- Email: [email protected]
CONVULSIONS DUE TO HYPOMAGNESÆMIA
1206 CALCIUM AND MAGNESIUM, AND RENAL STONES Evans and his co-workers (Nov. 4, p. 958) " conSIR,-Dr. sider that idiopathic hypercalciuria is an important cause of renal-stone formation," noting that I challenge this view. I have carried out comparative studies on patients with renal stones and normal White and Bantu subjects, and have not been able to demonstrate a cause-and-effect relation between the degree of calciuria and renal-stone formation. There is a considerable amount of evidence to support this conclusion. 1 2 A notable feature of my findings is that, although the Bantu do not form renal stones, the range of their daily urinary-calcium levels virtually extends over almost the whole range of daily urinarycalcium values observed in the patients with renal stones. In addition, only 8% of my patients with renal stones excreted more than 300 mg. of calcium per 24 hours, as compared with 68% of the patients examined by Dr. Evans and his co-workers. The widely differing proportions of hypercalciuria in these two groups of renal-stone patients seems to reinforce my view that hypercalciuria cannot in itself be a causal factor in renal-stone formation. It is highly improbable that the aetiological importance of hypercalciuria varies geographically. I have determined the 24-hour urinary excretion of magnesium in my three groups of subjects and, in conformity with the system adopted by Dr. Evans and his co-workers, have similarly divided each group into those with 24-hour urinarycalcium excretions of less than and more than 300 mg. The mean 24-hour urinary-magnesium values in 50 subjects in each group with a 24-hour urinary-calcium excretion of less than 300 me. were as follows: _
_
_
Whereas the mean 24-hour urinary-magnesium level was significantly lower in the patients with renal stone than in the White controls, in accord with the data of Dr. Evans and his co-workers, there was no significant difference in mean daily urinary-magnesium concentration between the stone patients and the Bantu who do not form renal stones. This is in accord with my previously reported data in which the daily level of urinary calcium was disregarded. This finding casts considerable doubt on the validity of the suggestion of Dr. Evans and his co-workers that in " normocalciuric subjects low levels of daily urinary magnesium may be causal in renal-stone formation. The further suggestion of Dr. Evans and his co-workers, that in patients with a low urinary-magnesium concentration there is possibly a primary metabolic defect responsible for the impared intestinal absorption, requires to be critically reexamined in relation to previous reports that in laboratory animals at least decreased absorption of magnesium can be produced by high levels of dietary phosphate.34 Success has been claimed in clinical trials for the use of high levels of dietary phosphate as a means of decreasing renal-stone recurrence.6If the effect of high levels of dietary phosphate on magnesium absorption in man were similar to that in animals these therapeutic benefits would have been obtained in the presence of diminished urinary excretion of magnesium. In testing the hypotheses of Dr. Evans and his co-workers, elucidation of this point seems to be essential. In the clinical trials mentioned above, the oral supplement of phosphate was administered in the form of the sodium salt. Since I have previously demonstrated the possible importance of a high daily urinary sodium/calcium ratio in the prevention of renal-stone formation,! the therapeutic effect claimed for "
1. 2. 3.
4. 5. 6.
Modlin, M. Ann. R. Coll. Surg. 1967, 40, 155. Modlin, M. Invest. Urol. 1967, 5, 49. O’Dell, B. L., Morris, E. R., Pickett, E. E., Hogan, A. G. J. Nutr. 1957, 63, 65. Bunce, G. E., Sauberlich, H. E., Reeves, P. G., Oba, T. S. ibid. 1965, 86, 406. Howard, J. E. Can. med. Ass. J. 1962, 86, 1001. Bernstein, D. S., Newton, R. Lancet, 1966, ii, 1105.
may well have been produced by the sodium component of the sodium-phosphate supplement.
phosphate
Endocrine Research Laboratory, University of Cape Town, South Africa.
MONTE MODLIN.
CONVULSIONS DUE TO HYPOMAGNESÆMIA interested to read the article by Dr. Savage and (July 29, p. 234) and the letter by Dr. Farmer (Nov. 4, p. 988). Stutzman and Amatuzio1 stressed the importance of hepatic cirrhosis as a cause of hypomagnesaemia. Since biliary cirrhosis is the main liver lesion in prolonged non-correctable cases of congenital biliary atresia (C.B.A.), the serum-magnesium is also reduced in this disorder.2 I have seen
SIR,-I
was
Dr. McAdam
a
male infant with
C.B.A.
who showed
a
very low level of serum-
magnesium and had clonic convulsions. The patient was admitted to the clinic of this department at the age of 2 months with the chief complaints of severe jaundice, which had appeared 4 days after birth and had gradually increased, and distended abdomen (due to hepatosplenomegaly). He was clinically diagnosed as C.B.A., and exploratory laparotomy at age 21/2 months revealed a surgically non-correctable type (atresia of ductus hepaticus). Ascites was present. Soon after the operation, the serum-magnesium level was 1-10 (normal 2.26::1: 0.15 3) mEq. per litre, but the patient remained symptom-free. Thereafter, the disease progressed gradually and the patient became very ill with generalised oedema, severe jaundice, and anaemia. He was therefore given 4 bloodtransfusions, each of 50 ml., and spironolactone, 50 mg. per day per os for 3 weeks. At the age of 4 months, right-sided clonic convulsions appeared abruptly and ceased 5 minutes later without any special treatment. Next day he had bilateral clonic convulsions for 5-minute periods, and he died that night. Retrospectively, the magnesium level of serum taken soon after the first convulsions was 0-79 mEq. per litre. In this patient the other factors responsible for convulsions, such as hypoglycaemia or cerebral vascular lesions, were not ruled out, nor was the effectiveness of magnesium administration tested. However, it is strongly suggested that the patient had convulsions due to hypomagnesaemia, on the ground that the observed seizures were not related to feeding and that neurological examination revealed no abnormalities. Department of Pædiatrics, University of Tokyo, Tokyo, Japan.
AKIO KOBAYASHI.
TRAINING IN MEDICAL LABORATORY TECHNOLOGY SIR,-May I support the plea of Mr. Wasley and Dr. Fraser Williams (Nov. 18, p. 1093) for a double wage-scale for medical laboratory technicians. I have recently had a hand in teaching them, and many medical students would shudder at the pressure they have to work under during their four-week period in class. The ground that they cover is hardly elementary. When tested, a small group of them had an average i.Q. of 138 (s.D.20), and this can be fairly contrasted with the Cattell-iii mean4 for physicians of 146. However, the standard of material to be learnt is well up to that of second M.B., and there are many, later lost to their profession as a result, who make excellent laboratory men but just cannot take the academic pace, and drop out. If a paper qualification is needed -and I do not see why-then a laboratory technician’s course, such as the one held in the Salisbury College of Further Education, might be suitable for this second grade (mean
i.Q.116). PATRICK F. JAMES. 1. 2. 3. 4.
Stutzman, F. L., Amatuzio, D. S. J. Lab. clin. Med. 1953, 41, 215. Kobayashi, A., Shiraki, K. Archs Dis. Childh. (in the press). Kobayashi, A. Lancet, July 8, 1967, p. 100. Cattell, R. B. A. Guide to Mental Testing. London, 1953.
_
_
Whereas the mean 24-hour urinary-magnesium level was significantly lower in the patients with renal stone than in the White controls, in accord with the data of Dr. Evans and his co-workers, there was no significant difference in mean daily urinary-magnesium concentration between the stone patients and the Bantu who do not form renal stones. This is in accord with my previously reported data in which the daily level of urinary calcium was disregarded. This finding casts considerable doubt on the validity of the suggestion of Dr. Evans and his co-workers that in " normocalciuric subjects low levels of daily urinary magnesium may be causal in renal-stone formation. The further suggestion of Dr. Evans and his co-workers, that in patients with a low urinary-magnesium concentration there is possibly a primary metabolic defect responsible for the impared intestinal absorption, requires to be critically reexamined in relation to previous reports that in laboratory animals at least decreased absorption of magnesium can be produced by high levels of dietary phosphate.34 Success has been claimed in clinical trials for the use of high levels of dietary phosphate as a means of decreasing renal-stone recurrence.6If the effect of high levels of dietary phosphate on magnesium absorption in man were similar to that in animals these therapeutic benefits would have been obtained in the presence of diminished urinary excretion of magnesium. In testing the hypotheses of Dr. Evans and his co-workers, elucidation of this point seems to be essential. In the clinical trials mentioned above, the oral supplement of phosphate was administered in the form of the sodium salt. Since I have previously demonstrated the possible importance of a high daily urinary sodium/calcium ratio in the prevention of renal-stone formation,! the therapeutic effect claimed for "
1. 2. 3.
4. 5. 6.
Modlin, M. Ann. R. Coll. Surg. 1967, 40, 155. Modlin, M. Invest. Urol. 1967, 5, 49. O’Dell, B. L., Morris, E. R., Pickett, E. E., Hogan, A. G. J. Nutr. 1957, 63, 65. Bunce, G. E., Sauberlich, H. E., Reeves, P. G., Oba, T. S. ibid. 1965, 86, 406. Howard, J. E. Can. med. Ass. J. 1962, 86, 1001. Bernstein, D. S., Newton, R. Lancet, 1966, ii, 1105.
may well have been produced by the sodium component of the sodium-phosphate supplement.
phosphate
Endocrine Research Laboratory, University of Cape Town, South Africa.
MONTE MODLIN.
CONVULSIONS DUE TO HYPOMAGNESÆMIA interested to read the article by Dr. Savage and (July 29, p. 234) and the letter by Dr. Farmer (Nov. 4, p. 988). Stutzman and Amatuzio1 stressed the importance of hepatic cirrhosis as a cause of hypomagnesaemia. Since biliary cirrhosis is the main liver lesion in prolonged non-correctable cases of congenital biliary atresia (C.B.A.), the serum-magnesium is also reduced in this disorder.2 I have seen
SIR,-I
was
Dr. McAdam
a
male infant with
C.B.A.
who showed
a
very low level of serum-
magnesium and had clonic convulsions. The patient was admitted to the clinic of this department at the age of 2 months with the chief complaints of severe jaundice, which had appeared 4 days after birth and had gradually increased, and distended abdomen (due to hepatosplenomegaly). He was clinically diagnosed as C.B.A., and exploratory laparotomy at age 21/2 months revealed a surgically non-correctable type (atresia of ductus hepaticus). Ascites was present. Soon after the operation, the serum-magnesium level was 1-10 (normal 2.26::1: 0.15 3) mEq. per litre, but the patient remained symptom-free. Thereafter, the disease progressed gradually and the patient became very ill with generalised oedema, severe jaundice, and anaemia. He was therefore given 4 bloodtransfusions, each of 50 ml., and spironolactone, 50 mg. per day per os for 3 weeks. At the age of 4 months, right-sided clonic convulsions appeared abruptly and ceased 5 minutes later without any special treatment. Next day he had bilateral clonic convulsions for 5-minute periods, and he died that night. Retrospectively, the magnesium level of serum taken soon after the first convulsions was 0-79 mEq. per litre. In this patient the other factors responsible for convulsions, such as hypoglycaemia or cerebral vascular lesions, were not ruled out, nor was the effectiveness of magnesium administration tested. However, it is strongly suggested that the patient had convulsions due to hypomagnesaemia, on the ground that the observed seizures were not related to feeding and that neurological examination revealed no abnormalities. Department of Pædiatrics, University of Tokyo, Tokyo, Japan.
AKIO KOBAYASHI.
TRAINING IN MEDICAL LABORATORY TECHNOLOGY SIR,-May I support the plea of Mr. Wasley and Dr. Fraser Williams (Nov. 18, p. 1093) for a double wage-scale for medical laboratory technicians. I have recently had a hand in teaching them, and many medical students would shudder at the pressure they have to work under during their four-week period in class. The ground that they cover is hardly elementary. When tested, a small group of them had an average i.Q. of 138 (s.D.20), and this can be fairly contrasted with the Cattell-iii mean4 for physicians of 146. However, the standard of material to be learnt is well up to that of second M.B., and there are many, later lost to their profession as a result, who make excellent laboratory men but just cannot take the academic pace, and drop out. If a paper qualification is needed -and I do not see why-then a laboratory technician’s course, such as the one held in the Salisbury College of Further Education, might be suitable for this second grade (mean
i.Q.116). PATRICK F. JAMES. 1. 2. 3. 4.
Stutzman, F. L., Amatuzio, D. S. J. Lab. clin. Med. 1953, 41, 215. Kobayashi, A., Shiraki, K. Archs Dis. Childh. (in the press). Kobayashi, A. Lancet, July 8, 1967, p. 100. Cattell, R. B. A. Guide to Mental Testing. London, 1953.