BY WHOLE—BODY COUNTING:

SCREENING OF PATIENT POPULATIONS

Pierre A. Delwaide

University of Liege, Liege, Belgium

A statistical study of body potassium measurements in the disease groups was undertakenwith correlations between repetitive measurements and the course of the disease.

Total-body potassium was measured in 750patients with a whole-body counter equipped

with 4ir plastifluor scintillators. Prelimitwrystudies on control subjects yielded reference

norms based on regression equations as a function of age and weight and demonstrated anexcellent correlation, in healthy subjects, between total-body potassium and total-body water or lean body mass. Results obtained in thepatients were expressed as a percentage of maxi

mally individualized reference norms, thusenabling comparisons to be made despite theheterogeneity of the data. Screening of patientsin ten disease groups showed that total-body po.tassium was frequently lowered. At least insofaras mean values are concerned, low potassiumlevels were characteristic not only of patientswith cirrhosis, amyotrophy, and obesity but alsoof those with heart failure, high blood pressure,renal failure, and even stabilized diabetes andtreated hyperthyroidism. Longitudinal studiesin cirrhotic patients also disclosed a marked instability of body potassium over time. Depictionis not necessarily irreversible but fatal issues

were preceded by a drastic fall. The system responsible for this potassium deficit appears tobe the skeletal musculature where the lossesseem to be a general and relatively nonspecificresponse.

The introduction of whole-body counting techniques into hospital use has facilitated the measurement of total-body potassium, a parameter of bodycomposition which is as significant in human pathology as in human physiology. Total-body potassiumshows a clear-cut tendency to be low in many dis

ease states, including uncontrolled diabetes, hepatic,cardiac, renal, and neuromuscular diseases, and themeasurement conditions are such that one is in practice determining intracellular potassium. The dataobtained can thus add significantly to our knowledgeconcerning the intracellular compartment. However,the wide range of absolute values of body potassiumin normals, the scatter of results even in homogeneous subject groups, the difficulty of finding a whollysatisfactory reference index for expressing the values,and the nonspecificity of the perturbations observedin a variety of diseases, all tend to complicate theissue. In particular, the distinction between “normal―and “pathologic―values is often a subtle one inindividual cases. It was thus felt that a statisticalapproach to the problem might prove useful. In thepresent study, 750 subjects in ten disease groupswere screened. An attempt was made to bring outthe particular characteristics of each group or condition without being too concerned with distinguishing on an individual basis between “normal―and“pathologic―.Also investigated was the possibilityof doing longitudinal studies of clinical course withthe same whole-body counting technique.

MATERIALS AND METHODS

The whole-body counter used at the Universityof Liege has been described previously ( 1 ) . Its 4irplastifluor detector is one of the few of its kind inthe world (2) . Efficiency and reproducibility areexcellent, although to the detriment of resolution.As a result, the counting time can be reduced to 200sec, but calibration must rely not on spectrometrybut on an algebraic technique based on the ratiobetween two channels (1 ) . The counter's technicalcharacteristics ( background, geometry, resolution,

Received Apr. 22, 1972; revision accepted Aug. 23, 1972.For reprints contact : Pierre A. Deiwaide, Laboratory of

Clinical Chemistry, I rue des Bonnes-Villes, B-4,000 Liege,Belgium.

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BODY POTASSIUM MEASUREMENTS

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and efficiency) are comparable to those of the morewidely used detectors with liquid scintillators (3).Accuracy has been verified using the double calibration method with a tracer dose of 42K. The effectof the subject's body build on his results has beenstudied with phantoms of increasing weight andvariable potassium concentrations; the use of severaltypes of phantoms, simulating individual somatotypemore closely, proved to be essential for good precision and has been adapted for routine use. Thecalibration technique as a whole is regularly subjected to quality control procedures based on dailymeasurements of the main parameters that serveto establish formulas : background, potassium standard (saturated solution of KHCO:3) , phantom (Greyand Marten, Ltd. ) containing 140 gm of potassiumand 3 nCi of 137Cs, and reference subjects. These procedures guarantee a technical reproducibility of 5%over time, which is better than that obtainable withisotopic dilution methods (4).

The problem of “referencenorms― is a complexone. To evaluate this complexity, 1,000 controls ofvarious ages and weights in good health were countedand distributed into cells based on sex, age, andweight.@(Computations showed that height is not anindependent factor. ) Computer processing of thesedata disclosed that the expression of results in termsof body weight (gm/kg or mEq/kg) was the mostappropriate method, making it possible to derive thefollowing linear regression equations:

For male subjects, Y = 3.396 —0.012 x1— 0.014 x2;

For female subjects, Y = 2.707 —0.010 x,— 0.011 x2,

where Y is the total potassium (gm/kg) , x1 the age(years), and x2 the weight (kg).

The 5 % confidence limits within homogeneouscells varied with the cell, ranging from 5 to 15% ofthe value estimated. Repeated counts on the samesubjects (ten men and ten women each measured20 times within 1 month) confirmed that interindividual variations are greater than intra-individualvariations and thus that the total-body potassiumvalue can be considered as a relative “constant―withrespect to individual subjects. These equations thusallow the prediction of individually fitted referencenorms for each patient. Recently, total potassiumwas very accurately measured with a highly sophisticated body counter (5) , yielding mean valuesslightly lower than ours (6) . However, this divergence is probably due to the selection of the controlpopulation which had higher mean body weights(6) than our subjects. As our body counter andcalibration methods provide an invariant response

relating to body size it was not thought necessary torelate the body potassium to an index of bodythickness, such as (weight/height) 1/2, useful forother types of body counter (7).

In healthy adult subjects there is an excellent correlation between total potassium and the values ofboth lean body mass as calculated from anthropometric measurements (8) and total-body water asmeasured by isotopic dilution. (Isotopic dilution alsoyields an estimate of lean body mass which is inexcellent agreement with anthropometric measurements.)

Figure 1 shows the correlations of body potassium, with (A) lean body mass and (B) with bodywater (75 young adult subjects) . However, it shouldbe stressed that these correlations were establishedin subjects in good health and thus presuppose thatthe potassium level in the lean body mass is a constant, or, in other words, that there are no potassiumabnormalities. Since this presupposition does notnecessarily hold under pathologic conditions, theapplication of such relationships to the ill requiresgreat caution. Although the reference to body weightalone is open to some criticism from a physiologicstandpoint (9) , it can be used for clinical purposesto establish “referencenorms―in the absence ofother criteria of demonstrably greater value. Thisapproach yields norms individualized for the age andbody build of the patients according to Eqs. 1and 2. The values obtained in pathologic casesmay thus be expressed as a percentage of the pre

(1) dictedvalue.In a number of cases total-body water and ex

changeable sodium were measured by the classic(2) isotope-dilution techniques. These results have also

been expressed as a percentage of reference normsdrawn from tables in the literature (10) . Latelythere is an important restriction on potassium measurements made by low-resolution whole-body counters : once the subject has been administered a radioisotope emitting gamma rays of energy greater than0.3 MeV, no counts can be made as long as theistope remains active.

A total of 750 patients were screened for bodypotassium; their distribution by disease groups isshown in Table 1 with the age and weight ranges.The choice of these disease groups was oriented byreports from the literature, based often on isotopicdilution of 42K but also on whole-body counting,that total potassium diminishes in diabetes (11,12),cirrhosis of the liver (13,14), heart failure (13,15),hyperthyroidism ( 16) , and neuromuscular diseasesaccompanied by wasting (13,17). The question ofpotassium deficit in uncomplicated hypertension( 18) and renal failure is more controversial. For

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RangeofagesRangeGroups

based on diagnosis No. of cases (yr)of weights Remarks

DELWAIDE

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FIG. 1. Correlationsbetweentotal-bodypotassium(mEq)and(A) lean body mass (kg) as calculated from anthropometric measurements (men : r : 0.7786, p < 0.001; women : r : 0.6307, p <

purposes of comparison, patients with angina pectoris or myocardial infarction without decompensation, neuromuscular diseases without atrophy, anddermatologic conditions were counted. Screening waslimited to patients in a generally satisfactory condition, most of them ambulatory and able to come tothe counting room, generally unassisted, from inpatient or outpatient services. The diabetic patientswere stabilized with either insulin or oral hypoglycemic agents; the hypertensives showed no majorcardiac or renal complications; the hyperthyroid patients had been treated at least 1 year earlier with131! and appeared clinically cured; and the heart

0.001) and (B) total water (liters) measured by tritiated water dilution (men : r : 0.6030, p < 0.001; women : r : 0.4959, p < 0.01)(healthy young adults).

disease patients had no clinically apparent edema.By excluding bedridden, cachectic, and very weakened subjects, we attempted to avoid the influenceof nonspecific factors such as severe dietary restriction, overall marasmus and the results of chronicimmobilization.

RESULTS

Table 2 provides some examples of our mannerof expressing results. It can be seen that the onlysignificant values are those which are based on individualized reference norms, computed from Eqs.

TABLE 1. CLASSIFICATION OF PATIENTS SCREENEDFOR TOTAL-BODY POTASSIUM

1.Diabetes1 15(58M;57F)16—7240—9627 treated withinsulin2.Essentialhypertension80(39M;41F)20—7050—10010 treated with diuretics,

slight meanoverweight3.Renalfailure80(38M;42F)18—7737—88Severe failure in need of

dialysis4.Cirrhosis75(SOM;25F)34-7540—945.Obesity60(15M;4SF)16-6760—1056.Heart

disease withdecompensation55(22M;33F)33—8041—97Anginaor infarction withoutdecompensation45(23M;22930—7944—847.Hyperthyroidism40(12M;28F)17—6744—81Treated

with 1@@l1 yrearlier8.Neuromusmular

diseases withoutatrophy35(1SM;20F)18—7545—92Neuromusculardiseases withatrophy30(18M;12F)18—7843—809.Adrenal

insuffIciency20(11M;9F)35—6544—8710.Misc.skin diseases115(62M;53F)17—8841—100Total750(363M;387F)

42 JOURNAL OF NUCLEAR MEDICINE

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WeightReferencevalues

from Eqs. 1 and 2Measuredvalues%ref.DiagnosisSex Age (kg)(mEq/kg) mEq (mEq/kg)value

Mean values in mEq/kgMe

%ofanvalues

referenceasnormMenWomen

BODY POTASSIUM MEASUREMENTS BY WHOLE-BODY COUNTING

TABLE 2. DATA PROCESSINGOF SOME INDIVIDUAL VALUES OF TOTAL-BODY POTASSIUM

VirilismAnorexia nervosaGastric ulcerIncipient pulmonary carcinoma

Ulcerative colitisGastric ulcerSpasmophiliaHyperadrenocorticismAdvanced pulmonary carcinomaRegional ileitisUlcerative colitisUlcerative colitisToxemia of pregnancyProstatic carcinoma with metastasesSevere malnutrition

These casesdo not belong to disease

FFMMMFFMMFMMFMF

22 7718 4167 4867 6942 8433 5422 4032 7240 6140 5066 5865 7232 9063 6824 41

42.153.249.241344.145j

52.551.452.945.145.941.235.843.351J

221523972495294938062244189531902692187621722374232220701222

47.159.051.843.045.342.047.244.344.137.537.532.925.630.529.1

11211110510310392908683838280727056

groups studied in Tables 1 and 3.

1 and 2. One of the advantages of this procedureis to permit intergroup comparison despite theheterogeneity of individual data.

In this light, Table 3 gives the mean values obtamed for the groups of Table 1. It will be observedfrom Table 3 that only by expressing the recordedvalues as a percentage of the reference norms (shortcircuiting sex differences) , were we able to demonstrate that the overall characteristic of most of thegroups was a reduction in total-body potassium.Mean potassium was very clearly lowered in casesof amyotrophy, cirrhosis, obesity, and heart failure.The mean deficit was less marked but still significantin patients with hypertension, diabetes, renal failure,and hyperthyroidism. In the diabetic patients, therewas a minimal difference between the insulin-treatedand noninsulin-treated patients. Scatter was not appreciably greater in the patients than in the pre

viously measured controls. Hence, the changes inpotassium, expressed in terms of a common index,do appear to be a characteristic of the disease groupsstudied and not an artifact of patient selection. Without having to introduce the difficult distinctionbetween “normal―and “pathologic―values of bodypotassium, we found that each group was characterized by a definite pattern insofar as mean potassiumvalue was concerned.

In Fig. 2A, the individual values (expressed as apercentage of the reference norms) are listed for themost significant disease groups studied. Figure 2Bgives the frequency distribution of total potassiumlosses as a function of magnitude expressed as apercentage of the reference norm. While the potassium loss is invariably present in amyotrophy, itsfrequency decreases as the mean values rise. Thispart of the figure demonstrates that the means ob

TABLE 3. MEAN VALUES OF TOTAL-BODY POTASSIUM

1. Neuromuscular diseases with atrophy2. Cirrhosis3. Obesity4. Heart diseases with decompensation5. Essential hypertension6. Diabetes (without insulin)7. Diabetes (with insulin)8. Renal failure9. Hyperthyroidism (treated)

10. Misc. skin diseases11. Neuromuscular diseases without atrophy12. Angina or myocardial infarction without decompensation

43.3 ±10.038.5± 7340.2± 7.144.1± 11.542.8± 9.344.1 ± 8.246.2± 9.446.4± 9.645.6 ± 11342.3± 8.949.7± 8.446.7± 7.8

273 ± 11.634.4± 8.331.4± 4.834.6± 8.235.6 ± 6.534.9± 9.039.2 ± 10.9393 ± 9.237.2± 8.132.6± 9.537.7 ± 7.438.2 ± 8.2

71.473.5

78.680.486.488.689.988.688.891.694.294J

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potassium values as function of relative degree of kaliopenia (cx.pressed as percentage of reference norms). While potassium loss ispresent in amyotrophy, its frequency decreases as mean values rise.

are negative : these patients constituted a homogeneous subgroup with severe renal failure of pyelonephritic origin (19).

It is well known that there is no correlation between serum potassium and total-body potassium.Figure 3 shows that this is true regardless of how

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FIG. 2. (A) individualvaluesof total-bodypotassium,cxpressed as percentage of reference norms, in various diseasegroups. (B) frequency distribution, in these groups, of total-body

tamed are associated with a general shift of the frequency distribution and not due to certain aberrantor discordant individual values. It will also be notedthat the renal failure group contains a small numberof significantly increased values, which are exceptions to the general rule that all potassium changes

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44 JOURNAL OF NUCLEAR MEDICINE

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BODY POTASSIUM MEASUREMENTS BY WHOLE-BODY COUNTING

total potassium is expressed (mEq/kg or relative toreference norm ) , notably in two diseases whereserum potassium levels are known to vary in bothdirections : cirrhosis and severe renal failure.

Simultaneous determinations of total water andexchangeable sodium by isotopic dilution were alsoperformed in some of the patients subjected towhole-body counting. Figure 4 attests to the complete absence of correlation between the results oftotal water and total potassium in the patients testedin contrast with the excellent correlation obtainedin healthy subjects (Fig. 1B) . Figure 5 similarlyconfirms the lack of correlation between total potassium and exchangeable sodium. It does thus appearthat knowledge of one of the parameters of water andmineral composition in no way helps to deduce, inindividual cases, the other parameters or even topredict in what direction they will be shifted.

The inter-individual variability of total-body potassium is greater, in healthy subjects, then the intraindividual variability over short periods of time;this is a recognized feature (20,21 ) . In patients also,longitudinal measurements are thus the logical complement . of the statistical approach which, althoughvaluable for the information it provides about meanbody potassium, furnishes essentially static data. Inchronic disease states, such data provide an “instantaneous― view at some point in a pathologicprocess where the stage of the disease may be ofgreat importance. Cirrhosis with its course markedby successive exacerbations and remissions is a goodcase in point. A total of 25 cirrhotic patients weresubjected to longitudinal measurements for as longas 24 months. Figure 6 shows the results obtainedin ten typical cases expressed as a percentage of thereference norms and compared to the potassium

changes occurring during the same time period in ahealthy reference subject. The short-term fluctuationswere even more marked than those previously described (14) . Over the long term, the fluctuationswere also very great and correlated with the overallclinical course of the patient as determined by hospital admission and discharges. However there wasno correlation with serum potassium. Thus, in addi

tion to the fact that body potassium is lowered incirrhotic patients, this parameter is also highly labileand subject to appreciable short-term variations, asopposed to its stability in the normal subject. It isparticularly interesting to note that the courses witha fatal outcome were preceded by a drastic fall in

potassium. However, even when the depletion is profound it is not necessarily irreversible, even thoughduring remissions potassium never reaches cornpletely normal levels.

DISCUSSION

The results of whole-body counting of potassiumin healthy and ill subjects show that this techniqueis suited rather for studies of populations than toindividual determinations. However, there are relatively few reports of mass screenings in the literature (22,23), and it was felt that a global approachcould clarify a host of questions. Some of the deviations found in the present study were confirmationsof data in the literature (11,17) ; others were eitherunexpected or of unexpected magnitude. Aside fromthe subgroup discussed above ( 19) , characterizedby a relative potassium excess, the deviations arealways negative. Another striking finding is that anappreciable number of patients, distributed in thevarious disease groups, had deficits of considerablemagnitude (Fig. 2A) : values as low as 50% of the

CI.

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FIG. 4. Absenceof correlationbetweentotal-bodypotassiumand total water in disease states (values expressed as a percentageof reference norms).

I, 4b Jo sb too ,@o TOTAL BODY POTASSIUM@ VII

FIG. 5. Absenceof correlationbetweentotal-bodypotassiumand exchangeable sodium (values expressed as percentage ofreference norms).

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DELWAIDE

% ref. val.

A @ek. B MonthsFIG. 6. Longitudinalstudiesof total-bodypotassiumin pa

tients with cirrhosis: (A) short-term study, and (B) long-term study(values expressed as a percentage of reference i@orms).f—death.f—hospitaldischarge. I—hospitalreadmission.

norm are not exceptional. This statistical approach

thus established an unequivocal decrease in totalbody potassium whose relative magnitude seems tobe characteristic of the diseases in question and notmerely a reflection of their chronicity. In contrast,certain conditions similar to the preceding diseases(e.g., rnyocardial infarction without decompensation,neuromuscular diseases without wasting) showbarely any change in total potassium. [The groupof patients with “neuromusculardiseases withoutwasting― deliberately did not include patients withmyasthenia gravis during the phase of exacerbation;in a previous study (24), 15 such patients provedto have a significantly depressed mean value.] Somecases deserve a further comment. In obese patients,the decrease in potassium is clear-cut and cannotbe explained simply by the excess body weight sincethe individual results are expressed in terms of normsderived from equations where weight is a negativefactor. In diabetes, insulin treatment was expectedto be a factor, since this hormone seems involvedin protein anabolism (25) . In our series there was aslight but statistically insignificant difference betweenthe insulin-treated patients and those stabilized without insulin. In renal failure, studies of patients similar

to ours (26) have attributed the decrease of bodypotassium to a reduction in the intracellular compartment. Nevertheless a drop in total-body potassium thus appears to be a rather nonspecific condition, which might almost be called “commonplace―;however, it is compensated for by the characteristicpatterns reflected in Fig. 2B, permitting the diseasesstudied to be rated on a well-defined scale in termsof their effects on body potassium. Total-body potassium disturbances are thus of unquestionablevalue in nosologic descriptions: kaliopenia should beadded to the usual symptoms of diseases such ascirrhosis, heart failure, obesity, and even hypertension, diabetes, and renal failure.

Longitudinal studies carried out in patients withcirrhosis and, as previously studied and reportedelsewhere, renal failure ( 19) and myasthenia gravis(24), reveal that, in addition to being generally low,total potassium in these disease states is markedlyunstable.

Repeated measurements of whole-body potassiumnot only provides a valuable index that parallels theclinical course (for the potassium depletion evenwhen profound is not necessarily irreversible) butalso draws attention to possible disturbances of the

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BODY POTASSIUM MEASUREMENTS BY WHOLE-BODY COUNTING

regulation of intracellular potassium stores and suggests that further studies may be of value.

However, it appears difficult to prove in thesecases a real “decreasein intracellular potassium concentration,― as distinct from a “reduction of leanbody mass―(main potassium store) (13,27) . As amatter of fact, the methods of determination of leanbody mass are subject to caution in severely ill persons and it seems dangerous to use this concept asa reference for potassium in our cases. Indeed the

system primarily responsible for the decrease in totalpotassium seems to be the skeletal musculature, sinceit contains 70% of body potassium (28), as cornpared with 3% for the liver ( 14) , and an evensmaller percentage for the kidneys and heart. Thetotal potassium loss observed in most disease statesis not a direct result of organic lesions but rather ageneral type of disturbance. The pathogenesis of thisdisturbance is still unclear, but it is thought to consist of a distant metabolic repercussion, particularlyvisible in organs having the largest potassium stores.[“Metabolic myopathy― has been described (29)as existing with certainty in endocrine diseases and

with great probability in heart, liver, and kidneyconditions.] Whole-body counting would thus provide a rapid, precise, and easy method of detectingthe magnitude of these repercussions. It should alsobe recalled that the courses ending fatally in ourseries were preceded by a drastic fall in total potassium.

CONCLUSION

The determination of total potassium by wholebody counting is especially useful when investigatinghomogeneous patient groups or performing longitudinal studies. This technique makes it possible tobring out the pattern characteristic of each diseasedespite the heterogeneity of the individual data. Onethus has a “marker―of the intracellular compartment, providing information about the body as awhole. This is an investigational tool of particularlygreat value in this field, where there are few tech

niques available for the study of the intracellularcompartment. For the clinician, the measurement ofwhole-body potassium is a highly useful approachto the pathophysiology of many diseases.

REFERENCES

1. DELWAIDE PA : 4,r plastic scintillator whole-bodycounter for clinical use. I Nuci Med 11: 19—24,1970

2. Directory of Whole Body Radioactivity Monitors, 2nded.Vienna,IAEA, 1970

3. BARNABI CF. JASANI BM : The calibration of a highsensitivity area whole body counter. Phys Med Biol 13: 561—572, 1968

4. PRICE WF, HAZELRIG JB, KREISBERG RA, et al: Reproducibility of body composition measurements in a singleindividual. I Lab Clin Med 74: 557—563, 1969

5. COHN SH, DOMBROWSKI CS, PATE HR. Ct at: A wholebody counter with an invariant response to radionuclide distribution and body size. Phys Med Biol 14: 645—658,1969

6. COHNSH, DOMBROWSKICS: Absolutemeasurementof whole-body potassium by gamma-ray spectrometry. INuci Med 11:239—246,1970

7. TYSONI, GENNAS, JONESRL, et at: Body potassiummeasurements with a total-body counter. I NucI Med 11:255—259,1970

8. CRENIERE: La prediction du poids corporel “normal―.BiométrieHumaine 1: 10—24,1966

9. FRANçOISB: Makeshiftdeterminationof total bodyfat. In Physiopathology of Adipose Tissue, Vague J, ed,Amsterdam, Excerpta, 1969, pp 349—358

10. BERNIERE, VmoN J: Valeurs normales de l'eau atdes Clectrolytes. MétabEau Electrol 7 : 5—51,1965

11. AIKAWA JK, FELT JH, HARREOL CT: Isotopic studiesof potassium metabolism in diabetics. I Clin Invest 32: 15—25, 1963

12. TELFLER N: Exchangeable potassium in diabetics.Metabolism15:502—509,1966

13. NAGANT DEDEUXCHAJSNESC, BUSSET R, COLLET RA,et at : Exchangeable potassium in wasting, amyotrophy,heart diseases and cirrhosis of the liver. Lancet 1: 681—687,1961

14. CASEY TH, SUMMERSKILL WHJ, BIcicFoRD MB:Body and serum potassium in liver disease. 1. Relationshipto hepatic function and associated factors. 2. Relationshipto arterial ammonia, blood pH and hepatic coma. Gastroenterology48: 198—215,1965

15. OLESEN KH : Body composition in heart disease.Total exchangeable potassium, total exchangeable sodium,total exchangeable chloride and derived values for bodycomposition in cardiac disease with and without edema.Acta Med Scan 175: 301—324,1964

16. SAv0IE JC, JUNGERSP: Intracellular potassium in hyperthyroidism. In Current Topics in Thyroid Research, NewYork, Academic Press, 1965, pp 1065—1073

17. KOSSMANN RJ, PETERSON DC, ANDREWS HL: Studiesin neuromuscular disease. I. Total body potassium in muscular dystrophy and related diseases. Neurology 15: 855—865,1965

18. HOLLANDER W, CHOBANIAN AV, BURROWS BA: Bodyfluids and electrolyte composition in arterial hypertension.I. Studies in essential hypertension and malignant hypertension.I ClinInvest40: 408—412,1961

19. DELWAIDE PA, RORIVE 0 : Etude du potassium totalchez des patients en insuffisance rénalechronique. Influencede Ia dialyse. Nephron 8: 173—190,1971

20. BODDY K, KING PC, TOTHILL P, et at : Measurementof total body potassium with a shadow-shield whole-bodycounter: calibration and errors. Phys Med Biol 16: 275—285,1971

21. J0HNv KV, WORTHLEY BW, LAWRENCE JR. et al:

A whole-body counter for serial studies of total body potassium.ClinSci39: 319—326,1970

22. HUGHESD, WILLIAMSRE, SMITH AH: Clinicalstudies in whole-body potassium content measured by

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DELWAIDE

gamma ray spectrometry in health and disease. Clin Sci 32:503—509,1967

23. TYSON I, GENNA 5, JONES RL, et al: Studies of potassium depletion using direct measurements of total-bodypotassium. I Nucl Med 11: 426—434,1970

24. DELWAIDE PA, DELWAIDE PJ, FENDERS CA: Isotopicstudies of body composition in neuromuscular diseases.I NeurolSci15:339—349,1972

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