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Organic hypoglycemia occurs in pancreatic and mesenchymal tumors. Thirty percent of extrapancreatic tumors are intrathoracic. A patient with hypoglycemic pleural mesothelioma was treated by surgical excision without recurrence five years after surgery. The mechanisms of hypoglycemia are not clearly established. The recurrence of hypoglycemia is a good sign of tumor recurrence.
Cerebral blood flow, plasma epinephrine, and plasma norepinephrine were measured in 25 spontaneously breathing, preterm neonates (mean gestational age 30.4 weeks) 2 hours after birth, during a routine screening for low blood glucose levels. Increased cerebral blood flow and plasma epinephrine values were observed when blood glucose levels were low, whereas plasma norepinephrine was constant throughout the blood glucose range. Hypoglycemia (defined as blood glucose concentration less than 30 mg/dL) was found in 13 neonates who were treated with intravenous glucose and milk enterally. Blood glucose levels were normal in the remaining 12 control neonates who received milk by a gastric line. Approximately 30 minutes after treatment with intravenous glucose and/or milk, cerebral blood flow had decreased by a mean of 11.3% in the 13 hypoglycemic neonates but was still 37.5% higher than cerebral blood flow in the control neonates despite normalization of plasma epinephrine concentration. Mean arterial blood pressure and blood gas values were identical between groups throughout the investigation. It is suggested that a normal coupling between cerebral metabolic demands and flow is present in very preterm neonates and that epinephrine may play a role in the cerebral hyperperfusion. Although none of the neonates had clinical signs of hypoglycemia, the data suggest that counterregulatory mechanisms are invoked when blood glucose values are less than 30 to 45 mg/dL.
The usual signs and symptoms of hypoglycemia include tachycardia and profound diaphoresis. These will progress to include an altered mental status that can advance in severe cases to coma, seizures, and death. Occasionally, hypoglycemia may present with focal neurologic signs that can include hemiparesis or hemiplegia with preservation of mental status. In patients with the latter signs, the possibility of a cerebrovascular accident or other intracranial abnormality must be considered. The authors describe an elderly patient with hypoglycemic hemiplegia secondary to insulin administration. Their report includes observations on clinical presentation, the various mechanisms involved, and guidelines for the management of this syndrome.
To assess the duration of Opuntia streptacantha Lem. hypoglycemic effect, two tests in fasting conditions, one with the intake of 500 g of broiled Opuntia stems and the other one with 400 ml of water as control, were performed in eight type II diabetics. Serum glucose levels were measured hourly during six hours. In the Opuntia test the decrease of serum glucose levels was more pronounced at the fourth hour (P less than 0.01 vs control test), serum glucose levels remained unchanged the following two hours. No significant changes on glycemia occurred in the control test. Difference between both tests was significant from the second to the sixth hour.
The results of the experimental investigation on 15 rabbits are presented here. Hypoglycemic action of the standard exogenic insulin dose strengthened after performing transcerebral lateral electrostimulation on the right side with the weak current impulse.
The clinical course of hypoglycemic acetonuria (in 27 children) and acute appendicitis accompanied by acetonuria (in 12) was analysed. The signs permitting to perform the differential diagnosis were distinguished.
Short-term hypoglycemic effect of thymosin was found in intact mice and in animals with alloxan diabetes: single intramuscular administration of 5 mg/kg of thymosin was accompanied by a decrease in glucose content in blood within 15-30 min. Increase in content of immunoreactive insulin in blood was responsible for the hypoglycemia, while the direct insulinotropic effect of thymosin was not observed in isolated pancreas.
Different doses of insulin incorporated into liposomes were administered to normal animals and to those with certain forms of experimental diabetes. Lecithin-cholesterol liposomes in the molar ratio 9:1 were used. They were formed by the supersound treatment of the lipid suspension with the crystalline insulin in the buffer containing 140 mM NaCl and 10 mM tris-HCl (pH 7.4). Incorporation of insulin into liposomes was 16.2% in determination by [125I] insulin and 9.7% in determination of immunoreactive insulin after destruction of liposomes. Dynamics of glycemia and insulinemia was studied in these animals. It is established that insulin from liposomes being per os administered to animals evokes an expressed hypoglycemic effect and hyperinsulinemia. Effective sugar-lowering doses of liposomal insulin for animals with the experimental diabetes were from 6 ME/kg and for normal animals--from 30 ME/kg.
The auto-immune hypoglycemic syndrome is characterized by the association of hypoglycemia (clinical and/or biological) and anti-insulin antibodies in patients who have never received exogenous insulin. Initially this syndrome was most often described in Japanese patients some of whom were treated with drugs containing a sulfydril group. We now recall the case of a female caucasian patient treated with Pyritinol for rhumatoid polyarthritis and who presented severe spontaneous hypoglycemia linked with the presence of anti-insulin antibodies in her serum. The level of her antibodies decreased abruptly on suspension of the drug. The recent and more developed characterization techniques of the different forms of circulating insulin and of their antibodies may help to differenciate an auto-immune hypoglycemia from hypoglycemia due to the secret auto-administration of bovine and porcine insuline, and permit us to suggest that an abnormality in the structure of the molecule of insulin might be a cause of this syndrome. However, the exact mechanism of hypoglycemia linked with the presence of anti-insulin auto-antibodies is not yet clear as is the predisposition of a drug with a sulfydril group to induce such an auto-immune phenomenon.
The levels of immunoreactive insulin and C-peptide were determined against a background of the GTT and GTT + prednisolone in patients with glucose intolerance before and 3-6 mos. after sulfanilamide therapy to study the effect of a prolonged use of glibenclamide (manilil) on compensatory-reserve function of beta-cells. The hypoglycemic effect of these drugs was determined by their extrahepatic action. The normalization of the body sensitivity to insulin was established. A prolonged use of sugar lowering sulfanilamides did not make a depleting effect on beta-cell function. The results obtained were in favor of the administration of glibenclamide to patients with disturbed glucose tolerance.
A comparative study of glibenclamide (G) effect on glucose and IRI levels in rats aged 4 to 5 and 24 to 28 mos. following 18 h starvation was performed. One hour after administration of G at a dose of up to 1 mg/kg of body mass glycemia did not change but in 3 and 5 h it decreased more markedly in old rats. The elevation of a G dose up to 5 mg/kg of body mass raised the hypoglycemic effect in young animals causing no changes in old rats. Glibenclamide at a dose of 1 mg/kg of body mass did not change the IRI level in the young rats' blood and increased it in the old rats 2-3 h after administration. A dose of 5 mg determined a higher IRI level in the young rats' blood and decreased this effect in the old animals.
It has been shown that in animals with reduced heparin blood concentration the hypoglycemic insulin action was considerably low. This was established for rats with alloxan diabetes and ageing rats with depressed anticoagulation system and atherosclerosis enhanced by prolonged atherogenic diet. With insulin injection (0.2-0.3 U/200 g), blood sugar concentration in such animals was 2-2.5 times lower than in normal ones. The compensation of endogenous heparin deficiency by an intravenous injection of heparin normalizes the reaction of animals to exogenous insulin.
The University Group Diabetes Program is a long-term prospective clinical trial designed to evaluate the effects of various hypoglycemic agents on vascular complications in patients with asymptomatic adult-onset diabetes. Mortality and blood glucose levels were determined as well as certain nonfatal events for patients assigned to diet alone or to either of two insulin treatment regimens. Lower levels of blood glucose with mean values close to normoglycemia were achieved in the treatment group in which the insulin dosage was adjusted to achieve normoglycemia compared with the levels achieved in patients treated with diet alone or with a fixed dose of insulin. In spite of differences in blood glucose levels among the treatment groups, there were only minor differences in the occurrence of fatal or nonfatal events.
Different levels of pyruvate, citrate and alpha-ketoglutarate were investigated in the brain tissue of white rats exposed to insulin-induced coma or in various periods following its glucose-cutting. The emergence of pronounced hypoglycemic nervous disorders was followed by a significant decrease in the content of all mentioned acids. Glucose arrest of insulin-caused coma took place in the presence of inactive initial stages of Krebs cycle (citrate synthesis). Restoration of hypoglycemia-affected brain functions had no correlation with the activated citrate synthesis. The levels of citrate and alpha-ketoglutarate normalized 15 minutes after glucose injection and the pyruvate level augmented 30 minutes after the drug administration. It was suggested that the glucose arresting effect demonstrated in insulin coma was conditioned by transformations in glucose carbon lattice regarding pyruvate carboxylising into oxalacetate with further inclusion into brain amino acids and peptides.
Persistent, severe hypoglycemia due to inappropriate or excessive insulin secretion is an infrequent but devastating metabolic emergency in infancy and childhood. The primary therapeutic goal is to normalize blood glucose levels and to prevent the catastrophic sequelae of permanent brain damage and mental retardation due to refractory hypoglycemia. Overall, the use of diazoxide, the mainstay of medical treatment, has proved disappointing and has led to the reevaluation of aggressive, early surgical intervention. Currently, subtotal (80% to 90%) pancreatectomy is the most widely used operative procedure in the treatment of hyperinsulinism. It is, however, still associated with a relatively high failure rate, particularly in neonates or during early infancy when either nesidioblastosis or islet cell hyperplasia-both diffuse proliferative beta-cell disorders-is the most common cause of inappropriate insulin secretion. In these cases, "total" or "near-total" pancreatectomy may be necessary to control the hypoglycemic crisis.
The organic calcium-agonist CGP 28392 augmented insulin release evoked by D-glucose in rat pancreatic islets incubated in the presence or absence of gliclazide, but failed to stimulate insulin secretion in the absence of glucose or presence of diazoxide. Gliclazide, however, failed to augment insulin release evoked, in the presence of CGP 28392, by a high concentration of glucose (11.1 mM), and protected the B-cell against the inhibitory action of diazoxide. As judged from the relative magnitude of changes in 45Ca fractional outflow rate from prelabelled islets perifused at an intermediate glucose concentration (7.0 mM), CGP 28392 failed to affect the rapid cationic response to gliclazide, whereas this hypoglycemic sulfonylurea decreased the cationic response to CGP 28392. These results suggest that the functional response to gliclazide is attributable to a molecular mechanism distinct from the prolongation of the open time of calcium channels presumably provoked by the dihydropyridine.
Evidence is presented that the hypoglycemic action of the human growth hormone fragment, Ile-Pro-Leu-Ser-Arg-Leu-Phe-Asp-Asn-Ala (hGH 4-15) is due to the interaction of hGH 4-15 with plasma membrane resulting in a time- and temperature-dependent release of a cellular mediator which acts to increase insulin binding and hexose transport with consequent potentiation of insulin action. The findings suggest that the hGH 4-15 mediator is a low molecular weight (500-2000 daltons) peptide or has a small peptide moiety in its structure containing an aromatic residue but no arginine or lysine.
A patient with glucagonoma syndrome and hypoglycemic attack is presented. Total pancreatectomy was performed with splenectomy and excision of the metastatic nodule in the liver. Diagnosis of glucagon-secreting A cell carcinoma of the pancreas was confirmed by hormone assays and morphological studies with light and electron microscopy. Glucagon, insulin, and somatostatin were demonstrated immunohistochemically in the tumor tissue. Multihormonal features of the endocrine pancreatic tumors are discussed.