412 Medication-associated thrombocytopenia
must also be excluded, and the elderly use more medicine than any other age-group.13 Of the five most frequently prescribed drugs for the elderly in 1966,5 three (tolbutamide, chlorothiazide, and hydrochlorothiazide) have been associated with thrombocytopenia. Other diseases associated with thrombocytopenia are also more common among the elderly. Also affecting the age distribution in I.T.P. is the age distribution of the population at risk. Only about 0-5% of the population is 85 years of age or older.5 All these factors bias the age distribution; and this, combined with other factors already mentioned, makes I.T.P. appear, at least, to be rare in the very elderly. Until a definitive diagnostic test is developed, it must be considered that I.T.P. may occur at any age, and that its prevalence may be the same in all age-groups. Therefore, I.T.P. should be considered seriously in differential diagnosis of any patient with thrombocytopenia, irrespective of age. Clinicians must review their concept of I.T.P. and epidemiologists their data.
National Institutes of Health, Bethesda, Maryland 20014, U.S.A. University of California San Francisco, San Francisco, California 94143, U.S.A. 1144 Sonoma Avenue, Santa Rosa, California 95405, U.S.A.
STEROIDS AND
SiR,—Goodall
et
GARY B. WEISS.
JOHN C. KLOCK. HARRY B. RICHARDSON.
GUILLAIN-BARRÉ SYNDROME al.14 reported that corticosteroids have
the clinical course of the Guillain-Barre defined by the criteria of Osler and Sidell. 15 These do not apply to polyneuritis of less acute onset or of a chronic, relapsing nature, which is regarded by some as a form of Guillain-Barre syndrome. We report a case of slowly progressive polyneuritis of Guillain-Barre type which responded unequivocally to treatment with prednino
effect
syndrome
on
as
sone.
An 18-year-old man was well until August, 1973, when hypoaathesia developed in the fingers and toes and was soon followed by mild weakness in the extremities. Generalised weakness progressed slowly with slight fluctuation over the next 7 months until he was barely able to walk, and hypoaesthesia had ascended to the knees and elbows. He noted increasing dyspnrea on exertion and occasional episodes of tachycardia with abrupt onset and cessation. On March 3, 1974, he entered the hospital, where examination revealed pronounced weakness of all muscle groups in the arms and legs, which was greater distally; diminished sensation distal to the knees and elbows; and areflexia. A complete myelogram was normal, and the cerebrospinal fluid contained 252 mg. of protein and no cells. An electromyogram showed evidence of mild, chronic, partial denervation in both proximal and distal muscle groups in the arms and legs. Motor conduction was slowed in median, ulnar, and peroneal nerves, and there were no ascending sensory potentials in median and ulnar nerves. Prednisone, 40 mg. every other day, was begun on March 22, 1974, but the dosage was tapered off to 10 mg. every other day by April 8, 1974, while his weakness progressed to complete loss of movement against gravity. Vital capacity steadily diminished from 45 litres on admission to 3 litres. On April 12, 1974, prednisone 100 mg. every other day was begun, and objective improvement in strength was noted within 2 days. By April 16 vital capacity had increased to 3-75 litres, and the patient was feeding himself. His strength continued to improve steadily, progressing from proximal to distal muscle groups and more rapidly in the arms than in the legs. By May 16 he was able to walk with crutches, and at discharge on June 5 he could walk on Prescription Drugs. The Drug Users: Background Papers. Washington, D.C., 1968. 14. Goodall, J. A. D., Kosmidis, J. C., Geddes, A. M. Lancet, 1974, i,
13. U.S. Task Force
524. 16.
Osler, L. D., Sidell, A. D. New Engl. J. Med. 1960, 262, 964.
without assistance. The dose of prednisone was tapered off from May 12 and had fallen to 20 mg. every other day by midJuly, when an increase in weakness was noted. 2 weeks later the patient was barely able to walk with crutches, but increasing the prednisone dose to 100 mg. every other day resulted in slow increase in strength to his former level. He is now maintained on 100 mg. every other day and is able to walk a quarter of a mile with a cane.
Except for the slow, progressive onset, this case has all the clinical and laboratory features of the Guillain-Barré syndrome. Several of the diagnostic criteria of Osler and Sidell are lacking, but these have been criticised by some workers 16-18as being too restrictive in view of the variability of sensory findings, bladder symptoms, and clinical course reported in many series, including that of Guillain.6 There can be little doubt that the course of our patient’s disease was affected by prednisone. After a 7-month progression to almost total paralysis, recovery began within 2 days of starting high-dose therapy. Relapse coincided with tapering off the prednisone and was reversed by increasing the dose. This response is similar to that reported by others in treatment of slowly progressive 20,21 A trial of high-dose and recurrent 22,23 polyneuritis. corticosteroid treatment in these two categories of polyneuritis therefore seems justifiable. Division of Neurology, Dartmouth-Hitchcock Medical Center, R. L. SULLIVAN Hanover, New Hampshire 03755, A. G. REEVES. U.S.A.
NATURAL ŒSTROGENS AND ANTITHROMBIN-III LEVELS SiR,-The association of low serum-antithrombin-iii levels with the administration of oestrogens in the form of combination oral contraceptives was first noted by von Kaulla and von KauUa.24 Since then, several reports have confirmed this observation. 25-28 Antithrombin ill is believed to be the main antithrombin in plasma and serum. Egeberg 29 linked antithrombin-ni levels with thrombosis in a family with a hereditary thrombotic diathesis and very low antithrombin-ni levels. A similar family has been reported by others.30 The fall in antithrombin-ni activity during oestrogen therapy may therefore be relevant to the association between these drugs and thrombosis. To our knowledge antithrombin-ni levels in patients taking " natural" cestrogens have not been reported. Antithrombin-m levels were estimated by the method of von Kaulla and von Kaulla 24 in five groups of subjects. Nineteen healthy young White women receiving no medication and twenty healthy young White women on combination type oral contraceptives were studied. Various commercial preparations were used, but the cestrogen Wiederholt, W. C., Mulder, D. W., Lambert, E. H. Proc. Staff meet. Mayo Clin. 1964, 39, 427. 17. Marshall, J. Brain, 1963, 86, 55. 18. McFarland, H. R., Heller, G. L. Archs Neurol. 1966, 14, 196. 19. Guillain, G. Archs Neurol. Psychiat., Chicago, 1936, 36, 975. 20. Hinman, R. C., Magee, K. R. Ann. intern. Med. 1967, 67, 1007. 21. DeVivo, D. C., Engel, W. K. J. Neurol. Neurosurg. Psychiat. 1970, 33, 62. 22. Austin, J. H. Brain, 1958, 81, 157. 23. Thomas, P. K., Lascelles, R. G., Hallpike, J. F., Hewer, R. L. ibid. 1969, 92, 589. 24. von Kaulla, E., von Kaulla, K. N. Am. J. clin. Path. 1967, 48, 69. 25. Fagerhol, M. K., Abildgaard, U. Scand. J. Hœmat. 1970, 7, 10. 26. Fagerhol, M. K., Abildgaard, U., Bergsjo, P., Jacobsen, J. H. Lancet, 1970, i, 1175. 27. Howie, P. W., Mallinson, A. C., Prentice, C. R. M., Horne, C. H. W., McNicol, G. P. ibid. 1970, ii, 1329. 28. von Kaulla, E., Droegemeuller, W., Aoki, N., von Kaulla, K. N. Am. J. Obstet. Gynec. 1971, 109, 868. 29. Egeberg, O. Thromb. Diath. Hœmorrh. 1965, 13, 516. 30. van der Meer, J., Stoepman-van Dalen, E. A., Jensen, J. M. S. J. clin. Path. 1973, 26, 532. 16.
413 component was the same (ethinyloestradiol 0-05 mg.) in all except one patient who received’Ovanon ’, which contains mestranol 0-075 mg. A group of twenty menopausal women, none of whom had previously been treated with hormones, were studied as older controls. Their mean with a group of twenty menopausal women who had been on treatment withPremarin’ (conjugated equine oestrogen) for at least one year. The mean age of this group was 50-25 years. Treatment consisted of premarin 1-25 mg. daily in 3-week cyclic periods. The final group comprised twenty women in the third trimester of pregnancy. Antithrombin-III levels in the pregnant women were reduced below those recorded for normal young nonpregnant controls (38.5 ±3.3 69-3 ±3-6 seconds; p < 0’001); this reduction was of similar order to that seen in the group on oral contraceptives (38-5 ±3-3 vs 46-9 ±3’8 seconds). The value for the group on oral contraceptives did not differ significantly from that for the pregnant group (0-05 >?< 0-1). The antithrombin-in levels in the untreated menopausal women (59-7 ±4-8 seconds) showed no significant difference when compared with the levels in young women not taking oral contraceptives (69-3±3-6 seconds; r < 0°1). Premarin administration had no effect The values in the treated on the antithrombin-m level. and control menopausal groups were 57-1±5’4 and As expected, a 59-7±4-8 seconds, respectively (P>0-1). statistically significant fall (P< 0-001) in antithrombin-in level was induced by contraceptive steroids. The mean values decreased from 69-3±3-6 seconds in the young controls to 46-9 ±3-8 seconds in women on oral contraception. Thus, premarin seems to have no effect on the antithrombin-in levels in menopausal women. However, pregnant women demonstrated a striking reduction in age
was
66-9 years.
They
were
compared
antithrombin-m levels, as did young women on combination oral contraceptives. The depressant effect of pregnancy on antithrombin-in levels has been reported 31,32 and is presumably due to the endogenous production of natural oestrogen. The reason for this difference is not clear, and further studies are required. The observed lack of effect of exogenous natural cestrogens on antithrombin ill may The have important clinical implications, however. substitution of a natural oestrogen for.synthetic ones might minimise the risk of thrombosis associated with their use. Department of Hæmatology, Medical School, University of Natal, Durban, South Africa.
H. B. W. GREIG.
Chelmsford Medical Centre,
Durban, South Africa.
M. NOTELOWITZ.*
APLASTIC ANÆMIA ASSOCIATED WITH LITHIUM SIR,—Dr Lazarus and his colleagues (Jan. 18, p. 160), while commenting on the role of lithium in the treatment of thyrotoxicosis, mentioned that lithium-related blood dyscrasias have not been reported. I should like to call attention to a case discussed by Hussain et al. 33 A 50-yearold woman developed a fatal aplastic anaemia in association with the use of lithium carbonate. Although a causal relationship could not be established and although the usual " Present address: Department of Obstetrics and Gynecology, University of Florida College of Medicine, Gainesville, Florida, U.S.A 31. Peterson, R. A., Krull, P. E., Finley, P., Ettinger, M. G. Am. J. clin. Path. 1970, 53, 468. 32. Zuck, T. F., Bergin, J. J., Raymond, J. M., Dwyre, W. R. Surgery Gynec. Obstet. 1971, 133, 609. 33. Hussain, M. Z., Khan, A. G., Chaudry, Z. A. Can. med. Ass. J.
1973, 108,
724.
effect of lithium on the hsematopoietic systems is a benign, reversible leucocytosis,34,35 the possibility of severe reactions exists. Department of Psychiatry, University of Wisconsin Center for Health Sciences,
Madison, Wisconsin 53706, U.S.A.
J. W. JEFFERSON.
Obituary JOHN HAMILTON BARCLAY M.D., M.S.Durh., F.R.C.S. Prof. J. Hamilton Barclay, emeritus professor of surgery in the University of Durham, died on Feb. 3 at the age of 88. He received his medical education in the University of Durham College of Medicine, Newcastle upon Tyne, where he graduated M.B. in 1911, M.S. in 1915, and M.D. in 1919. He became F.R.c.s. in 1914, and served throughout the 1914-18 war in France, commissioned in the R.A.M.C., in field ambulance and casualty-clearing stations. He was appointed to the honorary staff of the Newcastle upon Tyne Royal Victoria Infirmary in 1920 as assistant surgeon, and from 1929 he served as full consultant until his retirement in 1947. During his career he was consulting surgeon to several other hospitals in the North-East, including the Fleming Memorial Hospital for Sick Children, the Princess Mary Maternity Hospital, Durham County Hospital, and the Ingham Infirmary, South Shields. He was professor in the University of Durham from 1944 to 1947, being the last of a distinguished line of parttime professors of surgery in Newcastle. After his retirement, at the inception of the National Health Service, he became pastoral visitor and surgical adviser to the Newcastle Regional Hospital Board. He was popular with students, and was a past president of their medical society. His ward-rounds and outpatient sessions were always well attended, and his teaching, in the Morisonian tradition essentially clinical and practical, was based on his personal experience. Trained in the days before specialisation, he gained a wide experience of all surgical conditions, and became a sound and successful general surgeon who was in constant demand by general practitioners for the treatment of themselves and their
families. He was an active member of several local medical societies and of the Association of Surgeons of Great Britain, and a past president of the North of England Surgical Society; he made valuable contributions to their discussions and was always a stimulus to his younger colleagues. Long after his retirement he maintained an intense interest in the advances of surgery, and his presence at clinical meetings ceased only when his total blindness made it impossible for him to attend. Professor Barclay was a kind and humane man, a practising Christian whose principles permeated all aspects of his life. His patients trusted him implicitly, and the nursing staff liked working with him and respected him. A man of the highest character, with a somewhat shy but friendly disposition, he was held in the greatest regard by all his colleagues, who valued his opinion and appreciated to the full all the contributions he had made to the work of the hospital. He is survived by one married daughter.
G. Y. F. 34. Shopsin, B., Friedmann, R.,
Gershon, S. Clin. Pharmac. Ther. 1971,
12, 923. 35.
Murphy,
D.
L., Goodwin, F. K., Bunney, W.
1971, 127, 1159.
E. Am.
J. Psychiat.
must also be excluded, and the elderly use more medicine than any other age-group.13 Of the five most frequently prescribed drugs for the elderly in 1966,5 three (tolbutamide, chlorothiazide, and hydrochlorothiazide) have been associated with thrombocytopenia. Other diseases associated with thrombocytopenia are also more common among the elderly. Also affecting the age distribution in I.T.P. is the age distribution of the population at risk. Only about 0-5% of the population is 85 years of age or older.5 All these factors bias the age distribution; and this, combined with other factors already mentioned, makes I.T.P. appear, at least, to be rare in the very elderly. Until a definitive diagnostic test is developed, it must be considered that I.T.P. may occur at any age, and that its prevalence may be the same in all age-groups. Therefore, I.T.P. should be considered seriously in differential diagnosis of any patient with thrombocytopenia, irrespective of age. Clinicians must review their concept of I.T.P. and epidemiologists their data.
National Institutes of Health, Bethesda, Maryland 20014, U.S.A. University of California San Francisco, San Francisco, California 94143, U.S.A. 1144 Sonoma Avenue, Santa Rosa, California 95405, U.S.A.
STEROIDS AND
SiR,—Goodall
et
GARY B. WEISS.
JOHN C. KLOCK. HARRY B. RICHARDSON.
GUILLAIN-BARRÉ SYNDROME al.14 reported that corticosteroids have
the clinical course of the Guillain-Barre defined by the criteria of Osler and Sidell. 15 These do not apply to polyneuritis of less acute onset or of a chronic, relapsing nature, which is regarded by some as a form of Guillain-Barre syndrome. We report a case of slowly progressive polyneuritis of Guillain-Barre type which responded unequivocally to treatment with prednino
effect
syndrome
on
as
sone.
An 18-year-old man was well until August, 1973, when hypoaathesia developed in the fingers and toes and was soon followed by mild weakness in the extremities. Generalised weakness progressed slowly with slight fluctuation over the next 7 months until he was barely able to walk, and hypoaesthesia had ascended to the knees and elbows. He noted increasing dyspnrea on exertion and occasional episodes of tachycardia with abrupt onset and cessation. On March 3, 1974, he entered the hospital, where examination revealed pronounced weakness of all muscle groups in the arms and legs, which was greater distally; diminished sensation distal to the knees and elbows; and areflexia. A complete myelogram was normal, and the cerebrospinal fluid contained 252 mg. of protein and no cells. An electromyogram showed evidence of mild, chronic, partial denervation in both proximal and distal muscle groups in the arms and legs. Motor conduction was slowed in median, ulnar, and peroneal nerves, and there were no ascending sensory potentials in median and ulnar nerves. Prednisone, 40 mg. every other day, was begun on March 22, 1974, but the dosage was tapered off to 10 mg. every other day by April 8, 1974, while his weakness progressed to complete loss of movement against gravity. Vital capacity steadily diminished from 45 litres on admission to 3 litres. On April 12, 1974, prednisone 100 mg. every other day was begun, and objective improvement in strength was noted within 2 days. By April 16 vital capacity had increased to 3-75 litres, and the patient was feeding himself. His strength continued to improve steadily, progressing from proximal to distal muscle groups and more rapidly in the arms than in the legs. By May 16 he was able to walk with crutches, and at discharge on June 5 he could walk on Prescription Drugs. The Drug Users: Background Papers. Washington, D.C., 1968. 14. Goodall, J. A. D., Kosmidis, J. C., Geddes, A. M. Lancet, 1974, i,
13. U.S. Task Force
524. 16.
Osler, L. D., Sidell, A. D. New Engl. J. Med. 1960, 262, 964.
without assistance. The dose of prednisone was tapered off from May 12 and had fallen to 20 mg. every other day by midJuly, when an increase in weakness was noted. 2 weeks later the patient was barely able to walk with crutches, but increasing the prednisone dose to 100 mg. every other day resulted in slow increase in strength to his former level. He is now maintained on 100 mg. every other day and is able to walk a quarter of a mile with a cane.
Except for the slow, progressive onset, this case has all the clinical and laboratory features of the Guillain-Barré syndrome. Several of the diagnostic criteria of Osler and Sidell are lacking, but these have been criticised by some workers 16-18as being too restrictive in view of the variability of sensory findings, bladder symptoms, and clinical course reported in many series, including that of Guillain.6 There can be little doubt that the course of our patient’s disease was affected by prednisone. After a 7-month progression to almost total paralysis, recovery began within 2 days of starting high-dose therapy. Relapse coincided with tapering off the prednisone and was reversed by increasing the dose. This response is similar to that reported by others in treatment of slowly progressive 20,21 A trial of high-dose and recurrent 22,23 polyneuritis. corticosteroid treatment in these two categories of polyneuritis therefore seems justifiable. Division of Neurology, Dartmouth-Hitchcock Medical Center, R. L. SULLIVAN Hanover, New Hampshire 03755, A. G. REEVES. U.S.A.
NATURAL ŒSTROGENS AND ANTITHROMBIN-III LEVELS SiR,-The association of low serum-antithrombin-iii levels with the administration of oestrogens in the form of combination oral contraceptives was first noted by von Kaulla and von KauUa.24 Since then, several reports have confirmed this observation. 25-28 Antithrombin ill is believed to be the main antithrombin in plasma and serum. Egeberg 29 linked antithrombin-ni levels with thrombosis in a family with a hereditary thrombotic diathesis and very low antithrombin-ni levels. A similar family has been reported by others.30 The fall in antithrombin-ni activity during oestrogen therapy may therefore be relevant to the association between these drugs and thrombosis. To our knowledge antithrombin-ni levels in patients taking " natural" cestrogens have not been reported. Antithrombin-m levels were estimated by the method of von Kaulla and von Kaulla 24 in five groups of subjects. Nineteen healthy young White women receiving no medication and twenty healthy young White women on combination type oral contraceptives were studied. Various commercial preparations were used, but the cestrogen Wiederholt, W. C., Mulder, D. W., Lambert, E. H. Proc. Staff meet. Mayo Clin. 1964, 39, 427. 17. Marshall, J. Brain, 1963, 86, 55. 18. McFarland, H. R., Heller, G. L. Archs Neurol. 1966, 14, 196. 19. Guillain, G. Archs Neurol. Psychiat., Chicago, 1936, 36, 975. 20. Hinman, R. C., Magee, K. R. Ann. intern. Med. 1967, 67, 1007. 21. DeVivo, D. C., Engel, W. K. J. Neurol. Neurosurg. Psychiat. 1970, 33, 62. 22. Austin, J. H. Brain, 1958, 81, 157. 23. Thomas, P. K., Lascelles, R. G., Hallpike, J. F., Hewer, R. L. ibid. 1969, 92, 589. 24. von Kaulla, E., von Kaulla, K. N. Am. J. clin. Path. 1967, 48, 69. 25. Fagerhol, M. K., Abildgaard, U. Scand. J. Hœmat. 1970, 7, 10. 26. Fagerhol, M. K., Abildgaard, U., Bergsjo, P., Jacobsen, J. H. Lancet, 1970, i, 1175. 27. Howie, P. W., Mallinson, A. C., Prentice, C. R. M., Horne, C. H. W., McNicol, G. P. ibid. 1970, ii, 1329. 28. von Kaulla, E., Droegemeuller, W., Aoki, N., von Kaulla, K. N. Am. J. Obstet. Gynec. 1971, 109, 868. 29. Egeberg, O. Thromb. Diath. Hœmorrh. 1965, 13, 516. 30. van der Meer, J., Stoepman-van Dalen, E. A., Jensen, J. M. S. J. clin. Path. 1973, 26, 532. 16.
413 component was the same (ethinyloestradiol 0-05 mg.) in all except one patient who received’Ovanon ’, which contains mestranol 0-075 mg. A group of twenty menopausal women, none of whom had previously been treated with hormones, were studied as older controls. Their mean with a group of twenty menopausal women who had been on treatment withPremarin’ (conjugated equine oestrogen) for at least one year. The mean age of this group was 50-25 years. Treatment consisted of premarin 1-25 mg. daily in 3-week cyclic periods. The final group comprised twenty women in the third trimester of pregnancy. Antithrombin-III levels in the pregnant women were reduced below those recorded for normal young nonpregnant controls (38.5 ±3.3 69-3 ±3-6 seconds; p < 0’001); this reduction was of similar order to that seen in the group on oral contraceptives (38-5 ±3-3 vs 46-9 ±3’8 seconds). The value for the group on oral contraceptives did not differ significantly from that for the pregnant group (0-05 >?< 0-1). The antithrombin-in levels in the untreated menopausal women (59-7 ±4-8 seconds) showed no significant difference when compared with the levels in young women not taking oral contraceptives (69-3±3-6 seconds; r < 0°1). Premarin administration had no effect The values in the treated on the antithrombin-m level. and control menopausal groups were 57-1±5’4 and As expected, a 59-7±4-8 seconds, respectively (P>0-1). statistically significant fall (P< 0-001) in antithrombin-in level was induced by contraceptive steroids. The mean values decreased from 69-3±3-6 seconds in the young controls to 46-9 ±3-8 seconds in women on oral contraception. Thus, premarin seems to have no effect on the antithrombin-in levels in menopausal women. However, pregnant women demonstrated a striking reduction in age
was
66-9 years.
They
were
compared
antithrombin-m levels, as did young women on combination oral contraceptives. The depressant effect of pregnancy on antithrombin-in levels has been reported 31,32 and is presumably due to the endogenous production of natural oestrogen. The reason for this difference is not clear, and further studies are required. The observed lack of effect of exogenous natural cestrogens on antithrombin ill may The have important clinical implications, however. substitution of a natural oestrogen for.synthetic ones might minimise the risk of thrombosis associated with their use. Department of Hæmatology, Medical School, University of Natal, Durban, South Africa.
H. B. W. GREIG.
Chelmsford Medical Centre,
Durban, South Africa.
M. NOTELOWITZ.*
APLASTIC ANÆMIA ASSOCIATED WITH LITHIUM SIR,—Dr Lazarus and his colleagues (Jan. 18, p. 160), while commenting on the role of lithium in the treatment of thyrotoxicosis, mentioned that lithium-related blood dyscrasias have not been reported. I should like to call attention to a case discussed by Hussain et al. 33 A 50-yearold woman developed a fatal aplastic anaemia in association with the use of lithium carbonate. Although a causal relationship could not be established and although the usual " Present address: Department of Obstetrics and Gynecology, University of Florida College of Medicine, Gainesville, Florida, U.S.A 31. Peterson, R. A., Krull, P. E., Finley, P., Ettinger, M. G. Am. J. clin. Path. 1970, 53, 468. 32. Zuck, T. F., Bergin, J. J., Raymond, J. M., Dwyre, W. R. Surgery Gynec. Obstet. 1971, 133, 609. 33. Hussain, M. Z., Khan, A. G., Chaudry, Z. A. Can. med. Ass. J.
1973, 108,
724.
effect of lithium on the hsematopoietic systems is a benign, reversible leucocytosis,34,35 the possibility of severe reactions exists. Department of Psychiatry, University of Wisconsin Center for Health Sciences,
Madison, Wisconsin 53706, U.S.A.
J. W. JEFFERSON.
Obituary JOHN HAMILTON BARCLAY M.D., M.S.Durh., F.R.C.S. Prof. J. Hamilton Barclay, emeritus professor of surgery in the University of Durham, died on Feb. 3 at the age of 88. He received his medical education in the University of Durham College of Medicine, Newcastle upon Tyne, where he graduated M.B. in 1911, M.S. in 1915, and M.D. in 1919. He became F.R.c.s. in 1914, and served throughout the 1914-18 war in France, commissioned in the R.A.M.C., in field ambulance and casualty-clearing stations. He was appointed to the honorary staff of the Newcastle upon Tyne Royal Victoria Infirmary in 1920 as assistant surgeon, and from 1929 he served as full consultant until his retirement in 1947. During his career he was consulting surgeon to several other hospitals in the North-East, including the Fleming Memorial Hospital for Sick Children, the Princess Mary Maternity Hospital, Durham County Hospital, and the Ingham Infirmary, South Shields. He was professor in the University of Durham from 1944 to 1947, being the last of a distinguished line of parttime professors of surgery in Newcastle. After his retirement, at the inception of the National Health Service, he became pastoral visitor and surgical adviser to the Newcastle Regional Hospital Board. He was popular with students, and was a past president of their medical society. His ward-rounds and outpatient sessions were always well attended, and his teaching, in the Morisonian tradition essentially clinical and practical, was based on his personal experience. Trained in the days before specialisation, he gained a wide experience of all surgical conditions, and became a sound and successful general surgeon who was in constant demand by general practitioners for the treatment of themselves and their
families. He was an active member of several local medical societies and of the Association of Surgeons of Great Britain, and a past president of the North of England Surgical Society; he made valuable contributions to their discussions and was always a stimulus to his younger colleagues. Long after his retirement he maintained an intense interest in the advances of surgery, and his presence at clinical meetings ceased only when his total blindness made it impossible for him to attend. Professor Barclay was a kind and humane man, a practising Christian whose principles permeated all aspects of his life. His patients trusted him implicitly, and the nursing staff liked working with him and respected him. A man of the highest character, with a somewhat shy but friendly disposition, he was held in the greatest regard by all his colleagues, who valued his opinion and appreciated to the full all the contributions he had made to the work of the hospital. He is survived by one married daughter.
G. Y. F. 34. Shopsin, B., Friedmann, R.,
Gershon, S. Clin. Pharmac. Ther. 1971,
12, 923. 35.
Murphy,
D.
L., Goodwin, F. K., Bunney, W.
1971, 127, 1159.
E. Am.
J. Psychiat.
