278
Since broad-brush ecological surveys have failed to do more than create fluctuating suspicion, perhaps, as Rutty et al suggest, a register of the causes of death in laboratory workers should be compiled. The various national systems of qualification and certification would greatly help retrospective and prospective cohort analyses of medical laboratory workers, and would show whether there is a real risk that we should be confronting or merely a statistical quirk. Rutty GN, Honavar M, Doshi B. Malignant glioma in laboratory workers. J Clin Pathol 1991; 44: 868-69. 2. Codd MB, Kurland LT. Descriptive epidemiology of primary intracranial neoplasms. Progr Exp Tumor Res 1985; 29: 1-11. 3. Russell DS, Rubinstein LJ. Pathology of tumours of the nervous system. 5th ed. London: Edward Arnold, 1989. 4. Alderson MR, ed. The prevention of cancer. London: Edward Arnold, 1.
1982. 5. Selikoff IJ, Hammond EC. Brain tumors in the chemical industry. Ann NY Acad Sci 1982; 381: 1-364. 6. Hall A, Harrington JM, Aw T-C. Mortality study of British pathologists. Am J Ind Med 1991; 20: 83-89. 7. Arnetz BB, Raymond LW, Nicholich MJ, Vargo L. Mortality among petrochemical science and engineering employees. Arch Environ Health 1991; 46: 237-48. 8. National Radiological Protection Board. NRPB/HSE workshop. Followup to Professor Gardner’s case-control study of leukaemia and lymphoma among young people near Sellafield Nuclear Plant in West Cumbria. NRPB-R242. London: HM Stationery Office, 1990. 9. Harrington JM, Shannon HS. Mortality study of pathologists and medical laboratory technicians. Br Med J 1975; i: 759-62. 10. Harrington JM, Oakes D. Mortality study of British pathologists. Br J Ind Med 1984; 41: 188-91. 12. Hill AB. The environment and disease: association or causation? Proc R Soc Med 1965; 58: 295-300.
Failure to treat heart failure Congestive heart failure (CHF) affects 3-5% of the population over 65 years.12 CHF greatly impairs the quality of life and leads to frequent hospital admissions; it seems to account for about 5% of all adult medical and geriatric admissions, and the annual admission rate in patients with established heart failure may be as high as 45%.3,4 Each admission lasts for 8 days on average. The probability of dying within 5 years of the onset of CHF is about 50%; in patients with severe heart failure, the annual mortality is as high as 60%.s There is now evidence that this morbidity and mortality can be lessened by treatment with an angiotensin-converting-enzyme (ACE) inhibitor.6,7 In 1986, the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS) study showed that enalapril reduced 1-year mortality by nearly one-third (to 36%) compared with maximum conventional therapy (52%).5 However, these severely ill patients in hospital represent a minority of patients with congestive failure. For a substantial impact to be made on CHF, benefit has to be shown in patients with milder symptoms, many of whom will not have been referred to hospital. The Studies of Left Ventricular Dysfunction (SOLVD) investigators recruited over 2500 patients with New York Heart Association (NYHA) class II and III (mild and moderate) CHF, who were randomised to receive
either
enalapril (mean daily dose taken 16-6 mg) or placebo as an adjunct to conventional therapy (ie, diuretics, digoxin, and other vasodilators) 4°6 Mean follow-up was 41-4 months. Overall mortality with enalapril was 35% vs 40% (overall risk reduction 16%, p < 0-004).6This benefit was all the more impressive when one considers that nearly one-third of patients randomised to placebo had been prescribed an "open label" ACE inhibitor by the last year of the study. Enalapril also improved NYHA class and reduced the hospital admission rate for CHF in these patients. 37% of patients in the placebo group and 26% in the analapril group were admitted at least once (a risk reduction of 30%). The respective figures for two or more admissions were
18% and 12%. The risk reduction for death or hospital admission for worsening CHF was 26%. These findings were reinforced by the results of the second Vasodilator Heart Failure Trial (V-HeFT II), which was a direct comparison of enalapril and the combination of hydralazine and isosorbide dinitrate, the only other treatment shown to improve outcome in CHF.7,8The ACE inhibitor was better tolerated and resulted in a significantly lower mortality. Clearly no treatment, however successful, will be widely accepted unless it is also safe and easy to use. It is here that there has been concern about ACE inhibitors, largely based on widely publicised reports of severe hypotension and renal dysfunction in early studies with large doses of these drugs in severely ill patients.9,10 This experience has left a residual
reluctance, especially among non-cardiologists, to use ACE inhibitors in CHF. SOLVD, V-HeFT II, and two other recently published studies11,12 should dispel these doubts. In SOLVD, of 7402 patients given open-label enalapril for 2-7 days, only 2-2% of patients experienced symptomatic hypotension and 0-2% showed a decline in renal function. In the 4-year double-blind trial the mean rise in potassium was 02
mmol/1 and the increase in creatinine was 8-8 µmol/l (compared with placebo, 3% more enalapril-treated patients had an increase in creatinine above 177 µmol/l and 3-9% more had an increase in potassium above 5-5 mmol/1). 7% more enalapril-treated patients complained of dizziness and fainting and 6% more of cough with enalapril than with placebo. V-HeFT II, and a comparison of enalapril and prazosin in 1210 patients with CHF, likewise confirmed a small excess of symptomatic hypotension, mild renal dysfunction, and cough in enalapril-treated patientsY1 These three studies, plus a third open study with captopril in 6669 patients, showed no excess of angio-oedema or taste disturbance.6,7,11,12 Thus, concern about frequent or serious adverse effects in mild to moderate CHF should not be a reason for depriving patients of life-prolonging therapy. The message from the trials is that all patients with CHF due to myocardial systolic dysfunction should be given an ACE inhibitor; there is no reason to suppose that one ACE inhibitor would confer any special benefit over another. To prescribea
279
diuretic and delay ACE inhibitor therapy is no longer
supportable. 1. Smith WM. Epidemiology of
congestive heart failure. Am J Cardiol 1985;
55: 3A-8A. 2. Kannel WB, Cupples A. Epidemiology and risk profile of cardiac failure. Cardiovasc Drugs Ther 1988; 2: 387-95. 3. Sutton GC. Epidemiologic aspects of heart failure. Am Heart J 1990; 120:
1538-40. 4. The SOLVD investigators. Studies of left ventricular dysfunction (SOLVD)—rationale, design and methods: two trials that evaluate the effects of enalapril in patients with reduced ejection fraction. Am J Cardiol 1990; 66: 315-22. 5. The CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure. N Engl J Med 1987; 316: 1429-35. 6. SOLVD investigators. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991; 325: 293-302. 7. Cohn JN, Johnson G, Ziesche S, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med 1991; 325: 303-10. 8. Cohn JN, Archibald DG, Ziesche S, et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure. N Engl J Med 1986; 314: 1547-52. 9. Packer M, Lee WH, Yushak M, Medina N. Comparison of captopril and enalapril in patients with severe chronic heart failure. N Engl J Med 1986; 315: 847. 10. Cleland JGF, Dargie HJ, McAlpine H, et al. Severe hypotension after first dose enalapril in heart failure. Br Med J 1985; 291: 1309 - 12. 11. Hasford J, Bussmann W-D, Delius W, Koepcke W, Lehmann K, Weber E. First dose hypotension with enalapril and prazosin in congestive heart failure. Int J Cardiol 1991; 31: 287-94. 12. Di Bianco R. A large-scale trial of captopril for mild to moderate heart failure in the primary care setting. Clin Cardiol 1991; 14: 676-82.
Psychogenic vomiting—a disorder of gastrointestinal motility? For many people psychogenic vomiting is an occasional event associated with severe emotional stress. For a few continuing emotional conflicts lead to a syndrome of persistent or recurrent vomiting serious enough to require medical intervention. Such patients are commonly young or middle-aged women with a history of chronic and intermittent vomiting stretching back to childhood; their lives have often been blighted by bereavement, separation, or abuse.1-3 If one excludes patients with anorexia and bulimia nervosa, few of the remainder exhibit a serious psychopathological disorder. They tend to have rather rigid, passive personalities2 and an intense dislike of confrontation despite hostile relations with those close to them. Vomiting usually interrupts meals and is not associated with nausea or retching; patients can control the urge while they rush to the bathroom. Most patients do not lose weight and they have no abnormal physical signs; a few experience bouts of vomiting severe enough to cause dehydration and hypokalaemia. The vomiting has been variously described as a symbolic communication, a learned behaviour, a means of escape, a means of displacing anger, a somatic equivalent of anxiety, and a wilful manipulative action. Upper gastrointestinal symptoms including nausea and vomiting can now be investigated with various techniques to elucidate motility, including gastric
emptying studies,4,5 upper gastrointestinal manometry,5-7 and electrophysiological studies with
internal5,8 or surface electrodes.4 Hypomotility in the gastric antrum, abnormal gastric electrical activity known as gastric dysrrhythmia or tachygastria, and delayed gastric emptying have been reported in 50-100% of patients in various studies.4-8 There is no relation between the patients’ complaints and these motility disorders. Some patients with persistent abnormalities of gastrointestinal motility have only intermittent vomiting ;5 Gonzalez-Heydrich and colleagues9 describe a child in whom gastric emptying was delayed during stressful family circumstances but returned to normal once the stress had been removed. Abnormalities in gastrointestinal motility have also been induced in healthy controls during stress induced by limb cooling or vertigo. 10 The neurohormonal basis of disordered motility continues to interest researchers’ 1,12 but there have been few attempts to relate disordered motility to a clinical diagnosis of psychogenic
vomiting. 13 It is time to abandon the belief that psychogenic vomiting is a diagnosis to be considered only after organic disorders have been excluded.1.14 We should work on the basis that each individual has the potential
experience vomiting, perhaps secondary to disorders of gastrointestinal motility as a result of psychological stress, but that the threshold varies from one person to another. Those presenting with unexplained vomiting may be experiencing high levels of stress or have a low threshold. This hypothesis to
could be extended to suggest that certain upper gastrointestinal abnormalities such as gastritis or gastro-oesophageal reflux might lower the threshold for stress-related vomiting. 1. Wruble LD, Rosenthal RH, Webb WL. Psychogenic vomiting—a review. Am J Gastroenterol 1982; 77: 318-21. 2. Morgan HG. Functional vomiting. J Psychosom Res 1985; 29: 341-52. 3. Hill OW. Psychogenic vomiting. Gut 1968; 9: 348-52. 4. Geldoff H, Van der Schee EJ, Van Brankenstein M, Grashuis JL. Electrogastrographic study of gastric myoelectrical activity in patients with unexplained nausea and vomiting. Gut 1986; 27: 799-808. 5. Abell TL, Kim CH, Malagelada J-R. Idiopathic cyclic nausea and vomiting-a disorder of gastrointestinal motility? Mayo Clin Proc 1988; 63: 1169-75. 6. Malagelada J-R, Stanghellini V. Manometric evaluation of functional upper gut symptoms. Gastroenterology 1985; 88: 1223-31. 7. Kerlin P. Postprandial antral hypomotility in patients with idiopathic nausea and vomiting. Gut 1989; 30: 54-59. 8. You CH, Lee KY, Chey WY. Electrogastric study of patients with unexplained nausea, bloating and vomiting. Gastroenterology 1980; 79: 311-14. 9. Gonzalez-Heydrich J, Kerner JA, Steiner H. Testing the psychogenic vomiting diagnosis: four pediatric patients. Am J Dis Child 1991; 145: 913-16. 10. Stanghellini V, Malagelada J-R, Zinzmeister AR, et al. Stress induced gastroduodenal motor disturbances in humans—possible humoral mechanisms. Gastroenterology 1983; 85: 83-91. 11. Greydanus MP, Vassallo M, Camilleri M, Nelson DK, Hanson RB, Thomforde GM. Neurohormonal factors in functional dyspepsia: insights on pathophysiological mechanisms. Gastroenterology 1991; 100: 1311-18. 12. Camilleri M, Foeley RD. Idiopathic autonomic denervation in eight patients presenting with functional gastrointestinal disease: a causal association. Dig Dis Sci 1990; 35: 609-16. 13. Clouse RE, Lustman PJ. Psychiatric illness and contraction abnormalities of the esophagus. N Engl J Med 1983; 309: 1337-42. 14. Hanson JS, McCallum RW. The diagnosis and management of nausea and vomiting: a review. Am J Gastroenterol 1985; 80: 210-18.
Since broad-brush ecological surveys have failed to do more than create fluctuating suspicion, perhaps, as Rutty et al suggest, a register of the causes of death in laboratory workers should be compiled. The various national systems of qualification and certification would greatly help retrospective and prospective cohort analyses of medical laboratory workers, and would show whether there is a real risk that we should be confronting or merely a statistical quirk. Rutty GN, Honavar M, Doshi B. Malignant glioma in laboratory workers. J Clin Pathol 1991; 44: 868-69. 2. Codd MB, Kurland LT. Descriptive epidemiology of primary intracranial neoplasms. Progr Exp Tumor Res 1985; 29: 1-11. 3. Russell DS, Rubinstein LJ. Pathology of tumours of the nervous system. 5th ed. London: Edward Arnold, 1989. 4. Alderson MR, ed. The prevention of cancer. London: Edward Arnold, 1.
1982. 5. Selikoff IJ, Hammond EC. Brain tumors in the chemical industry. Ann NY Acad Sci 1982; 381: 1-364. 6. Hall A, Harrington JM, Aw T-C. Mortality study of British pathologists. Am J Ind Med 1991; 20: 83-89. 7. Arnetz BB, Raymond LW, Nicholich MJ, Vargo L. Mortality among petrochemical science and engineering employees. Arch Environ Health 1991; 46: 237-48. 8. National Radiological Protection Board. NRPB/HSE workshop. Followup to Professor Gardner’s case-control study of leukaemia and lymphoma among young people near Sellafield Nuclear Plant in West Cumbria. NRPB-R242. London: HM Stationery Office, 1990. 9. Harrington JM, Shannon HS. Mortality study of pathologists and medical laboratory technicians. Br Med J 1975; i: 759-62. 10. Harrington JM, Oakes D. Mortality study of British pathologists. Br J Ind Med 1984; 41: 188-91. 12. Hill AB. The environment and disease: association or causation? Proc R Soc Med 1965; 58: 295-300.
Failure to treat heart failure Congestive heart failure (CHF) affects 3-5% of the population over 65 years.12 CHF greatly impairs the quality of life and leads to frequent hospital admissions; it seems to account for about 5% of all adult medical and geriatric admissions, and the annual admission rate in patients with established heart failure may be as high as 45%.3,4 Each admission lasts for 8 days on average. The probability of dying within 5 years of the onset of CHF is about 50%; in patients with severe heart failure, the annual mortality is as high as 60%.s There is now evidence that this morbidity and mortality can be lessened by treatment with an angiotensin-converting-enzyme (ACE) inhibitor.6,7 In 1986, the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS) study showed that enalapril reduced 1-year mortality by nearly one-third (to 36%) compared with maximum conventional therapy (52%).5 However, these severely ill patients in hospital represent a minority of patients with congestive failure. For a substantial impact to be made on CHF, benefit has to be shown in patients with milder symptoms, many of whom will not have been referred to hospital. The Studies of Left Ventricular Dysfunction (SOLVD) investigators recruited over 2500 patients with New York Heart Association (NYHA) class II and III (mild and moderate) CHF, who were randomised to receive
either
enalapril (mean daily dose taken 16-6 mg) or placebo as an adjunct to conventional therapy (ie, diuretics, digoxin, and other vasodilators) 4°6 Mean follow-up was 41-4 months. Overall mortality with enalapril was 35% vs 40% (overall risk reduction 16%, p < 0-004).6This benefit was all the more impressive when one considers that nearly one-third of patients randomised to placebo had been prescribed an "open label" ACE inhibitor by the last year of the study. Enalapril also improved NYHA class and reduced the hospital admission rate for CHF in these patients. 37% of patients in the placebo group and 26% in the analapril group were admitted at least once (a risk reduction of 30%). The respective figures for two or more admissions were
18% and 12%. The risk reduction for death or hospital admission for worsening CHF was 26%. These findings were reinforced by the results of the second Vasodilator Heart Failure Trial (V-HeFT II), which was a direct comparison of enalapril and the combination of hydralazine and isosorbide dinitrate, the only other treatment shown to improve outcome in CHF.7,8The ACE inhibitor was better tolerated and resulted in a significantly lower mortality. Clearly no treatment, however successful, will be widely accepted unless it is also safe and easy to use. It is here that there has been concern about ACE inhibitors, largely based on widely publicised reports of severe hypotension and renal dysfunction in early studies with large doses of these drugs in severely ill patients.9,10 This experience has left a residual
reluctance, especially among non-cardiologists, to use ACE inhibitors in CHF. SOLVD, V-HeFT II, and two other recently published studies11,12 should dispel these doubts. In SOLVD, of 7402 patients given open-label enalapril for 2-7 days, only 2-2% of patients experienced symptomatic hypotension and 0-2% showed a decline in renal function. In the 4-year double-blind trial the mean rise in potassium was 02
mmol/1 and the increase in creatinine was 8-8 µmol/l (compared with placebo, 3% more enalapril-treated patients had an increase in creatinine above 177 µmol/l and 3-9% more had an increase in potassium above 5-5 mmol/1). 7% more enalapril-treated patients complained of dizziness and fainting and 6% more of cough with enalapril than with placebo. V-HeFT II, and a comparison of enalapril and prazosin in 1210 patients with CHF, likewise confirmed a small excess of symptomatic hypotension, mild renal dysfunction, and cough in enalapril-treated patientsY1 These three studies, plus a third open study with captopril in 6669 patients, showed no excess of angio-oedema or taste disturbance.6,7,11,12 Thus, concern about frequent or serious adverse effects in mild to moderate CHF should not be a reason for depriving patients of life-prolonging therapy. The message from the trials is that all patients with CHF due to myocardial systolic dysfunction should be given an ACE inhibitor; there is no reason to suppose that one ACE inhibitor would confer any special benefit over another. To prescribea
279
diuretic and delay ACE inhibitor therapy is no longer
supportable. 1. Smith WM. Epidemiology of
congestive heart failure. Am J Cardiol 1985;
55: 3A-8A. 2. Kannel WB, Cupples A. Epidemiology and risk profile of cardiac failure. Cardiovasc Drugs Ther 1988; 2: 387-95. 3. Sutton GC. Epidemiologic aspects of heart failure. Am Heart J 1990; 120:
1538-40. 4. The SOLVD investigators. Studies of left ventricular dysfunction (SOLVD)—rationale, design and methods: two trials that evaluate the effects of enalapril in patients with reduced ejection fraction. Am J Cardiol 1990; 66: 315-22. 5. The CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure. N Engl J Med 1987; 316: 1429-35. 6. SOLVD investigators. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991; 325: 293-302. 7. Cohn JN, Johnson G, Ziesche S, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med 1991; 325: 303-10. 8. Cohn JN, Archibald DG, Ziesche S, et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure. N Engl J Med 1986; 314: 1547-52. 9. Packer M, Lee WH, Yushak M, Medina N. Comparison of captopril and enalapril in patients with severe chronic heart failure. N Engl J Med 1986; 315: 847. 10. Cleland JGF, Dargie HJ, McAlpine H, et al. Severe hypotension after first dose enalapril in heart failure. Br Med J 1985; 291: 1309 - 12. 11. Hasford J, Bussmann W-D, Delius W, Koepcke W, Lehmann K, Weber E. First dose hypotension with enalapril and prazosin in congestive heart failure. Int J Cardiol 1991; 31: 287-94. 12. Di Bianco R. A large-scale trial of captopril for mild to moderate heart failure in the primary care setting. Clin Cardiol 1991; 14: 676-82.
Psychogenic vomiting—a disorder of gastrointestinal motility? For many people psychogenic vomiting is an occasional event associated with severe emotional stress. For a few continuing emotional conflicts lead to a syndrome of persistent or recurrent vomiting serious enough to require medical intervention. Such patients are commonly young or middle-aged women with a history of chronic and intermittent vomiting stretching back to childhood; their lives have often been blighted by bereavement, separation, or abuse.1-3 If one excludes patients with anorexia and bulimia nervosa, few of the remainder exhibit a serious psychopathological disorder. They tend to have rather rigid, passive personalities2 and an intense dislike of confrontation despite hostile relations with those close to them. Vomiting usually interrupts meals and is not associated with nausea or retching; patients can control the urge while they rush to the bathroom. Most patients do not lose weight and they have no abnormal physical signs; a few experience bouts of vomiting severe enough to cause dehydration and hypokalaemia. The vomiting has been variously described as a symbolic communication, a learned behaviour, a means of escape, a means of displacing anger, a somatic equivalent of anxiety, and a wilful manipulative action. Upper gastrointestinal symptoms including nausea and vomiting can now be investigated with various techniques to elucidate motility, including gastric
emptying studies,4,5 upper gastrointestinal manometry,5-7 and electrophysiological studies with
internal5,8 or surface electrodes.4 Hypomotility in the gastric antrum, abnormal gastric electrical activity known as gastric dysrrhythmia or tachygastria, and delayed gastric emptying have been reported in 50-100% of patients in various studies.4-8 There is no relation between the patients’ complaints and these motility disorders. Some patients with persistent abnormalities of gastrointestinal motility have only intermittent vomiting ;5 Gonzalez-Heydrich and colleagues9 describe a child in whom gastric emptying was delayed during stressful family circumstances but returned to normal once the stress had been removed. Abnormalities in gastrointestinal motility have also been induced in healthy controls during stress induced by limb cooling or vertigo. 10 The neurohormonal basis of disordered motility continues to interest researchers’ 1,12 but there have been few attempts to relate disordered motility to a clinical diagnosis of psychogenic
vomiting. 13 It is time to abandon the belief that psychogenic vomiting is a diagnosis to be considered only after organic disorders have been excluded.1.14 We should work on the basis that each individual has the potential
experience vomiting, perhaps secondary to disorders of gastrointestinal motility as a result of psychological stress, but that the threshold varies from one person to another. Those presenting with unexplained vomiting may be experiencing high levels of stress or have a low threshold. This hypothesis to
could be extended to suggest that certain upper gastrointestinal abnormalities such as gastritis or gastro-oesophageal reflux might lower the threshold for stress-related vomiting. 1. Wruble LD, Rosenthal RH, Webb WL. Psychogenic vomiting—a review. Am J Gastroenterol 1982; 77: 318-21. 2. Morgan HG. Functional vomiting. J Psychosom Res 1985; 29: 341-52. 3. Hill OW. Psychogenic vomiting. Gut 1968; 9: 348-52. 4. Geldoff H, Van der Schee EJ, Van Brankenstein M, Grashuis JL. Electrogastrographic study of gastric myoelectrical activity in patients with unexplained nausea and vomiting. Gut 1986; 27: 799-808. 5. Abell TL, Kim CH, Malagelada J-R. Idiopathic cyclic nausea and vomiting-a disorder of gastrointestinal motility? Mayo Clin Proc 1988; 63: 1169-75. 6. Malagelada J-R, Stanghellini V. Manometric evaluation of functional upper gut symptoms. Gastroenterology 1985; 88: 1223-31. 7. Kerlin P. Postprandial antral hypomotility in patients with idiopathic nausea and vomiting. Gut 1989; 30: 54-59. 8. You CH, Lee KY, Chey WY. Electrogastric study of patients with unexplained nausea, bloating and vomiting. Gastroenterology 1980; 79: 311-14. 9. Gonzalez-Heydrich J, Kerner JA, Steiner H. Testing the psychogenic vomiting diagnosis: four pediatric patients. Am J Dis Child 1991; 145: 913-16. 10. Stanghellini V, Malagelada J-R, Zinzmeister AR, et al. Stress induced gastroduodenal motor disturbances in humans—possible humoral mechanisms. Gastroenterology 1983; 85: 83-91. 11. Greydanus MP, Vassallo M, Camilleri M, Nelson DK, Hanson RB, Thomforde GM. Neurohormonal factors in functional dyspepsia: insights on pathophysiological mechanisms. Gastroenterology 1991; 100: 1311-18. 12. Camilleri M, Foeley RD. Idiopathic autonomic denervation in eight patients presenting with functional gastrointestinal disease: a causal association. Dig Dis Sci 1990; 35: 609-16. 13. Clouse RE, Lustman PJ. Psychiatric illness and contraction abnormalities of the esophagus. N Engl J Med 1983; 309: 1337-42. 14. Hanson JS, McCallum RW. The diagnosis and management of nausea and vomiting: a review. Am J Gastroenterol 1985; 80: 210-18.
