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Screening Tests for Alcoholism?
1117
Screening Tests for Alcoholism? FEW British doctors can be unaware of the way alcoholism has increased over the past three decades. Britain is not, of course, unique in this. Alcoholism has increased in many industrialised countries,1 and Governments as ideologically distinct as those in France and the Soviet Union have mounted campaigns to limit its damage. By contrast successive British Governments since the 1950s have allowed the real price of alcohol to fall (relative to average wages), and the number of sales outlets has increased. Last year a report from the Royal College of Psychiatrists outlined the folly of this, and called for action to reverse the trend.2 There are, however, few votes in putting up taxes on alcohol, so it seems that the health services can look forward to further increases in alcohol-related illness. The pressure on services is already considerable: JARMAN and KELLETT3reported that 19.5% of people admitted to a London teaching hospital had a drinking problem while JARIWALLA et a1. found that alcohol was a direct or contributing factor in 27% of the illnesses which led to admission to a Manchester medical unit; and earlier this year HOLT et a1. reported that 32% of patients attending the accident and emergency department of the Royal Infirmary, Edinburgh, had a blood alcohol concentration of 17-4 mmol/1 (80 mg/dl) or more.
If prevention
through the tax system is ruled outby
political funk, then the next best thing is early detection by screening tests or through case-finding. The possibilities may be broadly divided into interviews and 1 Moser J. Problems and programmes related to alcohol and drug dependence in 33 countries. Geneva: World Health Organisation, 1974. 2 Royal College of Psychiatrists. Report on alcohol and alcoholism. London: Tavistock, 1979.
3. Jannan CMB, Kellett JM. Alcoholism
questionnaires, and laboratory tests. The first and best known of the former is the 25-item interview version of the Michigan Alcoholism Screening Test (MAST). In an initial study SELZER6 found that MAST correctly identified 98% of "alcoholics" in hospital while MOORE7 reported that the MAST missed only 2 out of 126 problem drinkers at a psychiatric hospital. Subsequently a self-administered 13-item version was widely used in American hospitals. In the most recent report HURT et al.gave this version to 1002 medical outpatients at the Mayo Clinic: 54 of the patients scored in the range of possible or probable alcoholics, although only 17 of these were known to medical staff as being "alcoholic". However, 14% of all the subjects refused to answer the questionnaire and a further 4% did not complete it satisfactorily, while a records search revealed a false-negative rate of 6.7%. EWING and ROUSE9 developed a four-question screening test which they call the CAGE. MAYFIELD et al.’° tried this on 366 psychiatric patients and found that 81% of known alcoholics answered two or more questions affirmatively compared with only 11% of non-alcoholics. The CAGE is easier to use and less intimidating than the MAST and when SAUNDERS and KERSHAW" compared the two in a community survey they found the CAGE more sensitive. Attempts to refine such screening interviews will undoubtedly continue, but their value is limited to those who recognise that alcohol plays a role in their difficulties and are willing to admit this fact. As any practising doctor knows, heavy drinkers are not always too keen to volunteer the cause of their problems. Could laboratory tests provide a way round this difficulty? Liver enzymes have been much studied. Aspartate aminotransferase (AST or SGOT) and - alanine aminotransferase (ALT or SGPT) are often transiently raised in the "alcoholic" being admitted to hospital but are usually normal in the less acutely ill, and also rise in volunteers given large amounts of alcohol for up to five weeks.12 Serum gamma glutamyl transpeptidase (GGTP) has, however, been reported as raised in between 60% and 80% of "alcoholics"’3-’’and has been used with some Michigan Alcoholism Screening Test. the quest for a new diagnostic instrument. Am J Psychiatry 1971; 127: 1653-58. 7. Moore RA. The diagnosis of alcoholism in a psychiatric hospital: a trial of the Michigan Alcoholism Screening Test (MAST). Am J Psychiatry 1972; 128: 1565-69. 8. Hurt RD, Morse RM, Swenson WM Diagnosis of alcoholism with a self-administered alcoholism screening test: results with 1002 consecutive patients receiving general examinations. Mayo Clin Proc 1980; 55: 365-70 9. Ewing JA, Rouse BA. Paper read at the 29th International Congress on Alcoholism and 6. Selzer ML. The
Drug Dependence, Sydney, Australia, 1970 Mayfield D, McLeod G, Hall P The CAGE questionnaire: validation of a new alcoholism screening instrument. Am J Psychiatry 1974; 131: 1121-23. 11. Saunders WM, Kershaw PW. Screening tests for alcoholism-findings from a community study Br J Addict 1980; 75: 37-41. 12. Jones DP. Biochemical abnormalities accompanying alcoholism. In. Maichrowicz E, Noble EP, eds. The biochemistry and pharmacology of alcohol. New York and 10.
London- Plenum Press, 1979: 677-91. 13.
in the
general hospital. Br Med J 1979;
ii:
469-72.
4. Jariwalla AG, Adams PH, Hore BD. Alcohol and acute general medical admissions to hospital. Health Trends 1979; 11: 95-97. 5 Holt S, Steward IC, Dixon JMJ, Elton RA, Taylor TV, Little K. Alcohol and the emergency service patient. Br Med J 1980; 281: 638-40.
Spencer-Peet J, Wood DCF, Glatt MM Screening test for alcoholism. Lancet 1975; ii:
1089-90. 14. Rosalki SB, Rau D. Serum-glutamyl transpeptidase activity in alcoholism. Clin Chim Acta 1972; 39: 41-47. 15. Boone DJ, Tietz NW, Weinstock A Significance of gamma-glutamyl transferase (GGT) activity measurements in alcohol-induced hepatic injury Ann Clin Lab Sci 1977, 7: 25-8.
1118
screening test in both general practice 16 and of routine health checksy,18 But, not all investigators have been able to correlate levels of GGTP with alcohol intake, 19 and drugs such as phenobarbitone which cause proliferation of the hepatic endoplasmic reticulum also raise GGTP, as do success as a
in the
course
many forms of liver disease. 12
Macrocytosis without anaemia can be a useful though non-specific pointer towards excessive alcohol consumption.20 SHAW et al. 21reported that the ratio of plasma amino-n-butyric acid to leucine ratio is raised in alcoholism, but MORGAN et al. 22 were unable to confirm this and believe instead that the finding merely indicates hepatic dysfunction. More recently the serum transferrin has emerged as a marker possibly more specific than GGTP,23,24 but as yet this test is only available in a few specialised laboratories. By contrast, the most underused investigation is the simple blood alcohol. Its great disadvantage is rapid decay. But when an individual who denies heavy drinking is found to have a grossly raised blood alcohol, this signifies not only that his denials should thereafter be regarded with some scepticism, but also that he must be highly tolerant to alcohol to sustain consciousness in the face of such a level. The successful application of tests of presymptomatic morbidity to disorders such as pulmonary tuberculosis has led some authorities to suggest similar population screening for alcoholism. Such a view ignores the fact that no one disputes the existence of pulmonary tuberculosis, while there remains considerable doubt as to whether alcoholism can be considered a discrete entity. Furthermore, before advocating such a policy one should consider the criteria which any viable screening programme should fulfil. Of ten such criteria outlined by the World Health
Organisation,25
whole-population screening profor alcoholism would totally fulfil only the gramme first-i.e., that the condition sought should be an important public health problem.26 The cost in money a
and manpower of such
a
justified if, as seems likely, 16. Baxter S.
programme could not be a substantial proportion of
Screening for heavy drinking University of Nottingham, 1979
m
general practice. M.Sc. dissertation,
Whitehead TP, Clarke CA, Whitfield AGW. Biochemical and haematological markers of alcohol intake. Lancet 1978; i: 978-81. 18. Whitfield JB, Hensley WJ, Bryden D, Gallagher H. Estimation of alcohol intake from laboratory results. Ann Clin Biochem 1978; 15: 304-06. 19. Robinson D, Monk C, Bailey A. The relationship between serum gamma-glutamyl transpeptidase level and reported alcohol consumption in healthy men. J Stud Alc 1979; 40: 896-901. 20. Wu A, Chanarin I, Levi AJ. Macrocytosis of chronic alcoholism. Lancet 1974; i: 17.
829-30. 21. Shaw S, Stimmel B, Lieber CS. Plasma alpha amino-n-butyric acid to leucine ratio: empirical biochemical marker of alcoholism. Science 1976; 194: 1057-58.
22.
an
Morgan MY, Milsom JP, Sherlock S. Ratio of plasma alpha amino-n-butyric acid to leucine as an empirical marker of alcoholism: diagnostic value. Science 1977; 197:
1183-85. 23. Stibler H, Borg S, Allgulander C. Clinical significance of abnormal heterogeneity of transferrin in relation to alcohol consumption. Acta Med Scand 1979; 206: 275-81. 24. Stibler H, Sydown O, Borg S. Paper presented at the 5th Biennial Symposium on Alcoholism, Cardiff, 1980. 25. Wilson JMG, Jungner G. The principles and practice of screening for disease. Geneva: World Health Organisation, 1968. 26. Murray RM. Early detection instruments in alcoholism. In: Edwards G. et al, eds. Alcohol-related disabilities. Geneva: World Health Organisation: 1977, 89-105.
the abnormal drinkers declined help. And what would one do with all the previously undeclared "alcoholics" who would be uncovered? The treatment services are already overstretched, and there are considerable doubts about how effective intervention would be. Selective screening offers a more economical use of resources.26 General and psychiatric hospital patients could be readily screened with particular attention to those who have attempted suicide, those attending accident and emergency units, and those with physical disorders associated with alcoholism-e.g., those atten. ding peptic-ulcer or liver clinics. High-risk patients visiting their general practitioners, vagrants, and drunken drivers could also be screened with advantage. and employees in predisposing occupations also merit special attention. In circumstances where a reasonable degree of compliance can be expected the CAGE and MAST questionnaires seem useful but, of course, laboratory tests such as GGTP, macrocytosis, and the blood alcohol are much more versatile. In everyday practice, there remains no substitute for the alert doctor with a high degree of suspicion, and yet sufficient tact to be able to take a good drinking history without alienating the patient.
Idiopathic Chronic Ulcerative Enteritis APART from duodenal ulcer disease the commonest of small-bowel ulceration in Britain is Crohn’s disease. Other causes are much rarer and include the
cause
Zollinger-Ellison syndrome, tuberculosis, syphilis, fungal infections, ingestion of enteric-coated potassium chloride tablets, corticosteroid therapy,., intestinal lymphoma, and rare manifestations of vascular lesions including arteriosc1erosis2 and
polyarteritis nodosa. When all these have been excluded there remains a small group in which non-specific small-bowel ulceration is associated with malabsorption. The first case was described in 1949,3 since when about 40 cases have been recorded. They are the subject of two reviews published this year, one from Europe4 and the other from America.5 The European workers used the term "idiopathic chronic ulcerative enteritis" to describe ulceration of unknown aetiology. and their series included few patients with welldocumented coeliac disease. The Americans used the broader term "intestinal ulceration associated with malabsorption" to describe a very similar clinical syndrome in which about half the cases were proven coeliacs. The disease is one of middle age and usually presents as a chronic illness with diarrhoea, colicky central ab DR, Brightmore T Idiopathic and drug induced ulceration of the small inBr J Surg 1970, 57: 134-39 Taylor NS, Gueft B, Lebowich RJ. Atheromatous embolization a cause of gastric ulcers and small bowel necrosis. Gastroenterology 1964. 47: 97-103
1. Davies
testine.
2 3.
Nyman E. Ulcerative jejuno-ileitis with symptomatic sprue
275-83. 4. Mills PR, Brown IL, Watkinson 1980; 194: 133-49.
Acta. Med Scand 1947;134:
G. Idiopathic chronic ulcerative enteritis. Quart J Med
Screening Tests for Alcoholism? FEW British doctors can be unaware of the way alcoholism has increased over the past three decades. Britain is not, of course, unique in this. Alcoholism has increased in many industrialised countries,1 and Governments as ideologically distinct as those in France and the Soviet Union have mounted campaigns to limit its damage. By contrast successive British Governments since the 1950s have allowed the real price of alcohol to fall (relative to average wages), and the number of sales outlets has increased. Last year a report from the Royal College of Psychiatrists outlined the folly of this, and called for action to reverse the trend.2 There are, however, few votes in putting up taxes on alcohol, so it seems that the health services can look forward to further increases in alcohol-related illness. The pressure on services is already considerable: JARMAN and KELLETT3reported that 19.5% of people admitted to a London teaching hospital had a drinking problem while JARIWALLA et a1. found that alcohol was a direct or contributing factor in 27% of the illnesses which led to admission to a Manchester medical unit; and earlier this year HOLT et a1. reported that 32% of patients attending the accident and emergency department of the Royal Infirmary, Edinburgh, had a blood alcohol concentration of 17-4 mmol/1 (80 mg/dl) or more.
If prevention
through the tax system is ruled outby
political funk, then the next best thing is early detection by screening tests or through case-finding. The possibilities may be broadly divided into interviews and 1 Moser J. Problems and programmes related to alcohol and drug dependence in 33 countries. Geneva: World Health Organisation, 1974. 2 Royal College of Psychiatrists. Report on alcohol and alcoholism. London: Tavistock, 1979.
3. Jannan CMB, Kellett JM. Alcoholism
questionnaires, and laboratory tests. The first and best known of the former is the 25-item interview version of the Michigan Alcoholism Screening Test (MAST). In an initial study SELZER6 found that MAST correctly identified 98% of "alcoholics" in hospital while MOORE7 reported that the MAST missed only 2 out of 126 problem drinkers at a psychiatric hospital. Subsequently a self-administered 13-item version was widely used in American hospitals. In the most recent report HURT et al.gave this version to 1002 medical outpatients at the Mayo Clinic: 54 of the patients scored in the range of possible or probable alcoholics, although only 17 of these were known to medical staff as being "alcoholic". However, 14% of all the subjects refused to answer the questionnaire and a further 4% did not complete it satisfactorily, while a records search revealed a false-negative rate of 6.7%. EWING and ROUSE9 developed a four-question screening test which they call the CAGE. MAYFIELD et al.’° tried this on 366 psychiatric patients and found that 81% of known alcoholics answered two or more questions affirmatively compared with only 11% of non-alcoholics. The CAGE is easier to use and less intimidating than the MAST and when SAUNDERS and KERSHAW" compared the two in a community survey they found the CAGE more sensitive. Attempts to refine such screening interviews will undoubtedly continue, but their value is limited to those who recognise that alcohol plays a role in their difficulties and are willing to admit this fact. As any practising doctor knows, heavy drinkers are not always too keen to volunteer the cause of their problems. Could laboratory tests provide a way round this difficulty? Liver enzymes have been much studied. Aspartate aminotransferase (AST or SGOT) and - alanine aminotransferase (ALT or SGPT) are often transiently raised in the "alcoholic" being admitted to hospital but are usually normal in the less acutely ill, and also rise in volunteers given large amounts of alcohol for up to five weeks.12 Serum gamma glutamyl transpeptidase (GGTP) has, however, been reported as raised in between 60% and 80% of "alcoholics"’3-’’and has been used with some Michigan Alcoholism Screening Test. the quest for a new diagnostic instrument. Am J Psychiatry 1971; 127: 1653-58. 7. Moore RA. The diagnosis of alcoholism in a psychiatric hospital: a trial of the Michigan Alcoholism Screening Test (MAST). Am J Psychiatry 1972; 128: 1565-69. 8. Hurt RD, Morse RM, Swenson WM Diagnosis of alcoholism with a self-administered alcoholism screening test: results with 1002 consecutive patients receiving general examinations. Mayo Clin Proc 1980; 55: 365-70 9. Ewing JA, Rouse BA. Paper read at the 29th International Congress on Alcoholism and 6. Selzer ML. The
Drug Dependence, Sydney, Australia, 1970 Mayfield D, McLeod G, Hall P The CAGE questionnaire: validation of a new alcoholism screening instrument. Am J Psychiatry 1974; 131: 1121-23. 11. Saunders WM, Kershaw PW. Screening tests for alcoholism-findings from a community study Br J Addict 1980; 75: 37-41. 12. Jones DP. Biochemical abnormalities accompanying alcoholism. In. Maichrowicz E, Noble EP, eds. The biochemistry and pharmacology of alcohol. New York and 10.
London- Plenum Press, 1979: 677-91. 13.
in the
general hospital. Br Med J 1979;
ii:
469-72.
4. Jariwalla AG, Adams PH, Hore BD. Alcohol and acute general medical admissions to hospital. Health Trends 1979; 11: 95-97. 5 Holt S, Steward IC, Dixon JMJ, Elton RA, Taylor TV, Little K. Alcohol and the emergency service patient. Br Med J 1980; 281: 638-40.
Spencer-Peet J, Wood DCF, Glatt MM Screening test for alcoholism. Lancet 1975; ii:
1089-90. 14. Rosalki SB, Rau D. Serum-glutamyl transpeptidase activity in alcoholism. Clin Chim Acta 1972; 39: 41-47. 15. Boone DJ, Tietz NW, Weinstock A Significance of gamma-glutamyl transferase (GGT) activity measurements in alcohol-induced hepatic injury Ann Clin Lab Sci 1977, 7: 25-8.
1118
screening test in both general practice 16 and of routine health checksy,18 But, not all investigators have been able to correlate levels of GGTP with alcohol intake, 19 and drugs such as phenobarbitone which cause proliferation of the hepatic endoplasmic reticulum also raise GGTP, as do success as a
in the
course
many forms of liver disease. 12
Macrocytosis without anaemia can be a useful though non-specific pointer towards excessive alcohol consumption.20 SHAW et al. 21reported that the ratio of plasma amino-n-butyric acid to leucine ratio is raised in alcoholism, but MORGAN et al. 22 were unable to confirm this and believe instead that the finding merely indicates hepatic dysfunction. More recently the serum transferrin has emerged as a marker possibly more specific than GGTP,23,24 but as yet this test is only available in a few specialised laboratories. By contrast, the most underused investigation is the simple blood alcohol. Its great disadvantage is rapid decay. But when an individual who denies heavy drinking is found to have a grossly raised blood alcohol, this signifies not only that his denials should thereafter be regarded with some scepticism, but also that he must be highly tolerant to alcohol to sustain consciousness in the face of such a level. The successful application of tests of presymptomatic morbidity to disorders such as pulmonary tuberculosis has led some authorities to suggest similar population screening for alcoholism. Such a view ignores the fact that no one disputes the existence of pulmonary tuberculosis, while there remains considerable doubt as to whether alcoholism can be considered a discrete entity. Furthermore, before advocating such a policy one should consider the criteria which any viable screening programme should fulfil. Of ten such criteria outlined by the World Health
Organisation,25
whole-population screening profor alcoholism would totally fulfil only the gramme first-i.e., that the condition sought should be an important public health problem.26 The cost in money a
and manpower of such
a
justified if, as seems likely, 16. Baxter S.
programme could not be a substantial proportion of
Screening for heavy drinking University of Nottingham, 1979
m
general practice. M.Sc. dissertation,
Whitehead TP, Clarke CA, Whitfield AGW. Biochemical and haematological markers of alcohol intake. Lancet 1978; i: 978-81. 18. Whitfield JB, Hensley WJ, Bryden D, Gallagher H. Estimation of alcohol intake from laboratory results. Ann Clin Biochem 1978; 15: 304-06. 19. Robinson D, Monk C, Bailey A. The relationship between serum gamma-glutamyl transpeptidase level and reported alcohol consumption in healthy men. J Stud Alc 1979; 40: 896-901. 20. Wu A, Chanarin I, Levi AJ. Macrocytosis of chronic alcoholism. Lancet 1974; i: 17.
829-30. 21. Shaw S, Stimmel B, Lieber CS. Plasma alpha amino-n-butyric acid to leucine ratio: empirical biochemical marker of alcoholism. Science 1976; 194: 1057-58.
22.
an
Morgan MY, Milsom JP, Sherlock S. Ratio of plasma alpha amino-n-butyric acid to leucine as an empirical marker of alcoholism: diagnostic value. Science 1977; 197:
1183-85. 23. Stibler H, Borg S, Allgulander C. Clinical significance of abnormal heterogeneity of transferrin in relation to alcohol consumption. Acta Med Scand 1979; 206: 275-81. 24. Stibler H, Sydown O, Borg S. Paper presented at the 5th Biennial Symposium on Alcoholism, Cardiff, 1980. 25. Wilson JMG, Jungner G. The principles and practice of screening for disease. Geneva: World Health Organisation, 1968. 26. Murray RM. Early detection instruments in alcoholism. In: Edwards G. et al, eds. Alcohol-related disabilities. Geneva: World Health Organisation: 1977, 89-105.
the abnormal drinkers declined help. And what would one do with all the previously undeclared "alcoholics" who would be uncovered? The treatment services are already overstretched, and there are considerable doubts about how effective intervention would be. Selective screening offers a more economical use of resources.26 General and psychiatric hospital patients could be readily screened with particular attention to those who have attempted suicide, those attending accident and emergency units, and those with physical disorders associated with alcoholism-e.g., those atten. ding peptic-ulcer or liver clinics. High-risk patients visiting their general practitioners, vagrants, and drunken drivers could also be screened with advantage. and employees in predisposing occupations also merit special attention. In circumstances where a reasonable degree of compliance can be expected the CAGE and MAST questionnaires seem useful but, of course, laboratory tests such as GGTP, macrocytosis, and the blood alcohol are much more versatile. In everyday practice, there remains no substitute for the alert doctor with a high degree of suspicion, and yet sufficient tact to be able to take a good drinking history without alienating the patient.
Idiopathic Chronic Ulcerative Enteritis APART from duodenal ulcer disease the commonest of small-bowel ulceration in Britain is Crohn’s disease. Other causes are much rarer and include the
cause
Zollinger-Ellison syndrome, tuberculosis, syphilis, fungal infections, ingestion of enteric-coated potassium chloride tablets, corticosteroid therapy,., intestinal lymphoma, and rare manifestations of vascular lesions including arteriosc1erosis2 and
polyarteritis nodosa. When all these have been excluded there remains a small group in which non-specific small-bowel ulceration is associated with malabsorption. The first case was described in 1949,3 since when about 40 cases have been recorded. They are the subject of two reviews published this year, one from Europe4 and the other from America.5 The European workers used the term "idiopathic chronic ulcerative enteritis" to describe ulceration of unknown aetiology. and their series included few patients with welldocumented coeliac disease. The Americans used the broader term "intestinal ulceration associated with malabsorption" to describe a very similar clinical syndrome in which about half the cases were proven coeliacs. The disease is one of middle age and usually presents as a chronic illness with diarrhoea, colicky central ab DR, Brightmore T Idiopathic and drug induced ulceration of the small inBr J Surg 1970, 57: 134-39 Taylor NS, Gueft B, Lebowich RJ. Atheromatous embolization a cause of gastric ulcers and small bowel necrosis. Gastroenterology 1964. 47: 97-103
1. Davies
testine.
2 3.
Nyman E. Ulcerative jejuno-ileitis with symptomatic sprue
275-83. 4. Mills PR, Brown IL, Watkinson 1980; 194: 133-49.
Acta. Med Scand 1947;134:
G. Idiopathic chronic ulcerative enteritis. Quart J Med