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At least 847 records · Page 47Linked to original sources
PubMed1998

High incidence of hypoglycemic episodes with neurologic manifestations in children with insulin dependent diabetes mellitus.

UNLABELLED: Hypoglycemia is a serious frequent complication of insulin therapy in type 1 diabetes. PATIENTS AND METHODS: We surveyed 139 IDDM patients. RESULTS: Forty-four patients (32%) reported at least one severe hypoglycemic episode. All patients with severe hypoglycemia experienced neurological manifestations. Symptoms included confusion and abnormal behavior, convulsions, coma, transient hemiparesis and one case of permanent hemiparesis. Most episodes occurred at night or during morning hours. 44% of episodes were related to delayed meal or snack, 11% to excess insulin administration and 13% to extra physical activity. HbA1c was significantly lower in patients with severe hypoglycemia compared with diabetic controls (7.33 +/- 1.09% and 9.45 +/- 4.32%, respectively).

Adolescent↗
PubMed1989

[Hypoglycemic polyneuropathy: report of a case with insulinoma].

A case of a young man who presented symptoms and clinical signs of polyneuropathy that occurred in connection with recurrent hypoglycemic episodes is reported. The hypoglycemia was probably caused by a pancreatic islet tumor. There were symmetric weakness and wasting of hands and feet, absent tendon reflexes and 'glove and stocking' loss of sensation. Electromyographic studies showed denervation potentials with slight reduction of nerve conduction velocities. Sural nerve biopsy studied by optic and electronic microscopy showed axonal degeneration without signs of demyelination or remyelination. There are only 30 similar cases reported in the literature. According to experimental findings, the authors believe that glucopenia is the mechanism responsible for the development of the neuropathy, and that at present time there is no evidence for a direct insulin effect.

Adenoma, Islet Cell↗
PubMed1980

Hypoglycemic effect of disopyramide in a case of diabetes mellitus under insulin treatment.

In a 41-year-old male with diabetes mellitus well controlled with insulin (50 units/day), hypoglycemia developed after starting disopyramide treatment (200 mg/day) for correction of tachycardia. Lower levels of blood glucose and smaller amounts of urinary sugar persisted until disopyramide was withdrawn even after reducing insulin to a minimum dose of 20 units/day. The insulin requirement increased again thereafter to the original dose. These results indicate that disopyramide had a hypoglycemic effect in this patient.

Adult↗
PubMed1994

Insulinoma with normal plasma insulin concentrations and insulin/glucose ratios during hypoglycemic episodes.

A patient with insulinoma had frequent hypoglycemic episodes with normal plasma insulin levels and insulin/glucose ratios. When immunoreactive insulin (IRI) concentrations in this patient were compared among plasma samples with the same C-peptide immunoreactivity (CPR) levels, the concentrations were significantly lower than in control patients with insulinoma and equal to or lower than those of normal subjects. In hepatic venous samples, CPR levels were significantly higher and the IRI/CPR molar ratios were lower than those in a control subject. These results may indicate that normoinsulinemia in this patient could be explained by increased hepatic extraction of insulin.

Adolescent↗
PubMed1996

Anorexia nervosa with recurrent hypoglycemic coma and cerebral hemorrhage.

A 22-year-old woman with anorexia nervosa showed recurrent hypoglycemic coma and cerebral hemorrhage (Weber's syndrome). She also showed marked liver dysfunction. However, the liver damage was unlikely the main cause of these complications, because liver function tests were improved, and platelet count and prothrombin time were normal when cerebral bleeding occurred. These complications could be induced by her severe malnutrition. Although she rejected any nutritional support before cerebral hemorrhage, she began to accept glucose infusion after the episode, and psychiatric and nutritional states were apparently improved. Cerebral hemorrhage was a turning point in her disease.

Adult↗
PubMed1984

Hypoglycemic brain injury in the rat. Correlation of density of brain damage with the EEG isoelectric time: a quantitative study.

Thirty-eight male Wistar rats were exposed to insulin-induced hypoglycemia resulting in periods of cerebral isoelectricity ranging from 10 to 60 min. Plasma glucose levels during cerebral isoelectricity ranged from 0.12 mM to 1.36 mM. Control rats were injected with insulin, but hypoglycemia was terminated with glucose at the stage of large delta-wave EEG slowing. After recovery, the rats were allowed to wake up and survive for 1 wk. The number of dying neurons was assessed with acid-fuchsin/cresyl-violet-stained, whole-brain, subserial sections using direct visual counting of acidophilic, cytoclastic neurons. Brains from control rats that were not allowed to become isoelectric showed no dying neurons. Ten minutes of cerebral isoelectricity produced very minimal brain damage. The density of neuronal necrosis was positively related to the number of minutes of cerebral isoelectricity up to the maximum examined period of 60 min, but showed no correlation with the blood sugar levels. The cerebral cortex, hippocampus, caudate nucleus, spinal cord, and, to a lesser extent, cerebellar Purkinje cells were affected. The distribution of neuronal necrosis was not identical with that seen in ischemia, but, rather, suggested a CSF-borne neurotoxin operant in contributing to the pathogenesis of neuronal necrosis in hypoglycemic brain damage. Neuronal death does not occur in hypoglycemia unless the EEG becomes isoelectric, whatever the blood sugar level. Serious brain damage does not occur until electrocerebral silence has been established for at least several minutes. Neuronal death accelerates after 30 min of EEG isoelectricity in the rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Hypoglycemic thresholds for cognitive dysfunction in IDDM.

Fourteen poorly controlled insulin-dependent diabetes mellitus (IDDM) patients (HbA1c 11 +/- 0.5%) with a mean +/- SE duration of disease of 15 +/- 2 yr were studied to evaluate the hypoglycemic threshold for cognitive dysfunction under insulin-induced hypoglycemia. The P300 event-related potential, a measure of cognitive function, and reaction time (RT) in response to visual stimuli under euglycemic conditions and at plasma glucose concentrations of 3.5 and 2.5 mM (63 and 45 mg/dl, respectively) during a constant insulin infusion were recorded. Baseline P300 latency was similar to that of a nondiabetic control group, but baseline RT was greater in the IDDM group. There was no increase in P300 latency or RT under euglycemic clamp conditions or at a plasma glucose level of 3.5 mM (63 mg/dl). However, when plasma glucose was lowered to 2.5 mM (45 mg/dl), there was an increase in P300 latency and a prolongation of RT. As plasma glucose returned to baseline, P300 latency and RT remained prolonged. After administration of intravenous glucose and a meal, P300 latency and RT returned to baseline. P140, an event-related potential reflecting sensory processes, was not altered. Because P300 latency changes paralleled RT changes, hypoglycemia appears to slow decision-making processes in IDDM. This study revealed that 1) baseline P300 latency is not elevated in poorly controlled IDDM patients, suggesting no cumulative cognitive dysfunction.

Blood Glucose↗
PubMed1995

Brainstem dysfunction is provoked by a less pronounced hypoglycemic stimulus in diabetic BB rats.

Recent studies suggest that moderate hypoglycemia impairs brainstem function in normal humans and rats. To examine whether diabetes alters this response, simultaneous auditory-evoked potentials were recorded directly from the inferior colliculus (IC) and from the brainstem before and after controlled hypoglycemia (clamp) in awake insulin-dependent diabetic BB/Wor rats. Hyperglycemic diabetic animals were studied either during hyperinsulinemic euglycemia (5.6 mmol/l, n = 4) or mild hypoglycemia (3.5 mmol/l, n = 9). Nondiabetic controls were also studied at 3.5 mmol/l (n = 7) and at 2.8 mmol/l (n = 6). Brainstem function was not affected during euglycemia in diabetic rats. However, when plasma glucose was lowered to 3.5 mmol/l, the diabetic rats showed a 10% delay in IC evoked potential (ICEP) latency, whereas nondiabetic animals did not. This occurred despite similar counterregulatory hormones in both groups. The brainstem auditory-evoked potential (BAEP) localized the defect in the diabetic group to an area in or near the IC. When glucose levels were lowered to 2.8 mmol/l, however, brain function was impaired in nondiabetic rats as well. Again the defect was restricted to an area in or near the IC. We conclude that mild hypoglycemia causes a functional impairment in the IC region of the brainstem in both nondiabetic and diabetic rats. However, in the diabetic rats, this alteration occurs after a less pronounced hypoglycemic stimulus. Our findings suggest that chronic hyperglycemia leads to metabolic adaptions that render the diabetic brain more susceptible to mild hypoglycemia.

Animals↗
PubMed2000

Hypoglycemic counterregulatory responses differ between men and women with type 1 diabetes.

The aim of this study was to determine whether sex-related differences occur in counterregulatory responses to hypoglycemia in adult type 1 diabetic patients. Experiments were carried out on 16 (8 men/8 women) type 1 diabetic patients and compared with 16 (8 men/8 women) age- and weight-matched normal individuals. Men and women with type 1 diabetes were matched for age (26+/-2 vs. 25+/-1 years), duration of diabetes (9+/-1 vs. 8+/-1 years), glycemic control (HbA1c 7.7+/-0.3 vs. 7.8+/-0.2%), and weight (BMI 22.8+/-1 vs. 22.1+/-1 kg/m2), respectively. After normalizing plasma glucose overnight, patients underwent a 2-h hyperinsulinemic-hypoglycemic clamp study. Plasma glucose (3.0+/-0.1 mmol/l) and insulin (510+/-48 pmol/l) levels were equated in all groups. Plasma epinephrine, norepinephrine, growth hormone (GH), muscle sympathetic nerve activity (MSNA), and endogenous glucose production (EGP) responses were significantly lower (P<0.01) in type 1 diabetic women compared with men. Autonomic symptom scores, lipid oxidation, nonesterified fatty acids (NEFAs), and glycerol responses were equivalent between men and women with type 1 diabetes despite significantly reduced sympathoadrenal and MSNA responses in women. Autonomic nervous system (ANS) and EGP responses were equivalent in type 1 diabetic and normal individuals. However, lipid oxidation (assessed by indirect calorimetry), glycerol, and NEFA responses were increased (P<0.01) in type 1 diabetic patients compared with normal control subjects. We conclude that counterregulatory responses to fixed hypoglycemia differ markedly in men and women with type 1 diabetes: 1) sympathetic nervous system, GH, and EGP responses are significantly reduced in type 1 diabetic women, 2) autonomic symptom awareness and lipolytic responses appear to be relatively increased in type 1 diabetic women compared with men, and 3) during conditions of similar hyperinsulinemic hypoglycemia and ANS drive, lipid oxidation and lipolytic responses can be increased in type 1 diabetic patients compared with normal individuals.

Adult↗
PubMedDate not supplied

Efficacy of glyburide in diabetics poorly controlled on first-generation oral hypoglycemics.

Twenty-four type II (non-insulin-dependent) diabetic patients poorly controlled on maximum doses of first-generation oral hypoglycemic agents were switched to glyburide. There was a significant decrease in glycosylated hemoglobin, but the level was normalized in only four patients; there was no correlation with age, weight, or duration of diabetes. The best predictor for improvement was initial failure on tolbutamide, as opposed to the other first-generation drugs. Patients not controlled with 500 mg/day of chlorpropamide were less likely to benefit from glyburide therapy.

Administration, Oral↗
PubMed1997

The psychosocial impact of severe hypoglycemic episodes on spouses of patients with IDDM.

OBJECTIVE: No previous studies have examined the psychosocial impact of severe hypoglycemic episodes in IDDM patients on their spouses. This study compared spouses of IDDM patients with and without a history of recent severe hypoglycemia (SH) using traditional measures of psychosocial status and marital conflict, as well as diabetes-specific measures. RESEARCH DESIGN AND METHODS: A total of 61 nondiabetic spouses (23 wives and 38 husbands) of IDDM patients participated in the study. Spouses completed a battery of traditional psychometric measures (depression, anxiety, marital conflict) and diabetes-specific measures (fear of hypoglycemia, marital conflict over diabetes, sleep disturbance caused by hypoglycemia). Scores of spouses of IDDM patients with and without a recent history of SH were compared with t tests. RESULTS: Spouses of IDDM patients with and without a recent history of SH showed no differences on traditional psychometric measures of depression, anxiety, and marital conflict. However, spouses of patients with a recent history of SH showed significantly more fear of hypoglycemia, marital conflict about diabetes management, and sleep disturbances caused by hypoglycemia. Exploratory analyses of variance (ANOVAs) found no differences on psychometric measures between wives and husbands, with the exception that husbands of SH patients reported more sleep disturbance. Nondiabetic spouses, on average, showed greater fear of hypoglycemia than their diabetic partners. CONCLUSIONS: Although SH in IDDM patients can have a significant impact on the psychosocial status of their spouses, in this study the negative impact was restricted to areas of life that are directly related to diabetes and its management. Thus, SH per se is not necessarily associated with significant increases in spousal anxiety, depression, or marital conflict, but may be associated with types of diabetes-specific psychosocial distress that are not easily identified by traditional psychometric measures.

Adult↗
PubMed1980

In vivo incorporation of [3H[ leucine and [3H] tryptophan into proinsulin-insulin and other islet cell proteins in normoglycemic, hyperglycemic, and hypoglycemic rats.

Rats were infused for brief periods with buffer, glucose, or insulin. L-[4,5-3H] leucine (2.5 mCi) or L-[2,3-3H]-tryptophan (0.5 mCi) was quickly injected intravenously 30 min after the onset of the infusion, when marked hyperglycemia or hypoglycemia had been established. Rats remained connected to the infusion system and were killed 30 min after the injection of the labeled amino acid. Pancreatic islets were isolated by enzymatic digestion of the pancreas. They were processed for radioautography or for the measurement of [3H] proinsulin and [3H] insulin by immunoprecipitation and of other islet [3H] proteins by TCA precipitation. Various tissues of the rats were also removed to measure TCA-precipitable-labeled proteins. Incorporation of [3H]-leucine into proinsulin and insulin was 9 to 20 times greater in the hyperglycemic than in the hypoglycemic rats. Incorporation of [3H]-tryptophan into sedentary beta-cell proteins, measured by thea density of silver grain in radioautographs, showed a sixfold difference. The great sensitivity of hormonal and nonhormonal protein biosynthesis of the pancreatic beta cell to plasma glucose was unique among tissues and among other pancreatic islet cells we studied.

Animals↗
PubMedDate not supplied

Hypoglycemic coma associated with subcutaneous insulin infusion by portable pump.

The incidence of hypoglycemia in insulin-dependent diabetic patients managed by continuous subcutaneous insulin infusion (CSII) has been reported to be very low. We report a case of hypoglycemia coma occurring in a highly compliant and intelligent patient while on CSII by a portable pump. Factors contributing to this episode included high risk off hypoglycemia due to tight control, failure to recognize early hypoglycemic symptoms, and maintenance of hypoglycemia for over 2 h by the open-loop device. Hypoglycemia is a complication of CSII by portable pump. We join others in recommending its use solely by experienced physicians. Constant supervision of patients while on CSII is important to eliminate this potentially lethal complication.

Adult↗
PubMed1984

Circannual rhythm of insulin release and hypoglycemic effect of tolbutamide stimulus in healthy man.

Four healthy non obese young volunteers were observed for a 24-hr period, every other month, over the course of one year. Tolbutamide was injected i.v. each day of the experiment every four hours. Tolbutamide-induced insulin secretion (T.I.I.S.) was evaluated by planimetrically measuring insulin areas above basal levels. Tolbutamide-induced hypoglycemic effect was evaluated by measuring the blood glucose difference between the 5th and 25th minute after the drug injection (delta G5'-25'). The macroscopic evaluation of T.I.I.S. and delta G5'-25' (mean chronograms) permitted the detection of the existence of a circannual variation of both variables. In particular the maximum level of the blood glucose drop (delta G5'-25') was registered in February. Subsequently the quantification of the rhythm of T.I.I.S. was obtained by fitting a sine curve, according to the Cosinor method. The highest insulin release was confirmed in winter. As previously documented, the existence of a statistically significant circadian rhythm of T.I.I.S. was confirmed in the morning, i.e. the same period of the day in which insulin-induced hypoglycemia occurs.

Adult↗
PubMed1992

Hypoglycemic emergencies.

Optimal control of blood glucose requires a balance of diet, exercise, and in some cases, medications. Many factors can cause a state of imbalance, resulting in extremes of glucose control. Hypoglycemia is defined generally as a blood glucose level lower than 50 mg/dL. Although the causes of hypoglycemic episodes are diverse, the management is always aimed at normalizing the plasma glucose concentration. Treatment ranges from simple carbohydrate ingestion in mild to moderate cases to intravenous administration of glucose when the reaction is severe and loss of consciousness occurs. Recognition of warning signs and prompt treatment is essential in all cases.

Acute Disease↗
PubMed2000

Anti-inflammatory and neuroprotective effects of magnolol in chemical hypoxia in rat cultured cortical cells in hypoglycemic media.

Our previous studies demonstrated that magnolol protects neurons against chemical hypoxia by KCN in cortical neuron-astrocyte mixed cultures (14). In the present study, we examined whether the neuroprotective effect of magnolol involve modulating inflammatory mediators, prostaglandin E2 (PGE2) and nitric oxide (NO), induced by KCN (hypoxia) or KCN plus lipopolysaccharide (LPS). In glucose-absent (hypoglycemia) media, KCN or KCN plus LPS induced increases in lactate dehydrogenase (LDH) activity by 32% and 34%, and PGE2 production by 12% and 32%, respectively. Both LDH and PGE2 increases were suppressed by 100 microM magnolol. In addition, although KCN or LPS alone did not increase NO generation, KCN plus LPS increased NO generation. This increase was reduced by 100 microM magnolol or 10 microM L-NAME, but the LDH increase and PGE2 production were not reduced by L-NAME. These findings suggest that the protective effects of magnolol against brain damage by KCN or KCN plus LPS in hypoglycemic media may involve inhibition of PGE2 production, but inhibition of NO generation may not be important.

Animals↗
PubMed1975

Hypoglycemic coma associated with benign pleural mesothelioma.

A case of hypoglycemic coma and benign pleural mesothelioma is described. Serum insulin levels, as measured by insulin radioimmunoassay, were appropriately suppressed and consistent with hypoglycemia. Assay of the tumor showed insulin to be undectable. The mechanisms for hypoglycemia probably included increased glucose consumption by the tumor and, more important, the inhibition of lipolysis and hepatic gluconegenesis caused by tumor release of L-tryptophan and its metabolites and/or possibly nonsuppressible insulin-like activity, soluble in acid-ethanol(NSILA-s).

Coma↗