Biomedical subjects

F Hofeldt

Publications and source records attributed to F Hofeldt.

7 recordsLinked to original sources

PubMed1991

The role of endogenous opiates in athletic amenorrhea.

We hypothesized that menstrual disturbances in female athletes arise from opioid-induced abnormalities in gonadotropin and/or prolactin (PRL) secretion. To investigate this hypothesis, we measured luteinizing hormone, follicle-stimulating hormone, and PRL levels in eumenorrheic and amenorrheic athletes during thyrotropin-releasing hormone and gonadotropin-releasing hormone tests at baseline, after naloxone infusions, after exercise to exhaustion, and after similar exercise during naloxone infusions. Contrary to our hypothesis, amenorrheic runners did not have significant alterations in basal, postexercise, or stimulated hormone levels compared with eumenorrheic runners. In addition, opioid blockade by naloxone did not enhance gonadotropin release by amenorrheic athletes.

Adult↗

PubMed1987

Proximal femoral fractures.

The absolute number of hip fractures is large, increasing, and related to osteoporosis as well as other factors. By 65 years of age, 50% of women will exhibit bone mineral below the fracture threshold; by age 85, 100%. Trabecular bone loss, which occurs before cortical bone loss, is characteristic of postmenopausal osteoporosis, while cortical bone loss, which increases with age (especially after the age of 70), is characteristic of senile osteoporosis. Estrogen treatment is reasonable for early postmenopausal osteoporosis, less so for the senile variety. The elderly often lose the renal ability to 1-alpha hydroxylate 25-OH vitamin D and thus lose the ability to absorb calcium; they are refractory to D3 therapy, and may require more expensive therapy with 1,25-(OH)2-vitamin D. "Trivial" trauma with falls caused by loose rugs, electric cords, and the like may often be the primary cause of proximal femoral fractures. Sedative drugs are also hazardous. The polyfactorial problem of proximal femoral fractures requires treatment by a multidisciplinary medical team.

Aged↗

PubMed1984

Obstructive sleep apnea in hypothyroidism.

To determine the incidence and frequency of sleep apnea in persons with hypothyroidism, 11 consecutive patients with newly diagnosed disease were studied before and during thyroid hormone replacement therapy. Nine patients had episodes of apnea, with the number of episodes per hour of sleep ranging from 17 to 176 (mean, 71.8). Six of the nine patients were obese and had 99.5 episodes per hour compared with 16.3 episodes per hour in the 3 nonobese patients (p less than 0.02). After 3 to 12 months of thyroxine replacement therapy, mean apnea frequency decreased from 71.8 +/- 18.0 (SE) to 12.7 +/- 6.1 episodes per hour, without reduction in body weight. There were fewer changes in sleep stage per hour during treatment (22.1 +/- 4.9) than pretreatment (57.6 +/- 14.5). Carbon dioxide response tests done under non-loaded and flow-resistive loaded conditions before and during thyroxine replacement therapy showed increases in the loaded respiratory effort and ventilation during thyroxine treatment. Sleep apnea episodes are common in persons with untreated hypothyroidism, even with normal lung function. Thyroxine replacement therapy decreases apnea frequency, even without change in body weight.

Adult↗

PubMed1981

Lack of effects of beta sympathetic blockade on the metabolic and respiratory responses to carbohydrate feeding.

Increases in metabolic rate, heart rate and ventilation occur following carbohydrate feeding or during beta sympathetic stimulation. Furthermore, insulin secretion and hypokalemia are features common to both which raises the question as to whether these effects of carbohydrate depend upon an intact sympathetic nervous system. Accordingly, in the present study, we measured the effects of carbohydrate feeding (250 gram meal) before and after chronic beta sympathetic blockade in sex normal men. Before blockade metabolic rate (O2 consumption) rose (P less than 0.05) from a fasting mean of 248 +/- 19.7 (SEM) ML O2/min to 292 +/- 15.2 at 1 hr. 269 +/- 13.7 at 2, and 262 +/- 18.0 at 3 hr following the meal. During blockade (oral propranolol 80 mg p.o. Q 6 h for 3 days) the post-prandial increase in O2 consumption was also significant (P less than 0.05) and almost identical to that found before blockade. A similar pattern was found for ventilation, heart rate, insulin secretion and hypokalemia, where the significant postprandial changes were not altered by blockade. A transient increase in serum triiodothyronine from a mean of 92 +/- 8.4 microgram/ML to 109 +/- 9.4 occurred at 1 hr (P less than 0.05) only during blockade. No other changes in thyroid hormonal concentrations occurred as a result of the meal. We conclude that although similarities exist between beta sympathetic stimulation and carbohydrate feeding, the post-prandial effects studied do not depend on intact beta sympathetic receptors.

Dietary Carbohydrates↗

PubMed1981

Comparison of oral glucose tolerance tests and mixed meals in patients with apparent idiopathic postabsorptive hypoglycemia: absence of hypoglycemia after meals.

The relationship between symptoms of idiopathic postabsorptive hypoglycemia and glucose homeostasis was evaluated by giving oral glucose tolerance tests (OGTT) and mixed meals to 18 patients and 16 controls. Chemical hypoglycemia after OGTT occurred as often in patients referred because of possible hypoglycemia symptoms, 18 out of 80 (23%), as in controls, 4 out of 16 (25%). After glucose, patients showed both clinical and chemical hypoglycemia (mean +/- SE plasma glucose, 48 +/- 3 mg/dl), but insulin, glucagon, and growth hormone responses were similar to controls. After mixed meals, no chemical hypoglycemia occurred in patients (mean plasma glucose, 79 +/- 3 mg/dl), yet 14 out of 18 (78%) had symptoms and/or signs consistent with hypoglycemia. No abnormality of glucose homeostasis was observed after meals that could account for symptoms or signs experienced by patients with idiopathic postabsorptive hypoglycemia. Since factors other than hypoglycemia appear to be involved, the disorder should be termed the idiopathic postprandial syndrome to avoid the connotation of chemical hypoglycemia.

Adult↗

PubMed1980

Serum thyroglobulin levels predict total body iodine scan findings in patients with treated well-differentiated thyroid carcinoma.

Forty-eight consecutive patients with treated thyroid carcinoma were studied with 131-I total body scans and serum thyroglobulin (hTg) levels. Serum hTg levels during thyroxine treatment accurately predicted scan results (chi square = 18.6, p < 0.001). All patients with negative scans (24 patients) had serum hTg levels (< 7 ng/ml whereas in patients with metastatic thyroid cancer (eight patients) they ranged from 11 to 690 ng/ml. In patients with iodine uptake confined to the thyroid bed (16 patients) serum hTg values ranged from 2 to 17 ng/ml. Serum hTg levels rose in patients with negative scans during hypothyroidism or after exogenous TSH suggesting that hTg levels are more sensitive than iodine scans in detecting residual thyroid tissue. Serum hTg levels could replace total body iodine scans in many patients with treated thyroid carcinoma.

Adult↗

PubMed1978

Thyrotoxicosis: comparison of effects of thyroid ablation and beta-adrenergic blockade on metabolic rate and ventilatory control.

To elucidate the role of the beta-sympathetic system in thyrotoxicosis (THY), we examined cardiac sensitivity to infused beta-agonist and compared the effect of beta-blockade with that of resolution of the hyperthyroid state. Beta-sympathetic (beta-SYM) sensitivity was measured as the heart rate response to isoproterenol in THY patients and in normal subjects. The patients with THY showed both lower threshold (P less than 0.05) and increased slope (P less than 0.05) of the heart rate-isoproterenol response, suggesting beta-SYM hypersensitivity. The beta-SYM like features of THY were measured in 7 patients before and 7 days after beta-SYM blockade with propranolol (mean dose 411 +/- 32 mg/day [SEM]) which was shown to block the heart rate response to isoproterenol. These results were compared with those in a similar group of thyrotoxic patients rendered euthyroid with 131I. During beta-SYM blockade, heart rate decreased from 101 +/- 6.3 to 78 +/- 4.6 (P less than 0.01), but the elevated metabolic rate (V02), resting ventilation (VE), and increased hypoxic and hypercapnic ventilatory responses were not significantly affected. In the group rendered euthyroid with 131I, heart rate decreased from 110 +/- 3.5 to 76 +/- 7.8 (P less than 0.02), but in contrast to the result of beta-SYM blockade, a 28% decrease in VO2 (P less than 0.01), 41% decrease in VE (P less than 0.05), a 38% decrease in hypercapnic ventilatory response (P less than 0.05), and a 66% decrease in hypoxic response (P less than 0.03) occurred. During THY, beta-SYM mechanisms are responsible for part of the tachycardia, but the metabolic and ventilatory abnormalities are not beta-SYM mediated.

Adult↗