- Email: [email protected]
SERUM-LACTIC DEHYDROGENASE IN DIAGNOSIS OF MYOCARDIAL INFARCTION
1232
experiments analogous inner sources propelling the responses must be postulated. And the same, of course, applies to " habits " of man. But this side of the picture appears blotted out in learning theory. In the cases recently published by adherents of behaviour therapy no attempt is In other
made
from what inner sources the habits of their have arisen and continued to be fed; not to speak
to uncover
patients of the tracing of conditioning influences which seems far less than convincing. And yet, the whole procedure ranks as aetiological within the meaning of learning theory. Lastly, a word about the transvestite treated by Dr. Barker et al. (March 4). In their comments the authors seem distinctly uneasy about what they have accomplished, and conclude’their letter by saying, at present we are unable to demonstrate the precise mechanisms which alleviated symptoms in our patient." They may perhaps be willing to accept that, shorn of all the medical trappings, what they have done was to submit their patient to a series of exquisite humiliations. Common sense understands if, as a sequel to this, he has given up his " bad habit ", at least for the time being. "
London, W.1.
JOSEPH ZELMANOWITS.
SIR,-I have waited in vain for someone else to emend an obvious error in the title of this recent correspondence.
Surely-since we are discussing science, not religion palmistry-it should read Pavlov and Freud ? Loughton, Essex.
or
ALEX COMFORT.
SERUM-LACTIC DEHYDROGENASE IN DIAGNOSIS OF MYOCARDIAL INFARCTION SIR,-Estimation of the serum-glutamyl-oxaloacetictransaminase (S.G.O.T.) has been widely used in the past three or four years for diagnosing myocardial infarction. Now serum-lactic dehydrogenase (S.L.D.H.) estimation is being used more and more. The medical firms at this hospital have been performing this test, in the past six months, together with the S.G.O.T. estimation, and I have compared the relative value of these two
investigations in diagnosing myocardial infarction. The graph is based on 45 S.L.D.H. estimations and 45 S.G.O.T. estimations on specimens from patients with myocardial infarction obtained within 72 hours of their admission to hospital. The 3 large groups are based on levels of circulating enzymes during the first, second, and third 24-hour period in
hospital. I took as the upper limits of normal 35 Sigma Frankel units for S.G.O.T., and 600 Berger& Broida units forS.L.D.H.; in the first 24-hour period the mean levels of both enzymes rose to about 150°o of their upper normal levels. During the second 24-hour period the mean S.G.O.T. level rose to approximately 300% and the S.L.D.H. to 200 %. In the third 24-hour period the S.G.O.T. fell to 140"i,, while the S.L.D.H. continued to rise to
approximately 250°;,. Thus both the S.L.D.H. and the S.G.O.T. levels rise rapidly during the first 24 hours, but whereas the former continues to rise slowly in the subsequent 24-hour periods, the S.G.O.T., after reaching a maximum in the second 24-hour period, commences to fall rapidly towards normal in the third.
For estimations carried out more than 72 hours after the of chest pain the s.L.D.H. appears the more satisfactory test.Our results support these findings. False negatives have been observed in approximately 9% of cases in which the S.G.O.T. alone was estimated.2 We found in 45 estimations that the s.L.D.H. was raised to pathological levels on 7 occasions on which the S.G.O.T. remained within normal limits. But the S.L.D.H. cannot be assumed to be the more sensitive test on these grounds as even slight haemolysis of the blood specimen will raise the s.L.D.H. appreciably, but the S.G.O.T. will remain unaltered. Erythrocyte-L.D.H. concentraonset
1. 2.
King, J., Waind, A. P. Dewar, H. A., Rowell,
B. Brit. med. J. 1960, ii, 1361. N. R., Smith, A. J. ibid. 1958, ii, 1121.
S.G.O.T. and S.L.D.H. levels in the first three 24-hour periods after admission in patients with myocardial infarction. (Each based on 45 estimations.)
tion is some hundreds of times greater than plasma-L.D.H. This is, therefore, a major source of error; and all specimens sent
for
s.L.D.H.
estimation should be
freshly
taken and
unhaemolysed. Both the S.G.O.T. and S.L.D.H. were estimated colorimetrically, and this takes 1111,to 2 hours. One of the reagents used for the S.L.D.H. test is reduced diphosphopyridine nucleotide, which is expensive: the materials for the S.L.D.H. test cost about 7s. compared with about ls. for s.G.o.T. estimation. North Middlesex Hospital, London, N.18.
ROSS S. MELLICK.
BRONCHODILATORS AND CORTICOSTEROIDS IN ASTHMA
SIR,-We are writing to answer Dr. Gandevia’s com(May 13) on our paper.’ Firstly, concerning our criteria for labelling patients
ments
emphysematous, a reference was given in our paper to the work published by Dr. Thomson and Dr. Hugh-Jones.2 They reported that serial one-second forced expiratory volume (F.E.V.I) and vital capacity (v.c.) tests before and after aerosol isoprenaline can differentiate between patients with pure asthma and those with asthma plus emphysema. Our patient B in fig. 2 (referred to by Dr. Gandevia) came into the latter category. The highest F.E.V’1 percentage of the v.c. that she has ever attained, during four years’ treatment with corticosteroids, has been 56%. At this time her F.E.V’1 was 1720 ml., her v.c. 3030 ml., and her forced vital capacity 2800 ml., indicating obstructive disease with a good v.c.-i.e., absence of restrictive disease. We feel that it is justifiable to use the term emphysema for patients who show this type of ventilatory defect in the absence of bronchial narrowing which will respond to a bronchodilator. We found that the group of patients who showed the haphazard response to bronchodilators (illustrated by our fig. 5), had advanced emphysema where bronchospasm coexisted as the less significant factor, in contrast to the type of disease referred to above. Attention was drawn in the test and the caption of the figure to the low ordinate scale which represents the degree of reversible bronchial narrowing. It is this group, as would be expected, in which we have found no improvement with corticosteroid therapy unless there has been some additional disabling factor-e.g., excessive mucoid
sputum-which improved King 1. 2.
with
Edward VII Sanatorium, Midhurst, Sussex.
drugs. K. M. HUME E. RHYS TONES.
Hume, K. M., Rhys Jones, E. Lancet, 1960, ii, 1319. Thomson, W. B., Hugh-Jones, P. Brit. med. J. 1958, i, 1093.
experiments analogous inner sources propelling the responses must be postulated. And the same, of course, applies to " habits " of man. But this side of the picture appears blotted out in learning theory. In the cases recently published by adherents of behaviour therapy no attempt is In other
made
from what inner sources the habits of their have arisen and continued to be fed; not to speak
to uncover
patients of the tracing of conditioning influences which seems far less than convincing. And yet, the whole procedure ranks as aetiological within the meaning of learning theory. Lastly, a word about the transvestite treated by Dr. Barker et al. (March 4). In their comments the authors seem distinctly uneasy about what they have accomplished, and conclude’their letter by saying, at present we are unable to demonstrate the precise mechanisms which alleviated symptoms in our patient." They may perhaps be willing to accept that, shorn of all the medical trappings, what they have done was to submit their patient to a series of exquisite humiliations. Common sense understands if, as a sequel to this, he has given up his " bad habit ", at least for the time being. "
London, W.1.
JOSEPH ZELMANOWITS.
SIR,-I have waited in vain for someone else to emend an obvious error in the title of this recent correspondence.
Surely-since we are discussing science, not religion palmistry-it should read Pavlov and Freud ? Loughton, Essex.
or
ALEX COMFORT.
SERUM-LACTIC DEHYDROGENASE IN DIAGNOSIS OF MYOCARDIAL INFARCTION SIR,-Estimation of the serum-glutamyl-oxaloacetictransaminase (S.G.O.T.) has been widely used in the past three or four years for diagnosing myocardial infarction. Now serum-lactic dehydrogenase (S.L.D.H.) estimation is being used more and more. The medical firms at this hospital have been performing this test, in the past six months, together with the S.G.O.T. estimation, and I have compared the relative value of these two
investigations in diagnosing myocardial infarction. The graph is based on 45 S.L.D.H. estimations and 45 S.G.O.T. estimations on specimens from patients with myocardial infarction obtained within 72 hours of their admission to hospital. The 3 large groups are based on levels of circulating enzymes during the first, second, and third 24-hour period in
hospital. I took as the upper limits of normal 35 Sigma Frankel units for S.G.O.T., and 600 Berger& Broida units forS.L.D.H.; in the first 24-hour period the mean levels of both enzymes rose to about 150°o of their upper normal levels. During the second 24-hour period the mean S.G.O.T. level rose to approximately 300% and the S.L.D.H. to 200 %. In the third 24-hour period the S.G.O.T. fell to 140"i,, while the S.L.D.H. continued to rise to
approximately 250°;,. Thus both the S.L.D.H. and the S.G.O.T. levels rise rapidly during the first 24 hours, but whereas the former continues to rise slowly in the subsequent 24-hour periods, the S.G.O.T., after reaching a maximum in the second 24-hour period, commences to fall rapidly towards normal in the third.
For estimations carried out more than 72 hours after the of chest pain the s.L.D.H. appears the more satisfactory test.Our results support these findings. False negatives have been observed in approximately 9% of cases in which the S.G.O.T. alone was estimated.2 We found in 45 estimations that the s.L.D.H. was raised to pathological levels on 7 occasions on which the S.G.O.T. remained within normal limits. But the S.L.D.H. cannot be assumed to be the more sensitive test on these grounds as even slight haemolysis of the blood specimen will raise the s.L.D.H. appreciably, but the S.G.O.T. will remain unaltered. Erythrocyte-L.D.H. concentraonset
1. 2.
King, J., Waind, A. P. Dewar, H. A., Rowell,
B. Brit. med. J. 1960, ii, 1361. N. R., Smith, A. J. ibid. 1958, ii, 1121.
S.G.O.T. and S.L.D.H. levels in the first three 24-hour periods after admission in patients with myocardial infarction. (Each based on 45 estimations.)
tion is some hundreds of times greater than plasma-L.D.H. This is, therefore, a major source of error; and all specimens sent
for
s.L.D.H.
estimation should be
freshly
taken and
unhaemolysed. Both the S.G.O.T. and S.L.D.H. were estimated colorimetrically, and this takes 1111,to 2 hours. One of the reagents used for the S.L.D.H. test is reduced diphosphopyridine nucleotide, which is expensive: the materials for the S.L.D.H. test cost about 7s. compared with about ls. for s.G.o.T. estimation. North Middlesex Hospital, London, N.18.
ROSS S. MELLICK.
BRONCHODILATORS AND CORTICOSTEROIDS IN ASTHMA
SIR,-We are writing to answer Dr. Gandevia’s com(May 13) on our paper.’ Firstly, concerning our criteria for labelling patients
ments
emphysematous, a reference was given in our paper to the work published by Dr. Thomson and Dr. Hugh-Jones.2 They reported that serial one-second forced expiratory volume (F.E.V.I) and vital capacity (v.c.) tests before and after aerosol isoprenaline can differentiate between patients with pure asthma and those with asthma plus emphysema. Our patient B in fig. 2 (referred to by Dr. Gandevia) came into the latter category. The highest F.E.V’1 percentage of the v.c. that she has ever attained, during four years’ treatment with corticosteroids, has been 56%. At this time her F.E.V’1 was 1720 ml., her v.c. 3030 ml., and her forced vital capacity 2800 ml., indicating obstructive disease with a good v.c.-i.e., absence of restrictive disease. We feel that it is justifiable to use the term emphysema for patients who show this type of ventilatory defect in the absence of bronchial narrowing which will respond to a bronchodilator. We found that the group of patients who showed the haphazard response to bronchodilators (illustrated by our fig. 5), had advanced emphysema where bronchospasm coexisted as the less significant factor, in contrast to the type of disease referred to above. Attention was drawn in the test and the caption of the figure to the low ordinate scale which represents the degree of reversible bronchial narrowing. It is this group, as would be expected, in which we have found no improvement with corticosteroid therapy unless there has been some additional disabling factor-e.g., excessive mucoid
sputum-which improved King 1. 2.
with
Edward VII Sanatorium, Midhurst, Sussex.
drugs. K. M. HUME E. RHYS TONES.
Hume, K. M., Rhys Jones, E. Lancet, 1960, ii, 1319. Thomson, W. B., Hugh-Jones, P. Brit. med. J. 1958, i, 1093.