- Email: [email protected]
Syndrome X
1247
public is the higher relative risk of cancer for children
irradiated urider the age of 10 years as compared with all other agesP At present, ICRP applies the same organ risk coefficients to all ages.1 It is to be hoped that ICRP’s decision to maintain for the present its recommended dose limits was not tempered by the financial and practical consequences of a reduction. The method of appointment of ICRP members and the composition of that membership have been criticised.21,Z2 There is an increasing tendency nowadays for "expert" opinion to be
questioned and the public is being helped 2321 to become better informed about radiation hazards. Even the British nuclear industry, with its historically dismal discharge record, has said that it foresees little difficulty in meeting the more stringent requirements now implied. The ICRP has in the past formulated recommendations from which national bodies have taken a lead: by vacillating, it risks losing that authority.
Syndrome X THE
diagnosis of angina is not always straightforward. When coronary angiography was introduced it appeared to provide the diagnostic yardstick-indeed it demonstrates the common anatomical cause of angina-but clinical suspicion soon grew that some patients might be experiencing true angina despite lack of demonstrable coronary disease. Kemp1 in an editorial comment in 1973 on a report of such patients coined the term "syndrome X", which has been widely adopted as a useful diagnostic filing category, pending resolution. The underlying explanation remains unknown. Is it small evidence has not been causal lesion missed on angiography?-no longer a reasonable possibility in experienced hands. Is the chest pain not cardiac at all ?-undoubtedly often the case. The wheel of fashion turned and coronary spasm became popular, but this condition is now known to be an extremely rare cause of characteristically episodic cardiac ischaemia and one that presents little diagnostic difficulty in this context.2 Syndrome X has therefore persisted as an intriguing but uncertain entity (not, as vessel
disease?-the Is the
forthcoming.
a
neurologist
once
thought,
as
"cardiologist-speke"
for hysteria!). The possibility of syndrome X is suggested by a history of effort angina with no demonstrable coronary stenosis or other obvious cause. As such, it is a condition all too familiar to clinicians, although nonetheless important for that-neither the Morgan KZ. ICRP risk estimates: an alternative view. In: Russell Jones R, Southwood R, eds. Radiation and health- the biological effects of low-level expsoure to ionising radiation. Chichester: John Wiley, 1987. 125-54. 22. Russell Jones R. Radiation, cancer risk, and the new dosimetry. Lancet 1987; ii: 1143. 23. National Radiological Protection Board. Living with Radiation, 3rd ed London: HM Stationery Office. 1987. Pp 53 £1.90. 24. Radiation Risks: an Evaluation. By David Sumner. Glasgow: Tarragon Press. 1987. Pp 191. £3.95. ISBN 1 870781 00 7. 1. Kemp HG. Left ventricular function in patients with the anginal syndrome and normal coronary arteriograms. Am J Cardiol 1973; 32: 375-76. 2 Arbogast R, Bourassa MG. Myocardial function during atrial pacing in patients with angina pectoris and normal coronary arteriograms Am J Cardiol 1973; 32: 257-63. 3. Kemp HG, Vokonas PS, Cohn PF, Gorlin R The angina syndrome associated with normal coronary arteriograms. Am J Med 1973; 54: 735-42.
21.
patient nor his doctor is so easily managed that, whatever its cause, statistical by is good.3 Most such patients will have a prognosis non-cardiac cause; a critically careful history should help to identify those with thoracic root pain and suggest oesophageal dysmotility as the possible cause in others.4 However, from this large pool of patients there is a small group (probably < 1 % of those presenting to a cardiac unit with possible angina) who fulfil the diagnostic criteria of a necessarily tighter, albeit empirical definition of syndrome X—(a) typical angina on effort; (b) positive exercise test; (c) no demonstrable coronary stenosis; (d) no other obvious cause (ie, normal resting cardiac function and no hypertension, valve disease, or overt cardiomyopathy). Neither of the first two positive criteria provides 100 % sensitivity or selectivity. An alternative method is to use a conceptual definition based on the generally accepted view that syndrome X represents inducible myocardial ischaemia. This approach also poses problems. What is ischaemia and how is it definitively demonstrated? Does syndrome X, so defined, exist at all in the middle of this diagnostic parcel, once all non-cardiac causes and false-positive exercise tests have been peeled away? An overview of the literature provides an inevitably untidy picture, given the lack of agreed hard diagnostic criteria. Each study has characterised its own group of patients with possible syndrome X by its individual
reassurances
of reference. Whilst not all individual in these studies fulfil either the empirical or patients the conceptual definition offered above, and the findings of the different studies are of course not correlated in the same patients, most of the studies have documented group mean differences relative to their control groups. Overall there is now convincing evidence that some patients have reduced coronary perfusion reserve5,6 and inducible myocardial ischaemia (as indicated by lactate production). 2,5,7 With the exception of a few somewhat atypical patients,8 no histological evidence of small-vessel lesions has been found-although this leaves a window of uncertainty with respect to arteries of about 200 J.lI11 in diameter, which lie between the reach of biopsy and angiographic evidence and which probably represent the major resistance vessels. Many patients also showed evidence of myocardial damage compatible with ischaemia or cardiomyopathy, as indicated by conduction defects,5 impaired ventricular systolic reserve and diastolic ftmction,5,6,9 own terms
4. Dart AM, Alban-Davies H, Dalal J, Ruttley M, Henderson AH ’Angina’ and normal coronary arteriograms. a follow-up study. Eur Heart J1980, 1: 97-98 5. Opherk D, Zebe H, Weihe E, et al. Reduced coronary dilatory capacity and ultrastructural changes of the myocardium in patients with angina pectoris but normal coronary arteriograms. Circulatzon 1981, 63: 817-25 6. Cannon RO, Bonow RO, Bacharach SL, et al Left ventricular dysfunction in patients with angina pectoris, normal epicardial coronary arteries, and abnormal vasodilator reserve. Circulation 1985; 71: 218-26. 7. Boudoulas H, Cobb TC, Leighton RF, Wilt SM. Myocardial lactate production in patients with angina-like chest pain and angiographically normal coronary arteries and left ventricle. Am J Cardiol 1974; 34: 501-05. 8. Mossen M, Yarom R, Gotsman MS, Hasin Y. Histologic evidence for small-vessel coronary artery disease in patients with angina pectoris and patent large coronary arteries. Circulation 1986; 74: 964-72. 9. Wieshammer S, Delagardelle C, Sigel HA, et al. Haemodynamic response to exercise in patients with chest pain and normal coronary angiograms Eur Heart J1986; 7: 654-61.
1248
histological abnormalities on biopsy samples.5,11 some (or all) of these patients have cardiomyopathy, or is the myocardial damage a consequence of ischaemia? Experimental and circumstantial clinical evidence has been presented in support of the view that some cardiomyopathies could result from cumulative focal necrosis secondary to arteriolar disease, possibly in the form of spasm. 12 Conversely, coronary perfusion reserve is reduced in congestive cardiomyopathy, although in direct and Do
relation to the raised left ventricular diastolic pressure from the resulting heart failure, which may thus be its mechanism.13 In the Heidelberg study, about half the patients with syndrome X had left bundle-branch block (LBBB) at rest or induced by exercise: these patients went on to show evidence of deteriorating left ventricular function some 4 years later in contrast to those without LBBB.14 Do they represent two different conditions or two different phases of the same disease? On the basis of anecdotal experience, treatment of this condition is less than satisfactory. Some symptomatic benefit can usually be achieved from sublingual glyceryl trinitrate and from therapeutic trials of calcium antagonists and nitrovasodilators but benefit may not be sustained. Curiously the response to beta-blockers seems less predictable. No other drug appears to help. Reassurance that the condition seems largely benign and carries no risk of acute infarction is obviously appropriate but symptoms can remain
disturbing.
TRANSPLANTATION FOR ACUTE LIVER FAILURE "A patient with jaundice is incurable if he develops blackish yellow discolouration of faeces and urine, severe anasarca, reddish discolouration of the eyes, oral cavity, vomitus anorexia, drowsiness, confusion, subnormal temperature and coma."-CARAKA SAMHITN
THE clinical picture and prognosis of acute liver failure well known to the ancient Ayurvedic physicians of India; progress over the subsequent three thousand years has been largely disappointing. Although many of the lethal complications, such as hypoglycaemia and renal failure, are now recognised and treated, fulminant hepatic failure leading to coma still carries an appalling prognosis, with a mortality of up to 85%. The sight of a young, previously healthy individual succumbing to hepatic failure within two were
10. Schofield PM, Brookes NH, Bennet DH. Left ventricular dysfunction in patients with angina pectons and normal coronary angiograms. Br Heart J 1986; 56: 327-33. 11. Richardson PJ, Livesley B, Oram S, Olsen E, Armstrong P. Angina pectoris with normal coronary arteries. Transvenous myocardial biopsy with diagnosis. Lancet 1974; ii: 677-80. 12. Factor SM, Sonnenblick EH. The pathogenesis of clinical and experimental congestive cardiomyopathies: recent concepts. Prog Cardiovasc Dis 1985; 27: 395-420. 13. Opherk D, Schwarz F, Mall G, Manthey J, Baller D, Kubler W. Coronary dilatory capacity in idiopathic dilated cardiomyopathy: analysis of 16 patients. Am J Cardiol 1983; 51: 1657-62. 14. Kubler W, Opherk D. Angina pectoris with normal coronary arteries. Acta Med Scand 1984; 694: 55-57. 1. Singhal GD, Tripatti SN, Sharma KR Ayurvedic clinical diagnosis. Part 1. Varanasi, India Smghal Publications, 1984: 166.
three weeks is an experience that tends to provoke all sorts of therapeutic manoeuvres. Regrettably, these efforts have to
been unrewarding—corticosteroids, exchange transfusion, plasmapheresis, extracorporeal pig-liver perfusion, haemodialysis, and heparin have not proved useful. Although charcoal haemoperfusion, particularly if
instituted before coma supervenes, has been advocated as an effective therapy, there are no controlled studies to support this contention and the procedure has not gained widespread acceptance. Desperate situations tend to inspire dramatic measures, and the increasing success of liver transplantation for chronic end-stage hepatic damage has encouraged transplant units to consider this technique as a means of treating acute liver failure. In Western Europe alone at least 75 such procedures have been carried out;3 the Paris group4 have now reported their experience of 23 patients, 17 of whom survived. Successful orthoptic liver transplantation for acute hepatic failure requires considerable skill, excellent organisation, and not a little good fortune. From a technical point of view, the operation is less difficult than in chronic liver disease since there are no collateral veins associated with portal hypertension; gross coagulation disturbances can be largely controlled by the use of plasma derivatives and platelets. Undoubtedly the major decision concerns the timing of transplantation-if carried out too early there must be a serious risk that some patients are subjected to this major form of surgery who would otherwise have survived, whereas undue delay may lead to brain death from irreversible cerebral oedema. It is generally agreed that a prerequisite is deep hepatic coma with no response to painful stimuli, together with severely abnormal coagulation tests. Bismuth’s group believe that a plasma factor V level of less than 20% is critical, while others have advocated a combination of deep coma for at least 24 hours together with progressively deteriorating coagulation measurements.sS However, such criteria are inevitably somewhat arbitrary. Once the decision to transplant is taken, the surgical and support facilities have to be mobilised rapidly since the time available to the patient may be very short. Moreover, the patient must not only be at a centre with such facilities but also a suitable donor liver must become available at precisely the right moment; some of the difficulties with matching can partly be overcome by the use of ABO incompatible organs which are often (but not invariably) accepted by the
recipient. Fulminant liver failure due to viral hepatitis is the indication for the procedure and such patients often have no serum markers for either hepatitis A or B. Acute hepatitis B infection (often with IgM anti-HBc and no HBeAg6 in the serum) or coexisting delta infection does not contraindicate transplantation, since, unlike chronic hepatitis B, the virus seldom persists in these cases. Drug hepatotoxicity is another possible indication, but the place of transplantation as a treatment for patients who have attempted suicide must be seriously questioned. commonest
2. Gimson
AES, Bravde S, Mellon PJ, Canalese J, Williams R. Earlier charcoal haemoperfusion in fulminant hepatic failure. Lancet 1982; ii: 681-83. 3. Bismuth H, Castaing D, Ericzon BG, et al. Hepatic transplantation in Europe. Lancet 1987; ii: 674-76. 4. Bismuth H, Samuel D, Gugenheim J, et al. Emergency liver transplantation for fulminant hepatitis. Ann Intern Med 1987; 10: 337-41. 5. Vickers C, Neuberger J, Buckels J, McMaster P, Elias E. Liver transplantation for fulminant hepatic failure. Gut 1987; 28: A1345. 6. Robinson WS. In: Zakim D, Boyer TD, eds. Hepatology Philadelphia: WB Saunders, 1982: 881.
public is the higher relative risk of cancer for children
irradiated urider the age of 10 years as compared with all other agesP At present, ICRP applies the same organ risk coefficients to all ages.1 It is to be hoped that ICRP’s decision to maintain for the present its recommended dose limits was not tempered by the financial and practical consequences of a reduction. The method of appointment of ICRP members and the composition of that membership have been criticised.21,Z2 There is an increasing tendency nowadays for "expert" opinion to be
questioned and the public is being helped 2321 to become better informed about radiation hazards. Even the British nuclear industry, with its historically dismal discharge record, has said that it foresees little difficulty in meeting the more stringent requirements now implied. The ICRP has in the past formulated recommendations from which national bodies have taken a lead: by vacillating, it risks losing that authority.
Syndrome X THE
diagnosis of angina is not always straightforward. When coronary angiography was introduced it appeared to provide the diagnostic yardstick-indeed it demonstrates the common anatomical cause of angina-but clinical suspicion soon grew that some patients might be experiencing true angina despite lack of demonstrable coronary disease. Kemp1 in an editorial comment in 1973 on a report of such patients coined the term "syndrome X", which has been widely adopted as a useful diagnostic filing category, pending resolution. The underlying explanation remains unknown. Is it small evidence has not been causal lesion missed on angiography?-no longer a reasonable possibility in experienced hands. Is the chest pain not cardiac at all ?-undoubtedly often the case. The wheel of fashion turned and coronary spasm became popular, but this condition is now known to be an extremely rare cause of characteristically episodic cardiac ischaemia and one that presents little diagnostic difficulty in this context.2 Syndrome X has therefore persisted as an intriguing but uncertain entity (not, as vessel
disease?-the Is the
forthcoming.
a
neurologist
once
thought,
as
"cardiologist-speke"
for hysteria!). The possibility of syndrome X is suggested by a history of effort angina with no demonstrable coronary stenosis or other obvious cause. As such, it is a condition all too familiar to clinicians, although nonetheless important for that-neither the Morgan KZ. ICRP risk estimates: an alternative view. In: Russell Jones R, Southwood R, eds. Radiation and health- the biological effects of low-level expsoure to ionising radiation. Chichester: John Wiley, 1987. 125-54. 22. Russell Jones R. Radiation, cancer risk, and the new dosimetry. Lancet 1987; ii: 1143. 23. National Radiological Protection Board. Living with Radiation, 3rd ed London: HM Stationery Office. 1987. Pp 53 £1.90. 24. Radiation Risks: an Evaluation. By David Sumner. Glasgow: Tarragon Press. 1987. Pp 191. £3.95. ISBN 1 870781 00 7. 1. Kemp HG. Left ventricular function in patients with the anginal syndrome and normal coronary arteriograms. Am J Cardiol 1973; 32: 375-76. 2 Arbogast R, Bourassa MG. Myocardial function during atrial pacing in patients with angina pectoris and normal coronary arteriograms Am J Cardiol 1973; 32: 257-63. 3. Kemp HG, Vokonas PS, Cohn PF, Gorlin R The angina syndrome associated with normal coronary arteriograms. Am J Med 1973; 54: 735-42.
21.
patient nor his doctor is so easily managed that, whatever its cause, statistical by is good.3 Most such patients will have a prognosis non-cardiac cause; a critically careful history should help to identify those with thoracic root pain and suggest oesophageal dysmotility as the possible cause in others.4 However, from this large pool of patients there is a small group (probably < 1 % of those presenting to a cardiac unit with possible angina) who fulfil the diagnostic criteria of a necessarily tighter, albeit empirical definition of syndrome X—(a) typical angina on effort; (b) positive exercise test; (c) no demonstrable coronary stenosis; (d) no other obvious cause (ie, normal resting cardiac function and no hypertension, valve disease, or overt cardiomyopathy). Neither of the first two positive criteria provides 100 % sensitivity or selectivity. An alternative method is to use a conceptual definition based on the generally accepted view that syndrome X represents inducible myocardial ischaemia. This approach also poses problems. What is ischaemia and how is it definitively demonstrated? Does syndrome X, so defined, exist at all in the middle of this diagnostic parcel, once all non-cardiac causes and false-positive exercise tests have been peeled away? An overview of the literature provides an inevitably untidy picture, given the lack of agreed hard diagnostic criteria. Each study has characterised its own group of patients with possible syndrome X by its individual
reassurances
of reference. Whilst not all individual in these studies fulfil either the empirical or patients the conceptual definition offered above, and the findings of the different studies are of course not correlated in the same patients, most of the studies have documented group mean differences relative to their control groups. Overall there is now convincing evidence that some patients have reduced coronary perfusion reserve5,6 and inducible myocardial ischaemia (as indicated by lactate production). 2,5,7 With the exception of a few somewhat atypical patients,8 no histological evidence of small-vessel lesions has been found-although this leaves a window of uncertainty with respect to arteries of about 200 J.lI11 in diameter, which lie between the reach of biopsy and angiographic evidence and which probably represent the major resistance vessels. Many patients also showed evidence of myocardial damage compatible with ischaemia or cardiomyopathy, as indicated by conduction defects,5 impaired ventricular systolic reserve and diastolic ftmction,5,6,9 own terms
4. Dart AM, Alban-Davies H, Dalal J, Ruttley M, Henderson AH ’Angina’ and normal coronary arteriograms. a follow-up study. Eur Heart J1980, 1: 97-98 5. Opherk D, Zebe H, Weihe E, et al. Reduced coronary dilatory capacity and ultrastructural changes of the myocardium in patients with angina pectoris but normal coronary arteriograms. Circulatzon 1981, 63: 817-25 6. Cannon RO, Bonow RO, Bacharach SL, et al Left ventricular dysfunction in patients with angina pectoris, normal epicardial coronary arteries, and abnormal vasodilator reserve. Circulation 1985; 71: 218-26. 7. Boudoulas H, Cobb TC, Leighton RF, Wilt SM. Myocardial lactate production in patients with angina-like chest pain and angiographically normal coronary arteries and left ventricle. Am J Cardiol 1974; 34: 501-05. 8. Mossen M, Yarom R, Gotsman MS, Hasin Y. Histologic evidence for small-vessel coronary artery disease in patients with angina pectoris and patent large coronary arteries. Circulation 1986; 74: 964-72. 9. Wieshammer S, Delagardelle C, Sigel HA, et al. Haemodynamic response to exercise in patients with chest pain and normal coronary angiograms Eur Heart J1986; 7: 654-61.
1248
histological abnormalities on biopsy samples.5,11 some (or all) of these patients have cardiomyopathy, or is the myocardial damage a consequence of ischaemia? Experimental and circumstantial clinical evidence has been presented in support of the view that some cardiomyopathies could result from cumulative focal necrosis secondary to arteriolar disease, possibly in the form of spasm. 12 Conversely, coronary perfusion reserve is reduced in congestive cardiomyopathy, although in direct and Do
relation to the raised left ventricular diastolic pressure from the resulting heart failure, which may thus be its mechanism.13 In the Heidelberg study, about half the patients with syndrome X had left bundle-branch block (LBBB) at rest or induced by exercise: these patients went on to show evidence of deteriorating left ventricular function some 4 years later in contrast to those without LBBB.14 Do they represent two different conditions or two different phases of the same disease? On the basis of anecdotal experience, treatment of this condition is less than satisfactory. Some symptomatic benefit can usually be achieved from sublingual glyceryl trinitrate and from therapeutic trials of calcium antagonists and nitrovasodilators but benefit may not be sustained. Curiously the response to beta-blockers seems less predictable. No other drug appears to help. Reassurance that the condition seems largely benign and carries no risk of acute infarction is obviously appropriate but symptoms can remain
disturbing.
TRANSPLANTATION FOR ACUTE LIVER FAILURE "A patient with jaundice is incurable if he develops blackish yellow discolouration of faeces and urine, severe anasarca, reddish discolouration of the eyes, oral cavity, vomitus anorexia, drowsiness, confusion, subnormal temperature and coma."-CARAKA SAMHITN
THE clinical picture and prognosis of acute liver failure well known to the ancient Ayurvedic physicians of India; progress over the subsequent three thousand years has been largely disappointing. Although many of the lethal complications, such as hypoglycaemia and renal failure, are now recognised and treated, fulminant hepatic failure leading to coma still carries an appalling prognosis, with a mortality of up to 85%. The sight of a young, previously healthy individual succumbing to hepatic failure within two were
10. Schofield PM, Brookes NH, Bennet DH. Left ventricular dysfunction in patients with angina pectons and normal coronary angiograms. Br Heart J 1986; 56: 327-33. 11. Richardson PJ, Livesley B, Oram S, Olsen E, Armstrong P. Angina pectoris with normal coronary arteries. Transvenous myocardial biopsy with diagnosis. Lancet 1974; ii: 677-80. 12. Factor SM, Sonnenblick EH. The pathogenesis of clinical and experimental congestive cardiomyopathies: recent concepts. Prog Cardiovasc Dis 1985; 27: 395-420. 13. Opherk D, Schwarz F, Mall G, Manthey J, Baller D, Kubler W. Coronary dilatory capacity in idiopathic dilated cardiomyopathy: analysis of 16 patients. Am J Cardiol 1983; 51: 1657-62. 14. Kubler W, Opherk D. Angina pectoris with normal coronary arteries. Acta Med Scand 1984; 694: 55-57. 1. Singhal GD, Tripatti SN, Sharma KR Ayurvedic clinical diagnosis. Part 1. Varanasi, India Smghal Publications, 1984: 166.
three weeks is an experience that tends to provoke all sorts of therapeutic manoeuvres. Regrettably, these efforts have to
been unrewarding—corticosteroids, exchange transfusion, plasmapheresis, extracorporeal pig-liver perfusion, haemodialysis, and heparin have not proved useful. Although charcoal haemoperfusion, particularly if
instituted before coma supervenes, has been advocated as an effective therapy, there are no controlled studies to support this contention and the procedure has not gained widespread acceptance. Desperate situations tend to inspire dramatic measures, and the increasing success of liver transplantation for chronic end-stage hepatic damage has encouraged transplant units to consider this technique as a means of treating acute liver failure. In Western Europe alone at least 75 such procedures have been carried out;3 the Paris group4 have now reported their experience of 23 patients, 17 of whom survived. Successful orthoptic liver transplantation for acute hepatic failure requires considerable skill, excellent organisation, and not a little good fortune. From a technical point of view, the operation is less difficult than in chronic liver disease since there are no collateral veins associated with portal hypertension; gross coagulation disturbances can be largely controlled by the use of plasma derivatives and platelets. Undoubtedly the major decision concerns the timing of transplantation-if carried out too early there must be a serious risk that some patients are subjected to this major form of surgery who would otherwise have survived, whereas undue delay may lead to brain death from irreversible cerebral oedema. It is generally agreed that a prerequisite is deep hepatic coma with no response to painful stimuli, together with severely abnormal coagulation tests. Bismuth’s group believe that a plasma factor V level of less than 20% is critical, while others have advocated a combination of deep coma for at least 24 hours together with progressively deteriorating coagulation measurements.sS However, such criteria are inevitably somewhat arbitrary. Once the decision to transplant is taken, the surgical and support facilities have to be mobilised rapidly since the time available to the patient may be very short. Moreover, the patient must not only be at a centre with such facilities but also a suitable donor liver must become available at precisely the right moment; some of the difficulties with matching can partly be overcome by the use of ABO incompatible organs which are often (but not invariably) accepted by the
recipient. Fulminant liver failure due to viral hepatitis is the indication for the procedure and such patients often have no serum markers for either hepatitis A or B. Acute hepatitis B infection (often with IgM anti-HBc and no HBeAg6 in the serum) or coexisting delta infection does not contraindicate transplantation, since, unlike chronic hepatitis B, the virus seldom persists in these cases. Drug hepatotoxicity is another possible indication, but the place of transplantation as a treatment for patients who have attempted suicide must be seriously questioned. commonest
2. Gimson
AES, Bravde S, Mellon PJ, Canalese J, Williams R. Earlier charcoal haemoperfusion in fulminant hepatic failure. Lancet 1982; ii: 681-83. 3. Bismuth H, Castaing D, Ericzon BG, et al. Hepatic transplantation in Europe. Lancet 1987; ii: 674-76. 4. Bismuth H, Samuel D, Gugenheim J, et al. Emergency liver transplantation for fulminant hepatitis. Ann Intern Med 1987; 10: 337-41. 5. Vickers C, Neuberger J, Buckels J, McMaster P, Elias E. Liver transplantation for fulminant hepatic failure. Gut 1987; 28: A1345. 6. Robinson WS. In: Zakim D, Boyer TD, eds. Hepatology Philadelphia: WB Saunders, 1982: 881.