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Biomedical subjects

M D Kogut

Publications and source records attributed to M D Kogut.

At least 37 records · Page 2Linked 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↗
PubMed1977

Surgical treatment of hyperthyroidism in children.

During the past ten years, subtotal thyroidectomy for hyperthyroidism was performed upon 43 children at Childrens Hospital of Los Angeles. There were no deaths, no recurrent laryngeal nerve injuries and no permanent hypoparathyroidism. During the one to ten year follow-up period, one patient had recurrent hyperthyroidism develop and was treated with 131I. Twenty-five patients are hypothyroid and require thyroid supplement; 14 are euthyroid and receiv no medication. Postoperative thyroid function did not correlate well with gland remnant size, degree of fibrosis or the extent of lymphoid follicle formation. Lymphocytic infiltration was more severe in patients who had hypothyroidism develop postoperatively. Transient hypocalcemia developed in 22 patients. The effectiveness and safety of the surgical treatment for hyperthyroidism in children is reaffirmed, and it is advocated for consideration over 131I or prolonged medical therapy.

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

Studies in a phenotypic female with 17-alpha-hydroxylase deficiency.

In a 19-year-old phenotypic female (46, XY) with hypertension and hypokalemia, studies confirmed 17-alpha-hydroxylase deficiency. Prior to diagnosis she had been considered to have testicular feminization. Increased plasma progesterone and urinary pregnanediol levels were present before treatment. Increased secretion rates of deoxycorticosterone and corticosterone and abnormally low production of cortisol and aldosterone were present. Following treatment with hydrocortisone, plasma progesterone, serum potassium, and urinary pregnanediol levels and DOC and B secretions were normal. Aldosterone secretion six months after treatment remained low. Normal blood pressure measurements were achieved during treatment with hydrocortisone and oral estrogen with the patient at rest; however, mild elevations in blood pressure (130/90 mm Hg) have been noted despite continued hydrocortisone therapy.

Adult↗
PubMed1976

Pathogenesis, diagnosis and treatment of diabetic ketoacidosis.

The diagnosis of diabetic ketoacidosis must be suspected and the initiation of treatment should be prompt to provide a satisfactory outcome in the treatment of diabetic ketoacidosis. Corrections of fluid and electrolyte deficiencies should be made slowly; rapid "push"injections or large infusions of sodium bicarbonate should avoided and ample amounts of potassium should be given early. Precautions should be taken so that blood glucose concentrations do not fall rapidly, and so that blood glucose levels of 250-300 mg/100 ml are maintained by the administration of 5-10% glucose solutions. Bicarbonate therapy is indicated only in severe acidosis (pH less than or equal to 7.1). Physicians who are trained in the care of diabetes mellitus should supervise the treatment. In our hospital the same staff physicians and fellows attend all patients with diabetes. In addition the efforts of our house staff and nurses have contributed significantly to the care of these patients.

Adult↗
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↗
PubMed1975

Short stature in an adolescent due to spondyloepiphysial dysplasia tarda.

A 15-year-old boy had normal growth until age 7 years and decreased growth velocity thereafter. His upper segment/lower segment (U/L) ratio was 0.8. Anterior pituitary function was normal. Roentgenograms revealed characteristic findings of spondyloepiphysial dysplasia tarda (SDT). The sitting height measurement or U/L segment ratio is important in identifying this condition. This condition should be considered in the differential diagnosis of short stature in males.

Adolescent↗
PubMed1975

Fructose-induced hyperuricemia: observations in normal children and in patients with hereditary fructose intolerance and galactosemia.

After the infusion of fructose, 0.25 g/kg body wt, the mean peak plasma uric acid level was 5.4 +/- 0.7 (SEM) mg/100 ml in six normal children and was not significantly increased compared with that of the mean basal value of 4.1 +/- 0.5 mg/100 ml. The mean blood inorganic phosphate (Pi) levels were significantly less than the mean fasting value after fructose. Blood glucose, lactic acid, and fructose levels were significantly increased after fructose, but serum magnesium levels did not change. In two patients with hereditary fructose intolerance (HFI) the peak blood uric acid levels were 12.1 and 7.6 mg/100 ml, respectively, after fructose. In both patients the blood glucose concentrations decreased 69 and 26 mg/100 ml below the fasting levels after fructose. The serum Pi level decreased 2.3 and 1.2 mg/100 ml below fasting values, decrements greater than the mean decrement in serum Pi of 0.8 +/- 0.2 mg/100 ml which occurred in six normal children. The mean uric acid excretion, expressed as milligrams per mg urinary creatinine, was 0.6 +/- 0.1 (SEM) before fructose in the normal children and increased significantly to 1.0 +/- mg/mg creatinine after fructose. In two patients with HFI the uric acid excretion increased four- to fivefold after fructose administration; the increased uric acid excretion in HFI exceeded that of normal children. In three patients with galactosemia, increases in blood uric acid levels after galactose ingestion were similar to those in normal children after fructose, but less than those in patients with HFI after fructose. The serum Pi levels decreased less in galactosemic patients after galactose administration than in patients with HFI after fructose infusion. These studies support the hypothesis that fructose-induced hyperuricemia results from degradation of adenosine monophosphate. This effect appears to be specific for fructose. The lack of hyperruricemia in galactosemia patients after galactose ingestion may be explained by the observation that galactose is phosphorylated more slowly than fructose.

Adult↗