Total Body Chlorine Research Articles

Comparison of total body chlorine, potassium, and water measurements in children with cystic fibrosis

Symptoms of cystic fibrosis (CF) may limit the utility of total body chlorine (TBCl) and total body potassium (TBK) measurements for assessing body fluid compartments of children. This study assessed relations among independent measurements of TBCl, TBK, and total body water (TBW) in children with CF. We compared cross-sectional measurements of TBCl by in vivo neutron activation analysis, TBK by whole-body counting of (40)K, TBW by D(2)O dilution [TBW(D(2)O)], and TBW from TBCl and TBK [TBW(Cl + K)] in 19 prepubertal children (13 boys) aged 7.6-12.5 y who had mild symptoms of CF. Body-composition measurements were compared with data from previous studies of healthy children. Subjects with CF had deficits in TBCl, TBK, TBW, and body weight compared with control reference data (P < 0.05). The ratios (TBCl + TBK)/TBW and TBCl/TBK were not significantly different from control reference values, and plasma chlorine and potassium concentrations were within control reference ranges. The sum of TBCl and TBK correlated with TBW(D(2)O) (r(2) = 0.79, P < 0.001), and TBW(Cl + K) correlated with TBW(D(2)O) (r(2) = 0.78, P < 0.001). TBW(Cl + K) was similar to TBW(D(2)O) (mean +/- SEM: 19.0 +/- 0.5 compared with 19.4 +/- 0.5 L; NS). Prepubertal children with mild symptoms of CF can develop deficits in TBCl, TBK, and TBW that reflect chronic energy malnutrition. Mild symptoms of CF do not appear to affect normal relations among TBCl, TBK, and TBW. Measurements of TBCl and TBK may be used to assess body fluid compartments in these patients.

In vivo total body chlorine measurements using prompt-gamma neutron activation analysis

Total body chlorine (TBC1) provides an estimate of extracellular water. We have examined the feasibility of measuring TBC1 using the 5.6, 6.1, and 8.6 MeV C1 peaks produced during in vivo prompt-gamma neutron activation (dose<0.3 mSv). In subjects, background interference permitted the use of only the 8.6 MeV peak in C1 analysis. Preliminary analyses of the prompt-gamma spectra for 33 healthy females (ages: 24–40 yr) provided a mean estimate of 0.85 g C1 per kg body weight. It is therefore feasible to measure TBC1 concurrently with body nitrogen using relatively low-dose prompt-gamma neutron activation analysis.

Total body chlorine: Calibration of the in vivo neutron activation measurement

Total body chlorine (TBCl), used to estimate the extracellular space, is measured by delayed-gamma neutron activation (DGNA) using the reaction 37Cl(n,γ) 38Cl, at Brookhaven National Laboratory. During the calibration process, we noticed that different values were obtained when different amounts of Cl were placed in the phantom. This non-linear relationship is due to the thermal neutron flux suppression by the thermal neutron capture reaction 35Cl(n,γ) 36Cl. Monte Carlo simulations confirm the results of phantom measurements showing an inverse relationship between the Cl content in the phantom and the γ-ray yield per gram Cl. Thus, it is important to calibrate the DGNA system for TBCl using phantom standards containing an amount of Cl close to that expected in the individual undergoing measurement.

Absolute measurements of total-body calcium using prompt gamma neutron analysis and internal chlorine standardization: results in renal patients

Measurement of total-body calcium (TBCa) is important in the study of several medical conditions. Neutron activation analysis (NAA) is sufficiently precise for serial measurements, but in order to provide single, absolute determinations of TBCa, it requires a correction for body habitus. A method is described for the absolute determination of TBCa by comparing the total-body chlorine, obtained by NAA, with that obtained by stable bromine dilution. The method is applied to a group of 30 patients who had been treated for chronic renal failure, and significant differences are found between measured values of TBCa and those predicted for 'normal' healthy subjects. The overall experimental error in the absolute determination of TBCa is estimated to be 8%, for a dose equivalent of 3.1 mSv (based on skin dose, and a quality factor of 10 for neutrons).

In vivo measurement of total body chlorine using the 8.57 MeV prompt de-excitation following thermal neutron capture

Prompt gamma neutron activation analysis with 238Pu/Be sources is used to measure total body chlorine (TBCl) in vivo following the reaction 35Cl(n, gamma )36Cl. The chlorine de-excitation at 8.57 MeV is used for calibration of the system for TBCl. Body hydrogen is used as an internal standard and TBCl is derived from the gamma-ray counts ratio of chlorine to hydrogen. The precision of the method, determined from replicate scans of a Bush-type phantom, is 4.9% (CV). To assess accuracy an anthropomorphic phantom consisting of minced meat was constructed. Replicate scans of this phantom yielded a mean total chlorine which was not significantly different from the chemical analysis value.

Performance of the bismuth germanate total body chlorine analyzer.

The initial method for in-vivo determination of body chlorine (BC1) was total body neutron activation followed by whole body counting of activated chlorine1. Efforts to analyze total body chlorine (TBC1) using prompt-gamma/NaI system were successful, but the background in the chlorine region of interest 5 to 7 MeV was high and therefore the precision suffered2.KeywordsAnorexia NervosaLean Body MassTotal Body WaterHeavy WaterPhantom MeasurementThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Total Body Electrolyte Composition in Patients with Heart Failure

Total body elemental composition was measured in 40 patients with well documented heart failure who were oedema-free on digoxin and diuretics. The results were compared with values for 20 patients with untreated essential hypertension matched for height, weight, age, and sex. Total body potassium alone was also measured in 20 normal subjects also matched for anthropomorphic measurements. Patients with hypertension had a very similar total body potassium content to that of normal subjects, but patients with heart failure had significantly reduced total body potassium. This could not be explained by muscle wasting because total body nitrogen, largely present in muscle tissue, was well maintained. When total body potassium was expressed as a ratio of potassium to nitrogen mass a consistent depletion of potassium was revealed in the group with heart failure. Potassium depletion was poorly related to diuretic dose, severity of heart failure, age, or renal function. Activation of the renin-angiotensin-aldosterone system was, however, related to hypokalaemia and potassium depletion. Such patients also had significantly lower concentrations of serum sodium and blood pressure. Serum potassium was related directly to total body potassium. Despite the absence of clinically apparent oedema total body chlorine was not consistently increased in heart failure, but the calculated extracellular fluid volume remained expanded in the heart failure group. Total body sodium was significantly increased in patients with heart failure, but less than half of this increase could be accounted for by extracellular fluid volume expansion. Potassium depletion in heart failure may account in part for the high frequency of arrhythmias and sudden death in this condition.

Total body electrolyte composition in patients with heart failure: a comparison with normal subjects and patients with untreated hypertension.

Total body elemental composition was measured in 40 patients with well documented heart failure who were oedema-free on digoxin and diuretics. The results were compared with values for 20 patients with untreated essential hypertension matched for height, weight, age, and sex. Total body potassium alone was also measured in 20 normal subjects also matched for anthropomorphic measurements. Patients with hypertension had a very similar total body potassium content to that of normal subjects, but patients with heart failure had significantly reduced total body potassium. This could not be explained by muscle wasting because total body nitrogen, largely present in muscle tissue, was well maintained. When total body potassium was expressed as a ratio of potassium to nitrogen mass a consistent depletion of potassium was revealed in the group with heart failure. Potassium depletion was poorly related to diuretic dose, severity of heart failure, age, or renal function. Activation of the renin-angiotensin-aldosterone system was, however, related to hypokalaemia and potassium depletion. Such patients also had significantly lower concentrations of serum sodium and blood pressure. Serum potassium was related directly to total body potassium. Despite the absence of clinically apparent oedema total body chlorine was not consistently increased in heart failure, but the calculated extracellular fluid volume remained expanded in the heart failure group. Total body sodium was significantly increased in patients with heart failure, but less than half of this increase could be accounted for by extracellular fluid volume expansion. Potassium depletion in heart failure may account in part for the high frequency of arrhythmias and sudden death in this condition.

Measurement of total body chlorine by prompt gamma in vivo neutron activation analysis

A method of measuring total body chlorine (TBCI) by prompt gamma in vivo neutron activation analysis is described which depends on the same NaI(Tl) spectra used for determinations of total body nitrogen. From these spectra counts ratios of chlorine to hydrogen are derived and TBCI is determined using a model of body composition which depends on measured body weight, total body water (by tritium dilution) and protein (6.25*nitrogen) as well as estimated body minerals and glycogen. The precision of the method based on scanning an anthropomorphic phantom is at present only approximately 9% (SD), for a patient dose equivalent of less than 0.30 mSv. It is suggested that an improvement in precision will be achieved by increasing the scanning time (thereby increasing the radiation dose equivalent) and by adding two more detectors.

Improved models for determination of body fat by in vivo neutron activation

In the present study, two different models of body composition, based on data obtained by nuclear techniques are used. Total body nitrogen, calcium, and chlorine were obtained by total body neutron activation. Total body chlorine was used to estimate extracellular water, and total body calcium to determine bone mineral and extracellular solids. Total body potassium was measured by whole body counting to obtain the body cell mass. In addition, total body water was measured by the tritium dilution technique. It was found that either model can be used equally well to measure total body fat in normal subjects. Estimation of body fat as the difference between body weight and the sum of total body nitrogen (protein), total body water, and bone ash (model 1) appears to have an advantage over model 2, which uses body cell mass, extracellular water, and extracellular solids, particularly for patients with metabolic disorders. This advantage is partly due to the fact that the parameter protein (total body nitrogen) is less affected in metabolic disorders than the more labile total body potassium. The closely correlated results obtained with the two models based on nuclear measurements support the conclusion that these techniques provide reliable measurements of total body fat.

Body elemental composition, with particular reference to total and exchangeable sodium and potassium and total chlorine, in untreated and treated primary hyperaldosteronism.

The whole body content of sodium, potassium, chlorine, calcium, phosphorus and nitrogen was measured by neutron activation analysis in 13 patients with untreated primary hyperaldosteronism (Conn's syndrome; aldosterone-secreting adenoma). Concurrently, exchangeable sodium and potassium were estimated by isotope dilution. Results were compared with values in the same patients during treatment with potassium-conserving diuretics and again after removal of the adenoma; and also with those in a series of 30 patients having untreated essential hypertension. Both total body and exchangeable sodium were high in Conn's syndrome before treatment and were reduced by spironolactone or amiloride and by subsequent surgery. There was no evidence of alteration in the proportion of non-exchangeable sodium in this disease, in contrast to earlier reports. Total body and exchangeable potassium were low in untreated Conn's syndrome and increased to normal after therapy: the proportion of non-exchangeable potassium was similar before and after treatment, and also similar to that in essential hypertension. Total body chlorine was increased before treatment in Conn's syndrome and returned to normal with therapy; body calcium, phosphorus and nitrogen were normal throughout.

Sodium excess in postmenopausal osteoporosis

The sodium excess (Na es) which represents the nonexchangeable sodium compartment of bone was calculated from the total body sodium and total body chlorine of 95 women with vertebral crush fracture syndrome. No evidence was found for a subpopulation with increased or decreased Na es or Na es:TBCa ratio (TBCa is total body calcium which reflects total skeletal mass). Correlations in the osteoporotic women were found between the Na es and serum alkaline phosphatase ( r = 0.31), PTH ( r = 0.53), urinary hydroxyproline excretion ( r = 0.42) and serum 250H vitamin D ( r = −0.32). These data suggest that the state of vitamin D nutrition as well as parathyroid hormone levels may influence the quantity of sodium in bone in osteoporotic women. It is of great interest that these relationships were not observed in two control populations consisting of elderly women and women who recently undewent spontaneous menopause.

Normal levels of total body sodium and chlorine by neutron activation analysis

In vivo neutron activation analysis was used to measure total body sodium and chlorine in 18 male and 18 female normal adults. Corrections for body size were developed. Normalisation factors were derived which enable the prediction of the normal levels of sodium and chlorine in a subject. The coefficient of variation of normalised sodium was 5.9% in men and 6.9% in women, and of normalised chlorine 9.3% in men and 5.5% in women. In the range examined (40-70 years) no significant age dependence was observed for either element. Total body sodium was correlated with total body chlorine and total body calcium. Sodium excess, defined as the amount of body sodium in excess of that associated with chlorine, also correlated well with total body calcium. In females there was a mean annual loss of sodium excess of 1.2% after the menopause, similar to the loss of calcium.

Total body sodium and chlorine in normal adults as determined by neutron activation analysis

Total body neutron activation analysis (TBNAA) has used to determine the absolute levels of total body sodium (TBNa) and total body chlorine (TBCl) in 81 normal adults. For the age span studied (30–90 years), the mean values of TBNa and TBCl remained relatively constant for males, but decreased slightly for females beyond sixty years of age. In order to reduce the variability in this cross-sectional study, the TBNa and TBCl values were normalized for body dimensions (weight, height, body surface area) as well as age and sex. In addition, TBNa was related to skeletal mass (total body calcium) and lean body mass (total body potassium). The quantity of body sodium in excess of the chlorine space was determined. This value, defined as sodium excess, was significantly correlated with total body calcium. The values for total body sodium, total body chlorine, and sodium excess obtained in the present study were compared with values previously reported in the literature.

Total body sodium and chlorine in normal adults

Absolute levels of total body sodium (TBNa) and total body chlorine (TBCl) were determined in 81 normal adults (39 males, 42 females) by means of total body neutron activation analysis (TBNAA). The ages of the subjects ranged from 30 to 90 yr. The mean values for both TBNa and TBCl remained relatively constant throughout the age span studied for males, but decreased slightly for females over 60 yr of age. In order for the absolute measurements of Na and Cl to be of clinical value, the values must be compared to a predicted value based on the sex and body habitus of the individual. Normalization of TBNa values relative to body dimensions (weight, height, body surface area) were evaluated. In addition, TBNa was related to total body calcium (TBCa), which reflects skeletal mass, and TBK, which reflects muscle, or lean body mass. Normalization in terms of a linear combination of the TBCa and TBK was found to be the most satisfactory of all those studied. Sodium excess, Na ES, defined as the amount of body sodium (mEq) in excess of body chlorine (mEq) was determined. Sodium excess correlated well with total body clacium. Values for total body sodium and chlorine obtained in the present study were compared with values previously reported in the literature.

Determination of body composition by neutron activation analysis in patient with renal failure.

Abstract In vivo neutron activation analysis and whole-body counting techniques were used to measure the body composition of patients with chronic renal failure. Levels of total body calcium, phosphorus, sodium, chlorine, nitrogen, and potassium were measured in uremic patients at various times prior to and during maintenance dialysis. The metabolic derangements in individuals with chronic renal failure often result in the development of overt secondary hyperparathyroidism. The action of PTH on bone is associated with osteodystrophy as well as with extensive metastatic calcification. These effects present major problems in the therapeutic management of uremic patients. The most interesting finding is that of normal total body calcium (Ca/height) measured in uremic patients both prior to and during hemodialysis. Presumably, this high total Ca, occurring simultaneously with a condition such as osteoporosis, reflects the translocation of Ca from skeletal tissue to soft-tissue depots. Uremic patients on dialysis usually experience a loss of total body Ca. TBNAA (total body neutron activation analysis) alone does not distinguish between Ca in bone and Ca in the soft tissue; hence data from tracer studies are required for this analysis. However, following parathyroidectomy in uremic patients with extensive metastatic Ca, TBNAA measurements show a decrease in total body Ca concurrent with reduction of metastatic calcification as indicated by roentgenographic evidence. With renal failure, phosphate is released from the skeleton, and hyperphosphatemia ensues. The P/Ca values for patients on hemodialysis are, on the average, slightly higher than those of normal persons and of uremic patients not on dialysis. The total body sodium in uremic patients was, on the average, higher than that observed in a normal contrast population, as well as higher than that of a group of osteoporotic patients. However, no causal relationship was established between the reduction of total body Na during dialysis and the observed improvement in the hypertensive condition. There was little evidence of K depletion in uremic patients maintained on chronic dialysis as determined by whole-body counting. With few exceptions, uremic patients were found to have body K levels grams of K per kilogram of body weight) normal for their age and sex. The mean total-body nitrogen levels of the uremic patients expressed in terms of body K were similar to those of the normal contrast population, but lower than that of osteoporotic patients. The new insights acquired by the application of in vivo neutron activation technique in studying chronic renal disease, particularly with patients on hemodialysis, are to date chiefly suggestive. However, the acquisition of further data appears to be of considerable value for the understanding of chronic renal failure and the managment of patients through hemodialysis, particularly with respect to associated osteodystrophic changes.

Whole-Body Counter for Neutron Activation Analysis

For the measurement of total-body calcium, sodium, chlorine, nitrogen and phosphorus by in-vivo neutron activation analysis, there are two basic requirements. First, it is necessary to achieve a uniform neutron flux through the human subject. It is also necessary to quantitatively measure the induced radionuclides in the body. The Brookhaven 54-detector whole-body counter with its on-line computer satisfies this latte requirement by providing an absolute measure of the induced activity in the subject, independent of its location in the body and the size of the body itself. The application of this whole-body counter in the in-vivo measurement of total body calcium, sodium, chlorine, nitrogen and phosphorus is described.