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PRECORDIAL THUMPING
569 not antibiotic-resistant, unless they were crossinfected by contaminated meat or, as your editorial suggests, from the shoes of the Smithfield porters. One means of eliminating these sources of resistant bacteria would be by providing meat analogues instead of or supplements to the meat in patients’ diets. These, when made from textured vegetable protein plus vitamin Bis, will have all the nutritive value of meat at less cost. They also have the great advantage of being free from cholesterol, bacterial contamination, antibiotics, and pesticides. Vegetarian Nutritional
probably
Research Unit, Watford, Herts.
FRANK WOKES.
loss of delayed hypersensitivity, presumably because the effect of the transfused cells was lost. While this experience indicates the potential value of immunological reconstitution in treatment of chronic moniliasis, it must be recognised that not all patients with the disorder have defects in delayed hypersensitivity. Each patient must be evaluated thoroughly in order to define clearly the impairment in host-resistance before proceeding with therapy. Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases. Human Tumor Cell Biology Branch, National Cancer Institute.
Immunology
TREATMENT OF CHRONIC MONILIASIS WITH LYMPHOCYTE TRANSFUSIONS SIR,-Dr. Valdimarsson and his associates1 described a young woman with chronic mucocutaneous moniliasis in whom there was an apparent defect in the production of macrophage-migration inhibition factor (M.l.F.). We wish to report briefly our findings in a similar patient, and to present the results of the therapeutic approach they
proposed. Our
patient was a 17-year-old man who developed muco-
moniliasis at age 9 months. At age 12 years he to have hypoparathyroidism; there was no other endocrinopathy. Investigation revealed no abnormalities of humoral immunity. Phagocytic, metabolic, and candidacidal functions of the patient’s polymorphonuclear leucocytes were normal. Impairment of cellular immune responses was demonstrated by negative skin-tests to Candida albicans, purified protein derivative (P.P.D.) streptokinase-streptodornase (S.K.-S.D.), and histoplasmin, and only 0-6 cm. of soft induration to mumps antigen. The patient could not be actively sensitised with dinitrochlorbenzene. However, his lymphocytes responded in vitro to phytohasmagglutinin and C. albicans with an increase in thymidine incorporation which was comparable to that in skin-testpositive controls. Concentrated supernatant fluids from C. albicans-stimulated lymphocyte cultures were assayed for M.l.F. using the guineapig-macrophage system of. Thor et al.,2and no activity was detectable. Control supernatants prepared from skin-test-positive subjects under identical conditions inhibited migration by 25-30%. In August, 1969, the patient was given 63 x 109 lymphocytes from a related donor with positive delayed skintests to C. albicans and S.K.-S.D. The donor possessed leucocyte antigens LC-17 and Fiske (Te60), which the recipient lacked. The recipient’s cutaneous responses to S.K.-S.D. and C. albicans promptly became positive and remained so at 220 days. At this time, concentrated supernatants from C.albicans stimulated lymphocytes inhibited macrophage migration by 22%. This period was associated with considerable clearing of the cutaneous lesions. In April, 1970, he noted the appearance of new lesions and relapse in areas that had regressed. When restudied in June, 1970, both the S.K.-S.D. and C. albicans skin-tests were negative, and M.I.F. activity was not found in the supernatants. It is concluded that the patient’s lymphocytes were able to respond to an antigenic stimulus by replication, but were incapable of expressing differentiative functions such as M.I.F. production. Following transfusion of lymphocytes from an immunocompetent donor, the recipient’s skintests became reactive, M.l.F. was produced, and the moniliasis cleared considerably. The remission was temporary, and exacerbation of the moniliasis was accompanied by cutaneous
was
1.
2.
found
Valdimarsson, H., Holt, L., Riches, H. R. C., Hobbs, J. R. Lancet, 1970, i, 1259. Thor, D. E., Jureziz, R. E., Veach, S. R., Miller, E., Dray, S. Nature, 1968, 219, 755.
CHARLES H. KIRKPATRICK ROBERT R. RICH. ROBERT G. GRAW, JR.
Branch.
National Cancer Institute.
G. NICHOLAS ROGENTINE.
National Institutes of Health, Bethesda, Maryland 20014.
KETAMINE AND POLYNEUROPATHY SIR,-Ketamine has been the subject of several communications in The Lancet. Recently, I saw a patient in whom a progressive polyneuropathy developed shortly after she received ketamine. The patient, a 33-year-old woman, was given 150 mg. of ketamine in May, 1970, when a benign breast cyst was removed. A few days later she began to have tingling of her legs and later her arms. Weakness in her feet followed. She was admitted to hospital in July, at which time she had severe distal weakness in the lower limbs and absent deep tendon reflexes. Median-nerve conduction velocities were 20 m. per second in July and August. Spinal-fluid examination revealed a protein of 228 mg. per 100 ml. and no cells. She is now showing slow improvement in her strength. This association may simply be fortuitous but further experiences with ketamine may show that the Guillain-Barre syndrome can be a complication of this
drug. Division of Neurology, University of Colorado Medical Center, Denver, Colorado.
MICHAEL CHERINGTON.
PRECORDIAL THUMPING SIR,-Having been interested in cardiac resuscitation for some years I enjoyed the paper by Dr: Wild and Dr. Grover (Aug. 29, p. 436). Several short publications have previously discussed and illustrated the technique of precordial thumping as an emergency method of stimulating arrested ventricles into activity.1-3 In some units it has become standard practice. I have frequently found that half-a-dozen closely spaced moderately vigorous thumps over the sternum have been more effective in restarting cardiac contraction than spaced single stimuli as commonly employed in external massage. Doubt has been placed on the efficacy of external massage in maintaining an effective circulation,4 and it has been suggested2 that success with precordial thumping could be attributable to induced cardiac contraction rather than to mechanical effects of changes in intrathoracic pressure which are more a feature of external massage. Dr. Wild and Dr. Grover have done a valuable service in again bringing this simple manoeuvre to the attention of doctors and others involved with resuscitation. Department of Medicine, Charing Cross Hospital Medical School, Ross R. BAILEY. Fulham Hospital, London W.6. 1. Scherf, D., Bornemann, C. Am. J. Cardiol. 1960, 5, 30. 2. Palmer, D. G. N.Z. med. J. 1965, 64, 710. 3. 4.
Bailey, R. R. ibid. 1966, 65, 53. MacKenzie, G. J., Taylor, S. H., McDonald, A. H., Donald, K. W. Lancet, 1964, i, 1342.
probably
Research Unit, Watford, Herts.
FRANK WOKES.
loss of delayed hypersensitivity, presumably because the effect of the transfused cells was lost. While this experience indicates the potential value of immunological reconstitution in treatment of chronic moniliasis, it must be recognised that not all patients with the disorder have defects in delayed hypersensitivity. Each patient must be evaluated thoroughly in order to define clearly the impairment in host-resistance before proceeding with therapy. Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases. Human Tumor Cell Biology Branch, National Cancer Institute.
Immunology
TREATMENT OF CHRONIC MONILIASIS WITH LYMPHOCYTE TRANSFUSIONS SIR,-Dr. Valdimarsson and his associates1 described a young woman with chronic mucocutaneous moniliasis in whom there was an apparent defect in the production of macrophage-migration inhibition factor (M.l.F.). We wish to report briefly our findings in a similar patient, and to present the results of the therapeutic approach they
proposed. Our
patient was a 17-year-old man who developed muco-
moniliasis at age 9 months. At age 12 years he to have hypoparathyroidism; there was no other endocrinopathy. Investigation revealed no abnormalities of humoral immunity. Phagocytic, metabolic, and candidacidal functions of the patient’s polymorphonuclear leucocytes were normal. Impairment of cellular immune responses was demonstrated by negative skin-tests to Candida albicans, purified protein derivative (P.P.D.) streptokinase-streptodornase (S.K.-S.D.), and histoplasmin, and only 0-6 cm. of soft induration to mumps antigen. The patient could not be actively sensitised with dinitrochlorbenzene. However, his lymphocytes responded in vitro to phytohasmagglutinin and C. albicans with an increase in thymidine incorporation which was comparable to that in skin-testpositive controls. Concentrated supernatant fluids from C. albicans-stimulated lymphocyte cultures were assayed for M.l.F. using the guineapig-macrophage system of. Thor et al.,2and no activity was detectable. Control supernatants prepared from skin-test-positive subjects under identical conditions inhibited migration by 25-30%. In August, 1969, the patient was given 63 x 109 lymphocytes from a related donor with positive delayed skintests to C. albicans and S.K.-S.D. The donor possessed leucocyte antigens LC-17 and Fiske (Te60), which the recipient lacked. The recipient’s cutaneous responses to S.K.-S.D. and C. albicans promptly became positive and remained so at 220 days. At this time, concentrated supernatants from C.albicans stimulated lymphocytes inhibited macrophage migration by 22%. This period was associated with considerable clearing of the cutaneous lesions. In April, 1970, he noted the appearance of new lesions and relapse in areas that had regressed. When restudied in June, 1970, both the S.K.-S.D. and C. albicans skin-tests were negative, and M.I.F. activity was not found in the supernatants. It is concluded that the patient’s lymphocytes were able to respond to an antigenic stimulus by replication, but were incapable of expressing differentiative functions such as M.I.F. production. Following transfusion of lymphocytes from an immunocompetent donor, the recipient’s skintests became reactive, M.l.F. was produced, and the moniliasis cleared considerably. The remission was temporary, and exacerbation of the moniliasis was accompanied by cutaneous
was
1.
2.
found
Valdimarsson, H., Holt, L., Riches, H. R. C., Hobbs, J. R. Lancet, 1970, i, 1259. Thor, D. E., Jureziz, R. E., Veach, S. R., Miller, E., Dray, S. Nature, 1968, 219, 755.
CHARLES H. KIRKPATRICK ROBERT R. RICH. ROBERT G. GRAW, JR.
Branch.
National Cancer Institute.
G. NICHOLAS ROGENTINE.
National Institutes of Health, Bethesda, Maryland 20014.
KETAMINE AND POLYNEUROPATHY SIR,-Ketamine has been the subject of several communications in The Lancet. Recently, I saw a patient in whom a progressive polyneuropathy developed shortly after she received ketamine. The patient, a 33-year-old woman, was given 150 mg. of ketamine in May, 1970, when a benign breast cyst was removed. A few days later she began to have tingling of her legs and later her arms. Weakness in her feet followed. She was admitted to hospital in July, at which time she had severe distal weakness in the lower limbs and absent deep tendon reflexes. Median-nerve conduction velocities were 20 m. per second in July and August. Spinal-fluid examination revealed a protein of 228 mg. per 100 ml. and no cells. She is now showing slow improvement in her strength. This association may simply be fortuitous but further experiences with ketamine may show that the Guillain-Barre syndrome can be a complication of this
drug. Division of Neurology, University of Colorado Medical Center, Denver, Colorado.
MICHAEL CHERINGTON.
PRECORDIAL THUMPING SIR,-Having been interested in cardiac resuscitation for some years I enjoyed the paper by Dr: Wild and Dr. Grover (Aug. 29, p. 436). Several short publications have previously discussed and illustrated the technique of precordial thumping as an emergency method of stimulating arrested ventricles into activity.1-3 In some units it has become standard practice. I have frequently found that half-a-dozen closely spaced moderately vigorous thumps over the sternum have been more effective in restarting cardiac contraction than spaced single stimuli as commonly employed in external massage. Doubt has been placed on the efficacy of external massage in maintaining an effective circulation,4 and it has been suggested2 that success with precordial thumping could be attributable to induced cardiac contraction rather than to mechanical effects of changes in intrathoracic pressure which are more a feature of external massage. Dr. Wild and Dr. Grover have done a valuable service in again bringing this simple manoeuvre to the attention of doctors and others involved with resuscitation. Department of Medicine, Charing Cross Hospital Medical School, Ross R. BAILEY. Fulham Hospital, London W.6. 1. Scherf, D., Bornemann, C. Am. J. Cardiol. 1960, 5, 30. 2. Palmer, D. G. N.Z. med. J. 1965, 64, 710. 3. 4.
Bailey, R. R. ibid. 1966, 65, 53. MacKenzie, G. J., Taylor, S. H., McDonald, A. H., Donald, K. W. Lancet, 1964, i, 1342.