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Biomedical subjects

R M Walter

Publications and source records attributed to R M Walter.

At least 55 records · Page 3Linked to original sources
PubMed1980

Hypercalcemia in the accelerated phase of chronic myelogenous leukemia.

Within a recent one-year period, 3 patients in the accelerated phase of chronic myelogenous leukemia were admitted to our medical center with severe hypercalcemia. Simultaneous determinations of ionized calcium and parathyroid hormone levels in 2 of the patients confirmed the hypercalcemia and revealed suppression of parathyroid hormone. We conclude that hypercalcemia in the accelerated phase of chronic myelogeneous leukemia may be more common than previously described and is not mediated by parathyroid hormone. An elevated parathyroid hormone level accompanying hypercalcemia in these patients should suggest the additional diagnosis of primary hyperparathyroidism. Mithramycin was necessary for control in 2 of our cases as well as in others reported in the medical literature and should be an early therapeutic consideration whenever saline diuresis is inadequate.

Adult↗
PubMed1980

Portal and peripheral vein concentrations of insulin and glucagon after arginine infusion in morbidly obese subjects.

Five morbidity obese subjects with fasting normoglycemia underwent catheterization of portal and peripheral veins immediately prior to jejunoileal bypass surgery. Levels of immunoreactive insulin (IRI), immunoreactive glucagon (IRG), and glucose were determined in simultaneously obtained serum samples before and after infusion of arginine. Portal levels exceeded peripheral levels by at least 50% with IRI and by 30%-40% with IRG. These results were similar to those reported in nonobese subjects and show that in morbid obesity as well as in nonobese states, peripheral insulin to glucagon molar ratios (I/G) underestimate portal I/G. Although hepatic extraction was not specifically measured, the data suggest that the peripheral levels of insulin and glucagon reported in morbid obesity result from alterations in secretion and not altered extraction.

Adult↗
PubMed1978

Agranulocytosis secondary to pentazocine therapy.

Agranulocytosis developed in three patients after prolonged oral pentazocine hydrochloride therapy. Two of the patients had a recurrence of their agranulocytosis within three weeks of reinstitution of pentazocine. Culture techniques in one patient indicate a probable metabolic effect.

Agranulocytosis↗
PubMed1976

Glucagon responses to hypoglycemia in adrenalectomized man.

In order to examine the possibility that epinephrine is involved in either the mediation or modulation of the enhanced glucagon release during glucopenia, glucagon responses to insulin-induced hypoglycemia were evaluated in four men with bilateral adrenalectomy in comparison with ten normal men. In the adrenalectomized patients, the mean nadir of plasma glucose and the rate of ascent to baseline levels were indistinguishable from those observed in normal subjects. Similarly, glucagon responses in the adrenalectomized group were not different from those encountered in the normal volunteers. We conclude that epinephrine does not contribute significantly to the augmented glucagon release during abrupt glucopenia in normal man and is not necessary for normal recovery from hypoglycemia.

Adolescent↗
PubMed1976

Arginine-stimulated acute phase of insulin and glucagon secretion in diabetic subjects.

To determine if both phases of glucagon secretion are excessive in diabetes, arginine was admimistered intravenously as pulses and as infusions to normal subjects, insulin-dependent diabetics, and noninsulin-requiring diabetics. The acute phase of glucagon secretion, in response to arginine pulses at four different doses (submaximal to maximal alpha-cell stimulating), was indistinguishable in terms of timing, peak levels attained, and total increments comparing controls and diabetics. During the first half of the arginine infusion (500 mg/kg over 30 min) the glucagon rise in controls and diabetics was similar (P greater than 0.1), whereas during the last half of the infusion excessive glucagon levels were seen in the diabetics. No difference in the glucagon responses to arginine administered as either a pulse or an infusion was observed between the two types of diabetics. The acute phase responses of insulin to intravenous, maximal stimulating doses of glucose (20 g) and arginine (2.5 g) were measured in five insulin-independent diabetics. Although the acute insulin response to arginine was normal, there was marked attentuation of the early beta-cell response upon stimulation by glucose. From these results we conclude that although in diabetes excessive glucagon levels are observed with chronic arginine stimulation, the acute phase of glucagon secretion in response to arginine is normal. In addition, the beta-cell in noninsulin-requiring diabetics, although acutely hyporesponsive to glucose, remains normally responsive to another stimulus, arginine.

Adolescent↗
PubMed1975

Arginine-stimulated acute phase of insulin and glucagon secretion. I. in normal man.

To document and characterize the immediate phase of glucogen secretion as detected in peripheral blood in man, we have given pulses of L-arginine (0.1 gm. to 10.0 gm.) intravenously over twenty to thirty seconds to twenty-three healthy young men. Peak glucagon and insulin levels averaging four and five times basal levels respectively were reached two to five minutes after arginine administration and had returned to baseline levels by fifteen to thirty minutes. Computing the area above basal for the initial ten minutes after arginine stimulation established a dose-response relationship for the acute phases of glucagon and insulin secretion. A maximal glucagon response was elicited by doses of arginine of 5.0 gm. or greater, whereas for insulin, the plateau was reached at 2.5 gm. of arginine. Sequential 5.0-gm. pulses of arginine administered every thirty minutes showed that there was no augmentation or attenuation of the timing, magnitude (area 0-10 minutes) or absolute peak values reached for either the glucogon or insulin responses. The effect of induced hyperglycemia on the acute phase of insulin and glucagon secretion was assessed by administering the arginine during marked elevation of ambient glucose concentration achieved by the intravenous administration of glucose. This resulted in marked suppression of the acute glucagon response and dramatic accentuation of the insulin response.

Adolescent↗
PubMed1974

The effect of adrenergic blockade on the glucagon responses to starvation and hypoglycemia in man.

In an attempt to ascertain whether the sympathetic nervous system modulates glucagon release in man during starvation and hypoglycemia, the influence of alpha and beta adrenergic blockade on glucagon responses was studied in young, healthy men subjected to fasting and insulin-induced hypoglycemia. Six volunteers fasted for 84 h on three separate occasions. Plasma immunoreactive glucagon (IRG), measured initially at 12 h, climbed gradually from mean levels of 54 pg/ml to a zenith of 124 pg/ml at 48 h, with maintenance of these levels for the duration of the fast. The infusion of propranolol or phentolamine throughout the terminal 24 h of the second and third fasts failed to alter the pattern of IRG release. After an overnight fast, five volunteers received insulin intravenously, which evoked a mean rise in plasma IRG levels from 63 pg/ml to a maximum of 256 pg/ml at 30 min. The concurrent administration of propranolol or phentolamine did not modify the glucagon responses to insulin-induced hypoglycemia. These data suggest that the augmented glucagon release in man during starvation or after hypoglycemia is not significantly regulated by signals from the adrenergic nervous system.

Adolescent↗
PubMed1970

Antitumor efficacy of 7 beta, 17 alpha-dimethyltestosterone (Calusterone) in advanced female breast cancer.

Twenty-two women with far advanced, hormone-refractory breast cancer were treated with 7beta,17alpha dimethyltestosterone (calusterone), 150 to 300 mg per day by mouth, to test its antitumor efficacy. Using the strict criteria of the Cooperative Breast Cancer Group, 14 of the women (64 percent) obtained objective regressions. Regressions lasted for from 3 to 20 months, averaging 7 months. Undesirable actions are those of a 17alpha-alkylated, weak androgen with inconstant bromsulphalein retention, but without elevation of serum bilirubin levels or of hepatic enzymes.This compound has potent antitumor efficacy in women with advanced breast cancer, is better tolerated than most chemotherapeutic or steroidal antitumor agents, and will probably assume an important position in the care of these patients.

Adult↗