- Email: [email protected]
" IRRITABLE COLON OF CHILDHOOD "
1333 in this disease as it is for patients to be of disease in distant relatives such as grandmothers, aunts, or cousins. Any progress likely to be made in this area will come from intensive investigation of families in which documentation is complete rather than from surveys of large numbers in which insufficient attention has been paid to detail. IAN F. KERR Western Infirmary, R. M. Ross. Glasgow W.2. into
FIBRINOLYSIS AND UROLITHIASIS SIR,-I was interested in Mr. Charlton’s Hypothesis
family histories
aware
ISLET-CELLS AND INSULIN SIR,-Your leading article (May 27, p. 1142) contains a number of dubious propositions and one clear factual error. It states that " adrenaline releases insulin," a view which runs directly counter to a large body of experimental data1 suggesting that adrenaline, in fact, inhibits insulin release. It should be emphasised that the statement attributing the action of insulin to processes following upon cleavage of S-S groups and binding to tissue is hypothetical, as are many of the other assertions made in the leader. We should like to know, for instance, of the observations which showed " a rapid change in the glycogen concentration of the p-cells " which, it is claimed, is stimulated by changes in blood-sugar concentration in normal people. The rather graphic account of insulin synthesis and release in the P-cell is based upon the interpretation of electron-microscope photographs rather than a motion film, which the confident tone of the description suggests. The synalbumin antagonist of Vallance-Owen, though an important contribution in the elucidation of diabetes, does not yet occupy the position of Holy Writ and, to our knowledge, VallanceOwen himself has never differentiated between juvenile and " mature " diabetes (your terminology) in the way that the leader implies. With regard to the articles on insulin-like activity (LL.A.) and the properties of diluted plasma in the same issue (pp. 1123 and 1138), Dr. Power and his colleagues’ interesting observations, which they use to support the idea of a direct islet origin of I.L.A., might equally be explained by the genesis of the material from the insulin molecule itself. We have already published some observations on this possibility,2 but feel that the hypothesis can best be directly tested by examining the material released from islets incubated by vitro. Should this material fail to contain " non-insulin l.L.A.", the strong presumption is that it arises elsewhere. We hope to publish such a study in the near future. Department of Medicine, R. J. JARRETT Guy’s Hospital Medical School, HARRY KEEN. London S.B.1. "
"
obliged to Dr. Jarrett and Dr. Keen for unceremoniously exposing our obvious error. We meant to say adrenaline antagonises the release of insulin ". We agree that the sentence on the appearance of glycogen in p-cells could have been more happily worded (the work we had in mind was that of Lazarow, quoted in the leader). We are less submissive in response to the other rebukes. Our account of Lacey’s electronmicroscope observations was necessarily condensed: naturally
* * * We
are
"
the conclusions need to be re-examined. We had no intention of suggesting that synalbumin is the only important insulin antagonist, though it is the substance on which some satisfactorily neat work has been done. Finally, how, in the name of Langerhans, are we to write about insulin without introducing hypotheses (or what Dr. Jarrett and Dr. Keen would call " dubious propositions ") ? Do they assert that our knowledge of the production and mode of action of insulin has passed the stage where hypothesis and speculation are in order ?-ED. L. 1.
2.
3.
Coore, H. G., Randle, P. J. Biochem. J. 1964, 93, 66. Karam, J. H., Grasso, S. G., Wegienka, L. C., Grodsky, G. M., Forsham, P. H. Diabetes, 1966, 15, 571. Porte, D. J. clin. Invest. 1967, 46, 86. Cameron, J. S., Boyns, D. R., Jarrett, R. J., Keen, H. Diabetologia, 1966, 2, 86 and 91. Keen, H. in Diabetes Mellitus (edited by L. J. P. Duncan). Edinburgh 1965. Keen, H., Sells, R., Jarrett, R. J. Diabetologia, 1965, 1, 28.
(June 3,
p. 1199). In a current study1 of seventeen subjects with no renal disease, it has been observed that the renal-vein blood has
greater fibrinolytic activity than arterial blood when estimated by the euglobulin-lysis method as described by von Kaulla,22 with slight modification. These findings suggest that kidney parenchyma produces fibrinolytic activators which are passed on to the circulation. It is also possible that some of these activators find their way into the urine. This latter assumption seems to be reasonable, since Bjerrehuus 4 observed that urokinase concentrations in the bladder and renal pelvis were similar. Department of Medicine, Royal Victoria Infirmary, Newcastle upon Tyne
1.
I. S. MENON.
TREATMENT OF HÆMORRHAGIC DIATHESIS SIR,-Captain Dennis and his colleagues (May 20, p. 1088) demonstrate the importance of early recognition and rapid treatment of states of increased intravascular coagulation. I have jointly reported5 multiple coagulation defects in association with a dissecting aneurysm of the aorta. One of the mechanisms suggested was clotting within the dissecting haematoma with consumption of coagulation factors and secondary increase in fibrinolysis. These findings suggest that complete coagulation studies, including tests for increased fibrinolysis and assays of individual clotting factors, should be an essential part of the investigation of these patients. Wheat et al. have proposed initial medical management in most patients with acute dissecting aneurysms. These workers successfully used trimetaphan camsylate (’ Arfonad ’), reserpine, and guanethidine. Wheat et al.’s favourable results support the contention that medical therapy has an important role in the management of patients with dissecting aneurysms. The timely use of heparin, fibrinogen, and aminocaproic acid may be a valuable addition to the initial medical therapy of patients with a dissecting aneurysm and concomitant increased intravascular coagulation. Maimonides Medical Center, Maimonides Hospital, 4802 Tenth Avenue, New York 11219.
"
NORMAN L. FINE.
IRRITABLE COLON OF CHILDHOOD
"
SIR,-The recent paper by Davidson and Wassermanhas provoked editorial comment or annotation in both The Lancet8 and the British Medical Journal.9 Although paediatricians are well aware of the condition, it is remarkable that this exceedingly common clinical syndrome has not been described more clearly hitherto. Davidson and Wasserman were able to collect 186 cases in 10 years. I estimate that in my own hospital outpatient clinics I see roughly one case per month, comprising perhaps 1% of all new pmdiatric outpatient referralsfrom family doctors. Personally I have usually applied the term " intestinal hurry of the toddler," but " irritable colon " is probably a better and neater description. In many of my cases a mild intercurrent gastroenteritis seems to have been a precipitating factor, followed by recurrent loose stools for months. It is very important to recognise the condition for what 1.
2.
3. 4. 5. 6. 7. 8. 9.
it is
and
not
subject these
children and their
Menon, I. S. Br. med. J. 1967, ii, 110. Menon, I. S., Dewar, H. A. First International Symposium on Tissue Factors in the Homœostasis of the Coagulation-fibrinolysis System, Florence, May, 1967. von Kaulla, K. N. Chemistry of Thrombolysis: Human Fibrinolytic Enzymes; p. 79. Springfield, Illinois, 1963. Menon, I. S. Lab. Pract. 1967, 16, 574. Bjerrehuus, I. Scand. J. clin. Lab. Invest. 1952, 4, 179. Fine, N., Appelbaum, J., Elguezabal, A., Castleman, L. Archs intern. Med. 1967, 119, 522. Wheat, M., Palmer, R., Bartley, T., Seelman, R. J. thorac. cardiovasc. Surg. 1965, 50, 364. Davidson, M., Wasserman, R. M. J. Pœdiat. 1966, 69, 1027. Lancet, May 27, 1967, p. 1146. Br. med. J. April 15, 1967, p. 127.
1334 parents to the trial of unnecessary investigations. The main clue, of course, is the fact that health, vitality, appetite, and growth remain unimpaired-as Davidson and Wasserman have so clearly demonstrated. Where there is an element of doubt after the first assessment, periodic weight checks will define those cases which merit further investigation for a
malabsorption syndrome. Although, as pointed out in your annotation, a temporary enzyme deficiency is still a notional possibility, the clinical picture strongly suggests that absorption from the small intestine is unimpaired. Bedford General
Hospital (South Wing), Kempston Road, Bedford.
ARTHUR W. FERGUSON.
CLASSIFYING PROTEIN-CALORIE MALNUTRITION SIR,łThe hypothesis described by Dr. Islam (April 22, p. 898) to explain the fatty liver of kwashiorkor was outlined by us last year, together with some experimental support. 1 2 We found that serum P-lipoprotein cholesterols were lower in patients with severe fatty liver than in those with mild fatty liver. However, a-lipoprotein cholesterols were not reduced in most of our kwashiorkor patients. Full details will be published elsewhere. The scoring method suggested by Professor McLaren and his colleagues (March 11, p. 533) is a welcome attempt to classify syndromes" objectively within the protein-calorie malnutrition (P.C.M.) spectrum ". The method has the virtue of simplicity and uses serum-albumin, which seems to be the most reliable biochemical index of protein deficiency.3 Details will need to be worked out. For example, electrophoresis and scanning gives rather lower serum-albumin values than by salting out and biuret.4 Should the oedema be diagnosed on admission, when children are often dehydrated, or after fluid therapy ? 5 Oedema may sometimes reflect potassium deficiency.The method deserves trial by workers in different parts of the world when they report groups of patients with P.C.M. Hyperlipasmia, which Professor McLaren and his colleagues point out to be a biochemical change characteristic of marasmus, was reported in atrophic " infants by Ludmany et al.,’7and can be seen in the data for marasmus in the paper by Lewis et al.8 After serum-albumin, the following biochemical values might be useful for diagnostic classifications:
DAMAGES Dr. S. P. B. DONNAN and Dr. K. H. SUTTON, write: " The Press recently carried reports of a young house-surgeon who has been ordered in the High Court to pay damages of E31,383 to a nurse who was injured in 1963. She was a passenger in a car driven by him when it collided with a lorry, but, as the car was hired and was not insured for passenger liability, he has to pay the whole sum himself. Currently this is at E3per week, but the rate will increase with his income. In this tragic situation the innocent victim has to wait a lifetime before she receives the compensation the court has awarded, whilst the newly qualified doctor is faced with a debt, perhaps amounting to a fifth of his total career earnings, which he will work all his life to pay off. Doctors may be willing to help both these unfortunate people by subscribing to a fund to pay part at least of the damages. Accordingly we have set up a trust fund to which we invite members of the profession to subscribe. Contributions should be sent to us c/o Westminster Bank, 292 Wimborne Road, Bournemouth. To avoid expenses acknowledgements will only be sent on
request."
Parliament QUESTION TIME Capital Expenditure on Psychiatric Hospitals Capital expenditure on special hospitals, N.H.S. psychiatric hospitals, and psychiatric facilities at other N.H.S. hospitals during 1967-68 is estimated at about m’5 million or just over 10% of the total capital expenditure on N.H.S. hospitals. Cost of Antidepressive Drugs The ingredient cost of antidepressive drugs in 1966, as analysed in the Ministry of Health statistics and dispensed by chemists, was E3-13 million, compared with E2-78 million in 1965 and E2.37 million in 1964. Women Medical Students The number of women entering medical schools in 1966 was 570, compared with 523 in 1962.
Appointments
"
1. Serum- total-cholesterol.-This is the easiest lipid to measure in and gives some idea of lipoprotein synthesis. Levels are relatively higher in marasmus than in kwashiorkor.9 2. Urinary-creatinine/height index.- This has been proposed for grading the severity of protein depletion in P.c.m.10 It reflects muscle mass but has the disadvantage of requiring a 24-hour-urine collection. 3. We suggest that the serum-uric-acid level should be looked into as well. It has recently been reported significantly above normal in marasmus, but not in kwashiorkor.1’ It rises very high in fasting adults.12 We wish to make acknowledgements to C.S.I.R., and for U.S. Public Health Service grant AM 03995. serum
Departments of Medicine and Child Health, University of Cape Town, South Africa. 1. 2. 3. 4.
5. 6. 7. 8. 9. 10.
11. 12.
A. S. TRUSWELL J. D. L. HANSEN.
Truswell, A. S., Hansen, J. D. L., Wittmann, W., Wannenburg, P., Roberts, B., Watson, C. E. S. Afr. med. J. 1966, 40, 887. Truswell, A. S., Hansen, J. D. L., Wittmann, W. Int. Congr. Nutr. 1966, abstracts, p. 223. Truswell, A. S., Wannenburg, P., Wittmann, W., Hansen, J. D. L. Lancet, 1966, i, 1162. Truswell, A. S., Hansen, J. D. L., Freeseman, C., Smidt, T. F. S. Afr. med. J. 1963, 37, 527. Hansen, J. D. L. Proceedings of Colloquium on Protein Deficiencies and Calorie Deficiencies, Cambridge, 1967 (in the press). Hansen, J. D. L., Jenkinson, V. S. Afr. J. Lab. clin. Med. 1956, 2, 206. Ludmany, K., Csorba, S., Jezernicky, J. Z. Kinderheilk. 1965, 92, 299. Lewis, B., Hansen, J. D. L., Wittmann, W., Krut, L. H., Stewart, F. Am. J. clin. Nutr. 1964, 15, 161. Pretorius, P. J., Wehmeyer, A. S. S. Afr. med. J. 1966, 40, 240. Viteri, F. E., Arroyave, G., Béhar, M. Int. Congr. Nutr. 1966, abstracts, p. 46. Khalil, M., El-Khateeb, S., Aref, G. H., Gurgis, F. K. J. trop. Med. Hyg. 1967, 70, 11. Thomson, T. J., Runcie, J., Miller, V. Lancet, 1966, ii, 992.
M.B. Lond.: consultant clinical pathologist, Chelmsford hospital group. BRIERLEY, J. S. W., M.B. Leeds, D.P.H.: M.o.H., Huddersfield. NOALL, E. W. P., M.B. Lond., M.R.C.P., D.P.M.: consultant physician, Thames hospital group. PILKINGTON, T. L., M.R.C.S., D.P.M.: consultant psychiatrist, Gogarburn Hospital, Edinburgh. SMITH, R. S., M.B. Cantab., M.C.PATH. : consultant haematologist, Children’s Hospital, Sheffield.
ANTCLIFF, A. C.,
Manchester
Regional Hospital Board:
M.B. Baghdad, M.R.C.P., D.C.H.; consultant paediatrician, Oldham and district and Ashton, Hyde and Glossop hospital groups. ALLCOCK, E. A., M.B. Manc., M.SC. Minnesota, F.R.C.S., F.R.A.C.S., F.D.S. R.c.s.: consultant surgeon, South Cheshire hospital group. ATA, MOHAMMAD, M.B. Punjab, M.R.C.P.E., M.C.PATH. : consultant pathologist, with special experience in haematology, Rochdale and district
ABRAHAM, J. M.,
hospital group. GREEN, J. H., M.CH.ORTH. Lpool, F.R.C,S.E.: consultant traumatic and orthopxdic surgeon, Salford hospital group. MADDOCK, SHEILA G., M.B. Lpool: consultant geriatric physician, Salford hospital group. PITKEATHLEY, D. A., M.B. St. And., M.R.C.P.E., M.R.C.P.G.: consultant rheumatologist, R.H.B. hospitals and United Manchester Hospitals.
Regional Hospital Board, Scotland: CARLISLE, J. M., M.B. Glasg., D.P.M.: consultant psychiatrist, Leverndale Hospital. DONALD, J. R., M.B. Glasg., F.F.A. R.c.s.: consultant anxsthetist, Law and
Western
Stonehouse
Hospitals.
LINTON, A. L., M.B. Edin., M.R.C.P.E., M.R.C.P.G. renal disease, Western Infirmary, Glasgow.
Liverpool Regional Hospital
:
consultant
physician
in
Board:
CONWAY, C. F., M.B. N.u.I., F.F.A. R.C.S.: D.P.H., consultant anaathetist, Chester Royal Infirmary. D’NETTO, PHYLLIS E., M.R.C.P.E., M.R.C.P.G., D.OBST.: consultant geriatrician, Deva and Moston Hospitals. HARPER, PATRICK, M.B. Belf., D.P.M.: consultant psychiatrist, Rainhill Hospital. HART, S. M., M.B. N.U.I., F.F.A. R.c.s.: consultant anesthetist, Broadgreen Hospital.
FIBRINOLYSIS AND UROLITHIASIS SIR,-I was interested in Mr. Charlton’s Hypothesis
family histories
aware
ISLET-CELLS AND INSULIN SIR,-Your leading article (May 27, p. 1142) contains a number of dubious propositions and one clear factual error. It states that " adrenaline releases insulin," a view which runs directly counter to a large body of experimental data1 suggesting that adrenaline, in fact, inhibits insulin release. It should be emphasised that the statement attributing the action of insulin to processes following upon cleavage of S-S groups and binding to tissue is hypothetical, as are many of the other assertions made in the leader. We should like to know, for instance, of the observations which showed " a rapid change in the glycogen concentration of the p-cells " which, it is claimed, is stimulated by changes in blood-sugar concentration in normal people. The rather graphic account of insulin synthesis and release in the P-cell is based upon the interpretation of electron-microscope photographs rather than a motion film, which the confident tone of the description suggests. The synalbumin antagonist of Vallance-Owen, though an important contribution in the elucidation of diabetes, does not yet occupy the position of Holy Writ and, to our knowledge, VallanceOwen himself has never differentiated between juvenile and " mature " diabetes (your terminology) in the way that the leader implies. With regard to the articles on insulin-like activity (LL.A.) and the properties of diluted plasma in the same issue (pp. 1123 and 1138), Dr. Power and his colleagues’ interesting observations, which they use to support the idea of a direct islet origin of I.L.A., might equally be explained by the genesis of the material from the insulin molecule itself. We have already published some observations on this possibility,2 but feel that the hypothesis can best be directly tested by examining the material released from islets incubated by vitro. Should this material fail to contain " non-insulin l.L.A.", the strong presumption is that it arises elsewhere. We hope to publish such a study in the near future. Department of Medicine, R. J. JARRETT Guy’s Hospital Medical School, HARRY KEEN. London S.B.1. "
"
obliged to Dr. Jarrett and Dr. Keen for unceremoniously exposing our obvious error. We meant to say adrenaline antagonises the release of insulin ". We agree that the sentence on the appearance of glycogen in p-cells could have been more happily worded (the work we had in mind was that of Lazarow, quoted in the leader). We are less submissive in response to the other rebukes. Our account of Lacey’s electronmicroscope observations was necessarily condensed: naturally
* * * We
are
"
the conclusions need to be re-examined. We had no intention of suggesting that synalbumin is the only important insulin antagonist, though it is the substance on which some satisfactorily neat work has been done. Finally, how, in the name of Langerhans, are we to write about insulin without introducing hypotheses (or what Dr. Jarrett and Dr. Keen would call " dubious propositions ") ? Do they assert that our knowledge of the production and mode of action of insulin has passed the stage where hypothesis and speculation are in order ?-ED. L. 1.
2.
3.
Coore, H. G., Randle, P. J. Biochem. J. 1964, 93, 66. Karam, J. H., Grasso, S. G., Wegienka, L. C., Grodsky, G. M., Forsham, P. H. Diabetes, 1966, 15, 571. Porte, D. J. clin. Invest. 1967, 46, 86. Cameron, J. S., Boyns, D. R., Jarrett, R. J., Keen, H. Diabetologia, 1966, 2, 86 and 91. Keen, H. in Diabetes Mellitus (edited by L. J. P. Duncan). Edinburgh 1965. Keen, H., Sells, R., Jarrett, R. J. Diabetologia, 1965, 1, 28.
(June 3,
p. 1199). In a current study1 of seventeen subjects with no renal disease, it has been observed that the renal-vein blood has
greater fibrinolytic activity than arterial blood when estimated by the euglobulin-lysis method as described by von Kaulla,22 with slight modification. These findings suggest that kidney parenchyma produces fibrinolytic activators which are passed on to the circulation. It is also possible that some of these activators find their way into the urine. This latter assumption seems to be reasonable, since Bjerrehuus 4 observed that urokinase concentrations in the bladder and renal pelvis were similar. Department of Medicine, Royal Victoria Infirmary, Newcastle upon Tyne
1.
I. S. MENON.
TREATMENT OF HÆMORRHAGIC DIATHESIS SIR,-Captain Dennis and his colleagues (May 20, p. 1088) demonstrate the importance of early recognition and rapid treatment of states of increased intravascular coagulation. I have jointly reported5 multiple coagulation defects in association with a dissecting aneurysm of the aorta. One of the mechanisms suggested was clotting within the dissecting haematoma with consumption of coagulation factors and secondary increase in fibrinolysis. These findings suggest that complete coagulation studies, including tests for increased fibrinolysis and assays of individual clotting factors, should be an essential part of the investigation of these patients. Wheat et al. have proposed initial medical management in most patients with acute dissecting aneurysms. These workers successfully used trimetaphan camsylate (’ Arfonad ’), reserpine, and guanethidine. Wheat et al.’s favourable results support the contention that medical therapy has an important role in the management of patients with dissecting aneurysms. The timely use of heparin, fibrinogen, and aminocaproic acid may be a valuable addition to the initial medical therapy of patients with a dissecting aneurysm and concomitant increased intravascular coagulation. Maimonides Medical Center, Maimonides Hospital, 4802 Tenth Avenue, New York 11219.
"
NORMAN L. FINE.
IRRITABLE COLON OF CHILDHOOD
"
SIR,-The recent paper by Davidson and Wassermanhas provoked editorial comment or annotation in both The Lancet8 and the British Medical Journal.9 Although paediatricians are well aware of the condition, it is remarkable that this exceedingly common clinical syndrome has not been described more clearly hitherto. Davidson and Wasserman were able to collect 186 cases in 10 years. I estimate that in my own hospital outpatient clinics I see roughly one case per month, comprising perhaps 1% of all new pmdiatric outpatient referralsfrom family doctors. Personally I have usually applied the term " intestinal hurry of the toddler," but " irritable colon " is probably a better and neater description. In many of my cases a mild intercurrent gastroenteritis seems to have been a precipitating factor, followed by recurrent loose stools for months. It is very important to recognise the condition for what 1.
2.
3. 4. 5. 6. 7. 8. 9.
it is
and
not
subject these
children and their
Menon, I. S. Br. med. J. 1967, ii, 110. Menon, I. S., Dewar, H. A. First International Symposium on Tissue Factors in the Homœostasis of the Coagulation-fibrinolysis System, Florence, May, 1967. von Kaulla, K. N. Chemistry of Thrombolysis: Human Fibrinolytic Enzymes; p. 79. Springfield, Illinois, 1963. Menon, I. S. Lab. Pract. 1967, 16, 574. Bjerrehuus, I. Scand. J. clin. Lab. Invest. 1952, 4, 179. Fine, N., Appelbaum, J., Elguezabal, A., Castleman, L. Archs intern. Med. 1967, 119, 522. Wheat, M., Palmer, R., Bartley, T., Seelman, R. J. thorac. cardiovasc. Surg. 1965, 50, 364. Davidson, M., Wasserman, R. M. J. Pœdiat. 1966, 69, 1027. Lancet, May 27, 1967, p. 1146. Br. med. J. April 15, 1967, p. 127.
1334 parents to the trial of unnecessary investigations. The main clue, of course, is the fact that health, vitality, appetite, and growth remain unimpaired-as Davidson and Wasserman have so clearly demonstrated. Where there is an element of doubt after the first assessment, periodic weight checks will define those cases which merit further investigation for a
malabsorption syndrome. Although, as pointed out in your annotation, a temporary enzyme deficiency is still a notional possibility, the clinical picture strongly suggests that absorption from the small intestine is unimpaired. Bedford General
Hospital (South Wing), Kempston Road, Bedford.
ARTHUR W. FERGUSON.
CLASSIFYING PROTEIN-CALORIE MALNUTRITION SIR,łThe hypothesis described by Dr. Islam (April 22, p. 898) to explain the fatty liver of kwashiorkor was outlined by us last year, together with some experimental support. 1 2 We found that serum P-lipoprotein cholesterols were lower in patients with severe fatty liver than in those with mild fatty liver. However, a-lipoprotein cholesterols were not reduced in most of our kwashiorkor patients. Full details will be published elsewhere. The scoring method suggested by Professor McLaren and his colleagues (March 11, p. 533) is a welcome attempt to classify syndromes" objectively within the protein-calorie malnutrition (P.C.M.) spectrum ". The method has the virtue of simplicity and uses serum-albumin, which seems to be the most reliable biochemical index of protein deficiency.3 Details will need to be worked out. For example, electrophoresis and scanning gives rather lower serum-albumin values than by salting out and biuret.4 Should the oedema be diagnosed on admission, when children are often dehydrated, or after fluid therapy ? 5 Oedema may sometimes reflect potassium deficiency.The method deserves trial by workers in different parts of the world when they report groups of patients with P.C.M. Hyperlipasmia, which Professor McLaren and his colleagues point out to be a biochemical change characteristic of marasmus, was reported in atrophic " infants by Ludmany et al.,’7and can be seen in the data for marasmus in the paper by Lewis et al.8 After serum-albumin, the following biochemical values might be useful for diagnostic classifications:
DAMAGES Dr. S. P. B. DONNAN and Dr. K. H. SUTTON, write: " The Press recently carried reports of a young house-surgeon who has been ordered in the High Court to pay damages of E31,383 to a nurse who was injured in 1963. She was a passenger in a car driven by him when it collided with a lorry, but, as the car was hired and was not insured for passenger liability, he has to pay the whole sum himself. Currently this is at E3per week, but the rate will increase with his income. In this tragic situation the innocent victim has to wait a lifetime before she receives the compensation the court has awarded, whilst the newly qualified doctor is faced with a debt, perhaps amounting to a fifth of his total career earnings, which he will work all his life to pay off. Doctors may be willing to help both these unfortunate people by subscribing to a fund to pay part at least of the damages. Accordingly we have set up a trust fund to which we invite members of the profession to subscribe. Contributions should be sent to us c/o Westminster Bank, 292 Wimborne Road, Bournemouth. To avoid expenses acknowledgements will only be sent on
request."
Parliament QUESTION TIME Capital Expenditure on Psychiatric Hospitals Capital expenditure on special hospitals, N.H.S. psychiatric hospitals, and psychiatric facilities at other N.H.S. hospitals during 1967-68 is estimated at about m’5 million or just over 10% of the total capital expenditure on N.H.S. hospitals. Cost of Antidepressive Drugs The ingredient cost of antidepressive drugs in 1966, as analysed in the Ministry of Health statistics and dispensed by chemists, was E3-13 million, compared with E2-78 million in 1965 and E2.37 million in 1964. Women Medical Students The number of women entering medical schools in 1966 was 570, compared with 523 in 1962.
Appointments
"
1. Serum- total-cholesterol.-This is the easiest lipid to measure in and gives some idea of lipoprotein synthesis. Levels are relatively higher in marasmus than in kwashiorkor.9 2. Urinary-creatinine/height index.- This has been proposed for grading the severity of protein depletion in P.c.m.10 It reflects muscle mass but has the disadvantage of requiring a 24-hour-urine collection. 3. We suggest that the serum-uric-acid level should be looked into as well. It has recently been reported significantly above normal in marasmus, but not in kwashiorkor.1’ It rises very high in fasting adults.12 We wish to make acknowledgements to C.S.I.R., and for U.S. Public Health Service grant AM 03995. serum
Departments of Medicine and Child Health, University of Cape Town, South Africa. 1. 2. 3. 4.
5. 6. 7. 8. 9. 10.
11. 12.
A. S. TRUSWELL J. D. L. HANSEN.
Truswell, A. S., Hansen, J. D. L., Wittmann, W., Wannenburg, P., Roberts, B., Watson, C. E. S. Afr. med. J. 1966, 40, 887. Truswell, A. S., Hansen, J. D. L., Wittmann, W. Int. Congr. Nutr. 1966, abstracts, p. 223. Truswell, A. S., Wannenburg, P., Wittmann, W., Hansen, J. D. L. Lancet, 1966, i, 1162. Truswell, A. S., Hansen, J. D. L., Freeseman, C., Smidt, T. F. S. Afr. med. J. 1963, 37, 527. Hansen, J. D. L. Proceedings of Colloquium on Protein Deficiencies and Calorie Deficiencies, Cambridge, 1967 (in the press). Hansen, J. D. L., Jenkinson, V. S. Afr. J. Lab. clin. Med. 1956, 2, 206. Ludmany, K., Csorba, S., Jezernicky, J. Z. Kinderheilk. 1965, 92, 299. Lewis, B., Hansen, J. D. L., Wittmann, W., Krut, L. H., Stewart, F. Am. J. clin. Nutr. 1964, 15, 161. Pretorius, P. J., Wehmeyer, A. S. S. Afr. med. J. 1966, 40, 240. Viteri, F. E., Arroyave, G., Béhar, M. Int. Congr. Nutr. 1966, abstracts, p. 46. Khalil, M., El-Khateeb, S., Aref, G. H., Gurgis, F. K. J. trop. Med. Hyg. 1967, 70, 11. Thomson, T. J., Runcie, J., Miller, V. Lancet, 1966, ii, 992.
M.B. Lond.: consultant clinical pathologist, Chelmsford hospital group. BRIERLEY, J. S. W., M.B. Leeds, D.P.H.: M.o.H., Huddersfield. NOALL, E. W. P., M.B. Lond., M.R.C.P., D.P.M.: consultant physician, Thames hospital group. PILKINGTON, T. L., M.R.C.S., D.P.M.: consultant psychiatrist, Gogarburn Hospital, Edinburgh. SMITH, R. S., M.B. Cantab., M.C.PATH. : consultant haematologist, Children’s Hospital, Sheffield.
ANTCLIFF, A. C.,
Manchester
Regional Hospital Board:
M.B. Baghdad, M.R.C.P., D.C.H.; consultant paediatrician, Oldham and district and Ashton, Hyde and Glossop hospital groups. ALLCOCK, E. A., M.B. Manc., M.SC. Minnesota, F.R.C.S., F.R.A.C.S., F.D.S. R.c.s.: consultant surgeon, South Cheshire hospital group. ATA, MOHAMMAD, M.B. Punjab, M.R.C.P.E., M.C.PATH. : consultant pathologist, with special experience in haematology, Rochdale and district
ABRAHAM, J. M.,
hospital group. GREEN, J. H., M.CH.ORTH. Lpool, F.R.C,S.E.: consultant traumatic and orthopxdic surgeon, Salford hospital group. MADDOCK, SHEILA G., M.B. Lpool: consultant geriatric physician, Salford hospital group. PITKEATHLEY, D. A., M.B. St. And., M.R.C.P.E., M.R.C.P.G.: consultant rheumatologist, R.H.B. hospitals and United Manchester Hospitals.
Regional Hospital Board, Scotland: CARLISLE, J. M., M.B. Glasg., D.P.M.: consultant psychiatrist, Leverndale Hospital. DONALD, J. R., M.B. Glasg., F.F.A. R.c.s.: consultant anxsthetist, Law and
Western
Stonehouse
Hospitals.
LINTON, A. L., M.B. Edin., M.R.C.P.E., M.R.C.P.G. renal disease, Western Infirmary, Glasgow.
Liverpool Regional Hospital
:
consultant
physician
in
Board:
CONWAY, C. F., M.B. N.u.I., F.F.A. R.C.S.: D.P.H., consultant anaathetist, Chester Royal Infirmary. D’NETTO, PHYLLIS E., M.R.C.P.E., M.R.C.P.G., D.OBST.: consultant geriatrician, Deva and Moston Hospitals. HARPER, PATRICK, M.B. Belf., D.P.M.: consultant psychiatrist, Rainhill Hospital. HART, S. M., M.B. N.U.I., F.F.A. R.c.s.: consultant anesthetist, Broadgreen Hospital.