Biomedical subjects
Publications and source records attributed to M T Buckman.
In four depressed patients with abnormal dexamethasone suppression test results before treatment, plasma prolactin levels significantly increased after successful amitriptyline therapy. Such an increase did not take place in five depressed patients with normal dexamethasone suppression test findings.
Ten patients with clinical, laboratory and radiographic evidence compatible with the diagnosis of prolactinoma were treated with two dopamine agonists. One group (N = 6) took bromocriptine and the other group (N = 4) used pergolide, a longer-acting agent. Both medications were found to reduce prolactin levels significantly from baseline, but an oscillatory pattern with significant fluctuation was seen in the mean prolactin levels in the patients taking bromocriptine. Three patients did not achieve euprolactinemia on bromocriptine, 2.5 mg qid, the maximum dose used in this study. All of the study group taking pergolide became euprolactinemic rapidly; no more than a single dose of 100 micrograms/day was required. Tumor reduction was noted in two patients taking bromocriptine and two taking pergolide. The duration of side effects was shorter and compliance was improved on pergolide therapy.
Nine women with prolactinomas studied over 20 weeks were depressed as determined by three separate self-rating scales. The depression improved with bromocriptine or pergolide. Acute depression recurred and prolactins increased after discontinuation of the medication.
Results of preparathyroidectomy and postparathyroidectomy studies in a patient with multiple endocrine neoplasia type I and gastrinoma suggest that hyperparathyroidism unmasks occult gastrinoma and related secretory abnormalities. Three of four diagnostic findings were later obscured by parathyroidectomy and normalization of serum calcium concentration. Basal acid output, basal acid output/maximal acid output ratio, and serum gastrin concentration were decreased from values consistent with gastrinoma to normal. The secretin stimulation test, though still positive, was attenuated. These observations suggest that in multiple endocrine neoplasia type I, normal values for serum gastrin concentration, gastric secretion, and secretin stimulation may not exclude gastrinoma. The investigations clarify the interpretation of a voluminous but confusing literature on the interrelationship between hyperparathyroidism and altered gastric function in the presence or absence of Zollinger-Ellison syndrome.
In order to evaluate the possible role of prostaglandins in pituitary prolactin (PRL) secretion, PRL was serially measured following perphenazine (Trilafon) ingestion in 8 men before and after 5 days of indomethacin administration. Since estrogens have been shown to modulate prolactin secretion in man, serum steroids including estrone (E1), estradiol (E2), progesterone (P) and testosterone (T) were measured before and after indomethacin ingestion. Serum E1, P and T levels were similar during the pre- and post-indomethacin study periods: 56 +/- 4 (1 SEM) vs 48 +/- 5 pg/ml, 298 +/- 28 vs 315 +/- 32 pg/ml, and 8.1 +/- 0.7 vs 8.6 +/- 0.7 ng/ml, respectively. Serum E2 levels were slightly, but significantly, lower following indomethacin treatment at 30 +/- 3 vs 37 +/- 3 pg/ml (p less than .01). Basal serum PRL concentrations were unaffected by indomethacin administration (9 +/- 3 pre- vs 8 +/- 2 ng/ml post-drug treatment). Integrated perphenazine-induced PRL responses were likewise similar during the 2 study periods: 101 +/- 16 ng . hr/ml during the control period and 104 +/- 14 ng . hr/ml following indomethacin. Thus, short-term indomethacin treatment had no effect on basal or perphenazine-stimulated PRL secretion in men.
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A patient with an enlarged, asymmetric sella turcica and visual field defects suggestive of a pituitary or parasellar tumor underwent extensive roentgenographic and pituitary function studies. No abnormalities in pituitary luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, ACTH, prolactin or vasopressin secretion were detected. Growth hormone secretion was provoked by arginine infusion but not by hypoglycemia. Pneumoencephalography revealed air in the sella turcica, and no evidence of tumor. Thus, an enlarged sella turcica in a patient with visual field defects but normal pituitary function may suggest the presence of an "empty sella syndrome."
Renal handling of solute and water following oral water loading was determined in six subjects with small pituitary adenomas associated with nonsuppressible hyperprolactinemia. Compared to control subjects, urine volume and solute excretion were significantly diminished in the hyperprolactinemic group. This was attributable to a decrease in osmolar clearance. Free water clearances were not different from control subjects. Hypothyroidism and adrenal insufficiency as an explanation for the antidiuresis were excluded in each patient. The data supports the suggestion that prolactin influences renal function in man.
The role of endogenous estrogen in the regulation of serum prolactin concentration in man is controversial. To evaluate the possible effect of endogenous fluctuations in serum estrogen on the regulation of prolactin secretion, the authors determined phenothiazine stimulated prolactin secretion in 12 women in the early follicular phase of the menstrual cycle when estrogen levels were low (mean +/- SE E1 + E2 = 82 +/- 7 pg/ml) and compared it to the response during the late follicular phase when estrogen levels were higher (mean E1 + E2 = 320 +/- 63 pg/ml). Mean basal serum prolactin concentrations were similar in the early and late follicular phases of the cylcle (17 +/- 4 and 20 +/- 2 ng/ml, respectively). The integrated prolactin response following phenothiazine administration was significantly higher at mid-cycle (402 +/- 46 ng-hr/ml) than in the early follicular phase (317 +/0 46 ng-hr/ml, P less than .02). Thus, these studies suggest that endogenous estrogen secretion may play a role in the regulation of serum prolactin concentration in man.