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Original Studies |
Department of Endocrinology (Y.J., F.R.), Leiden University
Hospital, Leiden; and Department of Human Nutrition (P.D.), Wageningen
Agriculture University, Wageningen, The Netherlands
Eq 100-i (including
impedance index at 100 kHz): TBW (L) = (0.51 x
impedance index at 100 kHz)
1 6.3,
Eq 100-iwag (including
impedance index, weight, age, and
gender): TBW (L) = (0.35 x impedance index at 100
kHz)
2
(0.17 x weight) - (0.11 x age)
3 (2.66 x
gender)
4
7.7,
iEq 1-i (including impedance index at 1 kHz):
ECW (L) = (0.24 x impedance index at 1 kHz)
5
4.1.,
Eq
1-iwa (including impedance index, weight, and
age): ECW (L) = (0.20 x impedance index at 1 kHz)
6
(0.07 x weight) - (0.02 x age)
7 2.3
Address all correspondence and requests for reprints to: Dr. F. Roelfsema, Department of Endocrinology, Leiden University Hospital, Albinusdreef 2, 2333 AA Leiden, The Netherlands.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Patients with GHD had significantly lower ECW and TBW than healthy controls. In addition, the ECW to TBW ratio was significantly lower in GHD patients than in healthy controls. Four weeks of GH treatment significantly increased body weight, TBW, ECW, and ECW/TBW. A further increase in TBW, but not ECW, was found after 52 weeks of treatment. The mean increases in TBW and ECW from the baselines were 2.5 ± 0.3 and 2.0 ± 0.3 L, respectively.
The correlation coefficient and the estimated reliability between measured and estimated TBW and ECW at any time point were all high (>0.91 and >0.95, respectively). In general, both ECW and TBW were overestimated by multifrequency BIA in GHD adults. During treatment, the overestimation of both ECW and TBW diminished. The estimation error was correlated with the level of the body water compartment and the ratio of ECW to TBW. The estimated change in ECW with rhGH treatment was underestimated by multifrequency BIA.
We conclude that GHD adults have lower ECW and TBW and a lower ECW to TBW ratio, as measured by dilution techniques. The ECW to TBW ratio can be normalized within 4 weeks of rhGH treatment at a dose of 0.6 IU/day. Finally, we conclude that multifrequency impedance measurements do not give valid estimates of body water compartments in the follow-up of patients with GHD.
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In GHD adults, GH therapy appears to increase FFM and decrease fat mass, thereby improving body composition (7, 8). Bengtsson et al. (9) reported an increase in TBW, measured by dilution of tritiated water. Møller et al. (4) showed an increase in ECW within 41 h, but did not measure changes in TBW. We investigated the changes in both TBW and ECW, measured by dilution techniques, after 4 and 52 weeks of treatment with recombinant human GH (rhGH) in GHD adults. To prevent side-effects and supranormal serum insulin-like growth factor I (IGF-I) levels, a low, physiological dose of 0.6 IU/day was given for the first 4 weeks. The dose at 52 weeks of treatment was an individually tailored dose, using a range of 0.6–1.8 IU/day, to maintain the concentration of serum IGF-I within the normal laboratory range.
Dilution techniques are the most accurate methods for measuring body water compartments, but they are invasive, expensive, and thus difficult to apply to many subjects. Therefore, a second aspect of this study was to compare the results of the dilution techniques with those of the more convenient, multifrequency BIA method both at baseline and during rhGH therapy. Measuring impedance at multiple frequencies improves, at least in healthy controls, the accuracy of the estimation of ECW and TBW (10, 11, 12). In this study, TBW and ECW were estimated using the equations developed by Deurenberg et al. (12), which are based on measurements in apparently healthy subjects. The validity of these equations in patient populations, such as in adults with GHD in this study, has yet to be demonstrated. Therefore, the results using the multifrequency BIA method have been compared with those using the dilution techniques.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Five males and nine females (mean age, 48 yr; range, 33–67 yr) with adult-onset GHD, randomly selected from a study population of 60 patients (13), were studied. A peak serum GH response of less than 7 mU/L during insulin-induced hypoglycemia confirmed GH deficiency (GHD). None of the patients had a body mass index (BMI) greater than 32 kg/m2. The etiology of GHD was a pituitary adenoma in eight patients [nonfunctioning adenoma (n = 4), ACTH-producing adenoma (n = 3), and prolactinoma (n = 1)]. In the other six patients the etiology was trauma (n = 1), Sheehan’s syndrome (n = 1), or craniopharyngeoma (n = 4).
All patients received conventional substitution therapy as indicated. Substitution therapy was monitored during rhGH therapy, and doses were adjusted as requested. Twenty-eight healthy adult controls (10 men and 18 women) of comparable age, weight, and height were evaluated at the Department of Human Nutrition. Informed consent was obtained from all subjects, and the study was approved by the ethics committee of Leiden University Hospital.
Design of the study
All adults with GHD were treated with sc injections of rhGH
(Genotropin, Pharmacia & Upjohn, Peptide Hormones) given every evening
for 52 weeks. All patients started with a dose of 0.6 IU/day (
0.2
mg/day) for the first 4 weeks. After 52 weeks, the dose varied between
0.6–1.8 IU/day (0.2–0.6 mg/day), mainly based on individual serum
IGF-I levels.
At the start of the study and after 4 and 52 weeks of rhGH therapy, TBW and ECW were measured by both multifrequency BIA and dilution techniques.
Body composition
Body weight and height. With a minimum of clothes, weight was measured to the nearest 0.1 kg. Height was measured barefoot to the nearest 0.001 m. The BMI was calculated as weight (kilograms)/height (meters)2.
Dilution techniques. TBW and ECW were determined by dilution of deuterium oxide and potassium bromide, respectively. A cocktail of an accurately weighed dose of 15 g deuterium oxide and 900 mg bromide (1.34 g as potassium bromide) was orally administered. After 2.5–3 h of dilution, a venous blood sample was taken, and plasma was separated and stored at -20 C until analysis. Deuterium was determined in plasma after sublimation by infrared spectroscopy (14). TBW was calculated using a correction factor of 0.95 for nonaqueous dilution (15). Bromide in plasma was determined after ultrafiltration by high performance liquid chromatography (16). ECW was calculated using a correction factor of 0.9 for nonextracellular distribution and a correction of 0.95 for the Donnan effect (15). Intracellular water (ICW) can be calculated by subtracting ECW from TBW.
Impedance measurement. Patients were measured after voiding, using a tetrapolar electrode placement with a surface area of 5 cm2 at the left side of the body. Body impedance was measured with a Human-IM Scan impedance analyzer (Dietosystem, Milan, Italy). An impedance scan was made at frequencies ranging from 0.3–100 kHz. For clarity, only impedance values at 1, 5, 50, and 100 kHz are given. The impedance index was calculated as height (centimeters)2/impedance (ohms). TBW and ECW were calculated using the equations developed by Deurenberg et al. (12) based on a healthy control group (where weight is in kilograms, age is in years, and, where gender has a weight factor, females = 0 and male = 1):
Assays
The total serum IGF-I concentration was determined by RIA (Incstar, Stillwater, MN) after extraction and purification on ODS-silica columns. The interassay coefficient of variation was less than 11%. The detection limit was 1.5 nmol/L. Age-related normal data were determined in the same laboratory. IGF-I was also expressed as a SD score from age-related normal levels.
GH was measured with a time-resolved immunofluorescent assay (Wallac, Turku, Finland) specific for the 22-kDa GH protein. Standards were human biosynthetic GH (Pharmacia, Uppsala, Sweden) diluted in bovine calf serum and calibrated against the WHO First International Reference Preparation 80–505 (to convert micrograms per L to milliunits per L, multiply by 2.6). The detection limit of the assay was 0.03 mU/L (0.012 µg/L), and the intraassay coefficient of variation was less than 8.4%.
Statistical analysis
Statistical analysis was performed using SPSS for Windows (release 7.0, SPSS, Chicago, IL). Results are expressed as the mean ± SEM unless specified otherwise.
Differences between patients and controls were tested with Student’s unpaired t test. Differences in time and differences between measured and estimated body water were tested with Student’s paired t test. Pearson’s product-moment correlations were calculated. The level of significance is 0.05.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Some characteristics of the subjects and data on body water,
measured by dilution techniques and body impedance, are shown in Table 1
. No significant differences were found
for age, height, weight, or BMI between patients and controls. Female
GHD patients had significantly lower ECW, TBW, and ECW to TBW ratio
(ECW/TBW) than female healthy controls (P = 0.0005;
P = 0.0275, and P = 0.0035,
respectively). Both ECW and ECW/TBW were significantly lower
(P = 0.046; P = 0.003) in male GHD
patients than in healthy male controls. No differences in TBW were
found between male GHD patients and healthy controls (P
= 0.304). However, after correction for the small insignificant
difference in height, TBW was significantly lower in male GHD patients
than in healthy controls (P = 0.010).
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rhGH therapy
Table 2 shows the levels of serum
IGF-I and body water parameters, measured by dilution techniques and
multi-frequency BIA, at baseline and during rhGH treatment in patients
with GHD. Figure 1 shows the absolute
changes in body water, measured by dilution techniques. As there was no
difference with treatment between male and female patients in the
percent increase in TBW and ECW, results are given for the combined
group.
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All patients started with a dose of 0.6 IU rhGH for 4 weeks.
Serum IGF-I increased significantly (P < 0.0005),
reaching low normal values (Table 2
). Body weight and TBW significantly
increased with treatment (P = 0.001 and
P = 0.002, respectively). ECW increased from 12.9
± 0.7 to 14.9 ± 0.8 L (P < 0.0005), and ECW/TBW
increased from 0.39 ± 0.01 to 0.44 ± 0.01
(P < 0.0005). No significant differences were found
between the 4-week treatment levels of ECW, TBW, and ECW/TBW and those
in healthy controls.
The absolute increase in ECW (
ECW) was positively correlated
with both baseline weight (r = 0.711; P = 0.004)
and baseline body surface (r = 0.650; P = 0.012).
In addition, ECW tended to correlate with baseline ECW/TBW
(P = 0.054). The percent increase in ECW after 4 weeks
of treatment was not dependent on either body weight (P
= 0.258) or body surface (P = 0.414), but was dependent
on the ECW to TBW ratio (r = -0.581; P = 0.029).
Neither the absolute nor the percent increase in TBW was correlated
with any of the above-mentioned factors. A significant decrease in
impedance at all four frequencies was found after 4 weeks of
treatment.
52 weeks of treatment
One female GHD patient was withdrawn from the study because she expressed the wish to become pregnant.
After 52 weeks, the mean GH dose was 1.6 ± 0.1 IU/day, with a range of 0.6–1.8 IU/day. Serum IGF-I significantly increased to a mean SD score of +0.9 ± 0.4 based on age-related normal values (P < 0.0005).
A further increase in TBW was found after 52 weeks of treatment (P = 0.001). The mean increase in TBW from baseline was 2.5 ± 0.3 L (7.7 ± 0.8%; P < 0.0005). ECW did not change between 4 and 52 weeks of treatment. The ratio ECW to TBW decreased between 4 and 52 weeks of treatment, but was still significantly higher than baseline values. After 52 weeks of rhGH treatment in GHD adults, TBW, ECW, and ECW/TBW were no longer significantly different from levels in healthy controls.
The impedance at low (1 and 5 kHz), but not at high (50 and 100 kHz), frequencies was significantly decreased compared to 4-week treatment data (P = 0.224, P = 0.131, P = 0.012, and P = 0.004 at 1, 5, 50, and 100 kHz, respectively). All impedances were increased compared to baseline levels (P < 0.005).
Neither incremental values nor percent values of TBW and ECW were correlated with the GH dose or serum IGF-I levels after 52 weeks of treatment. The percent change in serum IGF-I after 4 and 52 weeks of treatment was correlated neither with the percent increase in ECW nor the percent increase in TBW.
Comparison of TBW and ECW determined by multifrequency BIA with dilution techniques
TBW and ECW were estimated using several regression equations
reported by Deurenberg et al. (12) and compared with TBW and
ECW, as determined by deuterium oxide and potassium bromide dilution,
respectively. There was a strong correlation between measured and
estimated levels (ECW, r > 0.91; TBW, r > 0.96). In
addition, the estimated reliability was 0.98 or higher for TBW and 0.95
or higher for ECW. The regression equations based on the impedance
index at 1 and 100 kHz were slightly better in estimating ECW and TBW,
respectively, than the equations based on the impedance indexes at 5
and 50 kHz, respectively. Therefore, only data based on the impedance
indexes at 1 and 100 kHz are reported. The difference between measured
and estimated levels in GHD adults are shown in Fig. 2.
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, the estimation error
(measured - estimated) significantly correlated with both the
level of TBW and the ECW/TBW ratio (r = 0.419 and r =
-0.608, respectively). The individual estimation errors ranged from
-16.4% to +9.0% (mean, -4.2 ± 0.8%). The change in TBW, as
measured by deuterium oxide, compared with the equation is shown in
Table 3. No significant differences were
found between the measured change and the estimated change after 4 and
52 weeks of treatment.
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). The measured change in TBW between baseline and 52
weeks of treatment, however, was significantly lower when estimated by
multifrequency BIA (P < 0.0005).
ECW was overestimated at baseline (-1.6 ± 0.3 L; P <
0.0005) using Eq 1-i in GHD patients, which disappeared after 4 and 52
weeks of rhGH treatment. The estimation error of this equation
significantly correlated with both the level of ECW (r = 0.639)
and the ECW/TBW ratio (r = 0.569; Fig. 3). The individual
estimation errors ranged from -31.5% to +10.8% (mean, -6.3 ±
1.4). The change in ECW after both 4 and 52 weeks was underestimated
with this regression equation compared with the change in ECW measured
by dilution of potassium bromide (Table 3).
The inclusion of weight and age in the equation (Eq 1-iwa) worsened the
estimation of ECW both at baseline and during treatment. The estimation
error of this equation was significantly correlated with both the level
of ECW (r = 0.328) and the ECW/TBW ratio (r = 0.652). The
individual estimation errors ranged from -35.2% to +7.0% (mean,
-8.1 ± 1.5%). The estimated change in ECW during rhGH therapy
was underestimated (Table 3).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In contrast to our results, Hoffman et al. (3) found a low ECW level, as suggested by sodium dilution, which corresponded to the decrease in FFSTM, estimated by dual energy x-ray absorptiometry. A disadvantage of dual energy x-ray absorptiometry is that changes in tissue hydration could affect the outcome (17); FFSTM will be underestimated when the hydration is decreased, and the ECW to FFSTM ratio will thus be overestimated. The results of Hoffman et al. (3) are, however, not in conflict with our results when the intracellular hydration, thus the ICW to body cell mass ratio, is increased in GHD patients. As Hoffman has also reported both an increase in ECW after just a few days of GH therapy in GHD adults (18) and an increase in the ECW to FFSTM ratio in acromegaly (19), we conclude that the level of ECW in GHD patients is lower than expected on the decreased BCM.
The frequently encountered side-effects during the first weeks of GH treatment are dose dependent and relate to the increment in ECW (7, 8, 18). Therefore, we were interested in the effect of a low dose of rhGH (0.6 IU/day) on TBW and, more importantly, ECW. We have recently shown that this dose can increase serum IGF-I into the low normal range (13). It was, therefore, not surprising that this dose increased ECW and the ECW/TBW ratio to normal values within 4 weeks of GH treatment. The mean increase in ECW of 2 L after 4 weeks of treatment did not change any further with the continuation of GH treatment at doses between 0.6–1.8 IU/day for another 48 weeks.
In addition to the lower dose, we also used a dose that was independent of weight or body surface. The reason for this was the reported negative correlation between physiological GH production and body fat (20, 21). Using a dose of rhGH based on weight is, therefore, nonphysiological. This study confirms this thought; no difference was found between heavy and light GHD patients in the percent change in ECW with 0.6 IU/day rhGH treatment for 4 weeks.
The expansion of ECW after GH administration was noticed by Ikkos in 1959 (22). The acute increase can be explained by the sodium-retaining effect of GH. The causal mechanisms are not yet fully known. GH (or IGF-I) could have a direct effect on the kidney. In addition, GH (or IGF-I) can influence, more or less indirectly, humoral factors influencing fluid homeostasis. The direct influence of GH (or IGF-I) on renal tubular function was already suggested by Biglieri (23) and Ludens (24), as it was demonstrated that GH administration also resulted in sodium retention in adrenalectomized humans and experimental animals. Further evidence that GH (or IGF-I) may act directly on renal function is the presence of receptors for both GH and IGF-I on the renal proximal tubular cell (25, 26, 27, 28). In addition to its direct effects, GH can influence the number of angiotensin II receptors in the kidney and, thus, the tubular reabsorption of sodium (29).
One of the most powerful mechanisms of sodium conservation is the activation of the renin-angiotensin-aldosterone system. The renin-angiotensin-aldosterone system has been reported to be suppressed in hypopituitary patients (30) and stimulated by GH in healthy humans (31) and in GHD patients (18, 32, 33). However, some studies could not demonstrate an increase in aldosterone with GH treatment (4, 18). Another humoral mediator in the sodium-retaining effect of GH could be the decreased levels of plasma atrial natriuretic peptide; decreased levels after rhGH therapy were found by Møller et al. (34), but could not be confirmed by others (4, 18).
The increase in ECW during the first 4 weeks of GH treatment fully explained the increase in TBW. We even found a small decrease in calculated ICW. However, caution should be used in the interpretation of these results, because ICW is indirectly determined by subtracting ECW from TBW. Moreover, for the calculation of ECW by dilution of bromide, corrections for the nonextracellular distribution and the Donnan factor, which are fixed at 0.9 and 0.95, respectively, are applied (15). A small decrease in ICW with rhGH treatment would be in agreement, however, with the hypothesis that GH influences the cellular water content, possibly by activating sodium-potassium-adenosine triphosphatase activity (35, 36). The increase in ICW found between 4–52 weeks of GH treatment is probably coupled with the increase in body cell mass.
Many investigators have reported data on the effect of GH on both TBW and ECW measured by BIA at a frequency of 50 kHz in adults with GHD. At this frequency, however, not all body water is responsible for the conductance of the current. The estimation of ECW and/or TBW is, therefore, based on the normally rather constant relation between ECW and TBW (13). The methodology has been recently improved by the introduction of multifrequency impedance analyzers, with which it is possible to distinguish between ECW and TBW (10, 11, 12). Theoretically, an alternating current with low frequency (1–5 kHz) is not able to penetrate the cell membrane because of the high capacitive resistance of the membrane. Consequently, the measured impedance at low frequencies is a measure of ECW only. At high frequencies (50–100 kHz) the capacitive resistance of the cell membrane diminishes, and the measured impedance will be related to TBW. In healthy young men and women, the multifrequency impedance method has recently been validated for the assessment of both ECW and TBW (10, 11, 12).
In this study the equations from the validation study by Deurenberg et al. (12), were used to estimate TBW and ECW in adults with GHD, and the estimated values were compared with the values obtained by dilution techniques. The equation based on the impedance index at 100 kHz (Eq 100-i) slightly overestimated TBW at baseline and during rhGH treatment in adults with GHD. Although the addition of factors such as weight, gender, and age improved the estimation of TBW at baseline, it decreased the usefulness of the measurement during rhGH treatment due to a significant change in the estimation error during treatment. Thus, an equation for TBW in which weight, age, and gender are included along with the impedance introduces an extra error in the analysis of data used to guide the follow-up of patients with GHD treated with rhGH.
At baseline, ECW was overestimated with multifrequency BIA, which could be explained by the lower levels of ECW and the lower ECW/TBW ratio in patients with GHD. As rhGH treatment increases, and thus normalizes, both ECW and ECW/TBW levels within 4 weeks, the estimation error of ECW diminished during rhGH treatment. The absolute change in estimated ECW with rhGH was, therefore, significantly lower than the measured change. The influence of body water distribution on the estimation error of ECW is thus not only apparent when measuring impedance at 50 kHz (37), but also when measuring impedance at multiple frequencies.
In conclusion, using dilution techniques for the measurement of both ECW and TBW, we found a low ECW/TBW ratio in adults with GHD, which can be normalized by 0.6 IU/day rhGH treatment. As this method is less convenient for clinical practice, we investigated whether both ECW and TBW could also be correctly estimated by multifrequency BIA. In adults with GHD, the quantitative estimation of changes in mainly ECW, but also in TBW, appeared to be unsatisfactory, however, when these changes coincided with changes in body water distribution, as during rhGH therapy.
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Acknowledgments |
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Footnotes |
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Received April 1, 1997.
Revised June 16, 1997.
Accepted June 27, 1997.
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References |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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) and TBW (
) during 4 and 52 weeks of
rhGH therapy. Both TBW and ECW increased significantly after 4 weeks of
rhGH (P = 0.002 and P <
0.0005, respectively) and after 52 weeks of rhGH treatment (both
P < 0.0005). The level of TBW, but not ECW, was
significantly higher at 52 weeks of treatment than at 4 weeks of rhGH
treatment (P = 0.001 and P =
0.696, respectively).
, 4 weeks of
rhGH treatment; *, 52 weeks of rhGH treatment. Values are the mean
± SEM. TBW is estimated by Eq 100-i, in which the
estimation is solely based on the impedance index at 100 kHz. TBW is
also estimated by Eq 100-iwag, in which weight, age, and gender along
with the impedance index at 100 kHz are included. ECW is estimated by
both Eq 1-i (based solely the impedance index at 1 kHz) and Eq 1-iwa
(based on the impedance index at 1 kHz and the weight and age of the
patient). a, P < 0.0005; b, P
< 0.001; c, P < 0.01.