Search PubMed⌕ Search

Biomedical subjects

G Costin

Publications and source records attributed to G Costin.

At least 55 records · Page 3Linked to original sources
PubMed1977

Carbohydrate metabolism and pancreatic islet-cell function in thalassemia major.

To investigate the development of diabetes mellitus in patients with thalassemia major, plasma glucose and immunoreactive insulin (IRI) levels following oral glucose and intravenous tolbutamide and glucose disappearance rates following intravenous insulin were measured in 10 patients before and during five years on a high transfusion program (HTP). Plasma immunoreactive glucagon (IRG) levels following oral glucose, intravenous insulin, and arginine were measured during the sixth year. Serial percutaneous liver biopsies were performed on seven patients. The oral glucose tolerance tests (OGAT) and mean peak IRI levels were normal in nine of 10 patients before HTP. After HTP was begun a progressive deterioration of OGTT occurred despite normal IRI levels. Following tolbutamide, the mean per cent fall in plasma glucose in the patients before HTP was significantly less than in controls (p less than 0.01) and similar to that of controls during five years of HTP in spite of higher than normal peak IRI levels. Of seven survivors after six years of HTP, three had normal OGTT and four had chemical diabetes; mean peak IRI levels were normal, but fasting IRG levels were significantly higher than in controls (p less than 0.05). In all seven patients, plasma IRG failed to increase following insulin-induced hypoglycemia and was significantly higher than in controls after arginine (p less than 0.01); after oral glucose, plasma IRG fell significantly below that of fasting only in the patients with chemical diabetes (p less than 0.03). Following intravenous insulin, the mean per cent fall in glucose before and during HTP was significantly less than in controls (p less than 0.01). Hemosiderosis and cirrhosis were present in all biopsied patients. Four patients died; two had chemical and two had nonketotic insulin-dependent diabetes. These data suggest that diabetes mellitus occurs frequently in patients with thalassemia on HTP and that insulin resistance and hyperglucagonemia, possibly due to cirrhosis, are important etiologic factors.

Adolescent↗
PubMed1976

Laron dwarfism: growth and immunoreactive insulin following treatment with human growth hormone.

A 13 1/2-year-old boy with features of growth hormone deficiency had elevated fasting plasma GH levels (5.7 to 66 ng/ml). Serum somatomedin values remained low despite treatment with human growth hormone. Plasma GH values were suppressed following oral administration of glucose and increased following insulin-induced hypoglycemia, L-dopa, and arginine. Chlorpromazine suppressed GH, both fasting and during IIH. These results suggest that the neuroendocrine mechanisms mediating GH secretion seemed to be intact. Peak plasma insulin levels increased in response to glucose administration after HGH suggesting that GH has a direct effect on the pancreatic beta cell which is not mediated by Sm. Plasma testosterone values increased to adult male levels, but there was inadequate secondary sexual response. Growth was enhanced by HGH and may have been due to testosterone and/or insulin. Although Laron dwarfism may result from a receptor defect, an abnormality in GH structure is also possible.

Adolescent↗
PubMed1976

Craniopharyngioma: the role of insulin in promoting postoperative growth.

To elucidate the mechanism for growth following surgery in children with craniopharyngioma, serum somatomedin and prolactin levels, and plasma insulin (IRI) levels in response to oral glucose and intravenous tolbutamide, were determined in 5 and 8 children, respectively, at variable intervals following removal of the tumor. All patients had growth hormone (GH) deficiency following surgery. Seven of 8 children had normal growth (5 cm per year or greater) postoperatively for varying periods of time; 2 children continued to grow normally 6 and 8 years after surgery. Mean (+/- SE) somatomedin level was 0.78 +/- 0.1 U/ml (normal 0.4-1.5 U/ml). Serum somatomedin was normal in 4 children with normal postoperative growth and was also normal in a child who grew poorly. Mean (+/- SE) prolactin level was 6.9 +/- 3.3 ng/ml (normal 0-20 ng/ml). In 5 non-obese children with craniopharyngioma mean (+/- SE) peak IRI level was 104.4 +/- 24.4 muU/ml after oral glucose and 56.7 +/- 8.4 muU/ml after intravenous tolbutamide. These values are similar to mean (+/- SE) peak IRI levels following glucose and tolbutamide in normal children, and significantly higher (P less than 0.05) than those of idiopathic hypopituitary children. In 2 obese children with craniopharyngioma peak IRI levels were 255 and 107 muU/ml after glucose and 208 and 103 muU/ml after tolbutamide, respectively. The patient with suboptimal growth had low IRI responses to stimuli similar to hypopituitary children. Although there was a significant correlation between peak IRI levels following glucose (r = 0.63, P less than 0.025) and tolbutamide (r = 0.75, P less than 0.01) and the rates of growth of the combined data from obese and non-obese patients, no correlation was found between the growth rates of only the non-obese craniopharyngioma patients and their peak IRI levels. No significant correlation was found between mean somatomedin level and mean rate of growth. Normal postoperative growth in all children with craniopharyngioma was associated with normal serum somatomedin activity and pancreatic beta-cell responsiveness to stimuli despite GH deficiency. The results suggest that insulin may be important in the control of somatomedin and growth in these children.

Antigens↗
PubMedDate not supplied

Perioperative management with prolonged intravenous insulin infusion versus subcutaneous insulin in children with type I diabetes mellitus.

Our objective was to retrospectively evaluate glycemic excursion and insulin dosage in the perioperative period in children and adolescents with type I diabetes mellitus receiving prolonged intravenous insulin infusion for 2-3 days compared to conventional subcutaneous insulin treatment. A retrospective review of surgical admissions at the Children's Hospital of Los Angeles in patients with type I diabetes mellitus was conducted for the 3-year period from July 1989 to June 1992, to evaluate two treatment protocols used during that period. For the nine admissions in group 1, patients received 0.06-0.1 units regular insulin/kg/h beginning 2 h prior to surgery and lasting for 2-3 days postoperatively; while, for the ten admissions in group 2 subjects were given subcutaneous regular and intermediate-acting insulin as 2-4 injections daily, with the regular insulin dose prior to surgery decreased to 66-75% of usual. Blood glucose levels were determined at the bedside at hourly intervals and insulin dose adjustment done with the aim of achieving blood glucose levels between 5.5 and 8.3 mmol/L (100-150 mg/dL). The mean bedside blood glucose levels for group 2 were significantly higher 1 h prior to surgery and during the intraoperative period (p < 0.05). In the postoperative period, group 2 blood glucose levels were significantly higher at multiple times for up to 3 days with multiple levels greater than 11.1 mmol/L (200 mg/dL), which was not seen in group 1. The mean insulin dosage (units/kg) prior to admission was not different for the two groups. On the day of surgery and during postoperative days 1 and 2, patients in group 1 received a greater insulin dosage than group 2 subjects (p < 0.025). In group 1, insulin dosage was increased 23% and 15% over baseline for postoperative days 1 and 2, respectively, then, by day 3, was decreased back toward the baseline. In group 2 subjects, a 13.8% increase occurred on the day of surgery due to extra insulin given immediately following the procedures, followed by a 5.4, 44.2, and 66.6% increase over baseline for postoperative days 1 through 3, respectively. In conclusion, meticulous glycemic control was readily achieved in the perioperative period with a constant intravenous insulin infusion for up to 3 days in children and adolescents with type I diabetes. To achieve glycemic control, insulin dosage needs to be increased on the day of surgery and for approximately 2 postoperative days.

Adolescent↗
PubMedDate not supplied

Brain infarction in children with diabetic ketoacidosis.

During the last 10 years, five children were treated at Childrens Hospital Los Angeles for acute, persistent neurologic loss during diabetic ketoacidosis (DKA). Four were transferred from local hospitals after the neurologic crisis. Computed tomography (CT) studies showed one or more areas of brain infarction in each patient, and none had evidence of diffuse cerebral edema. As three of the five patients had been treated for cerebral edema before their CT, brain edema may have been present initially. Our findings emphasize the importance of brain infarction as a cause of persistent neurologic loss in children with DKA.

Cerebral Infarction↗