1216
veloped. A perforated Meckel’s diverticulum was found at laparotomy and this was removed. She continued to be seriously ill, and on Jan. 17 she was seen by one of us (G.D.O.) Treatment with plasma and blood transfusion improved her general condition, but on Jan. 22 a faecal fistula developed and she was transferred to the General Hospital, Birmingham. On Jan. 25, Clostridium spp and Bacteroides spp were isolated fluid from an abdominal drain, and Escherichia coli and
from
Proteus spp. from her wound. She had required transfusion at the Women’s Hospital, and grouping and cross-matching for this were evidently uneventful. By Jan. 26th she had again become anaemic and blood was needed. At this time mixed-field
agglutination in blood-grouping tests was noticed. The second example was detected in a Kansas City patient who had septic complications of a caesarean section. B. melaninogenicus was grown in blood culture. Although the red cells of both patients were agglutinated by the peanut lectin, they were not agglutinated either by the soya-bean lectin, which reacts powerfully with T-transformed red cells, or by the BS II lectin which reacts powerfully with Tk erythrocytes (table). Agglutination of the red cells of both patients by the peanut lectin was greatly depressed after the cells were treated with papain. Papain has little or no effect on T erythocytes and enhances activity against Tk erythrocytes. Furthermore, the sera of both patients contained anti-T and anti-Tk, and the serum of each patient did not agglutinate the
Beta-adrenergic blocking drugs may induce cold hands and feet and the Raynaud’s phenomenon.23 Our two cases indicate that peripheral gangrene may also develop. White and Udwadia,4 have suggested that alpha-adrenoceptor agonist potentiation by beta-adrenoceptor blockade is the mechanism by which these effects are produced. Beta-adrenegic blocking drugs should be used with caution in patients with peripheral vascular disease.I We thank Dr C. L. Joiner for tient under his care.
allowing us
to
report details of a pa-
J. A. VALE D. B. JEFFERYS
Guy’s Hospital, London SE1 9RT
SERUM ALPHA1-ANTITRYPSIN IN CHILDREN WITH BRONCHIOLITIS
SIR,-A deficiency of alphaantitrypsin (o-A.T.), a major alpha-globulin which in vitro inhibits chymotrypsin, elastase, and neutral protease,5 is a congenital error of metabolism associated with chronic diseases of the respiratory tract and liver.6 Transitory low levels of o-A.T. have been found in newborns with idiopathic respiratory diseases.’ We have stuserum
died o-A.T. in The newborns
from 68 newborn and 29 older children. 15 full-term, 22 premature, and 14 small-
serum were
red cells of the other. The red cells had normal sialic-acid levels and were therefore strongly aggregated by ’polybrene’ (hexadimethrine bromide). We propose the notation Th for this new form of red cell polyagglutination. The microbial basis of exposure of the Th receptor will be the subject of further studies. G. W. G. BIRD Regional Blood Transfusion Service, Birmingham B15 2SG JUNE WINGHAM Community Blood Center of Greater Kansas City, Kansas City, Missouri, U.S.A.
M. L. BECK S. R. PIERCE
General Hospital,
G. D. OATES A. POLLOCK
Birmingham
PERIPHERAL GANGRENE COMPLICATING BETA-BLOCKADE
SIR,-In 1977
we reported a patient with peripheral ganafter she had been prescribed beta-adrenergic blocking grene drugs (propranolol and metoprolol). We have now seen a further patient with this complication. The patient was a 58-year-old woman with a history of moderately severe hypertension. Between 1963 and 1977 she had received a variety of antihypertensive agents including diuretics, methyldopa, bethanidine, and guanoxan..In April, 1977, metoprolol 100 mg twice a day was substituted for guanoxan and she continued to take methyldopa. Within 3 days the patient had intermittent claudication and cold hands and feet for the first time. She accepted these symptoms as part of her disease until October, 1977, when she noticed a purpleblack discoloration of the right 2nd-5th toes. She was seen in outpatients two days later and admitted forthwith. Early gangrene and absent peripheral pulses were confirmed. The patient was advised to stop smoking. Metoprolol was discontinued and dextran, ethanol and phenoxybenzamine were infused. On this regimen the circulation improved, and when she was discharged 2 weeks later all the gangrenous changes had resolved. Since metoprolol was discontinued the patient had not had cold hands and feet, nor has she had intermittent claudication.
1. Vale, J. A., and others Lancet, 1977, ii, 412. 2. Zacharias, F. J., and others Am. Heart J. 1972, 83, 755. 3. Marshall, A. J., Roberts, C. J. C., Barritt, D. W. Br. med.
Serum-«,-A.T. concentrations. A-E newborns: A, full term; B, premature; C, small-for-date; D, with hyaline membrane disease; E, with respiratory aspiration syndrome with or without bronchopneumonia. From F to I older children with: F, upper respiratory infection; G, bronchopneumonia; H, bronchial asthma; I, bronchiolitis. Individual values and mean ± s.D. are shown.
for-date children without acute respiratory disease, 11 with hyaline membrane disease (H.M.D.), and 6 with aspiration syndrome with or without bronchopneumonia. Of the 29 older children, 4 had upper respiratory infection, 7 had bronchopneumonia, 3 had bronchial asthma, and 15 had bronchiolitis. Serum o-A.T. was measured by radial immunodiffusion,-8 In newborn without acute respiratory disease, regardless of gestational age, birth-weight and intrauterine growth rate, the serum o-A.T. concentration was approximately 400 mg/3! (see figure). As reported by others9.10 the mean value in infants White, C. de B., Udwadia, B. P. Br. J. clin. Pharmac. 1975, 2, 99. Ohlsson, K. Scand. J. clin. lab. Invest. 1971, 28, 251. Glasgow, J. F. T., Matthew, F. L., Hercz, A., Levison, H., Sass-Kortsak, A. Am. J. Med. 1973, 54, 181. 7. Evans, H. E., Levi, M., Mandl, I. Am. Rev. resp. Dis. 1970, 101, 359. 8. Mancini, G., Carbonara, A. D., Heremans, J. F. Immunochemistry, 1965, 4. 5. 6.
2, 235. J. 1976, i, 1498.
9. Kotas, R. V., Fazen, L. E., Moore, T. E. J. Pediat. 1972, 10. El Bareesy, M. W., Johnson, A. M. ibid. 579.
81, 593.
veloped. A perforated Meckel’s diverticulum was found at laparotomy and this was removed. She continued to be seriously ill, and on Jan. 17 she was seen by one of us (G.D.O.) Treatment with plasma and blood transfusion improved her general condition, but on Jan. 22 a faecal fistula developed and she was transferred to the General Hospital, Birmingham. On Jan. 25, Clostridium spp and Bacteroides spp were isolated fluid from an abdominal drain, and Escherichia coli and
from
Proteus spp. from her wound. She had required transfusion at the Women’s Hospital, and grouping and cross-matching for this were evidently uneventful. By Jan. 26th she had again become anaemic and blood was needed. At this time mixed-field
agglutination in blood-grouping tests was noticed. The second example was detected in a Kansas City patient who had septic complications of a caesarean section. B. melaninogenicus was grown in blood culture. Although the red cells of both patients were agglutinated by the peanut lectin, they were not agglutinated either by the soya-bean lectin, which reacts powerfully with T-transformed red cells, or by the BS II lectin which reacts powerfully with Tk erythrocytes (table). Agglutination of the red cells of both patients by the peanut lectin was greatly depressed after the cells were treated with papain. Papain has little or no effect on T erythocytes and enhances activity against Tk erythrocytes. Furthermore, the sera of both patients contained anti-T and anti-Tk, and the serum of each patient did not agglutinate the
Beta-adrenergic blocking drugs may induce cold hands and feet and the Raynaud’s phenomenon.23 Our two cases indicate that peripheral gangrene may also develop. White and Udwadia,4 have suggested that alpha-adrenoceptor agonist potentiation by beta-adrenoceptor blockade is the mechanism by which these effects are produced. Beta-adrenegic blocking drugs should be used with caution in patients with peripheral vascular disease.I We thank Dr C. L. Joiner for tient under his care.
allowing us
to
report details of a pa-
J. A. VALE D. B. JEFFERYS
Guy’s Hospital, London SE1 9RT
SERUM ALPHA1-ANTITRYPSIN IN CHILDREN WITH BRONCHIOLITIS
SIR,-A deficiency of alphaantitrypsin (o-A.T.), a major alpha-globulin which in vitro inhibits chymotrypsin, elastase, and neutral protease,5 is a congenital error of metabolism associated with chronic diseases of the respiratory tract and liver.6 Transitory low levels of o-A.T. have been found in newborns with idiopathic respiratory diseases.’ We have stuserum
died o-A.T. in The newborns
from 68 newborn and 29 older children. 15 full-term, 22 premature, and 14 small-
serum were
red cells of the other. The red cells had normal sialic-acid levels and were therefore strongly aggregated by ’polybrene’ (hexadimethrine bromide). We propose the notation Th for this new form of red cell polyagglutination. The microbial basis of exposure of the Th receptor will be the subject of further studies. G. W. G. BIRD Regional Blood Transfusion Service, Birmingham B15 2SG JUNE WINGHAM Community Blood Center of Greater Kansas City, Kansas City, Missouri, U.S.A.
M. L. BECK S. R. PIERCE
General Hospital,
G. D. OATES A. POLLOCK
Birmingham
PERIPHERAL GANGRENE COMPLICATING BETA-BLOCKADE
SIR,-In 1977
we reported a patient with peripheral ganafter she had been prescribed beta-adrenergic blocking grene drugs (propranolol and metoprolol). We have now seen a further patient with this complication. The patient was a 58-year-old woman with a history of moderately severe hypertension. Between 1963 and 1977 she had received a variety of antihypertensive agents including diuretics, methyldopa, bethanidine, and guanoxan..In April, 1977, metoprolol 100 mg twice a day was substituted for guanoxan and she continued to take methyldopa. Within 3 days the patient had intermittent claudication and cold hands and feet for the first time. She accepted these symptoms as part of her disease until October, 1977, when she noticed a purpleblack discoloration of the right 2nd-5th toes. She was seen in outpatients two days later and admitted forthwith. Early gangrene and absent peripheral pulses were confirmed. The patient was advised to stop smoking. Metoprolol was discontinued and dextran, ethanol and phenoxybenzamine were infused. On this regimen the circulation improved, and when she was discharged 2 weeks later all the gangrenous changes had resolved. Since metoprolol was discontinued the patient had not had cold hands and feet, nor has she had intermittent claudication.
1. Vale, J. A., and others Lancet, 1977, ii, 412. 2. Zacharias, F. J., and others Am. Heart J. 1972, 83, 755. 3. Marshall, A. J., Roberts, C. J. C., Barritt, D. W. Br. med.
Serum-«,-A.T. concentrations. A-E newborns: A, full term; B, premature; C, small-for-date; D, with hyaline membrane disease; E, with respiratory aspiration syndrome with or without bronchopneumonia. From F to I older children with: F, upper respiratory infection; G, bronchopneumonia; H, bronchial asthma; I, bronchiolitis. Individual values and mean ± s.D. are shown.
for-date children without acute respiratory disease, 11 with hyaline membrane disease (H.M.D.), and 6 with aspiration syndrome with or without bronchopneumonia. Of the 29 older children, 4 had upper respiratory infection, 7 had bronchopneumonia, 3 had bronchial asthma, and 15 had bronchiolitis. Serum o-A.T. was measured by radial immunodiffusion,-8 In newborn without acute respiratory disease, regardless of gestational age, birth-weight and intrauterine growth rate, the serum o-A.T. concentration was approximately 400 mg/3! (see figure). As reported by others9.10 the mean value in infants White, C. de B., Udwadia, B. P. Br. J. clin. Pharmac. 1975, 2, 99. Ohlsson, K. Scand. J. clin. lab. Invest. 1971, 28, 251. Glasgow, J. F. T., Matthew, F. L., Hercz, A., Levison, H., Sass-Kortsak, A. Am. J. Med. 1973, 54, 181. 7. Evans, H. E., Levi, M., Mandl, I. Am. Rev. resp. Dis. 1970, 101, 359. 8. Mancini, G., Carbonara, A. D., Heremans, J. F. Immunochemistry, 1965, 4. 5. 6.
2, 235. J. 1976, i, 1498.
9. Kotas, R. V., Fazen, L. E., Moore, T. E. J. Pediat. 1972, 10. El Bareesy, M. W., Johnson, A. M. ibid. 579.
81, 593.
