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COMBINING THE ANTIDEPRESSANT DRUGS
904 A considerable proportion of consultants are incapable of teaching because of poor technique, and inadequate preparation, or unwillingness to admit ignorance of some aspect, of a subject; so that they have to rely on bluff or dogmatic statements which permit no questioning. Some are just not interested or find that teaching interferes with their private practice-teaching is thus left to the senior registrars and registrars who are often closer to the academic fold than their chiefs (and many are therefore better teachers). It is not hard to understand the reluctance of teachinghospital consultants to give up their posts, which hold out greater opportunities for referred private practice, for a merit
award, and for travel-and which offer less chance of a disturbed night. I believe that much of the present discontent among doctors in Britain stems from the stranglehold which the teaching hospitals hold on medicine; and until there is a radical reform this discontent will continue to smoulder in spite of an occasional sop in the way of increased remuneration. I believe that private practice should be prohibited in teaching hospitals (a suitable salary scale could be introduced), and since most valuable research is carried out before the age of forty the posts should be vacated between the ages of forty and fortyfive. I hope that the new medical school at Nottingham may be bold enough to escape from the rut into which so many of the British medical schools have fallen. Vancouver 9, British Columbia, LAWRENCE S. DEANE. Canada. HYPOKALÆMIA WITH SKIN ANÆSTHESIA SIR,-So far as we can discover, anaesthesia of the skin has not been reported in patients with hypokalaemia. We have treated a hypokalaemic patient in whom such a disturbance was found. The patient, a 23-year-old man, had undergone ureterosigmoidostomy in 1957 after a gunshot wound in the urinary bladder. He was admitted to hospital owing to extreme weakness. Hypokalaemia was diagnosed (serum-potassium levels below 3-5 mEq. per litre and characteristic electrocardiographic [E.C.G.] changes). The patient responded well to treatment with potassium chloride. On his second admission, 5 months later, he was apparently paraplegic. Punctilious examination revealed complete sensory loss in the left half of his body, left extremities, and scalp. The E.C.G. revealed very prominent u wave, and the serumpotassium was 3-0 mEq. per litre. The patient was treated with potassium chloride 5 g. by mouth, and 12 hours later the paralysis and the sensory disturbances had disappeared completely. The serumpotassium rose to 4-5 mEq. per litre, and the E.C.G. became normal. Medical Department A, N. LEVY Rothschild Municipal Hospital, D. DIENGOTT. Haifa, Israel. HYPOKALÆMIA AND THE ELECTROCARDIOGRAM
SIR,-Iagree (though for somewhat different reasons) with Dr. Swales (Aug. 7) that hyperkalxmia cannot be conclusively ruled out as a cause of heart-block in his patient. The " peaked T waves " referred to by him are not T waves but p waves superimposed on the u waves. The supraventricular tachycardia at this stage is not incompatible with the Zwaardemaker-Libbrecht (z.-L.) phenomenon, as suggested by him. The bradycardia following cardiac arrest in the intact anaesthetised dog lasted only for less than 50 seconds.2 A normal E.C.G. in severe hyperkalasmia has occasionally been reported in Simmond’s disease, in severe alkalosis,3 and in the2 presence of induced hyperca1caemia. Surawicz and Mazzoleni Swales, J. D. Lancet, 1964, ii, 1365. Surawicz, B., Mazzoleni, A. in Sudden Cardiac Death; York, 1964. 3. Lepeschkin, E. Adv. Cardiol. 1959, 2, 189. 4. Chamberlain, M. J. Lancet, 1964, i, 464. 1. 2.
p. 90. New
have demonstrated that bradycardia, heart-block, hypotension, and cardiac arrest occurred after rapidly induced hyperkalaemia in potassium-depleted dogs, although the characteristic E.C.G. changes of hyperkalaemia were not seen. These changes have been found to resemble the z.-L. phenomenon noticed in the isolated perfused heart of the rabbit. At the time of my previous letter,5 I was not aware of this work.The dissociated effect on the E.C.G. of a possible hyperkalasmia in his case, suggested by Dr. Swales, could therefore be a reflection of the
phenomenon alone. Thus heart-block in relation to plasma-potassium levels may possibly result from four different causes as against the three I mentioned earlier 5: (1) hypokalaemia 7; (2) suddenly induced normokalxmia, or, in the presence of previous potassium Z.-L.
depletion, (3) suddenly-induced hyperkalasmia 6or (4) hyperkalsemia of gradual or rapid onset, in a previously normal heart, showing characteristic E.C.G. changes of hyperkalxmia affecting P, Q, R, s, and T waves. The heart-block in the case reported by Dr. Swales1 could be due to cause (2) or (3). In a personal series of 15 cases of potassium depletion, I administered potassium chloride intravenously at rates of 50-135 mEq. per litre over a minimum period of one hour under E.c.G. monitoring alone, and I found no evidence either of the z.-L. phenomenon or of Q, R, s widening or peaked T waves. The same work is being continued, with blood controls. My series, however, does not include cases of diabetes mellitus. It may be perhaps more than a coincidence that the present caseand the cases of cardiac arrest in hypokalaemia previously reported 8have occurred in relation to diabetes mellitus and insulin therapy. Offerijns et a1.1o reported a direct effect of insulin on muscular paralysis, other than through changes in plasma-potassium. Sri Venkateswara Medical College, R. N. SARMA. Tirupati, India.
COMBINING THE ANTIDEPRESSANT DRUGS SIR,-Dr. Gander’s article and your leading article (July 17) are interesting since they show that inhibitors of monoamine oxidase (M.A.O.) can be used beneficially in combination with
antidepressant drugs such as imipramine or amitriptyline without necessarily producing severe or dangerous side-effects. Dr. Gander goes on to suggest that amitriptyline may be safer than imipramine when used in combination with an M.A.o. inhibitor, although he gives no comparative data on the incidence of side-effects with the two drugs and does not state which M.A.o. inhibitors were used in every case. Mr. Loveless and I have carried out experiments in the rabbit to study the toxic interaction between M.A.o. inhibitors and other antidepressant drugs. Our results 11 showed that the administration of imipramine to rabbits premedicated with a high dose of tranylcypromine, nialamide, or phenelzine was followed by fatal hyperpyrexia, accompanied by hyperexcitement, in a large proportion of animals. Similar results were obtained after administering amitriptyline to rabbits premedicated with phenelzine or nialamide, but the incidence of fatal hyperpyrexial responses was lower in rabbits premedicated with tranylcypromine. The administration of trimipramine to rabbits premedicated with the same three M.A.o. inhibitors was not followed by hyperpyrexia or hyperexcitement. Our data in the rabbit thus accord with Dr. Gander’s suggestion, in that the incidence of hyperpyrexia and hyperexcitement is less pronounced with amitriptyline than with imipramine, although half of Dr. Gander’s patients were treated with a 5. Sarma, R. N. ibid. 1965, i, 1221. 6. Surawicz, B., Gettes, L. S. Circulation Res. 1963, 12, 415. 7. Paes de Carvalho, A., Langan, W. B. Am. J. Physiol. 1963, 295, 375. 8. Guyer, P. B. Br. med. J. 1964, ii, 427. 9. Paulley, J. W. Lancet, 1965, i, 218. 10. Offerijns, F. G. I., Westerink, D. G., Willebrands, A. F. J. Physiol., Lond. 1958, 141, 377. 11. Loveless, A. H., Maxwell, D. R. Br. J. Pharmac. Chemother. 1965, 25, 158.
905 combination of amitriptyline and phenelzine-which in the rabbit produces toxic effects. Our data also emphasise that not only do imipramine, amitriptyline, and trimipramine differ in their ability to produce this side-effect but also the particular M.A.O. inhibitor used may be important. A careful selection of antidepressant drugs for use in combination may therefore be required if the greatest therapeutic effect and least side-effects are to be achieved. Further, it is important to specify the particular drugs used when reporting any such combined-antidepressant study. Research Laboratories, May & Baker Ltd., D. R. MAXWELL. Dagenham, Essex. SPLEEN IRRADIATION AND LYMPHOCYTES SIR,-It is known that peripheral-blood lymphocytes from patients with chronic lymphocytic leukaemia (C.L.L.) generally give a low proportion (7-85-8%) of blast-like cells after 3-4 days of tissue culture with phytohaemagglutinin (P.H.A.), whereas blood-lymphocytes from healthy persons give high proportions of these cells (68-05-2%) when cultured in the same conditions. It seems that this defect in blast-development shown by C.L.L.-lymphocytes depends on a plasma factor, rather than on the innate biology of the leukaemic lymphocytes. We have proved that the development into blast-like cells of
of blasts had developed after 72 hours of tissue culture with P.H.A. After irradiation of the spleen (480r administered in 6 doses during 14 days), the proportion of blast-like cells rose to 76%-a normal value. But this effect was transient: the proportions of blasts began to decrease 3 weeks after the end of irradiation, and reached the values obtained before irradiation after 5 weeks. To explain these results, one can assume that X rays destroy the P.H.A.-non-responsive lymphocytes (the leuksemic ones ?), and spare the P.H.A.-responsive ones (the normal ones ?). But this hypothesis does not seem in agreement with the relation observed between the proportions of the blast-like cells obtained in tissue-culture with P.H.A., and the leucocyte-counts in the peripheral blood. The figure shows that 5-8 weeks after spleen irradiation the lymphocytes became P.H.A.-non-responsive again while the leucocyte-count was still low. Thus we think that our results agree more with the hypothesis that spleen irradiation removes or destroys that factor observed in the c.L.L.-plasma which inhibits the blast-development of peri-
C.L.L.-behaviour-13%
pheral-blood lymphocytes.
The Blood Research Foundation Tortona Hospital, Italy.
Centre,
G. ASTALDI R. AIRÒ G. COSTA N. DUARTE.
COMMON COLD: CONTROLLED TRIALS
SIR,-Dr. Banks (Oct. 16) does not mention the doses of ascorbic acid used in his trials. Observations made over a number of years have led me to think that the effectiveness of ascorbic acid in preventing the development of a cold depends on the adequacy of the initial dose. I have always used 1000 mg. initially, followed by 500 mg. at approximately 8-hour intervals. AUDREY Z. BAKER. Tiverton, Devon. ’*’ ’*’ This letter was shown to Dr. Banks, who writes as follows: " In my first trial ascorbic acid, 50 mg. six-hourly, was intended to be the placebo control on the antibiotics. Since the result with this small dosage seemed surprisingly good the same dosage was maintained in the subsequent trials. I saw no reason to change it."-ED. L.
Leucocyte-counts and blast-development of peripheral-blood lymphocytes in tissue-culture with P.H.A. before and after X-irradiation of the spleen in chronic lymphocytic leukaemia.
blood-lymphocytes from healthy persons is inhibited when 5-20% ofc.L.L.-plasma is added to the tissue-culture medium.l On the other hand, we have recently found that the proportion of P.H.A.-responsive blood-lymphocytes from patients with C.L.L. may be increased to the normal values by irradiating the spleen of these patients. We have observed this effect in 4 such patients, submitted to X-irradiation with doses of 300600r given either in a single dose or in fractionated doses of 80-loot at intervals of 2-7 days. The tissue-culture medium consisted of N.C.T.C. 109 7-6 parts; plasma from the donor of the lymphocytes 2 parts; and P.H.A. (prepared in our laboratory) 0-4 parts. The accompanying figure shows blast-development before and after spleen irradiation in a patient with C.L.L. Before irradiation the peripheral-blood lymphocytes showed typical 1. Astaldi, G., Airò, R., Costa, G., Duarte, N. Lancet, 1965, i, 1394.
HYPOCHROMIC ANÆMIA annotation SiR,—Your (Aug. 7) and your reference to the review from Oxford1 indicate the frequency with which the terms " hypochromic anaemia " and " iron-deficiency anaemia " are regarded as practically synonymous. Although irondeficiency was the cause of hypochromic anaemia in 371 out of their 378 patients, Professor Witts and his colleagues emphasised that their group was " not fully representative of persons with hypochromic anxmia in the general population ", their patients being those in whom hypochromic anaemia was a major clinical feature. Some years ago we noted that hypochromia, as judged by the mean corpuscular haemoglobin concentration (M.C.H.C.), was often reported in our patients who were not suffering primarily from haematological diseases. We found this surprising in a hospital population composed largely of Africans, in whom iron stores are so frequently excessive.2 We therefore started a controlled investigation of patients admitted under our care with various chronic infections, and we demonstrated that hypochromic anaemia was quite common. Iron-deficiency was excluded as the cause in every case by demonstrating the presence of normal or increased amounts of hxmosiderin in the bone-marrow and by finding plasma-iron patterns typical of infection. Our results in the anaemia associated with amoebic liver abscess have already been recorded.3 We have since compared 1. 2. 3.
Beveridge, B. R., Bannerman, R. M., Evanson, J. M., Witts, L. J. Q. Jl Med. 1965, 34, 145. Bothwell, T. H., Isaacson, C. Br. med. J. 1962, i, 522. Mayet, F. G. H., Powell, S. J. Am. J. trop. Med. Hyg. 1964, 13, 790.
award, and for travel-and which offer less chance of a disturbed night. I believe that much of the present discontent among doctors in Britain stems from the stranglehold which the teaching hospitals hold on medicine; and until there is a radical reform this discontent will continue to smoulder in spite of an occasional sop in the way of increased remuneration. I believe that private practice should be prohibited in teaching hospitals (a suitable salary scale could be introduced), and since most valuable research is carried out before the age of forty the posts should be vacated between the ages of forty and fortyfive. I hope that the new medical school at Nottingham may be bold enough to escape from the rut into which so many of the British medical schools have fallen. Vancouver 9, British Columbia, LAWRENCE S. DEANE. Canada. HYPOKALÆMIA WITH SKIN ANÆSTHESIA SIR,-So far as we can discover, anaesthesia of the skin has not been reported in patients with hypokalaemia. We have treated a hypokalaemic patient in whom such a disturbance was found. The patient, a 23-year-old man, had undergone ureterosigmoidostomy in 1957 after a gunshot wound in the urinary bladder. He was admitted to hospital owing to extreme weakness. Hypokalaemia was diagnosed (serum-potassium levels below 3-5 mEq. per litre and characteristic electrocardiographic [E.C.G.] changes). The patient responded well to treatment with potassium chloride. On his second admission, 5 months later, he was apparently paraplegic. Punctilious examination revealed complete sensory loss in the left half of his body, left extremities, and scalp. The E.C.G. revealed very prominent u wave, and the serumpotassium was 3-0 mEq. per litre. The patient was treated with potassium chloride 5 g. by mouth, and 12 hours later the paralysis and the sensory disturbances had disappeared completely. The serumpotassium rose to 4-5 mEq. per litre, and the E.C.G. became normal. Medical Department A, N. LEVY Rothschild Municipal Hospital, D. DIENGOTT. Haifa, Israel. HYPOKALÆMIA AND THE ELECTROCARDIOGRAM
SIR,-Iagree (though for somewhat different reasons) with Dr. Swales (Aug. 7) that hyperkalxmia cannot be conclusively ruled out as a cause of heart-block in his patient. The " peaked T waves " referred to by him are not T waves but p waves superimposed on the u waves. The supraventricular tachycardia at this stage is not incompatible with the Zwaardemaker-Libbrecht (z.-L.) phenomenon, as suggested by him. The bradycardia following cardiac arrest in the intact anaesthetised dog lasted only for less than 50 seconds.2 A normal E.C.G. in severe hyperkalasmia has occasionally been reported in Simmond’s disease, in severe alkalosis,3 and in the2 presence of induced hyperca1caemia. Surawicz and Mazzoleni Swales, J. D. Lancet, 1964, ii, 1365. Surawicz, B., Mazzoleni, A. in Sudden Cardiac Death; York, 1964. 3. Lepeschkin, E. Adv. Cardiol. 1959, 2, 189. 4. Chamberlain, M. J. Lancet, 1964, i, 464. 1. 2.
p. 90. New
have demonstrated that bradycardia, heart-block, hypotension, and cardiac arrest occurred after rapidly induced hyperkalaemia in potassium-depleted dogs, although the characteristic E.C.G. changes of hyperkalaemia were not seen. These changes have been found to resemble the z.-L. phenomenon noticed in the isolated perfused heart of the rabbit. At the time of my previous letter,5 I was not aware of this work.The dissociated effect on the E.C.G. of a possible hyperkalasmia in his case, suggested by Dr. Swales, could therefore be a reflection of the
phenomenon alone. Thus heart-block in relation to plasma-potassium levels may possibly result from four different causes as against the three I mentioned earlier 5: (1) hypokalaemia 7; (2) suddenly induced normokalxmia, or, in the presence of previous potassium Z.-L.
depletion, (3) suddenly-induced hyperkalasmia 6or (4) hyperkalsemia of gradual or rapid onset, in a previously normal heart, showing characteristic E.C.G. changes of hyperkalxmia affecting P, Q, R, s, and T waves. The heart-block in the case reported by Dr. Swales1 could be due to cause (2) or (3). In a personal series of 15 cases of potassium depletion, I administered potassium chloride intravenously at rates of 50-135 mEq. per litre over a minimum period of one hour under E.c.G. monitoring alone, and I found no evidence either of the z.-L. phenomenon or of Q, R, s widening or peaked T waves. The same work is being continued, with blood controls. My series, however, does not include cases of diabetes mellitus. It may be perhaps more than a coincidence that the present caseand the cases of cardiac arrest in hypokalaemia previously reported 8have occurred in relation to diabetes mellitus and insulin therapy. Offerijns et a1.1o reported a direct effect of insulin on muscular paralysis, other than through changes in plasma-potassium. Sri Venkateswara Medical College, R. N. SARMA. Tirupati, India.
COMBINING THE ANTIDEPRESSANT DRUGS SIR,-Dr. Gander’s article and your leading article (July 17) are interesting since they show that inhibitors of monoamine oxidase (M.A.O.) can be used beneficially in combination with
antidepressant drugs such as imipramine or amitriptyline without necessarily producing severe or dangerous side-effects. Dr. Gander goes on to suggest that amitriptyline may be safer than imipramine when used in combination with an M.A.o. inhibitor, although he gives no comparative data on the incidence of side-effects with the two drugs and does not state which M.A.o. inhibitors were used in every case. Mr. Loveless and I have carried out experiments in the rabbit to study the toxic interaction between M.A.o. inhibitors and other antidepressant drugs. Our results 11 showed that the administration of imipramine to rabbits premedicated with a high dose of tranylcypromine, nialamide, or phenelzine was followed by fatal hyperpyrexia, accompanied by hyperexcitement, in a large proportion of animals. Similar results were obtained after administering amitriptyline to rabbits premedicated with phenelzine or nialamide, but the incidence of fatal hyperpyrexial responses was lower in rabbits premedicated with tranylcypromine. The administration of trimipramine to rabbits premedicated with the same three M.A.o. inhibitors was not followed by hyperpyrexia or hyperexcitement. Our data in the rabbit thus accord with Dr. Gander’s suggestion, in that the incidence of hyperpyrexia and hyperexcitement is less pronounced with amitriptyline than with imipramine, although half of Dr. Gander’s patients were treated with a 5. Sarma, R. N. ibid. 1965, i, 1221. 6. Surawicz, B., Gettes, L. S. Circulation Res. 1963, 12, 415. 7. Paes de Carvalho, A., Langan, W. B. Am. J. Physiol. 1963, 295, 375. 8. Guyer, P. B. Br. med. J. 1964, ii, 427. 9. Paulley, J. W. Lancet, 1965, i, 218. 10. Offerijns, F. G. I., Westerink, D. G., Willebrands, A. F. J. Physiol., Lond. 1958, 141, 377. 11. Loveless, A. H., Maxwell, D. R. Br. J. Pharmac. Chemother. 1965, 25, 158.
905 combination of amitriptyline and phenelzine-which in the rabbit produces toxic effects. Our data also emphasise that not only do imipramine, amitriptyline, and trimipramine differ in their ability to produce this side-effect but also the particular M.A.O. inhibitor used may be important. A careful selection of antidepressant drugs for use in combination may therefore be required if the greatest therapeutic effect and least side-effects are to be achieved. Further, it is important to specify the particular drugs used when reporting any such combined-antidepressant study. Research Laboratories, May & Baker Ltd., D. R. MAXWELL. Dagenham, Essex. SPLEEN IRRADIATION AND LYMPHOCYTES SIR,-It is known that peripheral-blood lymphocytes from patients with chronic lymphocytic leukaemia (C.L.L.) generally give a low proportion (7-85-8%) of blast-like cells after 3-4 days of tissue culture with phytohaemagglutinin (P.H.A.), whereas blood-lymphocytes from healthy persons give high proportions of these cells (68-05-2%) when cultured in the same conditions. It seems that this defect in blast-development shown by C.L.L.-lymphocytes depends on a plasma factor, rather than on the innate biology of the leukaemic lymphocytes. We have proved that the development into blast-like cells of
of blasts had developed after 72 hours of tissue culture with P.H.A. After irradiation of the spleen (480r administered in 6 doses during 14 days), the proportion of blast-like cells rose to 76%-a normal value. But this effect was transient: the proportions of blasts began to decrease 3 weeks after the end of irradiation, and reached the values obtained before irradiation after 5 weeks. To explain these results, one can assume that X rays destroy the P.H.A.-non-responsive lymphocytes (the leuksemic ones ?), and spare the P.H.A.-responsive ones (the normal ones ?). But this hypothesis does not seem in agreement with the relation observed between the proportions of the blast-like cells obtained in tissue-culture with P.H.A., and the leucocyte-counts in the peripheral blood. The figure shows that 5-8 weeks after spleen irradiation the lymphocytes became P.H.A.-non-responsive again while the leucocyte-count was still low. Thus we think that our results agree more with the hypothesis that spleen irradiation removes or destroys that factor observed in the c.L.L.-plasma which inhibits the blast-development of peri-
C.L.L.-behaviour-13%
pheral-blood lymphocytes.
The Blood Research Foundation Tortona Hospital, Italy.
Centre,
G. ASTALDI R. AIRÒ G. COSTA N. DUARTE.
COMMON COLD: CONTROLLED TRIALS
SIR,-Dr. Banks (Oct. 16) does not mention the doses of ascorbic acid used in his trials. Observations made over a number of years have led me to think that the effectiveness of ascorbic acid in preventing the development of a cold depends on the adequacy of the initial dose. I have always used 1000 mg. initially, followed by 500 mg. at approximately 8-hour intervals. AUDREY Z. BAKER. Tiverton, Devon. ’*’ ’*’ This letter was shown to Dr. Banks, who writes as follows: " In my first trial ascorbic acid, 50 mg. six-hourly, was intended to be the placebo control on the antibiotics. Since the result with this small dosage seemed surprisingly good the same dosage was maintained in the subsequent trials. I saw no reason to change it."-ED. L.
Leucocyte-counts and blast-development of peripheral-blood lymphocytes in tissue-culture with P.H.A. before and after X-irradiation of the spleen in chronic lymphocytic leukaemia.
blood-lymphocytes from healthy persons is inhibited when 5-20% ofc.L.L.-plasma is added to the tissue-culture medium.l On the other hand, we have recently found that the proportion of P.H.A.-responsive blood-lymphocytes from patients with C.L.L. may be increased to the normal values by irradiating the spleen of these patients. We have observed this effect in 4 such patients, submitted to X-irradiation with doses of 300600r given either in a single dose or in fractionated doses of 80-loot at intervals of 2-7 days. The tissue-culture medium consisted of N.C.T.C. 109 7-6 parts; plasma from the donor of the lymphocytes 2 parts; and P.H.A. (prepared in our laboratory) 0-4 parts. The accompanying figure shows blast-development before and after spleen irradiation in a patient with C.L.L. Before irradiation the peripheral-blood lymphocytes showed typical 1. Astaldi, G., Airò, R., Costa, G., Duarte, N. Lancet, 1965, i, 1394.
HYPOCHROMIC ANÆMIA annotation SiR,—Your (Aug. 7) and your reference to the review from Oxford1 indicate the frequency with which the terms " hypochromic anaemia " and " iron-deficiency anaemia " are regarded as practically synonymous. Although irondeficiency was the cause of hypochromic anaemia in 371 out of their 378 patients, Professor Witts and his colleagues emphasised that their group was " not fully representative of persons with hypochromic anxmia in the general population ", their patients being those in whom hypochromic anaemia was a major clinical feature. Some years ago we noted that hypochromia, as judged by the mean corpuscular haemoglobin concentration (M.C.H.C.), was often reported in our patients who were not suffering primarily from haematological diseases. We found this surprising in a hospital population composed largely of Africans, in whom iron stores are so frequently excessive.2 We therefore started a controlled investigation of patients admitted under our care with various chronic infections, and we demonstrated that hypochromic anaemia was quite common. Iron-deficiency was excluded as the cause in every case by demonstrating the presence of normal or increased amounts of hxmosiderin in the bone-marrow and by finding plasma-iron patterns typical of infection. Our results in the anaemia associated with amoebic liver abscess have already been recorded.3 We have since compared 1. 2. 3.
Beveridge, B. R., Bannerman, R. M., Evanson, J. M., Witts, L. J. Q. Jl Med. 1965, 34, 145. Bothwell, T. H., Isaacson, C. Br. med. J. 1962, i, 522. Mayet, F. G. H., Powell, S. J. Am. J. trop. Med. Hyg. 1964, 13, 790.