tant in diminishing the toxic effect of carbon monoxide in our patient. The reduction in central oxidative metabolism by barbiturates might also be important. Such protection is an interesting possibility that merits further investigation. References 1. WHITLOCK FA: Suicide in Brisbane, 1956 to 1973; the drug-death epidemic. Med I Aust 1: 737, 1975 2. SHILLITO
FH,
DRINKER
CK,
SHAUOHNESSY
TJ: The problem of nervous and mental
sequelac in carbon monoxide poisoning. JAMA 106: 669, 1936 3. SMITH JS, BRANDON 5: Acute carbon monoxide poisoning - 3 years of experience in a defined population. Postgrad Med J 46: 65, 1970 4. WEir.smi. EA, KAHN RL: Denial of Illness, Springfield IL CC Thomas, 1955, pp 96-100 5. CRITCHLEY' M:' .The Parietal Lobes, London, Edward Arnold, 1953, p 254 6. Ibid, p 388 7. RICHARDSON JC, CHAMBERS RA, HEYWOOD PM: Encephalopathies of anoxia and hypoglycemia. Arch Neurol 1: 178, 1959 8. GINSBERG R, ROMANO J: Carbon monoxide poisoning: need for appropriate treatment. Am I Psychiatry 133: 317, 1976 9. JEFFERSON JW: Subtle neuropsychiatric sequelae of carbon monoxide intoxication: two case reports. Ibid, p 961
10. SMITH JS, BRANDON S: Morbidity from acute carbon monoxide poisoning at three-year follow-up. Br Med J 1: 318, 1973 11. GINSBERG MD, MYERS RE: Experimental carbon monoxide encephalopathy in the primate. Arch Neurol 30: 202, 1974 12. SLUJJTER ME: The treatment of carbon monoxide poisoning by administration of oxygen at high atmospheric pressure, in Progress in Brain Research, vol 24, Boua H, LEDINGHAM IM (eds), Amsterdam, Elsevier, 1967, pp 123-82 13. FORBES WH,
SARGENT F,
ROUGHTON FJW:
The rate of carbon monoxide uptake by normal men. Am J Physiol 143: 594, 1945 14. FORBEs WH: Carbon monoxide uptake via the lungs. Ann NY Acad Sci 174: 72, 1970 15. BRODY JS, COBURN RF: Effects of elevated carboxyhemoglobin on gas exchange in the lung. Ibid, p 255
Two-year follow-up study of patients with known serum concentrations of carcinoembryonic antigen P.R. BAND,* MD, FRCP[C]; I.T. BECK,f MD, PH D, FACP, FRCP[C]; P.J. DINNER,* M Sc; AB. MILLER,* MB, FRCP[C]
Between 1970 and 1972 five university centres in Canada and the United States collaborated in a study of a test for carcinoembryonic antigen (CEA) in the serum, with the Montreal General Hospital's laboratory acting as the reference laboratory, examining duplicate halves of specimens examined in local laboratories. The National Cancer Institute of Canada acted as the coordinating centre. The first report gave results for 503 patients admitted to the study between June 1971 and April 1972, 146 of whom had cancer of the colon or recturn.1 Discrimination between colorectal cancer and "other" conditions was good at a CEA value of 2.5 ng/mL or more, such a result being obtained in 66% of the patients with colorectal cancer in the local laboratories and 62% in the reference laboratory, compared with 39% and 33%, respectively, of patients with "other" conditions. Patients with Dukes' C lesions of the colon or rectum From *University of Alberta, Edmonton; tQueen's University, Kingston; and .epidemiology unit, National Cancer Institute of Canada, University of Toronto Reprint requests to: Dr. AB. Miller, Director, Epidemiology unit, National Cancer Institute of Canada, University of Toronto, 121 St. Joseph St., Toronto, Ont. M5S 2R9
(those with metastases in regional lymph nodes) were more likely to have elevated CEA values than patients with more localized lesions. CEA was also more commonly found in patients with other cancers or with liver disease than in patients with other (benign) conditions. It was concluded that the test for CEA can be reproduced in other laboratories and that it or another simple technique could become an important diagnostic aid for colorectal cancer. It was also suggested that the CEA value might be an important prognostic indicator and that, for the 33% of patients with elevated CEA values but no colorectal cancer, follow-up might show an abnormally high incidence of colorectal cancer in subsequent years. Follow-up of the original 503 cases (and a smaller number reported after April 1972), at 6, 12, 18 and 24 months after admission to the study, was attempted to examine these hypotheses. A lack of resources severely restricted the extent of documentation of followup in the three American centres, but a special effort was made to determine the status of patients in the two Canadian centres at 24 months. Contact with
the patient at any time up to 3 months before or after this date was accepted as the required 24-month follow-up contact. Results Of the 103 patients admitted to the study from Kingston and the 96 from Edmonton, follow-up forms were returned for 102 and 91, respectively; of these, 14 were lost to follow-up at 2 years. CEA values were reported on the basis of the initial results from the Montreal laboratory to avoid differences between laboratories. As CEA values were not available for 14 of the patients followed up, results are presented for only 165 patients. The prognostic value of the initial CEA value in the 36 patients with colorectal cancer is shown in Table I. If values of 2.5 ng/mL or more are taken as positive the difference in terms of disease-free status and survival at 2 years is significant at the 5% level (X2 = 6.47 and 5.73, respectively, with Yates' continuity correction). If values of 5.0 ng/mL or more are taken as positive the difference in disease-free status does not attain statistical signif-
Table I-Status at 2 years of patients with colorectal cancer according to initial serum concentration of carcinoembryonic antigen (CEA) and Dukes' classification2 CEA concentration (ng/mL) and Dukes' classification*
FH,
DRINKER
CK,
SHAUOHNESSY
TJ: The problem of nervous and mental
sequelac in carbon monoxide poisoning. JAMA 106: 669, 1936 3. SMITH JS, BRANDON 5: Acute carbon monoxide poisoning - 3 years of experience in a defined population. Postgrad Med J 46: 65, 1970 4. WEir.smi. EA, KAHN RL: Denial of Illness, Springfield IL CC Thomas, 1955, pp 96-100 5. CRITCHLEY' M:' .The Parietal Lobes, London, Edward Arnold, 1953, p 254 6. Ibid, p 388 7. RICHARDSON JC, CHAMBERS RA, HEYWOOD PM: Encephalopathies of anoxia and hypoglycemia. Arch Neurol 1: 178, 1959 8. GINSBERG R, ROMANO J: Carbon monoxide poisoning: need for appropriate treatment. Am I Psychiatry 133: 317, 1976 9. JEFFERSON JW: Subtle neuropsychiatric sequelae of carbon monoxide intoxication: two case reports. Ibid, p 961
10. SMITH JS, BRANDON S: Morbidity from acute carbon monoxide poisoning at three-year follow-up. Br Med J 1: 318, 1973 11. GINSBERG MD, MYERS RE: Experimental carbon monoxide encephalopathy in the primate. Arch Neurol 30: 202, 1974 12. SLUJJTER ME: The treatment of carbon monoxide poisoning by administration of oxygen at high atmospheric pressure, in Progress in Brain Research, vol 24, Boua H, LEDINGHAM IM (eds), Amsterdam, Elsevier, 1967, pp 123-82 13. FORBES WH,
SARGENT F,
ROUGHTON FJW:
The rate of carbon monoxide uptake by normal men. Am J Physiol 143: 594, 1945 14. FORBEs WH: Carbon monoxide uptake via the lungs. Ann NY Acad Sci 174: 72, 1970 15. BRODY JS, COBURN RF: Effects of elevated carboxyhemoglobin on gas exchange in the lung. Ibid, p 255
Two-year follow-up study of patients with known serum concentrations of carcinoembryonic antigen P.R. BAND,* MD, FRCP[C]; I.T. BECK,f MD, PH D, FACP, FRCP[C]; P.J. DINNER,* M Sc; AB. MILLER,* MB, FRCP[C]
Between 1970 and 1972 five university centres in Canada and the United States collaborated in a study of a test for carcinoembryonic antigen (CEA) in the serum, with the Montreal General Hospital's laboratory acting as the reference laboratory, examining duplicate halves of specimens examined in local laboratories. The National Cancer Institute of Canada acted as the coordinating centre. The first report gave results for 503 patients admitted to the study between June 1971 and April 1972, 146 of whom had cancer of the colon or recturn.1 Discrimination between colorectal cancer and "other" conditions was good at a CEA value of 2.5 ng/mL or more, such a result being obtained in 66% of the patients with colorectal cancer in the local laboratories and 62% in the reference laboratory, compared with 39% and 33%, respectively, of patients with "other" conditions. Patients with Dukes' C lesions of the colon or rectum From *University of Alberta, Edmonton; tQueen's University, Kingston; and .epidemiology unit, National Cancer Institute of Canada, University of Toronto Reprint requests to: Dr. AB. Miller, Director, Epidemiology unit, National Cancer Institute of Canada, University of Toronto, 121 St. Joseph St., Toronto, Ont. M5S 2R9
(those with metastases in regional lymph nodes) were more likely to have elevated CEA values than patients with more localized lesions. CEA was also more commonly found in patients with other cancers or with liver disease than in patients with other (benign) conditions. It was concluded that the test for CEA can be reproduced in other laboratories and that it or another simple technique could become an important diagnostic aid for colorectal cancer. It was also suggested that the CEA value might be an important prognostic indicator and that, for the 33% of patients with elevated CEA values but no colorectal cancer, follow-up might show an abnormally high incidence of colorectal cancer in subsequent years. Follow-up of the original 503 cases (and a smaller number reported after April 1972), at 6, 12, 18 and 24 months after admission to the study, was attempted to examine these hypotheses. A lack of resources severely restricted the extent of documentation of followup in the three American centres, but a special effort was made to determine the status of patients in the two Canadian centres at 24 months. Contact with
the patient at any time up to 3 months before or after this date was accepted as the required 24-month follow-up contact. Results Of the 103 patients admitted to the study from Kingston and the 96 from Edmonton, follow-up forms were returned for 102 and 91, respectively; of these, 14 were lost to follow-up at 2 years. CEA values were reported on the basis of the initial results from the Montreal laboratory to avoid differences between laboratories. As CEA values were not available for 14 of the patients followed up, results are presented for only 165 patients. The prognostic value of the initial CEA value in the 36 patients with colorectal cancer is shown in Table I. If values of 2.5 ng/mL or more are taken as positive the difference in terms of disease-free status and survival at 2 years is significant at the 5% level (X2 = 6.47 and 5.73, respectively, with Yates' continuity correction). If values of 5.0 ng/mL or more are taken as positive the difference in disease-free status does not attain statistical signif-
Table I-Status at 2 years of patients with colorectal cancer according to initial serum concentration of carcinoembryonic antigen (CEA) and Dukes' classification2 CEA concentration (ng/mL) and Dukes' classification*
