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DIABETIC COMA WITHOUT KETOACIDOSIS
828
hyperglycsmia, hypernatrasmia, and uraemia—not following a stroke ?Their coexistence would of course produce the very picture we are discussing. Perhaps only in true diabetics could the blood-sugar rise as high as 1°0 or more after a stroke. Nevertheless it would be inadvisable, I believe, to describe as diabetic" the coma followinga cerebrovascular accident, notwithstanding a complicating hyperglycxmia.
investigated the celluria which follows the administration of aspirin and found that the desquamation of renal tubular cells was a transient change which ceased even though the drug was continued. This interesting property of salicylates may perhaps be part of a widespread action on epithelial surfaces, but it certainly cannot be cited as evidence for an ability to cause chronic renal damage. All this is rather confusing and unsatisfactory, and one must sympathise with Dr. Gilman when he demands " much more sophisticated epidemiologic studies ". Meanwhile we can only act according to the clues before us, which point to phenacetin-and not to aspirin-as the
-coma,
culprit.
of the
Postgraduate Medical School, London, W.12.
J. T. SCOTT.
HYSTERIA
SlR,—The second peripatetic correspondent in your issue of March 28 apparently still assumes that hysterical symptoms are a form of deliberate deceit requiring only " to be easily exposed " by the doctor. Even if he is as complacently naive and dangerously ignorant as this, why does this lamentable and obsolete error have to receive editorial sanction ? Guy’s Hospital, London, S.E.1.
D. STAFFORD CLARK.
DIABETIC COMA WITHOUT KETOACIDOSIS
SIR,-The condition described as "diabetic coma without ketoacidosis " is evidently not rare, for six cases have been reported in your pages in the past year.I-5 I want to express my misgivings about this designation before it becomes entrenched. I believe that the apparent contradiction-in-terms, though it makes for an arresting label, may prove to be a glaring misnomer. We already have enough of those. The term " diabetic coma " implies that the coma results from a metabolic disorder characteristic of diabetes. The claim that the coma in these cases results from extreme hyperglycxmia is not specially convincing-indeed a syrupy 2100 mg. per 100 ml. (i.e., more than twice the mean bloodsugar in this series of cases) has been encountered in a noncomatose patient. However, even if this claim should be substantiated, the designation " diabetic coma ", no matter how qualified, would be unfortunate, for an apparently very different condition has prior claim to the term. Apart from the stated difference of ketoacidosis, there are other conspicuous dissimilarities. Hyperglycsmia is common to both conditions, to be sure; but even in this shared feature there is apparently a large difference in degree. Some of these differences are tabulated below (values are approximate).
Some of the patients were known to be diabetic before their episode of coma. None the less is there not the danger in these cases of confusing coma in a diabetic with diabetic coma ? I am suggesting, in fact, that some or all of these " patients were suffering from something other than " diabetic coma. The something else might well have been a combination of derangements which, at least separately, may occur in patients who have just suffered a stroke. Can these sequelx8 Grant, N., Daily, W. J., Reaven, G. M. Lancet, 1963, i, 75. W. P. U. ibid. p. 394. Jackson, Ward, F. G. ibid. p. 450. White, J. C. ibid. p. 1052. Bergoz, R., Hausser, E. ibid. Jan 11. 1964, p, 116. Dtsch. med. Wschr. 1961, von Rossier, P. H., Reutter, F., Frick, P. 86, 2145. 7. Joslin, E. P., Root, H. F., White, P., Marble, A. The Treatment of Diabetes Mellitus. Philadelphia, 1959. 8. Baker, A. B. Clinical Neurology. New York, 1962. 1. Lucas, C. P.,
2. 3. 4. 5. 6.
coexist
"
possibility that your contributors may have been writing about patients some of whom had suffered a stroke is strengthened by some other features of their The
cases.
For instance, in four of the six
cases at
least
one
following phenomena was present1 24aa Babinski reflex, hemiplegia, or encephalomalacia at necropsy. The high mortality-rate, the severe azotaanis in every case, and the hyperelectrolytaemia in four of the cases 135 are, in my view, features which further support the proposition that at least some of the patients in " diabetic coma without ketoacidosis " may in fact have been victims of strokes. Other possibilities are also worth considering-the " diabetes " of urxmia, for instance, could conceivably present a similar picture. I should like to be able to propose a suitable descriptive term, but can do no better than " hyperglycasmic coma ", which is unsatisfactory, but seems to me to be an improvement in that it begs the question of aetiology. I hope someone more inventive will make good this deficiency in nosology, but until the setiology of this condition is established, tendentious labels should be avoided. All physicians interested in diabetes would agree that it is difficult enough to pick one’s way among the assumptions, empiricisms, and just plain fallacies in this field without compounding the difficulties by more
misleading terminology. Departments of Medicine, Northwestern University and Cook
County Hospital, Chicago, Ill.
ROBERT METZ.
ELEVATION OF SERUM-CHOLESTEROL BY AN ANABOLIC STEROID
SIR,-Iwas interested in the report of Dr. Jose and Dr. Mitchell (Feb. 29) concerning the effect ofmethandrostenolone on the serum-cholesterol. I have used this drug in one case of hypercholesterolaemic xanthomatosis, in a dose of 5 mg. twice daily, and I also found a rise in serum-cholesterol (see accompanying table). On the EFFECT OF ANABOLIC AGENTS IN FOUR CASES OF HYPERCHOLESTEROLae.B1IC
XANTHOMATOSIS
other hand, in this and three other cases of the same condition, I have found that the closely related anabolic agent, norethandrolone, in a dose of 10 mg. twice daily, has consistent lowered the serum-cholesterol (see table). No other form of treatment was given. Apart from a history of angiria of effort before treatment was begun in case 3 (but never subsequently’. no cardiovascular abnormalities were discovered after full investigation. By the end of the treatment the cutaneous lesions had cleared completely in case 3, and had decreased 12 size and number in the others by approximately 75°;. Xc side-effects were encountered.
hyperglycsmia, hypernatrasmia, and uraemia—not following a stroke ?Their coexistence would of course produce the very picture we are discussing. Perhaps only in true diabetics could the blood-sugar rise as high as 1°0 or more after a stroke. Nevertheless it would be inadvisable, I believe, to describe as diabetic" the coma followinga cerebrovascular accident, notwithstanding a complicating hyperglycxmia.
investigated the celluria which follows the administration of aspirin and found that the desquamation of renal tubular cells was a transient change which ceased even though the drug was continued. This interesting property of salicylates may perhaps be part of a widespread action on epithelial surfaces, but it certainly cannot be cited as evidence for an ability to cause chronic renal damage. All this is rather confusing and unsatisfactory, and one must sympathise with Dr. Gilman when he demands " much more sophisticated epidemiologic studies ". Meanwhile we can only act according to the clues before us, which point to phenacetin-and not to aspirin-as the
-coma,
culprit.
of the
Postgraduate Medical School, London, W.12.
J. T. SCOTT.
HYSTERIA
SlR,—The second peripatetic correspondent in your issue of March 28 apparently still assumes that hysterical symptoms are a form of deliberate deceit requiring only " to be easily exposed " by the doctor. Even if he is as complacently naive and dangerously ignorant as this, why does this lamentable and obsolete error have to receive editorial sanction ? Guy’s Hospital, London, S.E.1.
D. STAFFORD CLARK.
DIABETIC COMA WITHOUT KETOACIDOSIS
SIR,-The condition described as "diabetic coma without ketoacidosis " is evidently not rare, for six cases have been reported in your pages in the past year.I-5 I want to express my misgivings about this designation before it becomes entrenched. I believe that the apparent contradiction-in-terms, though it makes for an arresting label, may prove to be a glaring misnomer. We already have enough of those. The term " diabetic coma " implies that the coma results from a metabolic disorder characteristic of diabetes. The claim that the coma in these cases results from extreme hyperglycxmia is not specially convincing-indeed a syrupy 2100 mg. per 100 ml. (i.e., more than twice the mean bloodsugar in this series of cases) has been encountered in a noncomatose patient. However, even if this claim should be substantiated, the designation " diabetic coma ", no matter how qualified, would be unfortunate, for an apparently very different condition has prior claim to the term. Apart from the stated difference of ketoacidosis, there are other conspicuous dissimilarities. Hyperglycsmia is common to both conditions, to be sure; but even in this shared feature there is apparently a large difference in degree. Some of these differences are tabulated below (values are approximate).
Some of the patients were known to be diabetic before their episode of coma. None the less is there not the danger in these cases of confusing coma in a diabetic with diabetic coma ? I am suggesting, in fact, that some or all of these " patients were suffering from something other than " diabetic coma. The something else might well have been a combination of derangements which, at least separately, may occur in patients who have just suffered a stroke. Can these sequelx8 Grant, N., Daily, W. J., Reaven, G. M. Lancet, 1963, i, 75. W. P. U. ibid. p. 394. Jackson, Ward, F. G. ibid. p. 450. White, J. C. ibid. p. 1052. Bergoz, R., Hausser, E. ibid. Jan 11. 1964, p, 116. Dtsch. med. Wschr. 1961, von Rossier, P. H., Reutter, F., Frick, P. 86, 2145. 7. Joslin, E. P., Root, H. F., White, P., Marble, A. The Treatment of Diabetes Mellitus. Philadelphia, 1959. 8. Baker, A. B. Clinical Neurology. New York, 1962. 1. Lucas, C. P.,
2. 3. 4. 5. 6.
coexist
"
possibility that your contributors may have been writing about patients some of whom had suffered a stroke is strengthened by some other features of their The
cases.
For instance, in four of the six
cases at
least
one
following phenomena was present1 24aa Babinski reflex, hemiplegia, or encephalomalacia at necropsy. The high mortality-rate, the severe azotaanis in every case, and the hyperelectrolytaemia in four of the cases 135 are, in my view, features which further support the proposition that at least some of the patients in " diabetic coma without ketoacidosis " may in fact have been victims of strokes. Other possibilities are also worth considering-the " diabetes " of urxmia, for instance, could conceivably present a similar picture. I should like to be able to propose a suitable descriptive term, but can do no better than " hyperglycasmic coma ", which is unsatisfactory, but seems to me to be an improvement in that it begs the question of aetiology. I hope someone more inventive will make good this deficiency in nosology, but until the setiology of this condition is established, tendentious labels should be avoided. All physicians interested in diabetes would agree that it is difficult enough to pick one’s way among the assumptions, empiricisms, and just plain fallacies in this field without compounding the difficulties by more
misleading terminology. Departments of Medicine, Northwestern University and Cook
County Hospital, Chicago, Ill.
ROBERT METZ.
ELEVATION OF SERUM-CHOLESTEROL BY AN ANABOLIC STEROID
SIR,-Iwas interested in the report of Dr. Jose and Dr. Mitchell (Feb. 29) concerning the effect ofmethandrostenolone on the serum-cholesterol. I have used this drug in one case of hypercholesterolaemic xanthomatosis, in a dose of 5 mg. twice daily, and I also found a rise in serum-cholesterol (see accompanying table). On the EFFECT OF ANABOLIC AGENTS IN FOUR CASES OF HYPERCHOLESTEROLae.B1IC
XANTHOMATOSIS
other hand, in this and three other cases of the same condition, I have found that the closely related anabolic agent, norethandrolone, in a dose of 10 mg. twice daily, has consistent lowered the serum-cholesterol (see table). No other form of treatment was given. Apart from a history of angiria of effort before treatment was begun in case 3 (but never subsequently’. no cardiovascular abnormalities were discovered after full investigation. By the end of the treatment the cutaneous lesions had cleared completely in case 3, and had decreased 12 size and number in the others by approximately 75°;. Xc side-effects were encountered.