- Email: [email protected]
SEVERITY OF RESPIRATORY FAILURE
490
plete the dynamic testing of glucocorticoid reserve capacity by corticotrophin, using another functional test of mineralocorticoid reserve capacity. Our unpublished work shows its value in this respect. But risk must be taken into account as with many similar drugs. Third Medical Clinic, Laboratory for Endocrinology and Metabolism,
Charles University, Prague, Czechoslovakia.
OTO KÜCHEL KAREL HORKÝ MILAN PAZOUREK INGE GREGOROVÁ.
URINARY SODIUM/POTASSIUM RATIO AFTER CHLOROTHIAZIDE IN ADDISON’S DISEASE SIR,-We read with great interest the preliminary communication by Dr. Küchel and his colleagues1 on the lack of effect of angiotensin on the blood-pressure and urinary sodium/potassium ratio in patients with Addison’s disease. They suggested the use of angiotensin infusion for detecting hypoaldosteronism. In a recent study2 we found that in Addison’s disease the not decrease in response short-term chlorothiazide treatment; in normal persons, after giving chlorothiazide,1 ’0 g. twice daily, there is a profound decrease in this ratio on the third day, which persists for some time. The excretion of calcium follows the same pattern.34 We suggested that the renal handling of sodium, potassium, and calcium was dependent on the renin-angiotensin-aldosterone system. Chlorothiazide stimulates granulation in the juxtaglomerular cells5 in animals and aldosterone excretion in man," and more recently it has been shown that sodium restriction7 and treatment with chlorthalidone9 increases the plasma-renin concentration in man. In Addison’s disease, the plasma-renin seems to be increased,possibly in response to deficient aldosterone secretion. For this reason we feel that short-term treatment with a thiazide compound could be used as a screening test for the detection of hypoaldosteronism. A greatly accelerated aldosterone output would probably also result in a lack of response to thiazides.
urinary sodium/potassium ratio does
closing in, compressing my chest, and finally completely preventing my breathing. These always terminated in the same way-with my wife arousing me after having been herself awakened by my terrified screams. They vanished with the adoption of a restricted carbohydrate, high protein, and moderate fat diet, but occasionally recur when, against my better judgment, I eat sweets, not. adequately covered by protein. I have still to discover a rational explanation for the frank objective and subjective vertigo with tinnitus and developmental type nystagmus, sometimes associated with severe staggering, which, without the cardinal symptomatology of hypoglycasmia, many times leads to the diagnosis of simple functional or reactive prediabetic hypoglycaonia. Another more explicable discovery among hypoglycaemic cigarette smokers is the rarity walls
of those who smoke either before breakfast or before an hour after eating breakfast. This is due, I think, to the smoking/ adrenaline release/glycogen release/insulin stimulation/glycogen or glucose depletion cycle.
Another item of note is that only about one out of ten of those with hypoglyceemia volunteer complaints which suggest the proper diagnosis.
to
Further studies in centres where such cases are more abundant would be of great interest. B.-A. LAMBERG First Department of Medicine, P. TORSTI University of Helsinki, Helsinki, Finland.
J. PALOHEIMO.
F. B. STEINER. SEVERITY OF RESPIRATORY FAILURE
SiR,—In the middle column of table I in our article (Feb. 13) there is an unfortunate misprint, at a crucial stage of the argument, which may have confused those who had followed it up to this point. We are sure that all Lancet readers appreciate that even in respiratory physiology the subtraction of 15 from 50 does not yield 13; those who were mystified or disheartened, however, may be reassured that the arterial P02 predicted for an arterial Pco2 of 80 mm. Hg should read 35 mm. Hg. E. J. M. CAMPBELL Postgraduate Medical School, M. W. MCNICOL. London, W.12. ABDOMINAL PAIN OF SPINAL ORIGIN SiR,—The condition described by Mr. Daintree Johnson is almost certainly root pain due to a dorsal prolapsed intervertebral disc or dorsal spondylosis. Rapid relief can be given in the majority of cases by manipulation or spinal traction followed by mobilising exercises.
A. C. ELKIN.
SOME ASPECTS OF HYPOGLYCÆMIA
SIR,-Prof. Adam Patrick’s article 10 was indeed stimulating because of the vivid personal recollection it aroused concerning my own hypoglycsemic episodes. These were attacks of weakness, severe palpitation with a of pounding in the head, impending dread, and profuse perspiration, self-diagnosed as hypertensive episodes since they invariably came on about half an hour after eating my evening meal-the heaviest of the day. The diagnosis of hypoglycsemia was confirmed: after 3 days of carbohydrate loading, my 5thhour blood-glucose level in a glucose-tolerance test was 28 mg. per 100 ml. (Somogyi). This level was preceded by vomiting, diarrhoea, severe tachycardia, weakness approaching syncope, drenching sweats, violent erythematous tingling flushes, and voracious hunger. These symptoms lasted from 41/2 hours after the test was initiated until an hour later when I was fed. For years I havehad a stereotyped nightmare sequence of sense
1.
Kuchel, O., HorkÝ, K., Pazourek, M., Gregorová, I. Lancet, 1964, ii, 1316.
Lamberg, B.-A., Torsti, P. Acta med. scand. 1964, suppl. 412, p. 193. Lamberg, B.-A., Kulback, B. Scand. J. clin. Lab. Invest. 1959, 11, 351. Torsti, P., Lamberg, B.-A. Acta med. scand. 1964, suppl. 412, p. 181. Tobian, L. Circulation, 1962, 25, 189. Josephson, B., Bergstrom, J., Bucht, H., Hultman, E. Scand. J. clin. Lab. Invest. 1962, 14, 47. 7. Brown, J. J., Davies, D. L., Lever, A. F., Robertson, J. I. S. Lancet, 1963, ii, 278. 8. Brown, J. J., Davies, D. L., Lever, A. F., Robertson, J. I. S. Canad. med. Ass. J. 1964, 90, 201. 9. Veyrat, R., de Champlain, J., Boucher, R., Genest, J. ibid. p. 215. 10. Patrick, A. Lancet, 1964, ii, 1230. 2. 3. 4. 5. 6.
CORONARY THROMBOSIS PREVENTION ? SIR,-Following the fascinating article on linolenic acid for the prevention of thrombosis by Owren et al.1 many will await with interest the results of field-trials based on this work. Meanwhile, in view of doubt of the value of
long-term anticoagulant therapy, it
seems
that
potential
candidates for thrombosis-such as hypertensives, sufferers from angina, diabetics, and overweight executives-should take a drachm (5 ml.) of raw linseed oil daily. Even those already on anticoagulants might with advantage take this oil as well. It is unlikely to do harm and may well be life-saving. It is cheap, no laboratory supervision is required, and there is no danger of
haemorrhage. taste of linseed oil is quickly masked by other for those who dislike it a simple alternative is but foods, to take four times the quantity-i.e., 4 drachms (20 g.)of freshly ground linseed. One can grind linseed in a " coffee-grinder or liquidiser ". The powder so produced is palatable and can be taken as a cereal at breakfast with milk. The flavour is a little reminiscent ofBemax’. T. H. GILLISON.
The
1.
Owren, P. A., Hellem, A. J.,
Ödegaard,
A.
Lancet, 1964, ii,
975.
plete the dynamic testing of glucocorticoid reserve capacity by corticotrophin, using another functional test of mineralocorticoid reserve capacity. Our unpublished work shows its value in this respect. But risk must be taken into account as with many similar drugs. Third Medical Clinic, Laboratory for Endocrinology and Metabolism,
Charles University, Prague, Czechoslovakia.
OTO KÜCHEL KAREL HORKÝ MILAN PAZOUREK INGE GREGOROVÁ.
URINARY SODIUM/POTASSIUM RATIO AFTER CHLOROTHIAZIDE IN ADDISON’S DISEASE SIR,-We read with great interest the preliminary communication by Dr. Küchel and his colleagues1 on the lack of effect of angiotensin on the blood-pressure and urinary sodium/potassium ratio in patients with Addison’s disease. They suggested the use of angiotensin infusion for detecting hypoaldosteronism. In a recent study2 we found that in Addison’s disease the not decrease in response short-term chlorothiazide treatment; in normal persons, after giving chlorothiazide,1 ’0 g. twice daily, there is a profound decrease in this ratio on the third day, which persists for some time. The excretion of calcium follows the same pattern.34 We suggested that the renal handling of sodium, potassium, and calcium was dependent on the renin-angiotensin-aldosterone system. Chlorothiazide stimulates granulation in the juxtaglomerular cells5 in animals and aldosterone excretion in man," and more recently it has been shown that sodium restriction7 and treatment with chlorthalidone9 increases the plasma-renin concentration in man. In Addison’s disease, the plasma-renin seems to be increased,possibly in response to deficient aldosterone secretion. For this reason we feel that short-term treatment with a thiazide compound could be used as a screening test for the detection of hypoaldosteronism. A greatly accelerated aldosterone output would probably also result in a lack of response to thiazides.
urinary sodium/potassium ratio does
closing in, compressing my chest, and finally completely preventing my breathing. These always terminated in the same way-with my wife arousing me after having been herself awakened by my terrified screams. They vanished with the adoption of a restricted carbohydrate, high protein, and moderate fat diet, but occasionally recur when, against my better judgment, I eat sweets, not. adequately covered by protein. I have still to discover a rational explanation for the frank objective and subjective vertigo with tinnitus and developmental type nystagmus, sometimes associated with severe staggering, which, without the cardinal symptomatology of hypoglycasmia, many times leads to the diagnosis of simple functional or reactive prediabetic hypoglycaonia. Another more explicable discovery among hypoglycaemic cigarette smokers is the rarity walls
of those who smoke either before breakfast or before an hour after eating breakfast. This is due, I think, to the smoking/ adrenaline release/glycogen release/insulin stimulation/glycogen or glucose depletion cycle.
Another item of note is that only about one out of ten of those with hypoglyceemia volunteer complaints which suggest the proper diagnosis.
to
Further studies in centres where such cases are more abundant would be of great interest. B.-A. LAMBERG First Department of Medicine, P. TORSTI University of Helsinki, Helsinki, Finland.
J. PALOHEIMO.
F. B. STEINER. SEVERITY OF RESPIRATORY FAILURE
SiR,—In the middle column of table I in our article (Feb. 13) there is an unfortunate misprint, at a crucial stage of the argument, which may have confused those who had followed it up to this point. We are sure that all Lancet readers appreciate that even in respiratory physiology the subtraction of 15 from 50 does not yield 13; those who were mystified or disheartened, however, may be reassured that the arterial P02 predicted for an arterial Pco2 of 80 mm. Hg should read 35 mm. Hg. E. J. M. CAMPBELL Postgraduate Medical School, M. W. MCNICOL. London, W.12. ABDOMINAL PAIN OF SPINAL ORIGIN SiR,—The condition described by Mr. Daintree Johnson is almost certainly root pain due to a dorsal prolapsed intervertebral disc or dorsal spondylosis. Rapid relief can be given in the majority of cases by manipulation or spinal traction followed by mobilising exercises.
A. C. ELKIN.
SOME ASPECTS OF HYPOGLYCÆMIA
SIR,-Prof. Adam Patrick’s article 10 was indeed stimulating because of the vivid personal recollection it aroused concerning my own hypoglycsemic episodes. These were attacks of weakness, severe palpitation with a of pounding in the head, impending dread, and profuse perspiration, self-diagnosed as hypertensive episodes since they invariably came on about half an hour after eating my evening meal-the heaviest of the day. The diagnosis of hypoglycsemia was confirmed: after 3 days of carbohydrate loading, my 5thhour blood-glucose level in a glucose-tolerance test was 28 mg. per 100 ml. (Somogyi). This level was preceded by vomiting, diarrhoea, severe tachycardia, weakness approaching syncope, drenching sweats, violent erythematous tingling flushes, and voracious hunger. These symptoms lasted from 41/2 hours after the test was initiated until an hour later when I was fed. For years I havehad a stereotyped nightmare sequence of sense
1.
Kuchel, O., HorkÝ, K., Pazourek, M., Gregorová, I. Lancet, 1964, ii, 1316.
Lamberg, B.-A., Torsti, P. Acta med. scand. 1964, suppl. 412, p. 193. Lamberg, B.-A., Kulback, B. Scand. J. clin. Lab. Invest. 1959, 11, 351. Torsti, P., Lamberg, B.-A. Acta med. scand. 1964, suppl. 412, p. 181. Tobian, L. Circulation, 1962, 25, 189. Josephson, B., Bergstrom, J., Bucht, H., Hultman, E. Scand. J. clin. Lab. Invest. 1962, 14, 47. 7. Brown, J. J., Davies, D. L., Lever, A. F., Robertson, J. I. S. Lancet, 1963, ii, 278. 8. Brown, J. J., Davies, D. L., Lever, A. F., Robertson, J. I. S. Canad. med. Ass. J. 1964, 90, 201. 9. Veyrat, R., de Champlain, J., Boucher, R., Genest, J. ibid. p. 215. 10. Patrick, A. Lancet, 1964, ii, 1230. 2. 3. 4. 5. 6.
CORONARY THROMBOSIS PREVENTION ? SIR,-Following the fascinating article on linolenic acid for the prevention of thrombosis by Owren et al.1 many will await with interest the results of field-trials based on this work. Meanwhile, in view of doubt of the value of
long-term anticoagulant therapy, it
seems
that
potential
candidates for thrombosis-such as hypertensives, sufferers from angina, diabetics, and overweight executives-should take a drachm (5 ml.) of raw linseed oil daily. Even those already on anticoagulants might with advantage take this oil as well. It is unlikely to do harm and may well be life-saving. It is cheap, no laboratory supervision is required, and there is no danger of
haemorrhage. taste of linseed oil is quickly masked by other for those who dislike it a simple alternative is but foods, to take four times the quantity-i.e., 4 drachms (20 g.)of freshly ground linseed. One can grind linseed in a " coffee-grinder or liquidiser ". The powder so produced is palatable and can be taken as a cereal at breakfast with milk. The flavour is a little reminiscent ofBemax’. T. H. GILLISON.
The
1.
Owren, P. A., Hellem, A. J.,
Ödegaard,
A.
Lancet, 1964, ii,
975.