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Biomedical subjects

C H Chesnut

Publications and source records attributed to C H Chesnut.

84 records · Page 5Linked to original sources
PubMed1981

Total body bone mineral and lean body mass by dual-photon absorptiometry. II. Comparison with total body calcium by neutron activation analysis.

Total body bone mineral (TBBM) was measured in vivo using dual-photon absorptiometry (DPA) in 10 subjects. The total body calcium (TBCa) was measured in the same subjects using neutron activation analysis. The correlation between the two methods was very high (r greater than 0.99) and the standard error of estimate was low. The TBCa relative to TBBM was about 39%. The two noninvasive methods provided nearly identical indications of skeletal mass, but the radiation exposure with DPA was 500 to 5000 times smaller (0.6 mrem vs 300 to 3000 mrem). The radius shaft bone mineral content was highly correlated with the TBBM (0.97) and the TBCa (0.98) and could be used to estimate the latter variables with errors (1 SEE) of 9% and 6%, respectively.

Body Composition↗
PubMed1981

Improved method for quantitative determination in serum of alkaline phosphatase of skeletal origin.

In this quantitative method for detection of skeletal alkaline phosphatase (EC 3.1.3.1) activity in human serum, intestinal and placental alkaline phosphatase activities are recognized by their susceptibility to inhibition by L-phenylalanine, and skeletal and hepatic alkaline phosphatases are distinguished by their different sensitivities to inactivation by heat. Alkaline phosphatase isoenzymes prepared from organ sources may behave differently from the corresponding isoenzymes in serum. Our procedure allows us to include organ-derived internal standards of skeletal, intestinal, and biliary alkaline phosphatase to minimize between-assay variation. In preliminary applications, we have found that (a) total serum alkaline phosphatase activity is extremely variable in post-menopausal osteoporotic subjects and is not a reliable index of skeletal alkaline phosphatase activity; (b) seven osteoporotic patients responding to therapy with sodium fluoride with increased bone formation showed increased skeletal alkaline phosphatase activity in their serum as compared with age-matched controls (p less than 0.005); and (c) 10 post-menopausal osteoporotic patients responding to therapy with stanozolol with increased total body calcium showed an increase in circulating skeletal alkaline phosphatase activity (p less than 0.001).

Alkaline Phosphatase↗
PubMed1980

Basal plasma immunoreactive calcitonin in postmenopausal osteoporosis.

Calcitonin (CT) deficiency has been suggested as an etiologic factor in postmenopausal osteoporosis (PM-OP). Basal immunoreactive calcitonin (iCT) was measured with a sensitive radioimmunoassay (RIA) in 62 PM-OP women with compression fractures (CF) and in 28 normal age-matched women. Mean iCT values in the two groups were not significantly different (43.5 and 45.1 pg/ml, p greater than 0.10). In the 62 PM-OP females, no significant correlation was noted between basal plasma iCT levels and (1) age; (2) severity of disease as assessed by number of CF; (3) serum calcium, phosphorus, alkaline phosphatase, and immunoreactive parathyroid hormone; and (4) total bone mass as assessed by neutron activation analysis determinations of total body calcium (TBC). In 20 PM-OP patients treated for 24 mo with 100 Medical Research Council (MRC) units daily of synthetic salmon CT, no correlation was observed between basal plasma iCT and response of bone mass (TBC) to therapy. These data suggest that basal CT is not decreased in women with PM-OP, and that the level of circulating CT does not influence therapeutic changes in bone mass during CT therapy. CT is probably not a major etiologic or pathogenetic factor in PM-OP.

Aged↗
PubMed1977

Effect of methandrostenolone on postmenopausal bone wasting as assessed by changes in total bone mineral mass.

To assess the efficacy of methandrostenolone in the treatment of osteoporosis a 26-mo double-blind study was performed with 13 treated and 13 control (placebo) postmenopausal osteoporotic females. Drug effect was assessed primarily by determinations of total body calcium (TBC) by neutron activation analysis, essentially a measurement of total bone mineral mass. Results in the 16 patients completing the study (10 treated and 6 placebo), as well as in all 26 patients participating in the study, showed significant (p less than 0.01) differences in the change in TBC between treated and control groups. In patients dropping out, TBC changes through the time of dropout were similar to those in patients completing the study. In those patients completing the study, TBC increased 2% in the treated group and decreased 3% in the placebo group. An approximate sixfold difference in extraskeletal calcium balance would be required to explain the magnitude of the observed intergroup TBC difference. The drug effect appeared to persist throughout the 26-mo observation period. Thus these data strongly suggest that long-term use of methandrostenolone in postmenopausal osteoporosis prevented bone loss; the possibility that it increased bone mass above initial values is less certain.

Aged↗
PubMed1975

Relationship between local and total bone mass in osteoporosis.

The relationship between total body calcium (TBC) and local bone calcium mass (BCM) was studied in a group of osteoporotic patients (12 females and two males) with a wide range of body size. Two methods were used to estimate BCM: photon absorptiometry and radiographic morphometry. TBC was estimated by total-body neutron-activation analysis. Since 99 percent of TBC is located in the skeleton, it was assumed that TBC was essentially a measure of total skeletal (calcium) mass. TBC ranged from 482 to 1076 g. High correlations with r values from 0.84 to 0.94, p less than 0.001, were found between TBC and BCM measured by absorptiometry at six different sites of radius, ulna, and humerus. Additionally, high correlations with r values from 0.89 to 0.95, p less than 0.001, were found between BCM at the distal tenth of the radius and BCM at the five other sites. A high correlation was also found between body height and TBC, but partial correlations indicated that this accounted for very little of the correlation between TBC and BCM. In contrast to the above, correlations between BCM determined by radiographic morphometry and TBC were weak or nonsignificant. When TBC and BCM were expressed as percent of their mean value, the slopes of the estimating equations, describing the relationships between TBC and BCM, were essentially the same, but significantly less than one, which is the value of the slope expected if TBC and BCM had changed at the same relative rate. From these relationships, we conclude (1) that the rate of change in BCM was similar in the six sites examined, and (2) that the rate of change in these six sites was relatively more rapid than the change in total body calcium. Whether the change in rate of BCM was related to rate of increase during attainment of maximum BCM or subsequent rate of loss of BCM or both remains to be determined.

Activation Analysis↗
PubMedDate not supplied

Is osteoporosis a pediatric disease? Peak bone mass attainment in the adolescent female.

Osteoporosis in the elderly woman is determined by the amount of peak bone mass in adolescence, the premenopausal maintenance of such peak bone mass, and the rate of postmenopausal bone mass loss. The majority of research efforts in the past have been directed at defining the pathogenesis and treatment of postmenopausal osteoporotic bone loss. A comparatively new, and potentially fertile, area of research deals with factors responsible for attaining and augmenting peak bone mass in the adolescent female. Determinants of peak bone mass include genetic, nutritional, weight loading (exercise), and environmental factors. Nutritional factors, especially calcium, are potentially most amenable to therapeutic manipulation. Current data suggest that calcium deficiency exists in the adolescent female; and, although the current data are preliminary and not conclusive, they suggest that increasing calcium intake may be of value in increasing peak bone mass. However, assurance of compliance in the teenage female population in increasing calcium intake is difficult; relating a disease of the elderly, such as osteoporosis, to a teenage female population, a population that may experience the disease 40-50 years later, is frequently frustrating. Nevertheless, increased attention must be directed toward increasing calcium intake in this population of females. The amount of bone mass in adolescence may determine the amount of bone mass postmenopausally; a high or low peak bone mass may, therefore, contribute to protection against, or risk of, subsequent fracture. The ultimate target population for osteoporosis prophylaxis may indeed be the young, rather than the elderly, female.

Adolescent↗