induction of hypoglycemia, and there was no decrease in the degree of symptomatology on subsequent days. The multivariate analysis of variance showed no day to day differences in plasma glucose, counterregulatory hormones, or hypoglycemic symptoms. We conclude, firstly, that after short term hypoglycemic episodes, the neuroendocrine and symptomatic responses remain completely intact in normal individuals and, secondly, that short term periods of hypoglycemia are fundamentally different from prolonged periods, as described previously.

Adrenocorticotropic Hormone↗
PubMed1992

[A case of insulinoma with frequent hypoglycemic attacks not showing evident hyperinsulinemia].

Confirmation of inappropriate hyperinsulinemia is an indispensable requisite for the diagnosis of insulinoma. We report here a case of insulinoma without evident hyperinsulinemia at an early stage. The patient, a 49-year-old woman, had been admitted to our hospital for the evaluation of frequent hypoglycemic attacks. At that time, plasma immunoreactive insulin (IRI) after an overnight fast ranged from 7 to 16 microU/ml. The ratio of IRI/fasting blood sugar (FBS) (Fajans index; normal range, below 0.3) was always between 0.13 and 0.28 even at hypoglycemic states. In addition, because computed tomography and arteriography of the abdomen failed to settle the diagnosis of insulinoma, the patient was discharged and followed up at our outpatient clinic for 2 years. She was admitted to our hospital at 51 years of age for the re-evaluation of hypoglycemic attacks. Laboratory examinations revealed high fasting plasma levels of IRI ranging from 20 to 29 microU/ml. Fajans index also increased to 0.47-0.89. Celiac arteriography was able to confirm the existence of insulinoma. We suggest that insulinoma should be considered in the presence of unexplained hypoglycemic attacks even when there is no evident hyperinsulinemia.

Blood Glucose↗
PubMed2004

The use of a continuous glucose monitoring system in hypoglycemic disorders.

OBJECTIVE: To evaluate the use of a continuous glucose monitoring system (CGMS) in the evaluation and treatment of infants and children with hypoglycemic disorders. METHODS: Patients with hypoglycemic disorders wore the CGMS device in the Pediatric Clinic Research Center during their evaluation and treatment. Capillary blood glucose (CBG) values were obtained at least 3 times each day and entered into the device for calibration purposes. We evaluated the number of hypoglycemic episodes below 3.3 mmol/l (60 mg/dl) detected by CGMS compared to CBG values and characterized episodes by their duration and intensity. RESULTS: Five patients with hypoglycemic disorders were included in the study. There were a total of 13,369 sensor points, 343 paired sensor and CBG data points, and 57 days included. A total of 180 episodes of hypoglycemia occurred in these five patients, with an average duration of 55 +/- 13 minutes. Using a cut-off of 3.3 mmol/l (60 mg/dl) for hypoglycemia, the sensor had a sensitivity of 65.4%, specificity of 90.6%, and false positive rate of 42.9%. The positive and negative predictive values were 57.1% and 93.2%, respectively. CONCLUSION: CGMS is a useful adjunct in the diagnosis and evaluation of hypoglycemia, and for documentation of euglycemia in these patients following therapy.

Adolescent↗