- Email: [email protected]
HOW DOES THE KLOCKHOFF-LINDBLOM TEST WORK?
103 from the truth. The first attempts
(in the Phillipines) to develop a practical regimen rapidly followed Phillips’ balance studies, but failed because of inappropriate methods and solution concentrations. The problems to be solved included development of a formula and a simplified practical balance method avoiding too much or too little water and electrolyte absorption, and determining what to do about shocked patients, defining the role of oral rehydration v. oral maintenance, adapting the method to children as well as adults, deciding how much to give &c. For several years after the Philippine failures
no
practical regimen appeared,
and there the
matter
rested, until Dr David Sachar, Dr James Taylor, and Dr Ruth Hare and their co-workers initiated C.R.L.’s physiological studies of gut electric potentials and unidirectional intestinal sodium fluxes during cholera (using intestinal tubes and isotopes).5,6 When glucose was present in the intestinal perfusates they used, net salt and water absorption occurred, as Phillips (then director of C.R.L.) had reported earlier. This, together with an enormous cholera epidemic which strained the C.R.L.’s intravenous fluid production capacity, rekindled the issue and inspired Hirschhorn and co-workers7 to reconfirm and further develop Phillips’ work. Visits to C.R.L. by the Calcutta workers soon led to the similar confirmatory study in Calcutta’ noted by Islam et al. At Dacca, the reconfirmation of Phillips’ work led initially (1967) to another abortive attempt (50% failures) in Chittagong to develop a practical oral therapy maintenance method. Not until a redesigned study was completed (February-April, 1968) was the first effective and practical oral therapy method developed, as formally presented at the 1968 Tropical Medicine and Malariology Congress in Teheran and published that
August.4 As noted in my report to the then director, C.R.L., the late Phillips, in early May of 1968, having sent the report of C.R.L.’s practical oral therapy method to The Lancet,4 I visited Calcutta to discuss the method and results with the Calcutta investigators, and they expressed the opinion that the method involved impractical "heroic" quantities of oral fluids. Up to my visit, instead of progressing from their confirmatory study to develop a practical method using glucose, they had decided to test instead a maltose-electrolytes solution, believing that this would be practical. Like the Phillipine and Chittagong trials, the maltose trial turned out not to be useful. Between my visit and that of my colleague Dr Cash several months later, the Calcutta group shifted its efforts towards a valuable study (published in 1969)8 confirming our earlier work on the use of oral maintenance therapy, which included appropriate references to our work. Since confirmation is an essential part of scientific medical progress, their study was an important contribution. C.R.L. continued its leading role in this field,9 with the first papers on field use of oral therapy in rural areas,10 oral therapy in children," in patients with non-cholera diarrhoeas,’2 in patients treated with oral therapy alone (no intravenous fluids for rehydration),13 with glycine added, 14 and with adequate Dr
potassium. 15
The Calcutta studies, like the Dacca studies, were done with the assistance of foreign investigators, and the practical advances they generated are for many an ample benefit in return for the risks involved. It behooves us to turn our attention from the already extensive discussion of C.R.L.’s ethics to the vastly more important subject of the ethics of continued non-application of these methods in many endemic cholera and diarrhoea zones of developing countries, and to get on with the job of correcting current deficiencies in delivery of these advances to the populations at risk. Center for Vaccine Development, University of Maryland School
of Medicine, 29 South Greene Street,
Baltimore, Maryland 21201, U.S.A.
DAVID R. NALIN
HOW DOES THE KLOCKHOFF-LINDBLOM TEST WORK?
SiR,—The oral glycerol test devised by Klockhoff and Lindblom’ is often used to help in identifying patients with Meniere’s disease who might benefit from surgical decompression of the endolymphatic system. Glycerol 1.25-1.5 g/kg body-weight diluted with an equal volume of water is given by mouth. Audiograms are recorded before and 2-3 h after glycerol intake; and in patients whose hearing does improve, a temporary improvement of 15-20 dB at several frequencies occurs, often with a corresponding improvemment in speech discrimination. The mechanism is assumed to be by the osmotic action of the glycerol which causes a rise of some 18 mosmol/kg water in the plasma. We have observed this response clinically but we are not convinced that the mechanism of action is osmotic, or only osmotic. We have occasionally observed this improvement in threshold in patients with, not Meniere’s disease, but presenile deafness in whom there was no clinical indication of any hydrops of the endolymphatic space. Furthermore in patients with Meniere’s disease we have recorded a similar temporary improvement in hearing threshold in response to a fructose intake, instead of glycerol. The maximum concentration in the plasma of fructose after an oral intake of 1 g/kg body-weight seldom exceeds 1 mmol/1, and this increase is transient compared with the sustained concentration of glycerol in the
plasma. Blood-glucose in diabetes mellitus can rise above 25 mmol/1 (450 mg/dl)-i.e., an additional 15-20 mosmol/kg plasma water over
the renal-threshold value-but diabetes mellitus is said
to
predispose to fluctuant hearing loss (not to its alleviation) through its connection with hyperlipidamiia. In a non-diabetic patient who responded to glycerol and fructose with a temporarily improved hearing threshold, an equivalent dose of gluhad no effect. We concluded that this patient had a metabolic block in an actively respiring tissue in the cochlea, preventing glucose from entering the cell or due to failure of cose
hexosephosphate-isomerase activity. In searching for a metabolic explanation we have found, in agreement with previous investigators, that plasma lactate and Taylor, J. O., Saha, J. R., Phillips, R. A. Gastroenterology, 1969, 56, 512. 6. Taylor, J. O., Kinzie, J., Hare, R., Hare, K. Fed. Proc. 1968, 27, 386. 7. Hirschhorn, N., Kinzie, J., Sachar, D., Northrup, R., Taylor, J. O., Ahmad, S., Phillips, R. A. New Engl. J. Med. 1968, 279, 176. 8. Pierce, N. F., Sack, R. B., Mitra, R., Banwell, J., Brigham, K., Fedson, D., Mondal, A. Ann. intern. Med. 1969, 70, 1173. 9. Nalin, D. R , Cash, R. A. in Cholera, (edited by D. Barua and W. Burrows); p. 253. Philadelphia 1974. 10 Cash, R. A., Nalin, D. R., Rochat, R., Reller, B., Haque, Z., Rahman, M. Am J. trop Med. 1970, 19, 653. 11. Nalin, D. R., Cash, R. A. J. Pediat. 1971, 78, 355. 12. Nalin, D R., Cash, R. A., Trans. R. Soc. trop. Med. Hyg. 1970, 64, 769. 13 Cash, R.A , Nalin, D. R., Forrest, J., Abrutyn, E. Lancet, 1970, ii, 549. 14. Nalin, D R , Cash, R. A., Rahman, M., Yunus, M. Gut, 1970, 11, 768. 15. Nalin, D. R., Cash, R. A. Bull. Wld. Hlth Org. 1970, 43, 361. 5. Sachar, D. B.,
pyruvate rise sharply fructose ingestion. However, we observed no such rise in the plasma concentrations of these 3-carbon compounds after the administration of glycerol, despite, or because of, the considerable overloading of the hepatic machinery with this 3-carbon compound. In so far as glycerol is being metabolised, since it is a fully hydrogenated compound we considered that the N.A.D.N.A.D.P. system would be kept in the fully reduced state in the liver and that this might lead to fat synthesis. We have some evidence that the concentrations of plasma-triglycerides do rise after oral glycerol. 1. Klockhoff, I.,
Lindblom, U. Acta otolar. 1967, suppl. 224, p. 449.
-
104 A further consideration in the interpretation of the glycerol is the fact that the osmoreceptors respond to an increase of 6 mosmol/kg plasma water by initiating increased secretion of antidiuretic hormone.2 If the osmoreceptors respond to glycerol as an osmotic agent in the same way as they react to sodium chloride and sucrose, the effect of the glycerol intake may be through antidiuretic hormone acting on a water reabsorbing surface (e.g., the stria vascularis3). An added complication is the finding by Buckman and Peakethat plasma hyperosmosis leads to an increased prolactin secretion in the same time-span as the effect of glycerol intake. Prolactin has been shown to be a liporegulatory hormone.5 The glycerol test is of immediate clinical usefulness in otology, but the usual explanation of how it works-namely, by the osmotic action of glycerol-may be too simple. test
Department of Biochemistry, St George’s Hospital, Lincoln LN1 1EF
L. NAFTALIN
E.N.T.
Department, County Hospital, Lincoln
K. J. H. MALLETT
able 3 cm below the left costal margin, and a warm, swollen, tender left knee. His packed cell volume was 0-33, and a platelet-count was 23-Ox109/1. The leucocyte-count was 61 5109A with 90% myeloblasts, 1% neutrophils, and 9% lymphocytes. The blood smear revealed abnormal erythrocyte morphology morphology with anisocytosis, poikilocytosis, target cells, and many teardrop cells. An iliac-crest bone-marrow biopsy revealed a markedly fibrotic marrow infiltrated with leukaemic cells. The patient was treated with several regimens of combination chemotherapy with no improvement in his hxmatological indices. The patient died after a prolonged hospital course. Necropsy confirmed myelofibrosis. Our patient’s initial presentation did not fit into the group of patients described with the accelerated variant of myelofibrosis.8 He had an initial cellular marrow without increased fibrosis. He had had no prior chemotherapy, and no exposure to toxic chemicals. We believe that his prolonged pancytopenia and his bone-marrow fibrosis was most probably secondary to therapy with rubidazone. Rubidazone should probably be added to the list of chemical agents causing fibrosis of the bone-marrow. Department of Medicine, University of Utah Medical Center, Salt Lake City, Utah 84132, U. S.A.
DAVID S. CHENG HARMON J. EYRE
MYELOFIBROSIS ASSOCIATED WITH RUBIDAZONE an anthracycline antibiotic, is being in the treatment of haematological and solid extensively wish to report an unusual complication of We malignancies.6.7 this drug. A 57-year-old male was admitted to the University of Utah Medical Center in May, 1977, because of easy bruising. There was no history of exposure to irradiation or toxic chemicals. Physical examination revealed multiple ecchymoses and sternal tenderness, but no adenopathy or hepatosplenomegaly. The leucocyte-count was ll-2x010’’/l, with a differential of 83% myeloblasts, 1% neutrophils, and 16% lymphocytes. Auer rods were not seen. A bone-marrow aspirate and biopsy were diagnostic for acute myeloblastic leukaemia. On June 1 he was treated with a combination of rubidazone, cytarabine, vincristine, and prednisone on the South Western Oncology Group protocol 7626. Subsequently, prolonged pancytopenia developed. No consolidation chemotherapy was given. Repeated bone-marrow biopsies showed a hypoplastic marrow with no evidence of leukxmia. On Aug. 29, early fibrosis was noted for the first time in the bone-marrow. Repeated bloodcounts revealed persistent pancytopenia (table). The patient was readmitted on Feb. 13, 1978, because of fever and pain in the left knee. Physical examination revealed leukaemic cutaneous nodules, sternal tenderness, a spleen palp-
SIR,-Rubidazone,
used
Verney, E. B., Proc. R. Soc. B. 1947, 135, 25. 3. Naftalin, L. Otolar. Clin. N. Am. 1975, 8, 475. 4. Buckman, M. T., Peake, G. T. Science, 1973, 181, 755. 5. Meier, A. H. in Comparative Endocrinology of Prolactin (edited by H.-D. Dellman, J. A. Johnson, and D. M. Klachko); p. 153. New York, 1977. 6. Benjamin, R. S., Keating, M. J., McCredie, K. B., Luna, M A., Loo, T. L., Freireich, E. J. Proc. Am. Ass. Cancer Res. 1976, 72 7. Jacquillat, C., Weil, M., Gemon-Auclerc, M. F., Izrael, V., Bussel, A., Boiron, M., Jean Bernard. Cancer, 1976, 37, 653. 2.
CRYPTOCOCCUS IN BAGPIPES
SIR,-Dr Cobcroft and others9 may be overdogmatic in
warning of the dangers of playing the bagpipe. That fungal spores in the bag reach the player’s mouth by back-flow through the mouthpiece valve is a supposition for which they offer no evidence. In any case, valves vary greatly in efficiency. Some pipers use the tip of their tongue instead of a valve, which may virtually eliminate back-flow. Pipers may be classified into "wet" and "dry" blowers. The wet blower may require to replace his pipe-bag, because of rotting, more frequently than the dry blower. But a large proportion of saliva may be caught before it reaches the bag by putting a watertrap into the mouthpiece stock: such a trap can be improvised from a cork, the barrel of a 5 ml disposable plastic syringe, and some waterproof glue. Whether or not a patient is immunosuppressed, a prohibition on playing a favourite musical instrument may suppress morale-which can also be dangerous. Patients should be considered individually. An efficient valve, a water trap, perhaps a fungicide in the bag, are possible precautions. Undoubtedly some patients, because of reduced respiratory capacity or for other reasons, may become unable to play the Highland bagpipe. In such a case a patient might be advised to consider seeking a Lowland bagpipe as an alternative. This is similar to the Highland, but rather smaller and is blown by a bellows operated by the right elbow while the bag is under their
the left. These
can
be difficult
to
obtain, but
a
manufacturer
8. Douglas, R., Rasch, P. C. Am. J. clin. Path. 1977, 67, 334. 9. Cobcroft, R., Kronenberg, H., Wilkinson, T. Lancet, 1978,
HAMATOLOGICAL AND MARROW FINDINGS
i, 1309.
(in the Phillipines) to develop a practical regimen rapidly followed Phillips’ balance studies, but failed because of inappropriate methods and solution concentrations. The problems to be solved included development of a formula and a simplified practical balance method avoiding too much or too little water and electrolyte absorption, and determining what to do about shocked patients, defining the role of oral rehydration v. oral maintenance, adapting the method to children as well as adults, deciding how much to give &c. For several years after the Philippine failures
no
practical regimen appeared,
and there the
matter
rested, until Dr David Sachar, Dr James Taylor, and Dr Ruth Hare and their co-workers initiated C.R.L.’s physiological studies of gut electric potentials and unidirectional intestinal sodium fluxes during cholera (using intestinal tubes and isotopes).5,6 When glucose was present in the intestinal perfusates they used, net salt and water absorption occurred, as Phillips (then director of C.R.L.) had reported earlier. This, together with an enormous cholera epidemic which strained the C.R.L.’s intravenous fluid production capacity, rekindled the issue and inspired Hirschhorn and co-workers7 to reconfirm and further develop Phillips’ work. Visits to C.R.L. by the Calcutta workers soon led to the similar confirmatory study in Calcutta’ noted by Islam et al. At Dacca, the reconfirmation of Phillips’ work led initially (1967) to another abortive attempt (50% failures) in Chittagong to develop a practical oral therapy maintenance method. Not until a redesigned study was completed (February-April, 1968) was the first effective and practical oral therapy method developed, as formally presented at the 1968 Tropical Medicine and Malariology Congress in Teheran and published that
August.4 As noted in my report to the then director, C.R.L., the late Phillips, in early May of 1968, having sent the report of C.R.L.’s practical oral therapy method to The Lancet,4 I visited Calcutta to discuss the method and results with the Calcutta investigators, and they expressed the opinion that the method involved impractical "heroic" quantities of oral fluids. Up to my visit, instead of progressing from their confirmatory study to develop a practical method using glucose, they had decided to test instead a maltose-electrolytes solution, believing that this would be practical. Like the Phillipine and Chittagong trials, the maltose trial turned out not to be useful. Between my visit and that of my colleague Dr Cash several months later, the Calcutta group shifted its efforts towards a valuable study (published in 1969)8 confirming our earlier work on the use of oral maintenance therapy, which included appropriate references to our work. Since confirmation is an essential part of scientific medical progress, their study was an important contribution. C.R.L. continued its leading role in this field,9 with the first papers on field use of oral therapy in rural areas,10 oral therapy in children," in patients with non-cholera diarrhoeas,’2 in patients treated with oral therapy alone (no intravenous fluids for rehydration),13 with glycine added, 14 and with adequate Dr
potassium. 15
The Calcutta studies, like the Dacca studies, were done with the assistance of foreign investigators, and the practical advances they generated are for many an ample benefit in return for the risks involved. It behooves us to turn our attention from the already extensive discussion of C.R.L.’s ethics to the vastly more important subject of the ethics of continued non-application of these methods in many endemic cholera and diarrhoea zones of developing countries, and to get on with the job of correcting current deficiencies in delivery of these advances to the populations at risk. Center for Vaccine Development, University of Maryland School
of Medicine, 29 South Greene Street,
Baltimore, Maryland 21201, U.S.A.
DAVID R. NALIN
HOW DOES THE KLOCKHOFF-LINDBLOM TEST WORK?
SiR,—The oral glycerol test devised by Klockhoff and Lindblom’ is often used to help in identifying patients with Meniere’s disease who might benefit from surgical decompression of the endolymphatic system. Glycerol 1.25-1.5 g/kg body-weight diluted with an equal volume of water is given by mouth. Audiograms are recorded before and 2-3 h after glycerol intake; and in patients whose hearing does improve, a temporary improvement of 15-20 dB at several frequencies occurs, often with a corresponding improvemment in speech discrimination. The mechanism is assumed to be by the osmotic action of the glycerol which causes a rise of some 18 mosmol/kg water in the plasma. We have observed this response clinically but we are not convinced that the mechanism of action is osmotic, or only osmotic. We have occasionally observed this improvement in threshold in patients with, not Meniere’s disease, but presenile deafness in whom there was no clinical indication of any hydrops of the endolymphatic space. Furthermore in patients with Meniere’s disease we have recorded a similar temporary improvement in hearing threshold in response to a fructose intake, instead of glycerol. The maximum concentration in the plasma of fructose after an oral intake of 1 g/kg body-weight seldom exceeds 1 mmol/1, and this increase is transient compared with the sustained concentration of glycerol in the
plasma. Blood-glucose in diabetes mellitus can rise above 25 mmol/1 (450 mg/dl)-i.e., an additional 15-20 mosmol/kg plasma water over
the renal-threshold value-but diabetes mellitus is said
to
predispose to fluctuant hearing loss (not to its alleviation) through its connection with hyperlipidamiia. In a non-diabetic patient who responded to glycerol and fructose with a temporarily improved hearing threshold, an equivalent dose of gluhad no effect. We concluded that this patient had a metabolic block in an actively respiring tissue in the cochlea, preventing glucose from entering the cell or due to failure of cose
hexosephosphate-isomerase activity. In searching for a metabolic explanation we have found, in agreement with previous investigators, that plasma lactate and Taylor, J. O., Saha, J. R., Phillips, R. A. Gastroenterology, 1969, 56, 512. 6. Taylor, J. O., Kinzie, J., Hare, R., Hare, K. Fed. Proc. 1968, 27, 386. 7. Hirschhorn, N., Kinzie, J., Sachar, D., Northrup, R., Taylor, J. O., Ahmad, S., Phillips, R. A. New Engl. J. Med. 1968, 279, 176. 8. Pierce, N. F., Sack, R. B., Mitra, R., Banwell, J., Brigham, K., Fedson, D., Mondal, A. Ann. intern. Med. 1969, 70, 1173. 9. Nalin, D. R , Cash, R. A. in Cholera, (edited by D. Barua and W. Burrows); p. 253. Philadelphia 1974. 10 Cash, R. A., Nalin, D. R., Rochat, R., Reller, B., Haque, Z., Rahman, M. Am J. trop Med. 1970, 19, 653. 11. Nalin, D. R., Cash, R. A. J. Pediat. 1971, 78, 355. 12. Nalin, D R., Cash, R. A., Trans. R. Soc. trop. Med. Hyg. 1970, 64, 769. 13 Cash, R.A , Nalin, D. R., Forrest, J., Abrutyn, E. Lancet, 1970, ii, 549. 14. Nalin, D R , Cash, R. A., Rahman, M., Yunus, M. Gut, 1970, 11, 768. 15. Nalin, D. R., Cash, R. A. Bull. Wld. Hlth Org. 1970, 43, 361. 5. Sachar, D. B.,
pyruvate rise sharply fructose ingestion. However, we observed no such rise in the plasma concentrations of these 3-carbon compounds after the administration of glycerol, despite, or because of, the considerable overloading of the hepatic machinery with this 3-carbon compound. In so far as glycerol is being metabolised, since it is a fully hydrogenated compound we considered that the N.A.D.N.A.D.P. system would be kept in the fully reduced state in the liver and that this might lead to fat synthesis. We have some evidence that the concentrations of plasma-triglycerides do rise after oral glycerol. 1. Klockhoff, I.,
Lindblom, U. Acta otolar. 1967, suppl. 224, p. 449.
-
104 A further consideration in the interpretation of the glycerol is the fact that the osmoreceptors respond to an increase of 6 mosmol/kg plasma water by initiating increased secretion of antidiuretic hormone.2 If the osmoreceptors respond to glycerol as an osmotic agent in the same way as they react to sodium chloride and sucrose, the effect of the glycerol intake may be through antidiuretic hormone acting on a water reabsorbing surface (e.g., the stria vascularis3). An added complication is the finding by Buckman and Peakethat plasma hyperosmosis leads to an increased prolactin secretion in the same time-span as the effect of glycerol intake. Prolactin has been shown to be a liporegulatory hormone.5 The glycerol test is of immediate clinical usefulness in otology, but the usual explanation of how it works-namely, by the osmotic action of glycerol-may be too simple. test
Department of Biochemistry, St George’s Hospital, Lincoln LN1 1EF
L. NAFTALIN
E.N.T.
Department, County Hospital, Lincoln
K. J. H. MALLETT
able 3 cm below the left costal margin, and a warm, swollen, tender left knee. His packed cell volume was 0-33, and a platelet-count was 23-Ox109/1. The leucocyte-count was 61 5109A with 90% myeloblasts, 1% neutrophils, and 9% lymphocytes. The blood smear revealed abnormal erythrocyte morphology morphology with anisocytosis, poikilocytosis, target cells, and many teardrop cells. An iliac-crest bone-marrow biopsy revealed a markedly fibrotic marrow infiltrated with leukaemic cells. The patient was treated with several regimens of combination chemotherapy with no improvement in his hxmatological indices. The patient died after a prolonged hospital course. Necropsy confirmed myelofibrosis. Our patient’s initial presentation did not fit into the group of patients described with the accelerated variant of myelofibrosis.8 He had an initial cellular marrow without increased fibrosis. He had had no prior chemotherapy, and no exposure to toxic chemicals. We believe that his prolonged pancytopenia and his bone-marrow fibrosis was most probably secondary to therapy with rubidazone. Rubidazone should probably be added to the list of chemical agents causing fibrosis of the bone-marrow. Department of Medicine, University of Utah Medical Center, Salt Lake City, Utah 84132, U. S.A.
DAVID S. CHENG HARMON J. EYRE
MYELOFIBROSIS ASSOCIATED WITH RUBIDAZONE an anthracycline antibiotic, is being in the treatment of haematological and solid extensively wish to report an unusual complication of We malignancies.6.7 this drug. A 57-year-old male was admitted to the University of Utah Medical Center in May, 1977, because of easy bruising. There was no history of exposure to irradiation or toxic chemicals. Physical examination revealed multiple ecchymoses and sternal tenderness, but no adenopathy or hepatosplenomegaly. The leucocyte-count was ll-2x010’’/l, with a differential of 83% myeloblasts, 1% neutrophils, and 16% lymphocytes. Auer rods were not seen. A bone-marrow aspirate and biopsy were diagnostic for acute myeloblastic leukaemia. On June 1 he was treated with a combination of rubidazone, cytarabine, vincristine, and prednisone on the South Western Oncology Group protocol 7626. Subsequently, prolonged pancytopenia developed. No consolidation chemotherapy was given. Repeated bone-marrow biopsies showed a hypoplastic marrow with no evidence of leukxmia. On Aug. 29, early fibrosis was noted for the first time in the bone-marrow. Repeated bloodcounts revealed persistent pancytopenia (table). The patient was readmitted on Feb. 13, 1978, because of fever and pain in the left knee. Physical examination revealed leukaemic cutaneous nodules, sternal tenderness, a spleen palp-
SIR,-Rubidazone,
used
Verney, E. B., Proc. R. Soc. B. 1947, 135, 25. 3. Naftalin, L. Otolar. Clin. N. Am. 1975, 8, 475. 4. Buckman, M. T., Peake, G. T. Science, 1973, 181, 755. 5. Meier, A. H. in Comparative Endocrinology of Prolactin (edited by H.-D. Dellman, J. A. Johnson, and D. M. Klachko); p. 153. New York, 1977. 6. Benjamin, R. S., Keating, M. J., McCredie, K. B., Luna, M A., Loo, T. L., Freireich, E. J. Proc. Am. Ass. Cancer Res. 1976, 72 7. Jacquillat, C., Weil, M., Gemon-Auclerc, M. F., Izrael, V., Bussel, A., Boiron, M., Jean Bernard. Cancer, 1976, 37, 653. 2.
CRYPTOCOCCUS IN BAGPIPES
SIR,-Dr Cobcroft and others9 may be overdogmatic in
warning of the dangers of playing the bagpipe. That fungal spores in the bag reach the player’s mouth by back-flow through the mouthpiece valve is a supposition for which they offer no evidence. In any case, valves vary greatly in efficiency. Some pipers use the tip of their tongue instead of a valve, which may virtually eliminate back-flow. Pipers may be classified into "wet" and "dry" blowers. The wet blower may require to replace his pipe-bag, because of rotting, more frequently than the dry blower. But a large proportion of saliva may be caught before it reaches the bag by putting a watertrap into the mouthpiece stock: such a trap can be improvised from a cork, the barrel of a 5 ml disposable plastic syringe, and some waterproof glue. Whether or not a patient is immunosuppressed, a prohibition on playing a favourite musical instrument may suppress morale-which can also be dangerous. Patients should be considered individually. An efficient valve, a water trap, perhaps a fungicide in the bag, are possible precautions. Undoubtedly some patients, because of reduced respiratory capacity or for other reasons, may become unable to play the Highland bagpipe. In such a case a patient might be advised to consider seeking a Lowland bagpipe as an alternative. This is similar to the Highland, but rather smaller and is blown by a bellows operated by the right elbow while the bag is under their
the left. These
can
be difficult
to
obtain, but
a
manufacturer
8. Douglas, R., Rasch, P. C. Am. J. clin. Path. 1977, 67, 334. 9. Cobcroft, R., Kronenberg, H., Wilkinson, T. Lancet, 1978,
HAMATOLOGICAL AND MARROW FINDINGS
i, 1309.