BRITISH MEDICAL JOURNAL
16 OCTOBER 1976
The main components of timber-cellulose, hemicellulose, and lignin-are non-irritant and non-sensitising. Minor components such as resins, terpenes, and oils may cause allergic contact dermatitis in those handling and processing wood. In practice, chemicals such as preservatives, epoxy resins, polishes, varnishes, and dyes cause more dermatitis in woodworkers than the actual woods themselves. In general, allergies and both dermatitis and mucosal irritation from wood species are almost exclusively the prerogative of lumbermen and woodworkers. Handlers of the finished product are generally safe from toxic effects, though contact with aiticles made from highly allergic woods such as rosewood, rengas, or obeche has occasionally given rise to symptoms. The irritants of woods are mostly contained in the sap, so that the lumberjack bears the brunt of the chemical attack and may develop intense erythema and blistering of the exposed skin. The heartwood tends to contain the sensitisers, and allergic sensitivity is most commonly seen in woodworkers exposed to fine dust in enclosed spaces. The distribution is typical of airborne contact dermatitis, with selection of the dorsums of the hands and arms and swelling and erythema and scaling of eyelids, face, and genitalia. The eruption may become chronic after repeated exposure. Patch testing to moistened wood dust usually discloses the culprit sensitiser, but testing of controls is advisable. Mucosal irritation; sneezing, sore throat, conjunctivitis. and even epistaxis; nausea and vomiting may occur in susceptible individuals exposed to specific (and usually tropical) woods. Attacks of asthma may be delayed for several hours after exposure. This may reduce the degree of suspicion, and inhalation tests with aqueous extracts of dust seem to be the only really reliable way of establishing the diagnosis. Sequoia, cork oak, and maple may cause progressive pneumonitis, so that avoidance of established allergens should be mandatory. I 2
Kerdal-Vegas, F, Dermatologia Venezolana, 1965, 4, 10. Woods, B, and Calnan, C D, British of Dermatology, 1976, 94, suppl 13.
J7ournal
Juvenile rheumatoid arthritis-a viral disease? Of all the forms of polyarthritis which have been investigated for an infectious aetiology the most likely seems juvenile rheumatoid arthritis (Still's disease) in its acute form. Fever (often high), rash, lymphadenopathy, splenomegaly, pericarditis, pleuritis, and abdominal pain all occur,'-4 and may in very young children overshadow the joint manifestations. This clinical picture strongly suggests a disseminated infection. In terms of immunopathology juvenile rheumatoid arthritis has many features in common with the adult condition, including complement consumption in affected joints5 and often circulating autoantibodies,6 which may need special methods of detection.7 These findings, too, are entirely consistent with an infective aetiology.8 Nevertheless, like its adult counterpart, juvenile rheumatoid arthritis is a syndrome-an impression reinforced by epidemiological studies9 -and its heterogeneous nature means that clues to its pathogenesis may not apply to all forms of the disease. The evidence linking juvenile rheumatoid arthritis with any specific infection is still scanty. Isolated case reports do appear: illnesses like Still's disease have been described10 in a 16-year-old boy with a rise in antibody titres to Coxsackie
901
B3 and A9 viruses and in a 9-year-old girl from whom an adenovirus 7 was isolated. Furthermore, an increase in antibody titres to rubella virus has been reported in children with juvenile rheumatoid arthritis,"12 and rubella virus antigen was detected in 33% of the synovial effusions examined from these patients.'2 Sore throats are prominent in Still's disease of adults,'314 a disorder which clinically is almost identical with that seen in children in its most characteristic form.'5 All such observations must be interpreted with caution. A whole range of viral infections are accompanied by joint complaints,'6 and the diagnosis of juvenile rheumatoid arthritis can be made with confidence only when the clinical and laboratory features meet accepted criteria'7 18; of these the duration ofarthritis is especially relevant. In addition, antibody titres are often misleading: they may simply reflect the general increase in serum gammaglobulin concentrations commonly seen in connective tissue disorders.'9 Such patients produce an abnormally high secondary antibody response to diphtheria and tetanus toxoid20 so that an exaggerated anamnestic response to viral antigens might not be expected. More decisively, there is no evidence that the clinical course of rubella in patients with juvenile rheumatoid arthritis differs from that in normal children."l 21 Incrimination of common endemic viruses in the pathogenesis of juvenile rheumatoid arthritis is particularly difficult. After all, most children become infected with these, and reactivation may be a non-specific accompaniment of an entirely unrelated disease. The variable exposure to these viruses in different populations could account for the wide variation in viral antibody titres which have been recorded in children with juvenile rheumatoid arthritis." 1219 One possibility is that (as has been suggested22 in the demyelinating diseases) the cell-mediated immune responses to viruses may be defective in these children, so accounting for abnormal persistence of an inflammatory response. Nevertheless, there is little evidence that this sort of defect exists.23 24 The possibility of an infectious aetiology is also raised by the association which has been described between the HLA antigen B27 and juvenile rheumatoid arthritis.25-28 This association has not been found by all investigators29 30reflecting the varied nature of the diseases termed "juvenile rheumatoid arthritis." Nevertheless, B27 is probably commoner in those patients who have developed or are likely to develop ankylosing spondylitis,25 26 and indeed this observation was presaged by an earlier study which showed an increased incidence of ankylosing spondylitis in the families of children with juvenile rheumatoid arthritis.31 Furthermore, individuals who inherit the antigen show an increased susceptibility to polyarthritis after certain bacterial infections32; possibly HLA antigens on the cell surface may be modified by virus, thereby provoking an immune reaction by T-lymphocytes.33 Generally, attempts to identify viruses in long-term cultures of synovial membrane cells have been as fruitless in juvenile as in adult forms of rheumatoid arthritis.34 3 All the possible approaches have not yet been exhausted,36 however, and there may be a case for extending both virological and related immunological studies in juvenile rheumatoid arthritis. If this is to be done the children should be investigated in the acute stages of their illness37 with an open mind as to how it will eventually be classified. Ansell, B M, and Bywaters, E G L, in
Textbook of the Rheumatic Diseases, 4th ed, ed W S C Copeman, p 323. Edinburgh and London, Livingstone, 1969. 2 Schaller, J, and Wedgwood, R J, Pediatrics, 1972, 50, 940. 3Bujak, J S, et al, Medicine, 1973, 52, 431.
902
Goel, K M, and Shanks, R A, Annals of the Rheumatic Diseases, 1974, 33, 25. Rynes, R I, et al, Arthritis and Rheumatism, 1976, 19, 161. 6 Bianco, N E, et al, Arthritis and Rheumatism, 1971, 14, 685. 7Moore, T, Dorner, R W, and Zuckner, J, Annals of the Rheumatic Diseases, 1974, 33, 255. 8 Ziff, M, Federation Proceedings, 1973, 32, 131. 9 Sullivan, D B, Cassidy, J T, and Petty, R E, Arthritis and Rheumatism, 1975, 18, 251. 11 Rahal, J J, Millian, S J, and Noriega, E R,J7ournal of the American Medical Association, 1976, 235, 2496. 11 Linnemann, C C, Jr, et al, Annals of the Rheumatic Diseases, 1975, 34, 354. 12 Ogra, P L, et al, Lancet, 1975, 1, 1157. 13 Fabricant, M S, Chandor, S B, and Friou, G J, J'ournal of the American Medical Association, 1973, 225, 273. 14 Sills, E M, Medical Clinics of North America, 1975, 59, 1497. 11 Bywaters, E G L, Annals of the Rheumatic Diseases, 1971, 30, 121. 16 Smith, J W, and Sanford, J P, Annals of Internal Medicine, 1967, 67, 651. 17 Ansell, B M, and Bywaters, E G L, Bulletin on Rheumatic Diseases, 1959, 9, 189. 18 Brewer, E J, et al, Bulletin on Rheumatic Diseases, 1973, 23, 712. 19 Cassidy, J J, et al, Pediatrics, 1974, 54, 239. 20 H0yeraal, H M, and Mellbye, 0 J, Annals of the Rheumatic Diseases, 1974, 33, 248. 21 Schnitzer, T, Howard, A, and Ansell, B M, in preparation. 22 Medical Research Council, Multiple Sclerosis Research. London, HMSO, 1976. 23 H0yeraal, H M, Fr0land, S S, and Wisl0ff, F, Scandinavian J7ournal of Immunology, 1975, 4, 801. 24 Jennings, J, Annals of the Rheumatic Diseases, 1975, 34, 196. 25 Edmonds, J, et al, Annals of the Rheumatic Diseases, 1974, 33, 576. 26 Edmonds, J, et al, Annals of the Rheumatic Diseases, 1974, 33, 289. 27 Buc, M, Nyulassy, S, and Stefanovic, J, Tissue Antigens, 1974, 4, 395. 28 Rachelefsky, G S, et al, New England J'ournal of Medicine, 1974, 290, 892. 29 Nissila, M, Elomaa, L, and Tiilikainen, A, New England J3ournal of Medicine, 1975, 292, 430. 30 Gibson, D J, et al, New England Journal of Medicine, 1975, 293, 638. 31 Ansell, B M, Bywaters, E G L, and Lawrence, J S, Annals of the Rheumatic Diseases, 1962, 21, 243. 32 Brewerton, D A, ed, Annals of the Rheumatic Diseases, 1975, 34, suppl 1. 33 Doherty, P C, and Zinkernagel, R M, Lancet, 1975, 1, 1406. 34 Phillips, P E, Journal of Experimental Medicine, 1971, 134, 3135. 35 Middleton, P J, and Highton, T C, Annals of the Rheumatic Diseases, 1975, 34, 369. 36 Hamerman, D, Annals of the New York Academy of Sciences, 1975, 256, 25. 37 Schumacher, H R, and Kitridou, R C, Arthritis and Rheumatism, 1972, 15, 465.
Dealing with alcoholism Alcoholism provides a common ground for physicians, psychiatrists, accident surgeons, physiologists, and geneticists. Together with other experts representatives of these disciplines met last month at the Institute of Psychiatry in London to discuss their mutual interest. Despite the intense specialisation which each group is bringing to bear on its own facet of the problem, the impression left by the meeting was that these preoccupations were bringing the various workers closer together, rather than the opposite. Recent studies on mice had confirmed that acetaldehyde metabolism may hold the key to dependence and possibly to individual susceptibility to alcohol intoxication. Factors such as age and sex as well as the genetic strain seemed to be important. This added point to a full review of genetic factors
BRITISH MEDICAL JOURNAL
16 OCTOBER 1976
in human alcoholism, though the conclusion seemed to weigh against heredity's being a major determinant in an unclearly defined syndrome with social as well as medical features. A discussion of the medical markers of alcoholism (heavily weighted on reports of liver cirrhosis) suggested that these may be somewhat less reliable than is usually assumed. This lack of objective definition when it might most have been expected paved the way for a consideration of the role of habit, as seen by a psychologist, in controlling behaviour. Together with an acceptance of social and cultural pressures in the development of drinking habits early in life, it set the scene for a vigorous discussion on liquor licensing laws and the recent proposals1 2 to amend them. Dr Wolfgang Schmidt presented epidemiological evidence gathered at the Alcohol Research Foundation in Toronto which emphasised the association between per caput consumption of alcohol and harmful drinking, and the direct relation of both to availability of alcohol. This matter was raised in discussion during a session ofwhich Dr Christopher Clayson was chairman. Increased availability by extension of licensing hours, he argued, might not necessarily raise consumption nor increase drunkenness if it relieved "the pressure to drink," which Dr Clayson saw as such an undesirable feature of life in Scotland. Another controversial issue concerned the results of treatment, with particular reference to the analysis3 of largescale statistics concerning men attending community treatment centres in the Uniited States. This confirmed reports that remission (as evidenced by a return to normal drinking or reduced consumption attended by improved social relations) is far more frequent than total abstinence, the usual goal of treatment. Methods of working towards such remission were discussed, as well as the underlying psychological theories of learning which gave scientific ground to a re-educative approach to treatment. Learning theory contrasts sharply with the current preoccupation with psychodynamically orientated group work so evident in most alcohol treatment units in Britain and elsewhere. Nevertheless, the re-education of alcoholics to a different life style is now being tried in some practices. Another heartening trend is collaboration between physicians and psychiatrists, described by some speakers, even if it is only beginning to emerge here. Discussion of changes in the approach to treatment naturally led to a debate about the pattern of services needed in Britain if the rising tide of alcoholism is to be stemmed and the public is to be made more aware of the facts about the disease. Who is to compose the teams and who is to lead them? One point that should not need arguing is that whoever does head the team should have the relevant knowledge not only from his own field but also from that of his colleagues.
2 3
The Erroll Report: Report of the Departmental Committee on Liquor Licensing, Cmnd 5154. London, HMSO, 1972. The Clayson Report: Report of the Departmental Committee on Scottish Licensing Law, Cmnd 5354. Edinburgh, HMSO, 1973. Armor, D J, Polich, J M, and Stambul, H B, Alcoholism and Treatment, pp 1-216. Santa Monica, Rand Corporation, 1976.
16 OCTOBER 1976
The main components of timber-cellulose, hemicellulose, and lignin-are non-irritant and non-sensitising. Minor components such as resins, terpenes, and oils may cause allergic contact dermatitis in those handling and processing wood. In practice, chemicals such as preservatives, epoxy resins, polishes, varnishes, and dyes cause more dermatitis in woodworkers than the actual woods themselves. In general, allergies and both dermatitis and mucosal irritation from wood species are almost exclusively the prerogative of lumbermen and woodworkers. Handlers of the finished product are generally safe from toxic effects, though contact with aiticles made from highly allergic woods such as rosewood, rengas, or obeche has occasionally given rise to symptoms. The irritants of woods are mostly contained in the sap, so that the lumberjack bears the brunt of the chemical attack and may develop intense erythema and blistering of the exposed skin. The heartwood tends to contain the sensitisers, and allergic sensitivity is most commonly seen in woodworkers exposed to fine dust in enclosed spaces. The distribution is typical of airborne contact dermatitis, with selection of the dorsums of the hands and arms and swelling and erythema and scaling of eyelids, face, and genitalia. The eruption may become chronic after repeated exposure. Patch testing to moistened wood dust usually discloses the culprit sensitiser, but testing of controls is advisable. Mucosal irritation; sneezing, sore throat, conjunctivitis. and even epistaxis; nausea and vomiting may occur in susceptible individuals exposed to specific (and usually tropical) woods. Attacks of asthma may be delayed for several hours after exposure. This may reduce the degree of suspicion, and inhalation tests with aqueous extracts of dust seem to be the only really reliable way of establishing the diagnosis. Sequoia, cork oak, and maple may cause progressive pneumonitis, so that avoidance of established allergens should be mandatory. I 2
Kerdal-Vegas, F, Dermatologia Venezolana, 1965, 4, 10. Woods, B, and Calnan, C D, British of Dermatology, 1976, 94, suppl 13.
J7ournal
Juvenile rheumatoid arthritis-a viral disease? Of all the forms of polyarthritis which have been investigated for an infectious aetiology the most likely seems juvenile rheumatoid arthritis (Still's disease) in its acute form. Fever (often high), rash, lymphadenopathy, splenomegaly, pericarditis, pleuritis, and abdominal pain all occur,'-4 and may in very young children overshadow the joint manifestations. This clinical picture strongly suggests a disseminated infection. In terms of immunopathology juvenile rheumatoid arthritis has many features in common with the adult condition, including complement consumption in affected joints5 and often circulating autoantibodies,6 which may need special methods of detection.7 These findings, too, are entirely consistent with an infective aetiology.8 Nevertheless, like its adult counterpart, juvenile rheumatoid arthritis is a syndrome-an impression reinforced by epidemiological studies9 -and its heterogeneous nature means that clues to its pathogenesis may not apply to all forms of the disease. The evidence linking juvenile rheumatoid arthritis with any specific infection is still scanty. Isolated case reports do appear: illnesses like Still's disease have been described10 in a 16-year-old boy with a rise in antibody titres to Coxsackie
901
B3 and A9 viruses and in a 9-year-old girl from whom an adenovirus 7 was isolated. Furthermore, an increase in antibody titres to rubella virus has been reported in children with juvenile rheumatoid arthritis,"12 and rubella virus antigen was detected in 33% of the synovial effusions examined from these patients.'2 Sore throats are prominent in Still's disease of adults,'314 a disorder which clinically is almost identical with that seen in children in its most characteristic form.'5 All such observations must be interpreted with caution. A whole range of viral infections are accompanied by joint complaints,'6 and the diagnosis of juvenile rheumatoid arthritis can be made with confidence only when the clinical and laboratory features meet accepted criteria'7 18; of these the duration ofarthritis is especially relevant. In addition, antibody titres are often misleading: they may simply reflect the general increase in serum gammaglobulin concentrations commonly seen in connective tissue disorders.'9 Such patients produce an abnormally high secondary antibody response to diphtheria and tetanus toxoid20 so that an exaggerated anamnestic response to viral antigens might not be expected. More decisively, there is no evidence that the clinical course of rubella in patients with juvenile rheumatoid arthritis differs from that in normal children."l 21 Incrimination of common endemic viruses in the pathogenesis of juvenile rheumatoid arthritis is particularly difficult. After all, most children become infected with these, and reactivation may be a non-specific accompaniment of an entirely unrelated disease. The variable exposure to these viruses in different populations could account for the wide variation in viral antibody titres which have been recorded in children with juvenile rheumatoid arthritis." 1219 One possibility is that (as has been suggested22 in the demyelinating diseases) the cell-mediated immune responses to viruses may be defective in these children, so accounting for abnormal persistence of an inflammatory response. Nevertheless, there is little evidence that this sort of defect exists.23 24 The possibility of an infectious aetiology is also raised by the association which has been described between the HLA antigen B27 and juvenile rheumatoid arthritis.25-28 This association has not been found by all investigators29 30reflecting the varied nature of the diseases termed "juvenile rheumatoid arthritis." Nevertheless, B27 is probably commoner in those patients who have developed or are likely to develop ankylosing spondylitis,25 26 and indeed this observation was presaged by an earlier study which showed an increased incidence of ankylosing spondylitis in the families of children with juvenile rheumatoid arthritis.31 Furthermore, individuals who inherit the antigen show an increased susceptibility to polyarthritis after certain bacterial infections32; possibly HLA antigens on the cell surface may be modified by virus, thereby provoking an immune reaction by T-lymphocytes.33 Generally, attempts to identify viruses in long-term cultures of synovial membrane cells have been as fruitless in juvenile as in adult forms of rheumatoid arthritis.34 3 All the possible approaches have not yet been exhausted,36 however, and there may be a case for extending both virological and related immunological studies in juvenile rheumatoid arthritis. If this is to be done the children should be investigated in the acute stages of their illness37 with an open mind as to how it will eventually be classified. Ansell, B M, and Bywaters, E G L, in
Textbook of the Rheumatic Diseases, 4th ed, ed W S C Copeman, p 323. Edinburgh and London, Livingstone, 1969. 2 Schaller, J, and Wedgwood, R J, Pediatrics, 1972, 50, 940. 3Bujak, J S, et al, Medicine, 1973, 52, 431.
902
Goel, K M, and Shanks, R A, Annals of the Rheumatic Diseases, 1974, 33, 25. Rynes, R I, et al, Arthritis and Rheumatism, 1976, 19, 161. 6 Bianco, N E, et al, Arthritis and Rheumatism, 1971, 14, 685. 7Moore, T, Dorner, R W, and Zuckner, J, Annals of the Rheumatic Diseases, 1974, 33, 255. 8 Ziff, M, Federation Proceedings, 1973, 32, 131. 9 Sullivan, D B, Cassidy, J T, and Petty, R E, Arthritis and Rheumatism, 1975, 18, 251. 11 Rahal, J J, Millian, S J, and Noriega, E R,J7ournal of the American Medical Association, 1976, 235, 2496. 11 Linnemann, C C, Jr, et al, Annals of the Rheumatic Diseases, 1975, 34, 354. 12 Ogra, P L, et al, Lancet, 1975, 1, 1157. 13 Fabricant, M S, Chandor, S B, and Friou, G J, J'ournal of the American Medical Association, 1973, 225, 273. 14 Sills, E M, Medical Clinics of North America, 1975, 59, 1497. 11 Bywaters, E G L, Annals of the Rheumatic Diseases, 1971, 30, 121. 16 Smith, J W, and Sanford, J P, Annals of Internal Medicine, 1967, 67, 651. 17 Ansell, B M, and Bywaters, E G L, Bulletin on Rheumatic Diseases, 1959, 9, 189. 18 Brewer, E J, et al, Bulletin on Rheumatic Diseases, 1973, 23, 712. 19 Cassidy, J J, et al, Pediatrics, 1974, 54, 239. 20 H0yeraal, H M, and Mellbye, 0 J, Annals of the Rheumatic Diseases, 1974, 33, 248. 21 Schnitzer, T, Howard, A, and Ansell, B M, in preparation. 22 Medical Research Council, Multiple Sclerosis Research. London, HMSO, 1976. 23 H0yeraal, H M, Fr0land, S S, and Wisl0ff, F, Scandinavian J7ournal of Immunology, 1975, 4, 801. 24 Jennings, J, Annals of the Rheumatic Diseases, 1975, 34, 196. 25 Edmonds, J, et al, Annals of the Rheumatic Diseases, 1974, 33, 576. 26 Edmonds, J, et al, Annals of the Rheumatic Diseases, 1974, 33, 289. 27 Buc, M, Nyulassy, S, and Stefanovic, J, Tissue Antigens, 1974, 4, 395. 28 Rachelefsky, G S, et al, New England J'ournal of Medicine, 1974, 290, 892. 29 Nissila, M, Elomaa, L, and Tiilikainen, A, New England J3ournal of Medicine, 1975, 292, 430. 30 Gibson, D J, et al, New England Journal of Medicine, 1975, 293, 638. 31 Ansell, B M, Bywaters, E G L, and Lawrence, J S, Annals of the Rheumatic Diseases, 1962, 21, 243. 32 Brewerton, D A, ed, Annals of the Rheumatic Diseases, 1975, 34, suppl 1. 33 Doherty, P C, and Zinkernagel, R M, Lancet, 1975, 1, 1406. 34 Phillips, P E, Journal of Experimental Medicine, 1971, 134, 3135. 35 Middleton, P J, and Highton, T C, Annals of the Rheumatic Diseases, 1975, 34, 369. 36 Hamerman, D, Annals of the New York Academy of Sciences, 1975, 256, 25. 37 Schumacher, H R, and Kitridou, R C, Arthritis and Rheumatism, 1972, 15, 465.
Dealing with alcoholism Alcoholism provides a common ground for physicians, psychiatrists, accident surgeons, physiologists, and geneticists. Together with other experts representatives of these disciplines met last month at the Institute of Psychiatry in London to discuss their mutual interest. Despite the intense specialisation which each group is bringing to bear on its own facet of the problem, the impression left by the meeting was that these preoccupations were bringing the various workers closer together, rather than the opposite. Recent studies on mice had confirmed that acetaldehyde metabolism may hold the key to dependence and possibly to individual susceptibility to alcohol intoxication. Factors such as age and sex as well as the genetic strain seemed to be important. This added point to a full review of genetic factors
BRITISH MEDICAL JOURNAL
16 OCTOBER 1976
in human alcoholism, though the conclusion seemed to weigh against heredity's being a major determinant in an unclearly defined syndrome with social as well as medical features. A discussion of the medical markers of alcoholism (heavily weighted on reports of liver cirrhosis) suggested that these may be somewhat less reliable than is usually assumed. This lack of objective definition when it might most have been expected paved the way for a consideration of the role of habit, as seen by a psychologist, in controlling behaviour. Together with an acceptance of social and cultural pressures in the development of drinking habits early in life, it set the scene for a vigorous discussion on liquor licensing laws and the recent proposals1 2 to amend them. Dr Wolfgang Schmidt presented epidemiological evidence gathered at the Alcohol Research Foundation in Toronto which emphasised the association between per caput consumption of alcohol and harmful drinking, and the direct relation of both to availability of alcohol. This matter was raised in discussion during a session ofwhich Dr Christopher Clayson was chairman. Increased availability by extension of licensing hours, he argued, might not necessarily raise consumption nor increase drunkenness if it relieved "the pressure to drink," which Dr Clayson saw as such an undesirable feature of life in Scotland. Another controversial issue concerned the results of treatment, with particular reference to the analysis3 of largescale statistics concerning men attending community treatment centres in the Uniited States. This confirmed reports that remission (as evidenced by a return to normal drinking or reduced consumption attended by improved social relations) is far more frequent than total abstinence, the usual goal of treatment. Methods of working towards such remission were discussed, as well as the underlying psychological theories of learning which gave scientific ground to a re-educative approach to treatment. Learning theory contrasts sharply with the current preoccupation with psychodynamically orientated group work so evident in most alcohol treatment units in Britain and elsewhere. Nevertheless, the re-education of alcoholics to a different life style is now being tried in some practices. Another heartening trend is collaboration between physicians and psychiatrists, described by some speakers, even if it is only beginning to emerge here. Discussion of changes in the approach to treatment naturally led to a debate about the pattern of services needed in Britain if the rising tide of alcoholism is to be stemmed and the public is to be made more aware of the facts about the disease. Who is to compose the teams and who is to lead them? One point that should not need arguing is that whoever does head the team should have the relevant knowledge not only from his own field but also from that of his colleagues.
2 3
The Erroll Report: Report of the Departmental Committee on Liquor Licensing, Cmnd 5154. London, HMSO, 1972. The Clayson Report: Report of the Departmental Committee on Scottish Licensing Law, Cmnd 5354. Edinburgh, HMSO, 1973. Armor, D J, Polich, J M, and Stambul, H B, Alcoholism and Treatment, pp 1-216. Santa Monica, Rand Corporation, 1976.
