1147 amount of
electrolytes present in the body. However, sophisticated whole body-measurement of electrolytes is not possible in most clinical situations, and in practice the main problem is to know how far an observed serum-
calciferol. This conclusion is not supported by data from two of our patients, children with cystinosis and rickets. In these patients the steady-state plasma levels of 25-hydroxyvitamin D (25-OH D) were measured while 25-H.C.C. was being used in treatment. Later the levels were measured while vitamin Dand vitamin D3, respectively, were being administered. All medications were given orally. The findings were:
electrolyte
pattern should influence management in a particular case. If the " sick cell " hypothesis is correct, then it might be expected that many of the observed electrolyte disturbances would be corrected simply by treating the underlying illness. This is indeed often found to be the case. In many other instances, the addition of potassium supplements (or stopping thiazide diuretics if these drugs are being given) corrects not only hypokalsemia but also quite severe hyponatraemia. Trinity Hospital, 19 Trinity Road, Taunton, Somerset.
*
osteomalacia the curative dosages of native ergocalciferol and cholecalciferol or of 25 hydroxyergocalciferol and 25 hydroxycholecalciferol administered by the same route must be compared directly.
uraemic
In January of this year a 3-month-old child was sent into this hospital with a history of an apnoeic attack following a coughing spasm in the second week of what sounded like whooping-cough.
University College Hospital Medical School, University Street,
The elder sister of this child had had a similar illness for the previous three weeks. The mother had treated this apnoeic attack by placing the child under a cold water tap. By the time he was admitted he was well and the chest was clear apart from a few crepitations at the bases. Immediately after admission he had a generalised convulsion with clonic spasms of all limbs, for which he had to be intubated, given intravenous diazepam, and ventilated. Fundoscopy at this time was normal, as was the cerebrospinal fluid. It was thought that he may have had an intracerebral bleed (or possibly an encephalopathy) secondary to his whoopingcough. However, a sample of blood taken before this convulsion showed severe hyponatraemia (116 meq. per 1.) and severe hypochlorsemia (80 meq. per 1.). On requestioning the parents, it appeared that vomiting had been very frequent in the previous two weeks and it would appear likely that the child had developed hyponatrsemia secondary to the vomiting, which in turn was secondary to the pertussis, the hyponatraemia being responsible for the convulsion before admission and for the alarming convulsion in the He was treated with intermittent positive-pressure ward. ventilation and intravenous fluid therapy, and electrolytes rapidly returned to normal. Six hours after admission the convulsions had stopped, and the child was taken off the ventilator two days after admission. He was also given chloramphenicol and made a good recovery, although for the next two weeks he had obvious paroxysmal
PARACETAMOL MEASUREMENT SIR,—Prescott and Matthew2 believe that cysteamine is the treatment of choice for paracetamol poisoning, but the safety of cysteamine in man has yet to be established. Since only about 1% of those who take a paracetamol overdose die,3 it is important to ensure that cysteamine is only administered to those patients who really need it.4 The plasma-paracetamol level has been shown to be a reasonably reliable predictor for subsequent hepatic necrosis, and, since cysteamine should be given within 10 hours of paracetamol ingestion3asimple, reliable, and rapid method of estimating it is needed. The following is such a method, and is based on a recently reported colorimetric method.7 1 ml. of
plasma is added to a 25 ml. stoppered centrifuge containing 2 ml. 10% trichloroacetic acid. After thorough mixing, the tube is centrifuged briefly and the clear supernatant decanted into a 25 ml. test-tube containing 1 ml. 6N hydrochloric acid and 2 ml. 10% sodium nitrite. After allowing the contents to stand for 2 minutes, 2 ml. of 15% sulphamic acid is added carefully, followed by 5 ml. 10% NaOH. The ensuing yellow colour is measured at 430 nm. against a reagent blank
tube
seemed to be a minor epidemic of whooping-cough in this area at the time seem to confirm the diagnosis as pertussis complicated by hyponatraemic convulsions. ,
J. R. HARPER M. J. MAGUIRE.
VITAMIN-D METABOLISM IN CHRONIC RENAL FAILURE
SIR,-Dr Eastwood and Professor de Wardener (April 26, p. 981) found that the parenteral administration of 40 µg. per day of hydroxycholecalciferol (25-H.c.c.) healed
osteomalacia in chronic renal failure and imply that this is equivalent to giving the patients a similar dose of chole-
C. E. DENT MERCEDES DOMENECH J. M. GERTNER.
London WC1E 6JJ.
whooping-cough with, initially, frequent apnoeic attacks, paroxysms of coughing, and a typical whoop. A chest X-ray showed inflammatory changes throughout the right lung, which cleared. The diagnosis was not confirmed bacteriologically, but the child’s subsequent course, his sister’s illness, and what
Hospital,
Stamp.
In order to make a valid comparison of the relative efficacy of ergocalciferol (D2) and cholecalciferol (Dg) in
SIR,-Convulsions are a recognised complication of whooping-cough, as is vomiting and metabolic alkalosis, even to the point of tetany. These may, however, combine to present in an alarming fashion, as in the following case.
General
C. B.
Thus, in patient 1 the plasma level showed little change when 25 times by weight the dose of Da was substituted for 25-H.C.C.; while in patient 2 a six-fold increase in dosage led to a three-fold fall in plasma 25-OH D level. This is probably the result of poor conversion of vitamin D and D 3 to the 25 hydroxylated form as a result of feedback inhibition of hepatic calciferol 25-hydroxylase by the high circulating levels of 25-OH D.1
P. F. ROE.
HYPONATRÆMIA AND CONVULSIONS IN WHOOPING-COUGH
Northampton NN1 5BD.
Kindly determined by Dr T.
of water. The calibration jjLg. per ml. plasma.
curve
is linear
over
the range 100-500
The method takes 5-10 minutes and all reagents are standard laboratory issue, readily made up, and stable with the exception of the nitrite reagent, which should be made up immediately before use. The possibility of providing the reagents in the form of a test kit for rapid in-ward assays is being pursued. Olmdahl, J. L., De Luca, H. F. Physiol. Rev. 1973, 53, 327. Prescott, L. F., Matthew, H. Lancet, 1974, i, 998. Wright, N. Prescribers J. 1974, 14, 78. Gazzard, B. G., Murray-Lyon, I. M., Davis, M., Thompson, R. P. H., Williams, R., Goulding, R. Lancet, 1974, i, 864. 5. Stewart, M. J. ibid. p. 1162. 6. Prescott, L. F., Swainson, C. P., Forrest, A. R. W., Newton, R. W., Wright, N., Matthew, H. ibid. p. 588. 7. Chefetz, L., Daly, R. E., Schriftman, H., Lomner, J. J. J. pharm. Sci. 1971, 60, 463.
1. 2. 3. 4.
electrolytes present in the body. However, sophisticated whole body-measurement of electrolytes is not possible in most clinical situations, and in practice the main problem is to know how far an observed serum-
calciferol. This conclusion is not supported by data from two of our patients, children with cystinosis and rickets. In these patients the steady-state plasma levels of 25-hydroxyvitamin D (25-OH D) were measured while 25-H.C.C. was being used in treatment. Later the levels were measured while vitamin Dand vitamin D3, respectively, were being administered. All medications were given orally. The findings were:
electrolyte
pattern should influence management in a particular case. If the " sick cell " hypothesis is correct, then it might be expected that many of the observed electrolyte disturbances would be corrected simply by treating the underlying illness. This is indeed often found to be the case. In many other instances, the addition of potassium supplements (or stopping thiazide diuretics if these drugs are being given) corrects not only hypokalsemia but also quite severe hyponatraemia. Trinity Hospital, 19 Trinity Road, Taunton, Somerset.
*
osteomalacia the curative dosages of native ergocalciferol and cholecalciferol or of 25 hydroxyergocalciferol and 25 hydroxycholecalciferol administered by the same route must be compared directly.
uraemic
In January of this year a 3-month-old child was sent into this hospital with a history of an apnoeic attack following a coughing spasm in the second week of what sounded like whooping-cough.
University College Hospital Medical School, University Street,
The elder sister of this child had had a similar illness for the previous three weeks. The mother had treated this apnoeic attack by placing the child under a cold water tap. By the time he was admitted he was well and the chest was clear apart from a few crepitations at the bases. Immediately after admission he had a generalised convulsion with clonic spasms of all limbs, for which he had to be intubated, given intravenous diazepam, and ventilated. Fundoscopy at this time was normal, as was the cerebrospinal fluid. It was thought that he may have had an intracerebral bleed (or possibly an encephalopathy) secondary to his whoopingcough. However, a sample of blood taken before this convulsion showed severe hyponatraemia (116 meq. per 1.) and severe hypochlorsemia (80 meq. per 1.). On requestioning the parents, it appeared that vomiting had been very frequent in the previous two weeks and it would appear likely that the child had developed hyponatrsemia secondary to the vomiting, which in turn was secondary to the pertussis, the hyponatraemia being responsible for the convulsion before admission and for the alarming convulsion in the He was treated with intermittent positive-pressure ward. ventilation and intravenous fluid therapy, and electrolytes rapidly returned to normal. Six hours after admission the convulsions had stopped, and the child was taken off the ventilator two days after admission. He was also given chloramphenicol and made a good recovery, although for the next two weeks he had obvious paroxysmal
PARACETAMOL MEASUREMENT SIR,—Prescott and Matthew2 believe that cysteamine is the treatment of choice for paracetamol poisoning, but the safety of cysteamine in man has yet to be established. Since only about 1% of those who take a paracetamol overdose die,3 it is important to ensure that cysteamine is only administered to those patients who really need it.4 The plasma-paracetamol level has been shown to be a reasonably reliable predictor for subsequent hepatic necrosis, and, since cysteamine should be given within 10 hours of paracetamol ingestion3asimple, reliable, and rapid method of estimating it is needed. The following is such a method, and is based on a recently reported colorimetric method.7 1 ml. of
plasma is added to a 25 ml. stoppered centrifuge containing 2 ml. 10% trichloroacetic acid. After thorough mixing, the tube is centrifuged briefly and the clear supernatant decanted into a 25 ml. test-tube containing 1 ml. 6N hydrochloric acid and 2 ml. 10% sodium nitrite. After allowing the contents to stand for 2 minutes, 2 ml. of 15% sulphamic acid is added carefully, followed by 5 ml. 10% NaOH. The ensuing yellow colour is measured at 430 nm. against a reagent blank
tube
seemed to be a minor epidemic of whooping-cough in this area at the time seem to confirm the diagnosis as pertussis complicated by hyponatraemic convulsions. ,
J. R. HARPER M. J. MAGUIRE.
VITAMIN-D METABOLISM IN CHRONIC RENAL FAILURE
SIR,-Dr Eastwood and Professor de Wardener (April 26, p. 981) found that the parenteral administration of 40 µg. per day of hydroxycholecalciferol (25-H.c.c.) healed
osteomalacia in chronic renal failure and imply that this is equivalent to giving the patients a similar dose of chole-
C. E. DENT MERCEDES DOMENECH J. M. GERTNER.
London WC1E 6JJ.
whooping-cough with, initially, frequent apnoeic attacks, paroxysms of coughing, and a typical whoop. A chest X-ray showed inflammatory changes throughout the right lung, which cleared. The diagnosis was not confirmed bacteriologically, but the child’s subsequent course, his sister’s illness, and what
Hospital,
Stamp.
In order to make a valid comparison of the relative efficacy of ergocalciferol (D2) and cholecalciferol (Dg) in
SIR,-Convulsions are a recognised complication of whooping-cough, as is vomiting and metabolic alkalosis, even to the point of tetany. These may, however, combine to present in an alarming fashion, as in the following case.
General
C. B.
Thus, in patient 1 the plasma level showed little change when 25 times by weight the dose of Da was substituted for 25-H.C.C.; while in patient 2 a six-fold increase in dosage led to a three-fold fall in plasma 25-OH D level. This is probably the result of poor conversion of vitamin D and D 3 to the 25 hydroxylated form as a result of feedback inhibition of hepatic calciferol 25-hydroxylase by the high circulating levels of 25-OH D.1
P. F. ROE.
HYPONATRÆMIA AND CONVULSIONS IN WHOOPING-COUGH
Northampton NN1 5BD.
Kindly determined by Dr T.
of water. The calibration jjLg. per ml. plasma.
curve
is linear
over
the range 100-500
The method takes 5-10 minutes and all reagents are standard laboratory issue, readily made up, and stable with the exception of the nitrite reagent, which should be made up immediately before use. The possibility of providing the reagents in the form of a test kit for rapid in-ward assays is being pursued. Olmdahl, J. L., De Luca, H. F. Physiol. Rev. 1973, 53, 327. Prescott, L. F., Matthew, H. Lancet, 1974, i, 998. Wright, N. Prescribers J. 1974, 14, 78. Gazzard, B. G., Murray-Lyon, I. M., Davis, M., Thompson, R. P. H., Williams, R., Goulding, R. Lancet, 1974, i, 864. 5. Stewart, M. J. ibid. p. 1162. 6. Prescott, L. F., Swainson, C. P., Forrest, A. R. W., Newton, R. W., Wright, N., Matthew, H. ibid. p. 588. 7. Chefetz, L., Daly, R. E., Schriftman, H., Lomner, J. J. J. pharm. Sci. 1971, 60, 463.
1. 2. 3. 4.
