771
Fig. 2-Mesenteric lymph-node after treatment with disulfiram 120 mg/kg/day for 14 days showing heemosiderosis. (Perl’s method for ferric iron; reduced to 2/3 of x 160.) killed after 7 days of exposure, and the rest were killed after 14 days. Frozen sections of skeletal and cardiac muscle, liver, kidneys, and tongue were stained with scarletred. Embedded sections were stained with haematoxylin and eosin and Perl’s method for ferric iron. In all rats given disulfiram a focal acute-subacute myocardial degeneration was observed, characterised by swelling, disintegration, and fatty infiltration of the muscle fibres. Invasion by macrophages in degenerated areas was also seen (fig. 1). The degenerative changes occurred in animals exposed for 7 days as well as in those exposed for 2 weeks. In biceps and triceps brachii, quadriceps, and gastrocnemius muscles and in the tongue a qualitatively and quantitatively similar focal degeneration was observed in all exposed animals at both 7 and 14 sex were
days. The liver showed a slight fatty infiltration of hepatic cells in four out of ten animals after 7 days. At 14 days fatty infiltration was observed in sixteen out of twenty animals. These and varied between moderate All rats showed moderate or severe haemosiderosis in the mesenteric lymph-nodes after 14 days (fig. 2). The muscle degeneration observed was not associated with disturbances of behaviour or locomotion. It might, however, be followed by impairment of muscle function in animals exposed to higher doses or for a longer time to thiocarbamates or to carbon disulphide. The myocardial degeneration we found has not been described previously and might be associated with similar observations in dogs3 exposed to carbon disulphide or in rats’ subject to concomitant exposure to noradrenaline (norepinephrine) or phenobarbitone with carbon disulphide. Thiram produced muscle degeneration of the gastrocnemius in rats,’ and an increased risk of myocardial infarction has been associated with occupational exposure to carbon disulphide.8
changes were mainly peripheral and
severe.
S. EKVÄRN AB
Kabi, S-10425 Stockholm, Sweden
M. JÖNSSON N. G.
LINDQUIST
National Board of Occupational Safety and Health, S-100 26 Stockholm
B. HOLMBERG
National Veterinary Institute, S-104 05 Stockholm
T. KRONEVI
MECHANICAL METHODS AGAINST DEEP-VEIN THROMBOSIS
SiR,—Your editorial (Sept. 3, p. 490) ends on a note of caupractical limitations of mechanical methods of
tion about the 7. 8
Chandra, S V., Butter, W. H., Magos, L. Explmol. Pharmac. 1972, 17, 249. Hernberg, S., Tolonen, M., Nurminen, M. Scand. J. Work envir. Hlth, 1976. 2, 27.
preventing postoperative deep-vein thrombosis. In our experience these problems have been exaggerated. For the past six months we have been using below-knee graduated static compression stockings’ and pneumatic leggings2 in patients undergoing laparotomy, apart from those in lithotomy or lateral positions, who are fitted with electrical calf stimulators.3.4 In addition dextran-70s is given during and after the operation. The use of dextran-70 has resulted in one case of transient circulatory overloading, but the mechanical methods have been completely free of complications. We have encountered no problems in the application of compression leggings or calf stimulators. The time taken is no longer than that required to apply and connect the diathermy pad. The additional work is negligible, and there have been no storage problems. At other hospitals the routine application of compression leggings has been similarly problem-free. These have been used in about 4000 patients at St. Helier Hospital, Carshalton, among whom none has had signs of pulmonary embolism within three weeks of surgical operation.6 Recent reports of haemorrhage in patients receiving low-dose heparin 7,S may stimulate surgeons to look again at mechanical methods; our experience has dispelled any misgivings about difficulties or added work-load. DAVID NEGUS SYLVIA QUAILE DAVID WILMHURST Operating Theatres, VERNON ROBINSON Lewisham Hospital, London SE13 6LH RAY SMITH
TREATMENT OF EROSIVE LICHEN PLANUS OF THE ORAL MUCOSA WITH DEPOT STEROIDS
SIR,-The oral ulceration associated with erosive lichen causes considerable and sometimes protracted discomfort. The response to local applications of corticosteroids is variable probably because it is difficult to keep the drug in contact with the mucosal lesion for a sufficient time. Sometimes systemic administration of corticosteroids is resorted to. Intralesional steroid therapy does have a use in dermatology,9 and erosive lichen planus of the mouth has been treated with triamcinolone acetonide in a few patients’"’’’ Five patients with persistent ulceration of the oral mucosa were treated. Lichen planus was diagnosed clinically and confirmed histologically. The areas of ulceration varied from the tongue to the labial and buccal mucosa and the ulceration had not responded to conventional topical steroid therapy. One patient had had ulcers on the lateral margin of the tongue for about 3 months. An aqueous suspension containing methylprednisolone acetate 40 mg/ml (’Depo-Medrone’) was used and 0.5-1.0 ml was injected submucosally. The white suspension tended to leak from the injection site but this was overcome by inserting the needle at least 10 mm from the ulcerated area. The response was encouraging, improvement usually being evident by 48 h; and in four cases the lesions healed within a week. One patient required a second injection of 0-5ml after
planus
Holford, C. P. Br. J. Surg. 1976, 63, 157. Hills, N. H., Pflug, J. J., Jeyasingh, K., Boardman, L., Calnan, J. S. Br. med. J. 1972, i,131. 3. Doran, F. S. A., White, H. M., Drury, M. Br. J. Surg. 1970, 57, 20. 4. Browse, N. L., Negus, D. Br. med. J. 1970, iii, 615. 5. Kline, K., Hughes, L. E., Campbell, H., Williams, A., Zlosnick, J., Leach,
1. 2.
K. G. ibid. 1975, ii, 109.
Wells, B. W. Personal communication. Gruber, U. F., Duchert, F., Fridrich, R., Torhorst, J., Rem, J. Lancet, 1977, i, 207. 8. Britton, B. J., Finch, D. R. A., Gill, P. G., Kettlewell, M. G. W., Morris, P. J. ibid. 1977, ii, 604. 9. Verbov, J. Br. J. Derm. 1976, 94, suppl. 15, p. 51. 10. Taylor, A. Dent. Practit. 1966, 17, 56. 11. Sleeper, H. R. Yale J. Biol. Med. 1967, 40, 164. 6. 7.
772 week and the ulcer healed over the next week; this ulcer was cm in diameter and might have been subjected to trauma because it was on the lateral margin of the tongue. The frequency ot such injections must be carefully considered because they provide a significant systemic dose of corticosteroid. However, this has not been a problem in my series; minor erosions or atrophy responded to a mild astringent mouthwash (e.g., zinc sulphate). a
1
Department of Oral Medicine and Pathology, Dental Hospital and School, Glasgow G2 3JZ
M. M. FERGUSON
IMPORTED SHIGA DYSENTERY
SIR,-In the 1970s major epidemics of dysentery caused by antibiotic-resistant Shigella dysenteriae type 1 have been reported from Central Americal-s and Bangladesh.6,7 We have lately seen a case with many of the features observed in these epidemics and have isolated an organism with the same antibiotic resistances. An Asian boy, 3 years old, returned with his parents in midMay from Pakistan and became ill on May 23 with abdominal pain, fever, and diarrhoea. Stools became very frequent with passage of blood and mucopus and he was admitted to hospital on May 26. No amoeba: were seen in the stools and cultures were negative at first but 1 week after admission a strain of S. dysenteriae type 1 was identified which had failed to grow on desoxycholate-citrate medium but was present in the mixed growth on MacConkey agar. It was resistant to tetracycline, streptomycin, chloramphenicol, and sulphonamides but was sensitive to ampicillin, gentamicin, co-trimoxazole, and colistin. The white cell count, which was 11.7 x 109/1 on admission, rose to 32 x 109/1 in the following week with 91% neutrophils and shift to the left. Bacteraemia was suspected so, after a blood culture had been arranged, parenteral gentamicin was prescribed. There being no response, after three days oral colistin was added. This may have caused slight improvement, in that the stools became more formed, but general recovery did not begin until intramuscular ampicillin was started on June 11. Thereafter progress was rapid. The blood culture was
negative. The red-cell count fell from 5.43 x 10’Z/1 on June 1, to 3-79 x 10’Vl on June 13, the haematocrit from 37% to 26% and the haemoglobin from 11.9 to 9.2 g/1. We cannot say if haemolysis7 had contributed to the development of anaemia: a Coombs’ test and other investigations on June 15 were negative. Red cells were noted in the urine on June 11. Recovery has been complete and there has been no bacteriological relapse. The parents’ stools were negative. The difficulty experienced in isolating the pathogen,’,2,’,s its antibiotic resistances,2,3,6 failure to get a clinical response with antibiotics which were expected to be effective, 1.2 response to ampicillin 5,6 the high white cell countand the hmmaturia,7 all suggest that we have been dealing with a case of dysentery caused by a strain of Shiga’s bacillus like those responsible for overseas
epidemics.
Are such strains endemic in Asia now, or are there epidemics in areas of India and Pakistan which were previously untouched ? This organism could be a hazard to Asians in Britain who visit villages in their countries of origin, and even though outbreaks in Britain are not likely, individual cases may present problems to clinicians and laboratory workers.2 Laboratory workers need to bear this organism in mind in all cases where the history or the symptoms suggest shigellosis as a possibility,
and they should look for it on the usual selective media.
on
MacConkey plates,8
as
well
as
P. D. Moss W. M. DARLING
Royal Infirmary, Blackburn, Lancashire
HYPERVOLÆMIA IN PHENYLKETONURIA
SIR,-The effect of phenylketonuria (P.K.U.) on blood volume has hitherto not been described. We measured plasma volume in nine untreated infants and children with P.K.U. or hyperphenylalaninaemia using Evans blue.9 The blood volume was calculated from the plasma volume and microhaematocrit (P.c.v.). The plasma concentration of phenylalanine was measured by the method of McCamman and Robins. 10 BLOOD VOLUME AND PLASMA PHENYLALANINE CONCENTRATION
volume predicted from weight and of variation of normal blood volume is
* Percentage of normal blood
height." The coefficient approximately 10%. The blood volume
’
was
normal in four infants aged 2-4 two infants aged 5 weeks and increased in the older infants and
weeks, moderately increased in
8 weeks and considerably children (see table). The high concentrations of phenylalanine in our patients competitively inhibit the conversion of tyrosine to L-dopa by tyrosine hydroxylase 12 and so reduce formation of catecholamines.13 Thus, P.K.U. may have a similar effect to alphaadrenergic blocking agents, which also increase the blood volume. 14, 11 The more pronounced hypervolaenua in the older infants and children suggests an age-dependent effect, either of P.K.U. on the formation of catecholamines or of catecholamines on the blood volume. Department of Pædiatrics, University of Munich, D-8000 München 2, West Germany
O. LINDERKAMP
J. SCHAUB K. P. RIEGEL
PLASMA RENIN AND ANGIOTENSIN II IN ACUTE RENAL FAILURE
SiR,—We incorrectly cited some of the rèferences in our recent (Aug. 13, p. 328). Iaina et al.16 studied the hypoxic
paper
model of acute renal failure in the rat not the glycerol-induced model. Powell-Jackson et al.17 in Glasgow as well as Rauh et Rahaman, M. M., Huq, I., Dey, C. R. J. infect. Dis. 1975, 131, 700. Linderkamp, O., Mader, T., Butenandt, O., Riegel, K. P. Europ. J. Pediat. 1977, 125, 135. 10. McCamman, M., Robins, E. J. Lab. clin. Med. 1962, 59, 885. 11. Linderkamp, O., Versmold, H. T., Riegel, K. P., Betke, K. Eur. J. Pediat 1977, 125, 227. 12. Ikeda, M., Levitt, M., Udenfriend, S. Archs. Biochem. Biophys. 1967, 120, 8. 9.
420. 1. Vijil, C. Lancet, 1970, ii, 471. 2. Levine, M. M., DuPont, H. L., Formal, S. B., Gangarosa, E. J. ibid, p. 3. Reller, L. B. ibid. p. 661. 4. Mata, L. J., Cáceres, A., Torres, M. F. ibid. 1971, i, 600. 5. Vijil, C. ibid, 1971, ii, 823. 6. Rahaman, M. M. Huq, I., Dey, C. R., Kibriya, A. K. M. G., Curlin, G.
1974, i, 406. 7. Rahaman, M. M., Alam, A. K. M. J., Islam, M. R. ibid, p. 1004.
13.
A. Clin. chim. Acta.
1972, 42,
235.
607.
ibid,
Curtius, H. Ch., Baerlocher, K., Völlmin, J.
14. 15. 16. 17.
Weil, J. V., Chissey, C. A. Circulation, 1968, 37, 54. Linderkamp, O., Dehnert-Hilscher, A. Anœsthetist, 1977, 26, 349 laina, A., Solomon, S., Eliahou, H. E. Lancet, 1975, ii, 157. Powell-Jackson, J. D., Brown, J. J., Lever, A. F., MacGregor, J., Macadam, R. F., Titterington, D. M., Robertson, J. I. S., Waite, M. A. ibid. 1972, i, 774.
Fig. 2-Mesenteric lymph-node after treatment with disulfiram 120 mg/kg/day for 14 days showing heemosiderosis. (Perl’s method for ferric iron; reduced to 2/3 of x 160.) killed after 7 days of exposure, and the rest were killed after 14 days. Frozen sections of skeletal and cardiac muscle, liver, kidneys, and tongue were stained with scarletred. Embedded sections were stained with haematoxylin and eosin and Perl’s method for ferric iron. In all rats given disulfiram a focal acute-subacute myocardial degeneration was observed, characterised by swelling, disintegration, and fatty infiltration of the muscle fibres. Invasion by macrophages in degenerated areas was also seen (fig. 1). The degenerative changes occurred in animals exposed for 7 days as well as in those exposed for 2 weeks. In biceps and triceps brachii, quadriceps, and gastrocnemius muscles and in the tongue a qualitatively and quantitatively similar focal degeneration was observed in all exposed animals at both 7 and 14 sex were
days. The liver showed a slight fatty infiltration of hepatic cells in four out of ten animals after 7 days. At 14 days fatty infiltration was observed in sixteen out of twenty animals. These and varied between moderate All rats showed moderate or severe haemosiderosis in the mesenteric lymph-nodes after 14 days (fig. 2). The muscle degeneration observed was not associated with disturbances of behaviour or locomotion. It might, however, be followed by impairment of muscle function in animals exposed to higher doses or for a longer time to thiocarbamates or to carbon disulphide. The myocardial degeneration we found has not been described previously and might be associated with similar observations in dogs3 exposed to carbon disulphide or in rats’ subject to concomitant exposure to noradrenaline (norepinephrine) or phenobarbitone with carbon disulphide. Thiram produced muscle degeneration of the gastrocnemius in rats,’ and an increased risk of myocardial infarction has been associated with occupational exposure to carbon disulphide.8
changes were mainly peripheral and
severe.
S. EKVÄRN AB
Kabi, S-10425 Stockholm, Sweden
M. JÖNSSON N. G.
LINDQUIST
National Board of Occupational Safety and Health, S-100 26 Stockholm
B. HOLMBERG
National Veterinary Institute, S-104 05 Stockholm
T. KRONEVI
MECHANICAL METHODS AGAINST DEEP-VEIN THROMBOSIS
SiR,—Your editorial (Sept. 3, p. 490) ends on a note of caupractical limitations of mechanical methods of
tion about the 7. 8
Chandra, S V., Butter, W. H., Magos, L. Explmol. Pharmac. 1972, 17, 249. Hernberg, S., Tolonen, M., Nurminen, M. Scand. J. Work envir. Hlth, 1976. 2, 27.
preventing postoperative deep-vein thrombosis. In our experience these problems have been exaggerated. For the past six months we have been using below-knee graduated static compression stockings’ and pneumatic leggings2 in patients undergoing laparotomy, apart from those in lithotomy or lateral positions, who are fitted with electrical calf stimulators.3.4 In addition dextran-70s is given during and after the operation. The use of dextran-70 has resulted in one case of transient circulatory overloading, but the mechanical methods have been completely free of complications. We have encountered no problems in the application of compression leggings or calf stimulators. The time taken is no longer than that required to apply and connect the diathermy pad. The additional work is negligible, and there have been no storage problems. At other hospitals the routine application of compression leggings has been similarly problem-free. These have been used in about 4000 patients at St. Helier Hospital, Carshalton, among whom none has had signs of pulmonary embolism within three weeks of surgical operation.6 Recent reports of haemorrhage in patients receiving low-dose heparin 7,S may stimulate surgeons to look again at mechanical methods; our experience has dispelled any misgivings about difficulties or added work-load. DAVID NEGUS SYLVIA QUAILE DAVID WILMHURST Operating Theatres, VERNON ROBINSON Lewisham Hospital, London SE13 6LH RAY SMITH
TREATMENT OF EROSIVE LICHEN PLANUS OF THE ORAL MUCOSA WITH DEPOT STEROIDS
SIR,-The oral ulceration associated with erosive lichen causes considerable and sometimes protracted discomfort. The response to local applications of corticosteroids is variable probably because it is difficult to keep the drug in contact with the mucosal lesion for a sufficient time. Sometimes systemic administration of corticosteroids is resorted to. Intralesional steroid therapy does have a use in dermatology,9 and erosive lichen planus of the mouth has been treated with triamcinolone acetonide in a few patients’"’’’ Five patients with persistent ulceration of the oral mucosa were treated. Lichen planus was diagnosed clinically and confirmed histologically. The areas of ulceration varied from the tongue to the labial and buccal mucosa and the ulceration had not responded to conventional topical steroid therapy. One patient had had ulcers on the lateral margin of the tongue for about 3 months. An aqueous suspension containing methylprednisolone acetate 40 mg/ml (’Depo-Medrone’) was used and 0.5-1.0 ml was injected submucosally. The white suspension tended to leak from the injection site but this was overcome by inserting the needle at least 10 mm from the ulcerated area. The response was encouraging, improvement usually being evident by 48 h; and in four cases the lesions healed within a week. One patient required a second injection of 0-5ml after
planus
Holford, C. P. Br. J. Surg. 1976, 63, 157. Hills, N. H., Pflug, J. J., Jeyasingh, K., Boardman, L., Calnan, J. S. Br. med. J. 1972, i,131. 3. Doran, F. S. A., White, H. M., Drury, M. Br. J. Surg. 1970, 57, 20. 4. Browse, N. L., Negus, D. Br. med. J. 1970, iii, 615. 5. Kline, K., Hughes, L. E., Campbell, H., Williams, A., Zlosnick, J., Leach,
1. 2.
K. G. ibid. 1975, ii, 109.
Wells, B. W. Personal communication. Gruber, U. F., Duchert, F., Fridrich, R., Torhorst, J., Rem, J. Lancet, 1977, i, 207. 8. Britton, B. J., Finch, D. R. A., Gill, P. G., Kettlewell, M. G. W., Morris, P. J. ibid. 1977, ii, 604. 9. Verbov, J. Br. J. Derm. 1976, 94, suppl. 15, p. 51. 10. Taylor, A. Dent. Practit. 1966, 17, 56. 11. Sleeper, H. R. Yale J. Biol. Med. 1967, 40, 164. 6. 7.
772 week and the ulcer healed over the next week; this ulcer was cm in diameter and might have been subjected to trauma because it was on the lateral margin of the tongue. The frequency ot such injections must be carefully considered because they provide a significant systemic dose of corticosteroid. However, this has not been a problem in my series; minor erosions or atrophy responded to a mild astringent mouthwash (e.g., zinc sulphate). a
1
Department of Oral Medicine and Pathology, Dental Hospital and School, Glasgow G2 3JZ
M. M. FERGUSON
IMPORTED SHIGA DYSENTERY
SIR,-In the 1970s major epidemics of dysentery caused by antibiotic-resistant Shigella dysenteriae type 1 have been reported from Central Americal-s and Bangladesh.6,7 We have lately seen a case with many of the features observed in these epidemics and have isolated an organism with the same antibiotic resistances. An Asian boy, 3 years old, returned with his parents in midMay from Pakistan and became ill on May 23 with abdominal pain, fever, and diarrhoea. Stools became very frequent with passage of blood and mucopus and he was admitted to hospital on May 26. No amoeba: were seen in the stools and cultures were negative at first but 1 week after admission a strain of S. dysenteriae type 1 was identified which had failed to grow on desoxycholate-citrate medium but was present in the mixed growth on MacConkey agar. It was resistant to tetracycline, streptomycin, chloramphenicol, and sulphonamides but was sensitive to ampicillin, gentamicin, co-trimoxazole, and colistin. The white cell count, which was 11.7 x 109/1 on admission, rose to 32 x 109/1 in the following week with 91% neutrophils and shift to the left. Bacteraemia was suspected so, after a blood culture had been arranged, parenteral gentamicin was prescribed. There being no response, after three days oral colistin was added. This may have caused slight improvement, in that the stools became more formed, but general recovery did not begin until intramuscular ampicillin was started on June 11. Thereafter progress was rapid. The blood culture was
negative. The red-cell count fell from 5.43 x 10’Z/1 on June 1, to 3-79 x 10’Vl on June 13, the haematocrit from 37% to 26% and the haemoglobin from 11.9 to 9.2 g/1. We cannot say if haemolysis7 had contributed to the development of anaemia: a Coombs’ test and other investigations on June 15 were negative. Red cells were noted in the urine on June 11. Recovery has been complete and there has been no bacteriological relapse. The parents’ stools were negative. The difficulty experienced in isolating the pathogen,’,2,’,s its antibiotic resistances,2,3,6 failure to get a clinical response with antibiotics which were expected to be effective, 1.2 response to ampicillin 5,6 the high white cell countand the hmmaturia,7 all suggest that we have been dealing with a case of dysentery caused by a strain of Shiga’s bacillus like those responsible for overseas
epidemics.
Are such strains endemic in Asia now, or are there epidemics in areas of India and Pakistan which were previously untouched ? This organism could be a hazard to Asians in Britain who visit villages in their countries of origin, and even though outbreaks in Britain are not likely, individual cases may present problems to clinicians and laboratory workers.2 Laboratory workers need to bear this organism in mind in all cases where the history or the symptoms suggest shigellosis as a possibility,
and they should look for it on the usual selective media.
on
MacConkey plates,8
as
well
as
P. D. Moss W. M. DARLING
Royal Infirmary, Blackburn, Lancashire
HYPERVOLÆMIA IN PHENYLKETONURIA
SIR,-The effect of phenylketonuria (P.K.U.) on blood volume has hitherto not been described. We measured plasma volume in nine untreated infants and children with P.K.U. or hyperphenylalaninaemia using Evans blue.9 The blood volume was calculated from the plasma volume and microhaematocrit (P.c.v.). The plasma concentration of phenylalanine was measured by the method of McCamman and Robins. 10 BLOOD VOLUME AND PLASMA PHENYLALANINE CONCENTRATION
volume predicted from weight and of variation of normal blood volume is
* Percentage of normal blood
height." The coefficient approximately 10%. The blood volume
’
was
normal in four infants aged 2-4 two infants aged 5 weeks and increased in the older infants and
weeks, moderately increased in
8 weeks and considerably children (see table). The high concentrations of phenylalanine in our patients competitively inhibit the conversion of tyrosine to L-dopa by tyrosine hydroxylase 12 and so reduce formation of catecholamines.13 Thus, P.K.U. may have a similar effect to alphaadrenergic blocking agents, which also increase the blood volume. 14, 11 The more pronounced hypervolaenua in the older infants and children suggests an age-dependent effect, either of P.K.U. on the formation of catecholamines or of catecholamines on the blood volume. Department of Pædiatrics, University of Munich, D-8000 München 2, West Germany
O. LINDERKAMP
J. SCHAUB K. P. RIEGEL
PLASMA RENIN AND ANGIOTENSIN II IN ACUTE RENAL FAILURE
SiR,—We incorrectly cited some of the rèferences in our recent (Aug. 13, p. 328). Iaina et al.16 studied the hypoxic
paper
model of acute renal failure in the rat not the glycerol-induced model. Powell-Jackson et al.17 in Glasgow as well as Rauh et Rahaman, M. M., Huq, I., Dey, C. R. J. infect. Dis. 1975, 131, 700. Linderkamp, O., Mader, T., Butenandt, O., Riegel, K. P. Europ. J. Pediat. 1977, 125, 135. 10. McCamman, M., Robins, E. J. Lab. clin. Med. 1962, 59, 885. 11. Linderkamp, O., Versmold, H. T., Riegel, K. P., Betke, K. Eur. J. Pediat 1977, 125, 227. 12. Ikeda, M., Levitt, M., Udenfriend, S. Archs. Biochem. Biophys. 1967, 120, 8. 9.
420. 1. Vijil, C. Lancet, 1970, ii, 471. 2. Levine, M. M., DuPont, H. L., Formal, S. B., Gangarosa, E. J. ibid, p. 3. Reller, L. B. ibid. p. 661. 4. Mata, L. J., Cáceres, A., Torres, M. F. ibid. 1971, i, 600. 5. Vijil, C. ibid, 1971, ii, 823. 6. Rahaman, M. M. Huq, I., Dey, C. R., Kibriya, A. K. M. G., Curlin, G.
1974, i, 406. 7. Rahaman, M. M., Alam, A. K. M. J., Islam, M. R. ibid, p. 1004.
13.
A. Clin. chim. Acta.
1972, 42,
235.
607.
ibid,
Curtius, H. Ch., Baerlocher, K., Völlmin, J.
14. 15. 16. 17.
Weil, J. V., Chissey, C. A. Circulation, 1968, 37, 54. Linderkamp, O., Dehnert-Hilscher, A. Anœsthetist, 1977, 26, 349 laina, A., Solomon, S., Eliahou, H. E. Lancet, 1975, ii, 157. Powell-Jackson, J. D., Brown, J. J., Lever, A. F., MacGregor, J., Macadam, R. F., Titterington, D. M., Robertson, J. I. S., Waite, M. A. ibid. 1972, i, 774.
