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C-REACTIVE PROTEIN, LYMPHOCYTE TRANSFORMATION, AND PROTEIN-CALORIE MALNUTRITION
495 occasions when he might wish to influence his firm. The situation has not arisen, but it has been a safeguard. Over the years, in relation to the annual report of the Chief Inspector of Factories, I have objected to the clearly demonstrable fact that the statistics relating to the work of the A.F.D. were incomplete and grossly misleading. These valueless figures have been used as a basis of argument for abandoning care of young people. Even the provisions in the Bill are to be rendered useless by another Bill, not yet published, which plans the virtual destruction of the Youth Employment Service. The background of this E.M.A.S. Bill which is being revealed should be a matter for grave concern. The Bill, in its present form, is regressive and inoperable, and should be reframed. on
Ferneham, Farnham Royal, Bucks.
M. E. M. HERFORD.
PLATELET-COUNTING SIR,-Dr. Beard and his colleagues (Feb. 5, p. 317) accuse us of being prejudiced against " modern particle counting equipment (e.g., the Coulter S) Careless yes (for even in Leeds we have to use a Coulter B for platelet counting!), but not prejudiced. In fact we believe this machine is admirable for routine platelet-counts, but maintain that in the region of 20,000 and below it has the inaccuracy of other methods. Dr. Beard and his colleagues state that " accurate plateletcounts " are obtained. May we ask how does he know they are accurate ? Background and " carry-over " is significant at these low levels and, in a later paper than the one cited, Bulldescribes attempts to minimise these factors. It is our experience that many technicians using counting equipment prefer to perform a count by the traditional countingchamber method when very low counts are concerned. The point we made, and maintain is still valid, is that the 20,000 figure quoted in the editorial and by other workers is, in fact, an arbitrary one, and that if it is strictly adhered to as a guide to platelet therapy, many transfusions will be given which are unnecessary and could be disadvantageous to the patient because platelet antibodies may develop, or one of the other complications of any transfusion-serum hepatitis, for example. Regional Transfusion Laboratory, L. A. DERRICK TOVEY Bridle Path, Leeds LS15 7TW.
S. M.
MANOHITHARAJAH.
C-REACTIVE PROTEIN, LYMPHOCYTE TRANSFORMATION, AND PROTEIN-CALORIE MALNUTRITION SIR,-We were very interested in the observations of Smythe and his colleagues2 on deficiency of cell-mediated
immunity
in
protein-calorie malnutrition.
Further
corre-
lation of their immunological data may be possible in the light of an address by Pauk and his colleagues.33 These authors noted inhibition of phytohxmagglutinin (P.H.A.) stimulation of peripheral-blood lymphocytes by sera with elevated C-reactive protein (C.R.P.) and by purified C.R.P. One wonders if the decreased P.H.A. stimulation in proteincalorie malnutrition could not be explained in part by the elevation of C.R.P. noted by Smythe and his colleagues.’-1 Information about the preparation of leucocytes used, the 1. 2.
3.
Bull, B. S. Am. J. clin. Path. 1970, 54, 707. Smythe, P. M., Schonland, M., Brereton-Stiles, G. G., Coovadia, H. M., Grace, H. J., Loening, W. E. K., Mafoyane, A., Parent, M. A., Vos, G. H. Lancet, 1971, ii, 939. Pauk, Y. K., Kimura, L., Yanagihara, E., Ochiai, H., Tam, R., Muraoka, M., Hokama, Y. Paper presented at the Eighth National Meeting of the Reticuloendothelial Society, Detroit, 1971.
presence of autologous serum in cultures, and the C.R.P. levels of the sera would thus be important in determining whether the diminished lymphocyte transformation seen was a manifestation of a depletion of thymic-dependent
lymphocytes
or an
inhibition by
Division of Immunology-Allergy, Department of Pediatrics, University of Texas Medical Branch, Galveston, Texas 77550, U.S.A.
C.R.P.
RANDALL M. GOLDBLUM ARMOND S. GOLDMAN.
PHENYTOIN AFTER RECOVERY FROM MYOCARDIAL INFARCTION SiR,—The report by the collaborative group1 requires comment regarding methodology and conclusions. Its purpose, as stated, was to determine whether phenytoin had an anti-arrhythmic action, and whether survival twelve months after myocardial infarction was improved in the group treated with phenytoin. The efficacy of the drug as an anti-arrhythmic agent was determined at intervals of six weeks by observing " symptoms, signs " at clinic visits. In one of the hospitals, a one-minute electrocardiogram rhythm strip was recorded has shown that the subduring each visit. Experience " jective awareness of palpitations " is an exceedingly poor measure of arrhythmias. Many patients are unaware when extrasystoles or arrhythmias occur; others report " " palpitations which are unassociated with any change in cardiac rhythm; and others feel palpitations with only a few of their arrhythmic events. Furthermore, the distinction between disorders of atrial or ventricular origin cannot be made by most patients. The recording of a one-minute E.c.G. strip is better than no record at all; but it is insufficient by a factor of 600/1 in comparison with a continuous ten-hour recording obtained on tape by dynamic electrocardiography (Holter in active ambulatory patients. Our experience with over 3000 such recordings, and the experience of many others throughout the world with this straightforward, reliable technique is the basis for emphasising the unreliability of correlating patient-reported symptoms and
monitoring)
findings. We also feel that survival figures cannot be deduced from this study unless it is certain that two different groups were being compared. As emphasised by the wide range of plasma-phenytoin levels in the hospital that performed these studies, many of the " treated " patients may have received merely a large placebo dose. It would, therefore, be necessary to document that treatment with this (or any other) drug-altered arrhythmias of ventricular origin at a statistically significant level before one could conclude that the incidence of " sudden fatal arrhythmias " was
favourably or unfavourably affected. Since there is continuing evidence that ventricular extrasystoles may be an expression of myocardial ischxmiaand since there is a relationship between the frequency per minute, pairing, multifocal origin, and the R-on-T relationship to the development of ventricular tachycardia3 and probably ventricular fibrillationit is extremely important to identify the patients at risk and to provide effective therapy. Rox San Medical Building, 465 North Roxbury Drive,
Beverly Hills, California 90210, U.S.A.
DANIEL J. BLEIFER JOSEPH J. SHEPPARD HAROLD L. KARPMAN SELVYN B. BLEIFER.
Lancet, 1971, ii, 1055. Killip, T. Am. J. Cardiol. 1971, 28, 614. Karpman, H. L., Sheppard, J. J., Bleifer, S. B., Bleifer, D. J. Clinical Applications of Dynamic Electrocardiography; p. 4619. Rand Corporation, Santa Monica, California, 1971. 4. Han, J., Goel, B. G. Electrophysiologic Precursors of Ventricular Tachyarrhythmias. Albany, N.Y. 1. 2. 3.
Ferneham, Farnham Royal, Bucks.
M. E. M. HERFORD.
PLATELET-COUNTING SIR,-Dr. Beard and his colleagues (Feb. 5, p. 317) accuse us of being prejudiced against " modern particle counting equipment (e.g., the Coulter S) Careless yes (for even in Leeds we have to use a Coulter B for platelet counting!), but not prejudiced. In fact we believe this machine is admirable for routine platelet-counts, but maintain that in the region of 20,000 and below it has the inaccuracy of other methods. Dr. Beard and his colleagues state that " accurate plateletcounts " are obtained. May we ask how does he know they are accurate ? Background and " carry-over " is significant at these low levels and, in a later paper than the one cited, Bulldescribes attempts to minimise these factors. It is our experience that many technicians using counting equipment prefer to perform a count by the traditional countingchamber method when very low counts are concerned. The point we made, and maintain is still valid, is that the 20,000 figure quoted in the editorial and by other workers is, in fact, an arbitrary one, and that if it is strictly adhered to as a guide to platelet therapy, many transfusions will be given which are unnecessary and could be disadvantageous to the patient because platelet antibodies may develop, or one of the other complications of any transfusion-serum hepatitis, for example. Regional Transfusion Laboratory, L. A. DERRICK TOVEY Bridle Path, Leeds LS15 7TW.
S. M.
MANOHITHARAJAH.
C-REACTIVE PROTEIN, LYMPHOCYTE TRANSFORMATION, AND PROTEIN-CALORIE MALNUTRITION SIR,-We were very interested in the observations of Smythe and his colleagues2 on deficiency of cell-mediated
immunity
in
protein-calorie malnutrition.
Further
corre-
lation of their immunological data may be possible in the light of an address by Pauk and his colleagues.33 These authors noted inhibition of phytohxmagglutinin (P.H.A.) stimulation of peripheral-blood lymphocytes by sera with elevated C-reactive protein (C.R.P.) and by purified C.R.P. One wonders if the decreased P.H.A. stimulation in proteincalorie malnutrition could not be explained in part by the elevation of C.R.P. noted by Smythe and his colleagues.’-1 Information about the preparation of leucocytes used, the 1. 2.
3.
Bull, B. S. Am. J. clin. Path. 1970, 54, 707. Smythe, P. M., Schonland, M., Brereton-Stiles, G. G., Coovadia, H. M., Grace, H. J., Loening, W. E. K., Mafoyane, A., Parent, M. A., Vos, G. H. Lancet, 1971, ii, 939. Pauk, Y. K., Kimura, L., Yanagihara, E., Ochiai, H., Tam, R., Muraoka, M., Hokama, Y. Paper presented at the Eighth National Meeting of the Reticuloendothelial Society, Detroit, 1971.
presence of autologous serum in cultures, and the C.R.P. levels of the sera would thus be important in determining whether the diminished lymphocyte transformation seen was a manifestation of a depletion of thymic-dependent
lymphocytes
or an
inhibition by
Division of Immunology-Allergy, Department of Pediatrics, University of Texas Medical Branch, Galveston, Texas 77550, U.S.A.
C.R.P.
RANDALL M. GOLDBLUM ARMOND S. GOLDMAN.
PHENYTOIN AFTER RECOVERY FROM MYOCARDIAL INFARCTION SiR,—The report by the collaborative group1 requires comment regarding methodology and conclusions. Its purpose, as stated, was to determine whether phenytoin had an anti-arrhythmic action, and whether survival twelve months after myocardial infarction was improved in the group treated with phenytoin. The efficacy of the drug as an anti-arrhythmic agent was determined at intervals of six weeks by observing " symptoms, signs " at clinic visits. In one of the hospitals, a one-minute electrocardiogram rhythm strip was recorded has shown that the subduring each visit. Experience " jective awareness of palpitations " is an exceedingly poor measure of arrhythmias. Many patients are unaware when extrasystoles or arrhythmias occur; others report " " palpitations which are unassociated with any change in cardiac rhythm; and others feel palpitations with only a few of their arrhythmic events. Furthermore, the distinction between disorders of atrial or ventricular origin cannot be made by most patients. The recording of a one-minute E.c.G. strip is better than no record at all; but it is insufficient by a factor of 600/1 in comparison with a continuous ten-hour recording obtained on tape by dynamic electrocardiography (Holter in active ambulatory patients. Our experience with over 3000 such recordings, and the experience of many others throughout the world with this straightforward, reliable technique is the basis for emphasising the unreliability of correlating patient-reported symptoms and
monitoring)
findings. We also feel that survival figures cannot be deduced from this study unless it is certain that two different groups were being compared. As emphasised by the wide range of plasma-phenytoin levels in the hospital that performed these studies, many of the " treated " patients may have received merely a large placebo dose. It would, therefore, be necessary to document that treatment with this (or any other) drug-altered arrhythmias of ventricular origin at a statistically significant level before one could conclude that the incidence of " sudden fatal arrhythmias " was
favourably or unfavourably affected. Since there is continuing evidence that ventricular extrasystoles may be an expression of myocardial ischxmiaand since there is a relationship between the frequency per minute, pairing, multifocal origin, and the R-on-T relationship to the development of ventricular tachycardia3 and probably ventricular fibrillationit is extremely important to identify the patients at risk and to provide effective therapy. Rox San Medical Building, 465 North Roxbury Drive,
Beverly Hills, California 90210, U.S.A.
DANIEL J. BLEIFER JOSEPH J. SHEPPARD HAROLD L. KARPMAN SELVYN B. BLEIFER.
Lancet, 1971, ii, 1055. Killip, T. Am. J. Cardiol. 1971, 28, 614. Karpman, H. L., Sheppard, J. J., Bleifer, S. B., Bleifer, D. J. Clinical Applications of Dynamic Electrocardiography; p. 4619. Rand Corporation, Santa Monica, California, 1971. 4. Han, J., Goel, B. G. Electrophysiologic Precursors of Ventricular Tachyarrhythmias. Albany, N.Y. 1. 2. 3.