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Biomedical subjects

C A Verdonk

Publications and source records attributed to C A Verdonk.

11 recordsLinked to original sources
PubMed1989

Radioiodine uptake following iodine-131 therapy for Graves' disease: an early indicator of need for retreatment.

Forty-five patients with Graves' disease were studied prospectively to determine if 24-hour I-131 uptake measurements alone or in combination with serum thyroid hormone levels at six weeks would determine the necessity for retreatment of the thyrotoxicosis. All patients with an I-131 uptake greater than 30% at six weeks required retreatment. No patient with an I-131 uptake of less than 15% required retreatment. Patients with uptakes between 15% and 30% were variable. An elevated free thyroxin index at 6 weeks is not helpful to determine which patients will remain thyrotoxic. Patients with a free thyroxin index within the normal range at six weeks can be predicted to be euthyroid by 12 weeks if their 24-hour I-131 uptake is between 15% and 30% and to be hypothyroid if their 24-hour I-131 uptake is below 15%. There was no difference between patient groups treated initially with antithyroid medication and those who were not.

Adult↗
PubMed1987

Euthyroid hyperthyroxinemia and inappropriate secretion of thyrotropin. Recognition and diagnosis.

Various disease states associated with euthyroid hyperthyroxinemia and inappropriate thyrotropin secretion are becoming increasingly recognized. These diagnoses were established in six (11%) of 57 patients referred for evaluation of elevated free thyroxine index over an 11-month period. Failure to separate these entities from primary thyrotoxicosis may result in unnecessary thyroid ablative therapy and subsequent clinical confusion. Several illustrative patient summaries are presented to outline an approach to this clinical challenge.

Adolescent↗
PubMed1981

Pathogenesis of hypoglycemia in insulinoma patients: suppression of hepatic glucose production by insulin.

To determine the mechanism by which hyperinsulinemia causes hypoglycemia in insulinoma patients, rates of glucose production and utilization, and circulating levels of insulin, glucagon, alanine, lactate, and glycerol were measured in 6 insulinoma patients during development of fasting hypoglycemia and in 8 normal volunteers studied over an identical interval. Initially, insulinoma patients had a greater plasma insulin (42 +/- 9 versus 15 +/- 1 microunits/ml) and glucagon levels (214 +/- 31 versus 158 +/- 21 pg/ml) than normal subjects, P less than 0.05, but their plasma glucose levels (81 +/- 4 mg/dl) and rates of glucose production and utilization (1.71 +/- 0.08 and 1.74 +/- 0.08 mg/kg . min, respectively) were not significantly different from those of normal subjects (93 +/- 2 mg/dl, 1.93 +/- 0.11, and 1.92 +/- 0.13 mg/kg . min, respectively). During a subsequent 8-h fast, glucose production and glucose utilization decreased in both groups, but more markedly in insulinoma patients. Since glucose utilization exceeded glucose production to a greater extent in insulinoma patients than in normal subjects, plasma glucose decreased to 44 +/- 3 mg/dl in insulinoma patients, but only to 84 +/- 1 mg/dl in normal subjects (P less than 0.001). Glucose utilization in insulinoma patients never exceeded that of normal subjects. These results demonstrate that fasting hypoglycemia in the insulinoma patients is usually due to suppression of glucose production rather than to acceleration of glucose utilization, as is widely thought. A direct effect of insulin on the liver is probably responsible, since circulating levels of gluconeogenic precursors are normal and since plasma glucagon increases during development of hypoglycemia in insulinoma patients.

Adenoma, Islet Cell↗
PubMed1981

Effects of plasma glucose concentration on glucose utilization and glucose clearance in normal man.

Glucose clearance (glucose utilization divided by plasma glucose) is commonly used to assess glucose utilization under conditions in which plasma glucose concentrations vary. The validity of this practice requires that glucose clearance itself be independent of plasma glucose concentration. The present studies were, therefore, undertaken to determine the relationship between glucose clearance and plasma glucose concentration in man. Using the glucose clamp technique, rates of glucose utilization (measured isotopically with 3-3H-glucose) and glucose clearance were determined in 5 normal volunteers at steady-state plasma glucose concentrations of approximately 60, 95, 130, and 165 mg/dl, while plasma insulin concentrations were maintained constant (approximately 18 microU/ml) by infusion of insulin and somatostatin. Despite virtually identical 0.4 mg X kg-1 X min-1 increments in glucose utilization for each 35-mg/dl increment in plasma glucose, glucose clearance decreased as a function of plasma glucose concentration (r = -0.85, P less than 0.001). These results indicate that glucose clearance is not independent of changes in plasma glucose concentration and, thus, use of glucose clearance to evaluate glucose utilization of differing plasma glucose concentration is not valid. Whether this conclusion also applies to similar use of clearance for other substrates remains to be determined.

Adult↗
PubMed1981

Parathyroid "double adenomas": fact of fiction?

It has been suggested that primary hyperparathyroidism (HPT) may occasionally be caused by "multiple adenomas." If this is true, then selective excision of the enlarged glands should be curative in such cases. To examine this proposition, we reviewed the records of 1,962 patients with surgically proved HPT and culled all those who met the following criteria: (1) identification and excision of two enlarged and histologically hypercellular parathyroid glands, each weighing more than 70 mg, and (2) identification and preservation of two other normal-sized parathyroid glands. There were 38 such patients (1.9% of the total group). Thirty-seven patients were euparathyroid at follow-up (an average of 4.6 years postoperatively). Only one individual, a member of a kindred with multiple endocrine neoplasia (MEN), type 1, had persistent HPT; but four other patients with MEN syndromes were among the group cured by surgery. The findings of this study support the notion that more than one adenoma may occasionally be found in primary HPT, and that selective excision of the enlarged glands with preservation of the normal parathyroid glands constitutes adequate treatment. One possible exception to this rule is the patient with either familial HPT or one of the MEN syndromes; subtotal parathyroidectomy is preferred in this situation.

Adenoma↗
PubMed1980

Glucose clamping using the Biostator GCIIS.

The Biostator GCIIS was used to clamp circulating glucose at hypoglycemic (42 +/- 1 mg/dl), euglycemic (86 +/- 2 mg/dl), and hyperglycemic (142 +/- 1 mg/dl) levels in normal subjects during a concomitant infusion of insulin (0.1 U/kg/h). Because of limitations in maximal glucose infusion (1 g/min) from the Biostator, a supplementary infusion of glucose was required to accomplish euglycemic and hyperglycemic clamps. The coefficients of variation of blood glucose were 7.06 +/- 1.3%, 5.9 +/- 0.5%, and 6.1 +/- 0.9 for 120 minutes of hypoglycemic, euglycemic, and hyperglycemic clamps, respectively. Despite the occasional interruption of blood flow in the double-lumen catheter and the occasional poor correlation between Biostator and reference glucose method, satisfactory glucose clamps could be maintained for 2 hours.

Adult↗
PubMed1980

Effect of alpha-adrenergic stimulation and its blockade on glucose turnover in man.

Epinephrine (50 ng . kg-1 . min-1) was infused for 120 min in seven normal volunteers alone (combined alpha- and beta-adrenergic stimulation), with propranolol (alpha-adrenergic stimulation), and with propranolol plus phentolamine (alpha-adrenergic blockade superimposed on alpha-adrenergic stimulation). During alpha-adrenergic stimulation, plasma glucose and glucose production increased 32 and 42% less, respectively, than during infusion of epinephrine alone, whereas glucose clearance was suppressed comparably. Plasma insulin decreased during alpha-adrenergic stimulation but increased during infusion of epinephrine alone. Plasma epinephrine was threefold greater during infusion of epinephrine plus propranolol than during infusion of epinephrine alone. When alpha-adrenergic blockade was superimposed on alpha-adrenergic stimulation, the increases in plasma glucose and glucose production as well as the decreases in plasma insulin and glucose clearance observed during alpha-adrenergic stimulation were virtually abolished, whereas plasma epinephrine levels were unaltered. These results indicate that in man epinephrine can cause hyperglycemia via both alpha- and beta-adrenergic stimulation of glucose production and suppression of glucose clearance, either directly or indirectly. alpha-Adrenergic effects on glucose production and clearance may be mediated by inhibition of insulin secretion.

Adult↗
PubMed1980

Interaction of fat-stimulated gastric inhibitory polypeptide on pancreatic alpha and beta cell function.

Gastric inhibitory polypeptide (GIP) is considered to be the principal mediator of the enteroinsular axis. A glucose-insulin clamp technique was used to study the effects of differing blood glucose levels on the insulinotropic and glucagonotropic actions of fat-stimulated GIP in seven healthy subjects, as well as the effect of physiologic hyperinsulinemia on GIP secretion. Blood glucose levels were clamped for 4 h at 43+/-2 mg/dl (hypoglycemic clamp), 88+/-1 mg/dl (euglycemic clamp), and 141+/-2 mg/dl (hyperglycemic clamp) in the presence of a constant insulin infusion (100 m U/kg per h). Under hypoglycemic clamp conditions there was no increase in C-peptide nor glucagon after Lipomul ingestion, despite an increase of GIP of 51.7+/-8.7 ng/ml per 120 min. Under euglycemic clamp conditions, small and inconsistent increases in C-peptide and glucagon were observed after fat ingestion and a concomitant increase of GIP of 35.2+/-9.4 ng/ml per 120 min. Under hyperglycemic clamp conditions after fat ingestion and a GIP increase of 24.0+/-5.7 ng/ml per 120 min, C-peptide increased from 6.4+/-5 ng/ml to 11.0+/-1.1 ng/ml (P < 0.01) but glucagon did not change. These findings confirm that in healthy man GIP exerts its insulinotropic properties only under hyperglycemic conditions and indicate that GIP is not glucagonotropic. Under euglycemic clamp conditions (plasma glucose, 89+/-1 mg/dl) and physiologic hyperinsulinemia (serum immunoreactive insulin, 137+/-3 muU/ml) GIP responses to fat ingestion (39.7+/-9.8 ng/ml per 120 min) were not different from the GIP responses to fat ingestion in the absence of hyperinsulinemia (39.7+/-11.1 ng/ml per 120 min). Therefore, insulin under normoglycemic conditions does not exert an inhibitory effect on fat-stimulated GIP secretion. The higher GIP response to oral fat in the hypoglycemic clamp, and the lower GIP response in the hyperglycemic clamp compared to the response in the euglycemic clamp suggests an effect of glycemia itself on GIP secretion in the presence of hyperinsulinemia.

Adult↗
PubMed1975

Diabetic microangiopathy in patients with pancreatitic diabetes mellitus.

Clinically evident diabetic microangiopathy (retinopathy and nephropathy) occurred in 18% of diabetic patients with acute pancreatitis and 14% of diabetic patients with chronic pancreatitis. The presence of diabetic retinopathy and nephropathy in patients with pancreatitic diabetes without a family history of diabetes mellitus suggests that these patients have "primary" diabetes mellitus unmasked by the pancreatitis. The occurrence of diabetic microangiopathy is significantly correlated with the duration of diabetes. The frequency of these diabetic complications seems to increase when there is a family history of diabetes in patients whose pancreatitis is simultaneous with or precedes the onset of diabetes. The majority of patients with diabetic microangiopathy were on insulin therapy, but the need for insulin treatment is an indication of the severity of the diabetes, rather than the insulin being a causative factor of the microangiopathy. The degree of steatorrhea in diabetic patients with chronic pancreatitis did not protect against the development of microangiopathy.

Acute Disease↗