- Email: [email protected]
TREATMENT OF HEPATIC COMA
1092 raised plasma ultrafiltrable calcium, while reabsorption of calcium is not directly influenced; (c) the effects of castration on bone-mineral metabolism are apparently extrarenal and occur shortly after castration. Studies are now in progress influences calcium metabolism hormones. Department of Isotopes, Institute of Oncology, Warsaw 22, Poland.
to
determine whether castration of other
through intervention
JANUSZ SZYMENDERA STEFAN
MADAJEWICZ.
kg. per hour, and the output after 6 (1.g. per kg. per hour higher than after 12 (1.g. per kg. per hour.e In your leading article,12 commenting on the first reports on pentagastrin to appear in The Lancet,2—4 you concluded: "Its use in the testing of gastric function is, however, complicated by the side-effects, and it clearly does not fulfil the ideal of a secretory stimulant without undesirable activity". Pure gastrin has no side-effects on subcutaneous administration," and it is possible that the smallest molecule displaying the entire range of physiological properties of natural gastrin in animal experiments 14-the C terminal tetrapeptide, or tetragastrin "-may get closer to the ideal stimulant for clinical use than does pentagastrin. We have by now compared the effect of tetragastrin on gastric secretion with that of histamine diphosphate (40 (Jtg. per kg. subcutaneously) in 52 subjects.15 The effects of 2-5, 5, 10, and 20 (1.g. per kg. of subcutaneously injected tetragastrin have been studied in 6, 6, 19, and 21 subjects, respectively. With the 2-5 (1.g. per kg. dose the acid response was significantly lower than after histamine, while the mean acid output after 5 µg. per kg. (29-3 mEq. per hour) was similar to that after histamine (32-3 mEq. per hour). With the higher doses of tetragastrin the acid response corresponded closely to that after histamine. No side-effects were encountered in any of the 52 subjects studied. In this respect tetragastrin so far seems similar to pure gastrin; the effect of tetragastrin upon intrinsic factor and pepsin secretion 15 is also very similar to the effect of gastrin.16 per
"
GASTRIN ANALOGUES AND GASTRIC-SECRETION TESTS SIR,-The steadily increasing number of publications on the effect of the synthetic gastrin analogue I.C.I. 50,123 (N-t-
.
butyloxycarbonyl - p - alanyl - L - tryptophyl - L - methionyl - L amide, pentagastrin) on gastric secreaspartyl-L-phenylalanine tion 1-10 have apparently not provided the final answers to two fundamental questions: the frequency of side-effects, and the maximal " acid dose of pentagastrin which will elicit a "
response.
The side-effects of
abdominal
pentagastrin-sinking
sen-
sations, abdominal cramps, nausea, hypotension, faintness, headache, and general malaise-are reported to occur with widely differing frequencies.1-3 5 7-9 They seem to be more after intravenous than after subcutaneous administration.511 Although one group of investigators 10 found no side-effects after 1-5 and 7-5 g. per kg. per hour, side-effects were fairly common in other studies using 6 and 12 g. per kg. a However, the side-effects are by no means per hour.2 s restricted to intravenous administration, but have been reported after subcutaneous injections of 4-13 fLg. per kg. I-a5 7— apparently most often with doses above 6 µg. per kg., although one group of workers stated that " there was no apparent relationship between the dose and the severity of the symptoms ".5 maximal " acid The dose of pentagastrin needed for a 5 8-11 Most response has been discussed by several workers. 1 2 workers using subcutaneous or intramuscular injections found that 6 fLg. per kg. of pentagastrin elicited an acid response similar to that after augmented histamine stimulation, and that the acid output did not rise further after 8, 9, or 10 fLg. per kg.15 9 The doses of intravenously administered pentagastrin required for a maximal " acid response vary in the reports cited above. Wormsley et al.2 found peak acid outputs (similar to those after ametazole) in most subjects after pentagastrin doses ranging from 0-6 to 6 g. per kg. per hour; in some subjects, however, it was not certain that peak acid secretory capacity had been reached, since an increase in dose-rate produced side-effects. Konturek and Lankosz 10 found that 1-5 µg. per kg. per hour of pentagastrin gave an acid output significantly higher than that after a submaximal dose of histamine diphosphate (20 µg. per kg. per hour); and that a five-fold increase of the pentagastrin dose during the same experiment’s third hour did not result in a higher acid output, while the acid output after this dose was not significantly higher than the acid response to histamine diphosphate in a dose of 40 µg. per kg. per hour, in the same period. Another group5 found the acid response significantly higher after 5 µg. per kg. per hour of pentagastrin than after 2-5 as well as after 10 µg. common
"
"
Makhlouf, G. M., McManus, J. P. A., Card, W. I. Gastroenterology, 1966, 51, 455. 2. Wormsley, K. G., Mahoney, M. P., Ng, M. Lancet, 1966, i, 993. 3. Logan, C. J. H., Connell, A. M. ibid. p. 996. 4. Logan, C. J. H., Brick, I., Roddie, I. C. ibid. p. 999. 5. Multicentre Pilot Study. ibid. 1967, i, 291. 6. Bank, S., Marks, I. N., Louw, J. H., Tigler-Wybrandi, N. ibid. 1967, ii, 67. 7. Shearman, D. J. C., Finlayson, N. D. C., Murray-Lyon, I. M., Samson, R. R., Girdwood, R. H. ibid. p. 192. 8. Multicentre Study. ibid. p. 534. 9. Johnston, D., Jepson, K. ibid. p. 585. 10. Konturek, S. J., Lankosz, J. Scand. J. Gastroent. 1967, 2, 112. 11. Makhlouf, G. M. Lancet, Sept. 30, 1967, p. 720. Duthie, H. L., Jepson, K., Johnston, D. ibid. p. 841. 1.
Medical Department F, Glostrup Hospital, Copenhagen.
PAUL RØDBRO.
Surgical Department A, Bispebjerg Hospital, Copenhagen.
K. H. KØSTER.
TREATMENT OF HEPATIC COMA SIR,-We have read with interest your leading article (Aug. 5, p. 294). We describe here a successful exchange transfusion we have lately performed in a patient with hepatic coma due to infective hepatitis. Ten days before admission to the medical unit of this hospital, a 32-year-old policeman developed anorexia and malaise, followed by jaundice a couple of days later. Six days before he had started vomiting and. had developed upper abdominal pain. At this stage he had been admitted to the Police Hospital, where his condition rapidly deteriorated despite treatment; after four days he had become drowsy, LIVER-FUNCTION TESTS IN PATIENT WITH HEPATIC COMA BEFORE AND AFTER EXCHANGE BLOOD-TRANSFUSION
at times he was agitated and restless. Twelve hours before transfer here he had passed into a state of deep coma. The patient was of good physique, with yellow sclerae. Painful stimuli elicited no response. The plantar response was extensor on both sides. Liver-function tests done on various occasions are shown in the accompanying table. The patient was treated with prednisolone, 100 mg. daily,
though
12. 13. 14.
Lancet, 1966, i, 1022. Makhlouf, G. M., McManus, J. P. A., Card, W. I. ibid. 1964, ii, 485. Morley, J. S., Tracy, H. J., Gregory, R. A. Nature, Lond. 1965, 207, 1356.
Køster, K. H., Rødbro, P., Peterson, H. J. Scand. J. Gastroent. (in the press). Køster, K. H., Faber, V., Rødbro, P. ibid. 16. Wangel, A. G., Callender, S. T. Br. med. J. 1965, i, 1409. Makhlouf, G. M., McManus, J. P. A., Card, W. I. Gastroenterology, 1967, 52, 787. 15.
1093
paromomycin (’ Humatin ’), 500 mg. every 4 hours, through a Ryle’s tube, together with 15% glucose solution by intravenous drip transfusion, and parenteral vitamins. After 48 hours on this regimen the depth of coma was unchanged. At this stage (i.e., 60 hours after the onset of deep coma, and 108 hours after the onset of drowsiness) an exchange transfusion was performed with 10 pints of fresh heparinised blood. While making the skin incision and doing the dissection to identify the long saphenous vein, no local anxsthetic was needed because of deep coma; but as the transfusion was coming to an end, the patient seemed to have some awareness of pain in the groin. Twelve hours after the exchange transfusion the patient, who had been lying absolutely still, became extremely restless and was restrained in bed with great difficulty. Plantar response remained extensor on both sides. Later the depth of coma gradually lessened and 30 hours after the transfusion the patient complained of headache. At that time he was still confused and not fully orientated. His confused state gradually improved and 38 hours after the transfusion he was able to obey simple commands and answer simple questions. At this stage the plantar responses became flexor. Improvement was rapid during the next few hours and 50 hours after transfusion he was mentally alert and answered all questions rationally. Thereand
after his recovery was uneventful and he is now back at work, after a period of convalescence. Our experience is so far limited to this one case, but we feel that this form of treatment offers some hope in an otherwise hnmalPCe situation Dow Medical College and Civil Hospital, Karachi, Pakistan.
NAZIR A. CHAUDHARY NASEER AHMAD SHAIKH MUSHTAQ HASAN.
TRAINING IN MEDICAL LABORATORY TECHNOLOGY SIR The response in your correspondence columns to the statement from the Institute of Medical Laboratory Technology (Oct. 28, p. 935) reflects a widespread endeavour to maintain high standards of technology and efficiency. There is general agreement on a system of coordinated training conducted by experts and based on day or block release; and there should be close liaison between training institutes and working laboratories. However, laboratories must continue to function at all times as efficient working units, and the problem of providing full training facilities is linked with that of maintaining adequate work output of a high technical standard. Whether or not day release is made compulsory, there is little doubt that it is here to stay: it is also clear that the constraints imposed by regular staff absences can be overcome only by increases in technical establishments; but, because of present financial restrictions and shortage of labour, it is unlikely that early increases in senior establishments will come about or that, in any case, these would solve the immediate problem. In the recent correspondence, no account has been taken of those who are willing and capable of giving useful service in laboratories but who, for various reasons, have no wish to undergo training in depth or to acquire technological qualifications. Much of the work of medical laboratories-clinical, academic, or reference departments-is elementary or repetitive, and much of this can be carried out by people with comparatively little training. Is it not time, as a matter of national policy, to encourage employment of a quota of semiskilled labour in laboratories in order to permit greater flexibility in educational arrangements for those most suitable for advanced training ? Recruitment of such semiskilled labour should be based on recognised salary scales proportional to, but slightly less than, those of technicians in training; and increments could be based on age, length of service, and, possibly, degree of local responsibility. This suggestion in no way implies a lowering of technical standards. Most experienced laboratory workers are acquainted with technicians who are excellent at their daily work but pass examinations only with great difficulty, if at all.
Surely, employment and recognition of such workers would some of the obvious leaks in technical establishments, because many who are now deterred by academic handicaps would be encouraged to enter laboratory services. Contemporary proposals for technicians’ training are to be commended for their far-sighted aims and their optimism. But this optimism must be modified by the realities of the present situation. Only by paying due regard to the pressures on the
plug
lower echelons of laboratory workers will a future elite body of technologists be created. Department of Medical Microbiology, G. D. WASLEY St. Thomas’s Hospital Medical School, R. FRASER WILLIAMS. London S.E.1.
DERMATOGLYPHICS IN ECTODERMAL DYSPLASIA
SIR,—I wish to report briefly my dermatoglyphic analyses of families with hereditary anhydrotic ectodermal dysplasia, since there seem to be findings common to affected individuals two
and carriers. In this X-linked disorder there are decreased numbers of sweat-glands in the skin, hypotrichosis, and anodontia. The carrier female usually has symptoms. Since the skin is involved, one might expect to find characteristic dermatoglyphic changes, as in this short series. In family1 the father was clinically normal; the mother had thin hair, decreased sweating, and poor teeth; three sons were all severely affected. In family 2 the father was clinically normal; the mother had decreased sweating; three sons were severely involved and one son was normal. The dermatoglyphics of all these people were analysed; the affected ones had striking ridge disruption in all areas of palms and soles. There was also a tendency for the patterns to be vestigial, particularly in the third and fourth interdigital and plantar hallucal areas. The c and d digital triradii tended to be absent, vestigial, or displaced, and the C and D palmar lines were impossible to trace or stopped without going anywhere. The hypothenar patterns were usually too complex to describe by a single pattern name, and in addition the palmar axial triradius tended to be distal. The carriers (mothers) had some but not all of these patterns. The complex hypothenar patterns were present in both mothers. The normal people in this series had none of these findings. Thus dermatoglyphics may prove to be another clinical measure for diagnosis of patients with anhydrotic ectodermal dysplasia and of the carrier or less affected female. This work was aided by a grant from the National Foundation. Departments of Pathology and Pediatrics, University of Colorado Medical Center, Denver, Colorado 80220. JEAN H. PRIEST.
INSULIN AND GLUCOSE RESPONSE TO GLUCAGON IN DOWN’S SYNDROME
SIR,-Abnormal glucose tolerance has been reported 1-3 in patients with Down’s syndrome (D.S.). In children with D.S., other mentally retarded children, and normal children, we have found that the mean rise in plasma-immunoreactiveinsulin level after oral glucose is only about half that observed in adults.4 Since glucagon has been shown to promote insulin secretion in adults,5 6 we decided to measure the response to it of these children. 16 children (aged 20 months to 6 years 4 months) were studied: 6 had D.s., 5 were mentally retarded from other causes, and 5 were normal. All were taking a high-carbohydrate diet containing 1000-2000 calories per day. After an overnight fast 0-5 mg. glucagon was given intravenously during 1-2 1. O’Leary, W. D. Am. J. Dis. Child. 1931, 41, 544. Runge, G. H. Am. J. ment. Defic. 1959, 63, 822. Benda, C. E. The Child with Mongolism; p. 175. New York, 1960. Milunsky, A., Rubenstein, A. H., Lowy, C., Wright, A. D. Devl Med. Child Neurol (in the press). 5. Yalow, R. S., Black, H., Villazon, M., Berson, A. A. Diabetes, 1960, 9, 356. 6. Samols, E., Marri, G., Marks, V. Lancet, 1965, ii, 415. 2. 3. 4.
to
determine whether castration of other
through intervention
JANUSZ SZYMENDERA STEFAN
MADAJEWICZ.
kg. per hour, and the output after 6 (1.g. per kg. per hour higher than after 12 (1.g. per kg. per hour.e In your leading article,12 commenting on the first reports on pentagastrin to appear in The Lancet,2—4 you concluded: "Its use in the testing of gastric function is, however, complicated by the side-effects, and it clearly does not fulfil the ideal of a secretory stimulant without undesirable activity". Pure gastrin has no side-effects on subcutaneous administration," and it is possible that the smallest molecule displaying the entire range of physiological properties of natural gastrin in animal experiments 14-the C terminal tetrapeptide, or tetragastrin "-may get closer to the ideal stimulant for clinical use than does pentagastrin. We have by now compared the effect of tetragastrin on gastric secretion with that of histamine diphosphate (40 (Jtg. per kg. subcutaneously) in 52 subjects.15 The effects of 2-5, 5, 10, and 20 (1.g. per kg. of subcutaneously injected tetragastrin have been studied in 6, 6, 19, and 21 subjects, respectively. With the 2-5 (1.g. per kg. dose the acid response was significantly lower than after histamine, while the mean acid output after 5 µg. per kg. (29-3 mEq. per hour) was similar to that after histamine (32-3 mEq. per hour). With the higher doses of tetragastrin the acid response corresponded closely to that after histamine. No side-effects were encountered in any of the 52 subjects studied. In this respect tetragastrin so far seems similar to pure gastrin; the effect of tetragastrin upon intrinsic factor and pepsin secretion 15 is also very similar to the effect of gastrin.16 per
"
GASTRIN ANALOGUES AND GASTRIC-SECRETION TESTS SIR,-The steadily increasing number of publications on the effect of the synthetic gastrin analogue I.C.I. 50,123 (N-t-
.
butyloxycarbonyl - p - alanyl - L - tryptophyl - L - methionyl - L amide, pentagastrin) on gastric secreaspartyl-L-phenylalanine tion 1-10 have apparently not provided the final answers to two fundamental questions: the frequency of side-effects, and the maximal " acid dose of pentagastrin which will elicit a "
response.
The side-effects of
abdominal
pentagastrin-sinking
sen-
sations, abdominal cramps, nausea, hypotension, faintness, headache, and general malaise-are reported to occur with widely differing frequencies.1-3 5 7-9 They seem to be more after intravenous than after subcutaneous administration.511 Although one group of investigators 10 found no side-effects after 1-5 and 7-5 g. per kg. per hour, side-effects were fairly common in other studies using 6 and 12 g. per kg. a However, the side-effects are by no means per hour.2 s restricted to intravenous administration, but have been reported after subcutaneous injections of 4-13 fLg. per kg. I-a5 7— apparently most often with doses above 6 µg. per kg., although one group of workers stated that " there was no apparent relationship between the dose and the severity of the symptoms ".5 maximal " acid The dose of pentagastrin needed for a 5 8-11 Most response has been discussed by several workers. 1 2 workers using subcutaneous or intramuscular injections found that 6 fLg. per kg. of pentagastrin elicited an acid response similar to that after augmented histamine stimulation, and that the acid output did not rise further after 8, 9, or 10 fLg. per kg.15 9 The doses of intravenously administered pentagastrin required for a maximal " acid response vary in the reports cited above. Wormsley et al.2 found peak acid outputs (similar to those after ametazole) in most subjects after pentagastrin doses ranging from 0-6 to 6 g. per kg. per hour; in some subjects, however, it was not certain that peak acid secretory capacity had been reached, since an increase in dose-rate produced side-effects. Konturek and Lankosz 10 found that 1-5 µg. per kg. per hour of pentagastrin gave an acid output significantly higher than that after a submaximal dose of histamine diphosphate (20 µg. per kg. per hour); and that a five-fold increase of the pentagastrin dose during the same experiment’s third hour did not result in a higher acid output, while the acid output after this dose was not significantly higher than the acid response to histamine diphosphate in a dose of 40 µg. per kg. per hour, in the same period. Another group5 found the acid response significantly higher after 5 µg. per kg. per hour of pentagastrin than after 2-5 as well as after 10 µg. common
"
"
Makhlouf, G. M., McManus, J. P. A., Card, W. I. Gastroenterology, 1966, 51, 455. 2. Wormsley, K. G., Mahoney, M. P., Ng, M. Lancet, 1966, i, 993. 3. Logan, C. J. H., Connell, A. M. ibid. p. 996. 4. Logan, C. J. H., Brick, I., Roddie, I. C. ibid. p. 999. 5. Multicentre Pilot Study. ibid. 1967, i, 291. 6. Bank, S., Marks, I. N., Louw, J. H., Tigler-Wybrandi, N. ibid. 1967, ii, 67. 7. Shearman, D. J. C., Finlayson, N. D. C., Murray-Lyon, I. M., Samson, R. R., Girdwood, R. H. ibid. p. 192. 8. Multicentre Study. ibid. p. 534. 9. Johnston, D., Jepson, K. ibid. p. 585. 10. Konturek, S. J., Lankosz, J. Scand. J. Gastroent. 1967, 2, 112. 11. Makhlouf, G. M. Lancet, Sept. 30, 1967, p. 720. Duthie, H. L., Jepson, K., Johnston, D. ibid. p. 841. 1.
Medical Department F, Glostrup Hospital, Copenhagen.
PAUL RØDBRO.
Surgical Department A, Bispebjerg Hospital, Copenhagen.
K. H. KØSTER.
TREATMENT OF HEPATIC COMA SIR,-We have read with interest your leading article (Aug. 5, p. 294). We describe here a successful exchange transfusion we have lately performed in a patient with hepatic coma due to infective hepatitis. Ten days before admission to the medical unit of this hospital, a 32-year-old policeman developed anorexia and malaise, followed by jaundice a couple of days later. Six days before he had started vomiting and. had developed upper abdominal pain. At this stage he had been admitted to the Police Hospital, where his condition rapidly deteriorated despite treatment; after four days he had become drowsy, LIVER-FUNCTION TESTS IN PATIENT WITH HEPATIC COMA BEFORE AND AFTER EXCHANGE BLOOD-TRANSFUSION
at times he was agitated and restless. Twelve hours before transfer here he had passed into a state of deep coma. The patient was of good physique, with yellow sclerae. Painful stimuli elicited no response. The plantar response was extensor on both sides. Liver-function tests done on various occasions are shown in the accompanying table. The patient was treated with prednisolone, 100 mg. daily,
though
12. 13. 14.
Lancet, 1966, i, 1022. Makhlouf, G. M., McManus, J. P. A., Card, W. I. ibid. 1964, ii, 485. Morley, J. S., Tracy, H. J., Gregory, R. A. Nature, Lond. 1965, 207, 1356.
Køster, K. H., Rødbro, P., Peterson, H. J. Scand. J. Gastroent. (in the press). Køster, K. H., Faber, V., Rødbro, P. ibid. 16. Wangel, A. G., Callender, S. T. Br. med. J. 1965, i, 1409. Makhlouf, G. M., McManus, J. P. A., Card, W. I. Gastroenterology, 1967, 52, 787. 15.
1093
paromomycin (’ Humatin ’), 500 mg. every 4 hours, through a Ryle’s tube, together with 15% glucose solution by intravenous drip transfusion, and parenteral vitamins. After 48 hours on this regimen the depth of coma was unchanged. At this stage (i.e., 60 hours after the onset of deep coma, and 108 hours after the onset of drowsiness) an exchange transfusion was performed with 10 pints of fresh heparinised blood. While making the skin incision and doing the dissection to identify the long saphenous vein, no local anxsthetic was needed because of deep coma; but as the transfusion was coming to an end, the patient seemed to have some awareness of pain in the groin. Twelve hours after the exchange transfusion the patient, who had been lying absolutely still, became extremely restless and was restrained in bed with great difficulty. Plantar response remained extensor on both sides. Later the depth of coma gradually lessened and 30 hours after the transfusion the patient complained of headache. At that time he was still confused and not fully orientated. His confused state gradually improved and 38 hours after the transfusion he was able to obey simple commands and answer simple questions. At this stage the plantar responses became flexor. Improvement was rapid during the next few hours and 50 hours after transfusion he was mentally alert and answered all questions rationally. Thereand
after his recovery was uneventful and he is now back at work, after a period of convalescence. Our experience is so far limited to this one case, but we feel that this form of treatment offers some hope in an otherwise hnmalPCe situation Dow Medical College and Civil Hospital, Karachi, Pakistan.
NAZIR A. CHAUDHARY NASEER AHMAD SHAIKH MUSHTAQ HASAN.
TRAINING IN MEDICAL LABORATORY TECHNOLOGY SIR The response in your correspondence columns to the statement from the Institute of Medical Laboratory Technology (Oct. 28, p. 935) reflects a widespread endeavour to maintain high standards of technology and efficiency. There is general agreement on a system of coordinated training conducted by experts and based on day or block release; and there should be close liaison between training institutes and working laboratories. However, laboratories must continue to function at all times as efficient working units, and the problem of providing full training facilities is linked with that of maintaining adequate work output of a high technical standard. Whether or not day release is made compulsory, there is little doubt that it is here to stay: it is also clear that the constraints imposed by regular staff absences can be overcome only by increases in technical establishments; but, because of present financial restrictions and shortage of labour, it is unlikely that early increases in senior establishments will come about or that, in any case, these would solve the immediate problem. In the recent correspondence, no account has been taken of those who are willing and capable of giving useful service in laboratories but who, for various reasons, have no wish to undergo training in depth or to acquire technological qualifications. Much of the work of medical laboratories-clinical, academic, or reference departments-is elementary or repetitive, and much of this can be carried out by people with comparatively little training. Is it not time, as a matter of national policy, to encourage employment of a quota of semiskilled labour in laboratories in order to permit greater flexibility in educational arrangements for those most suitable for advanced training ? Recruitment of such semiskilled labour should be based on recognised salary scales proportional to, but slightly less than, those of technicians in training; and increments could be based on age, length of service, and, possibly, degree of local responsibility. This suggestion in no way implies a lowering of technical standards. Most experienced laboratory workers are acquainted with technicians who are excellent at their daily work but pass examinations only with great difficulty, if at all.
Surely, employment and recognition of such workers would some of the obvious leaks in technical establishments, because many who are now deterred by academic handicaps would be encouraged to enter laboratory services. Contemporary proposals for technicians’ training are to be commended for their far-sighted aims and their optimism. But this optimism must be modified by the realities of the present situation. Only by paying due regard to the pressures on the
plug
lower echelons of laboratory workers will a future elite body of technologists be created. Department of Medical Microbiology, G. D. WASLEY St. Thomas’s Hospital Medical School, R. FRASER WILLIAMS. London S.E.1.
DERMATOGLYPHICS IN ECTODERMAL DYSPLASIA
SIR,—I wish to report briefly my dermatoglyphic analyses of families with hereditary anhydrotic ectodermal dysplasia, since there seem to be findings common to affected individuals two
and carriers. In this X-linked disorder there are decreased numbers of sweat-glands in the skin, hypotrichosis, and anodontia. The carrier female usually has symptoms. Since the skin is involved, one might expect to find characteristic dermatoglyphic changes, as in this short series. In family1 the father was clinically normal; the mother had thin hair, decreased sweating, and poor teeth; three sons were all severely affected. In family 2 the father was clinically normal; the mother had decreased sweating; three sons were severely involved and one son was normal. The dermatoglyphics of all these people were analysed; the affected ones had striking ridge disruption in all areas of palms and soles. There was also a tendency for the patterns to be vestigial, particularly in the third and fourth interdigital and plantar hallucal areas. The c and d digital triradii tended to be absent, vestigial, or displaced, and the C and D palmar lines were impossible to trace or stopped without going anywhere. The hypothenar patterns were usually too complex to describe by a single pattern name, and in addition the palmar axial triradius tended to be distal. The carriers (mothers) had some but not all of these patterns. The complex hypothenar patterns were present in both mothers. The normal people in this series had none of these findings. Thus dermatoglyphics may prove to be another clinical measure for diagnosis of patients with anhydrotic ectodermal dysplasia and of the carrier or less affected female. This work was aided by a grant from the National Foundation. Departments of Pathology and Pediatrics, University of Colorado Medical Center, Denver, Colorado 80220. JEAN H. PRIEST.
INSULIN AND GLUCOSE RESPONSE TO GLUCAGON IN DOWN’S SYNDROME
SIR,-Abnormal glucose tolerance has been reported 1-3 in patients with Down’s syndrome (D.S.). In children with D.S., other mentally retarded children, and normal children, we have found that the mean rise in plasma-immunoreactiveinsulin level after oral glucose is only about half that observed in adults.4 Since glucagon has been shown to promote insulin secretion in adults,5 6 we decided to measure the response to it of these children. 16 children (aged 20 months to 6 years 4 months) were studied: 6 had D.s., 5 were mentally retarded from other causes, and 5 were normal. All were taking a high-carbohydrate diet containing 1000-2000 calories per day. After an overnight fast 0-5 mg. glucagon was given intravenously during 1-2 1. O’Leary, W. D. Am. J. Dis. Child. 1931, 41, 544. Runge, G. H. Am. J. ment. Defic. 1959, 63, 822. Benda, C. E. The Child with Mongolism; p. 175. New York, 1960. Milunsky, A., Rubenstein, A. H., Lowy, C., Wright, A. D. Devl Med. Child Neurol (in the press). 5. Yalow, R. S., Black, H., Villazon, M., Berson, A. A. Diabetes, 1960, 9, 356. 6. Samols, E., Marri, G., Marks, V. Lancet, 1965, ii, 415. 2. 3. 4.