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Biomedical subjects

D F Gardner

Publications and source records attributed to D F Gardner.

36 records · Page 2Linked to original sources
PubMed1982

Thyroid function tests in patients with acute and resolved hepatitis B virus infection.

Serum thyroid hormones and thyroid hormone binding were sequentially measured in 20 patients with acute hepatitis B infection. Criteria to select patients consisted of a positive test for hepatitis B surface antigen, aspartate aminotransferase (AsAT) concentration greater than 400 U/L during the acute illness, and available serum specimens after recovery. The mean serum thyroxine (T4) concentration (+/- SE) was 12.5 +/- 0.6 microgram/dL during acute infection and 7.4 +/- 0.3 microgram/dL after recovery (p less than 0.001), whereas mean free T4 index values did not significantly differ. The mean serum thyroxine-binding globulin (TBG) concentration was significantly increased (p less than 0.001) during acute illness and accounted for the reversible of serum and the increased serum T4 concentrations. The rise in serum TBG correlated with the rise in AsAT during the acute illness (p less than 0.04) suggesting nonspecific release of these proteins from injured hepatocytes. The mean free triiodothyronine (T3) index was decreased during acute hepatitis (p less than 0.001) and returned to normal after recovery, indicating that acute hepatitis B infection, like other nonthyroidal illnesses, is associated with decreased T4 to T3 conversion in peripheral tissues.

Acute Disease↗
PubMed1981

Sella turcica erosion and transient hypogonadism in the multiple endocrine deficiency syndrome.

A 42-year-old man presented with clinical and biochemical evidence of hypothyroidism, hypoadrenalism, and hypogonadism. Initial diagnostic studies suggested intrinsic pituitary disease and were supported by the finding of a roentgenographically abnormal sella turcica. Detailed endocrine evaluation subsequently showed normal pituitary function and primary target organ deficiencies. Adrenal and thyroid hormone replacement resulted in complete resolution of clinical symptoms and abnormalities of gonadal function. Thorough endocrine evaluation is needed in patients with multiple endocrine deficiencies.

Adult↗
PubMed1981

Effects of thyrotropin-releasing hormone and metoclopramide in patients with phenothiazine-induced hyperprolactinemia.

TRH and metoclopramide tests were performed in 10 female patients with presumed phenothiazine-induced hyperprolactinemia to define the serum PRL response to these agents. Our results show that the serum PRL response to metoclopramide is blunted in most patients with phenothiazine-induced hyperprolactinemia, and the serum PRL response to TRH is exaggerated in most patients during and 3 weeks after stopping phenothiazines.

Adult↗
PubMed1980

Persistent defect in regulation of prolactin secretion after successful pituitary tumor removal in women with the galactorrhea-amenorrhea syndrome.

TRH, metoclopramide (MCP), chlorpromazine (CPZ), and insulin (ITT) stimulation tests of PRL secretion were carried out in age-matched controls and before and after successful removal of pituitary prolactinomas in women with the galactorrhea-amenorrhea syndrome. In preoperative patients there was a blunted or absent PRL response to TRH in 87%, to MCP in 100%, to CPZ in 100%, and to ITT in 93%. Two to 6 months after successful tumor removal, serum PRL rose 2-fold (the usual criterion for a normal response) in 73% after TRH, in 100% after MCP, but in only 13% after CPZ and in only 14% on ITT. However, the PRL increment with all four tests was significantly lower than that in normal controls. One to 8 yr after successful surgery, the PRL increments after TRH and MCP were returning to normal, but the PRL responses to CPZ and ITT remained blunted. GH, ACTH, and TSH reserves were intact in all patients. The diminished PRL response to all stimulation tests observed up to 6 months postoperatively might be explained by the persistence of a negative feedback effect from high PRL levels associated with the tumor. The more persistent impairment of the PRL response to CPZ and ITT is unexplained but suggests a hypothalamic defect.

Amenorrhea↗
PubMed1979

Effect of tri-iodothyronine replacement on the metabolic and pituitary responses to starvation.

To determine the implication of decreased T3 production during fasting, seven normal men were fasted for 80 hours on two occasions; they received 5 microgram of T3 every three hours durnig the second fast. The mean serum T3 concentration declined during the control fast from 120 to 73 ng per deciliter (P less than 0.01), but remained slightly above base-line values during the T3 fast. Mean serum T4 concentrations did not change, and mean serum rT3 concentrations increased, during both fasts. The peak serum TSH increment after TRH was 11.1 micromicron per milliliter before fasting, 8.9 (not significant) after the control fast and 2.2 (P less than 0.01) after the T3 fast. Urea excretion was 9.1 per cent higher during the T3 fast; there were no differences in the changes in blood glucose, plasma fatty acids or other substrates during the two fasts. Pretreatment with potassium iodide lowered serum T4 concentrations and increased the serum TSH response to TRH after fasting. We conclude that the decrease in serum T3 concentrations during fasting spares muscle protein. Fasting is accompanied by a lower set point of TSH secretion, which remains sensitive to changes in serum thyroid hormone concentrations.

Adult↗
PubMed1979

Repetitive infusion of gonadotropin-releasing hormone distinguishes hypothalamic from pituitary hypogonadism.

Patients who have severe hypogonadotropic hypogonadism caused by presumed hypothalamic disease often have a subnormal LH response to a bolus dose of gonadotropin-releasing hormone (GnRH). To determine if this subnormal response is the result of lack of exposure of the pituitary gonadotroph cells to GnRH, five such men were given daily infusions of 500 microgram GnRH, for 7 days. A standard 250-microgram bolus test dose of GnRH was administered before and again immediately after the week of GnRH infusions. Five men who had severe hypogonadotropic hypogonadism as a result of presumed pituitary disease also received daily GnRH infusions for 1 week. The mean incremental LH responses (+/- SE) to GnRH of the men with presumed hypothalamic disease were 5.0 +/- 1.9 mIU/ml before and 56.9 mIU/ml after the week of infusions. The mean incremental LH responses of the men with presumed pituitary disease were 2.4 +/- 0.7 mIU/ml before and 3.7 +/- 2.9 mIU/ml after the week of infusions. These data suggest that the normal gonadotroph requires prolonged exposure to GnRH for LH responsiveness to become normal, but that the severely damaged gonadotroph cannot be stimulated to release LH normally even by the same prolonged stimulation with GnRH.

Adolescent↗
PubMedDate not supplied

Pancreatic venography and plasma ketone measurements in the diagnosis of hyperinsulinism.

Preoperative localization of an insulinoma was possible using a technique of transhepatic pancreatic venography, with measurement of insulin levels in six pancreatic veins. Surgical exploration confirmed the presence of an insulinoma at the site predicted by venography. Peripheral plasma insulin levels were only minimally elevated at the time of hypoglycemia. However, complete suppression of ketogenesis during a 74-hour fast was observed, and felt to be a biological marker for hyperinsulinism. These observations suggest that transhepatic pancreatic venography and the measurement of plasma ketones in addition to glucose and insulin during fasting, may be useful supplementary studies in the evaluation of patients with fasting hypoglycemia.

Adult↗
PubMedDate not supplied

Dietary pectin and glycemic control in diabetes.

Seventeen diabetic subjects requiring insulin and who exhibited glycemic stability over a 9-12-mo control period received 5 g of pectin with each meal and at bedtime for 3 mo. Hemoglobin A1c (HbA1c) and glycosylated serum protein were measured in each patient on multiple occasions to assess glycemic control. No clear-cut change in these measurements occurred during the period of pectin ingestion. These data are not consistent with a beneficial effect of high-pectin diets in people with diabetes.

Blood Glucose↗