I would like to hear from any physician who is treating a diabetic patient suffering from severe complications while undergoing therapy with metformin. I can be contacted by telephone at (514) 343-6329 (collect) or in writing (please include all relevant information). PIERRE BIRON, MD Coordinator - metformin monitoring do Department of pharmacology University of Montreal Montreal, PQ H3C 3J7
Indomethacin and aplastic anemia To the editor: In their letter entitled "Fatal aplastic anemia following indomethacin ingestion" (Can Med Assoc J 117: 118, 1977) Drs. E. Menkes and G.J. Kutas report a case of aplastic anemia following 3 days' standarddosage indomethacin therapy. They failed to consider the possible role of the patient's past drug therapy in this adverse effect. In the case described the patient was treated previously for rheumatoid arthritis with an unstated number of enteric-coated tablets of acetylsalicylic acid and had received a 10-month course of sodium aurothiomalate (total dose, 435 mg). Gold salts have been reported to be one of the agents most frequently associated with drug-induced aplastic anemia.' In their review, Swanson and Cook2 tabulated 80 reports of gold salt-induced aplastic anemia. They noted that aplastic anemia secondary to gold salt therapy may occur 3 days to 6 months after the cessation of treatment. As reported in the literature (C.A. Shearer, W.A. Parker: unpublished data, 1977), symptoms of aplastic anemia occur in over 50% of patients within the first 7 weeks after the final injection. The onset may be quite sudden and without warning,3 and may occur despite monthly blood counts (including platelet counts).4 Menkes and Kutas state that for their patient gold injections were discontinued 6 weeks prior to the onset of symptoms. Therefore, I believe that gold salt therapy should be considered a possible etiologic factor in inducing aplastic anemia in their patient. Fourteen cases of acetylsalicylic acid-induced aplastic anemia have been reported.2 In view of this low incidence, despite their widespread use, salicylates are less likely than gold salts to have caused aplastic anemia in this patient. The authors state that "there have been three reports of deaths due to progressive aplastic anemia with onset 3 to 10 days after the institution of therapy with indomethacin in the usual therapeutic doses." This statement may be misleading. Firstly, from a cursory look at this statement one might infer
that there have been three reports of aplastic anemia following 3 to 10 days of indomethacin therapy. These would appear to resemble the case presented by Menkes and Kutas. However, the patient in the report by Frederick and Tanaka5 was treated with indomethacin, 75 mg/d for 1 month, 1 year prior to admission for aplastic anemia. The patient later received indomethacin for 3 to 4 days and presented with symptoms of lethargy and weakness 2 weeks post-therapy, and with bruisability and petechiae 5 weeks post-therapy. Therefore, this case report does not conform to the criteria of onset 3 to 10 days after therapy was begun. Secondly, the authors cite a review1 of drug-induced aplastic anemia to justify the previously quoted statement. This review states only that indomethacin has been implicated in causing aplastic anemia; no information is provided to indicate dose, duration or time of onset of symptoms. The report by Menkes and Kutas highlights one of the major problems of iatrogenic blood dyscrasias - that is, the positive identification of the etiologic agent. The possibility exists that gold salts or, less likely, acetylsalicylic acid therapy, rather than indomethacin was responsible for this fatal adverse effect. The situation is further complicated in that approximately 50% of cases of aplastic anemia are idiopathic.1 CAMERON A. SHEARER, PHARM D Assistant professor College of pharmacy Dalhousie University Halifax, MS
References 1. WILLIAMS DM, LYNCH RE, CARTWRIGHT GE: Drug-induced aplastic anemia. Semin Hemato!
10: 195, 1973 2. SWANSON M, COOK R: Drugs, Chemicals and Blood Dvscrasias, Hamilton, Drug Jntelligence PubI, 1977, pp 126, 466 3. KAY AGL: Myelotoxicity of gold. Br Med I 1: 1266, 1976 4. Gold for rheumatoid arthritis (E). Br Med I 1: 471, 1971 5. FREDRICK GR, TANAKA KR: Indomethacin and aplastic anemia (C). N Engi I Med 279: 1291, 1968
What do family physicians see in practice? To the editor: I am surprised at the conclusions reached by Dr. A.M. Warrington and his colleagues in their article on this subject (Can Med Assoc J 117: 354, 1977) and also by the methodology they used in their study. The purpose of the investigation was to determine what Canadian physicians see in general practice. There is no way in which a self-selected group of seven physicians in a middle-income area of one city can be representative of all physicians. To make suggestions for training based on this biased sample seems inappropriate.
18 CMA JOURNAL/JANUARY 7, 1978/VOL. 118
(amoxicillin) AMOXIL. (amoxicillin). -. A new generation broad-spectrum penicillin. INDICATIONS: Infections due to susceptible strains of the following microorganisms: Gram-negative-H. influenzae, E. coli, R mirabilis and Ngonorrhoeae. Gram-positive-Streptococci, Dpneumoniae and penicillin-sensitive staphylococci. In emergency cases where the causative organism is not yet identified. therapy may be initiated with AMOXIL on the basis of clinical judgment while awaiting the results of bacteriologic studies. DOSAGE AND ADMINISTRATION: Infections of the ear, nose and throat due to streptococci, pneumococci, and penicillin-sensitive staphylococci; infections of the upper respiratory tract due to H. influenzae; in ections of the genitourinary tract due to E. coli, R mirabilis, and S. faecalis; infections of the skin and soft tissues due to streptococci, penicillin-sensitive staphyloc.occi and E. coil: Usual Dose: Adults-250 mg every 8 hours. Children-25 mg/kg/day in divided doses every 8 hours. This dosage should not exceed the recommended adult dosage. In severe infections or infections caused by less sensitive organisms: 500 mg every 8 hours for adults, and 50 mg/kg/day in divided doses every 8 hours for children. Infections of the lower respiratory tract due to streptococci, pneumococci, penicillin-sensitive staphylococci and H. influenzae: Usual Dose: Adults-SQO mg every 8 hours. Children-SO mg/kg/day in divided doses every 8 hours. This dosage should not exceed the recommended adult dosage. Urethritis due to N. gonorrhoeae: 3 g as a single oral dose. Patients with gonorrhea, with a suspected lesion of syphilis, should have darkfield examinations before receiving AMOXIL, and monthly serologic tests for a minimum of four months. For chronic urinary tract infections, frequent bacteriologic and clinical appraisals are necessary. Smaller doses than those recommended above should not be used. Stubborn infections may require several weeks' treatment, sometimes at higher doses than recommended above. Concurrent bacteriologic sensitivity monitoring is recommended. Continued clinical and/or bacteriologic follow-up for several months after cessation of therapy may be required. Treatment should continue for 48 to 72 hours beyond the time patient becomes asymptomatic or bacterial eradication is obtained. At least 10 days' treatment is recommended for infections caused by beta- hemolytic streptococci to prevent acute rheumatic fever or glomerulonephritis. CONTRAINDICATION: In patients with a history of allergy to the penicillins or the cephalosporins. PRECAUTIONS: Periodic assessment of renal, hepatic, and hematopoietic function should be made during prolonged AMOXIL therapy. AMOXIL is excreted mostly by the kidney. The dosage administered to patients with renal impairment should be reduced proportionately to the degree of loss of renal function. The possibility of superinfections with mycotic or bacterial organisms should be kept in mind during therapy. If superinfections occur (usually involving Aerobacter, Pseudomonas or Candida), the drug should be discontinued and aproriatethera instituted. ADVERSE R EAC. S.As with other penicillins, presumably the most common untoward reactions will be related to sensitivity phenomena, similar to those observed with ampicillin. They are more likely to occur in individuals who have previously demonstrated hypersensitivity to penicillins and in those with a history of allergy, asthma, hay fever or urticaria. (See Product Monograph which is available on request).SUPPLI ED: AMOXIL-250 Capsules (250 mg amoxicillin) in bottles of 100 and 500. AMOXIL-500 Capsules (500 mg amoxicillin) in bottles of 100.AMOXIL.l2sSuspension(125mg amoxicillin per 5 ml) in bottles of 75, 100 and 150 ml. AMOXIL-250 Suspension (250 mg amoxicillin per 5 ml) in bottles of 75, 100 and 150 ml. AMOXIL Pediatric Drops (50 mg amoxicillin per ml) in bottles of 15 ml. AYERST LABORATORIES Division of Ayerst, McKenna & Harrison Limited Montreal, Canada Made in Canada by arrangement with Reg'd BEECHAM, iNC.
I hope physicians are trained to cope with all the problems the patients have, not just the problems the physicians recognize. The Canadian study refers to the high level of recognition by physicians of hypertension in patients in the Virginia study; it comments on the similarities, not on the differences between the two investigations. I doubt whether people in Canada are significantly different from those in the United States. The Virginia.. study involved more physicians than 'the Canadian one and its results are similar in most respects to those of the national ambulatory care study of the US National Center for Health Statistics.1 The national ambulatory care study found the distribution of problems seen to be similar but not identical to that found in surveys of the US population. These surveys examined probability samples of the US public to verify the prevalence of common conditions such as hypertension, diabetes, coronary artery disease, gout and rheumatoid disease.24 Hypertension is the most common chronic disease in the US; its prevalence is between 15% and 18% .5,6 Coronary artery disease is the most common cause of morbidity and death. Diabetes affects 2% or more of the population. Similar studies show the prevalence of conditions in the general population to be greater than that recognized by family practitioners. One would expect persons with chronic disease to constitute a higher percentage of the physician's practice than of the general population. Conditions of "soft addiction", such as obesity, alcoholism and smoking are very common in the general population, although the last two were not recognized as problems in these studies. The article by Warrington and colleagues suggests to me the failure on the part of the physicians sampled to recognize common conditions and emotional problems in their patients. All chronic diseases have associated emotional problems that need special psychosocial skills and attitudes. Or perhaps, as I hope is true, they failed to code them. This is borne out by the article on the treatment of hypertension in a family practice by K.V. Rudnick and associates in a subsequent issue of the Journal (117: 492, 1977). C.M.G. BUTTERY, MD, MPH Associate professor Department of family medicine Eastern Virginia Medical School Norfolk, Va
3. Blood Pressure of Adults by Race and Area; United States 1960-1964, Public Health Service publ no 1000, ser 11, no 5, Washington, US Govt Printing Office, July 1964 4. Hypertension and Hypertensive Heart Disease in Adults; United States 1960-1962, Public Health Service pubi no 1000, ser 11, no 13, Washington, US Govt Printing Office, May 1966 5. Blood Pressure of Persons 6-74 Years of Age in the United States, advance data from vital and health statistics of the National Center for Health Statistics, no 1, Hyattsville, Md, NCHS, Oct 18, 1976 6. Hypertension; United States, 1974, advance data from vital and health statistics of the National Center for Health Statistics, no 2, Hyattsville, Md, NCHS, Nov. 8, 1976
Autopsy of an Egyptian mummy (Nakht-ROM I) To the editor: It was interesting to learn about the contributions of so many disciplines to the elaborate autopsy of the mummy of Nakht (ROM I), and about the use of advanced technologies to extract the greatest amount of information (Can Med Assoc J 117: 461, 1977). Some presumably highpriced equipment was used and no expense was spared to do a thorough job, even if the various experts' services were donated. It therefore seems a great pity that one extremely valuable means of research either was not reported or was omitted, namely carbon-14 dating of the body or the cloth wrappings. As little as 50 g of the body, and even less of the wrappings (maybe 20 g), would have had to be sacrificed. The article by N.B. Millet on the archeologic background (page 462) claims accurate dating of Nakht, but the only thing that seems certain is that this boy-weaver lived in the XXth Dynasty during the reign of the predecessor of Ramesses III. Conventional Egyptian chronology has long placed the start of the XXth Dynasty at about 1200 BC, but this is now being challenged strongly. As a matter of fact, the first person to put a date on Ramesses III's accession was J.C. Prichard, a Scottish psychiatrist, who, in 1819, stated that it was 1147 BC; that was before anybody had succeeded in deciphering a Single hieroglyph. The person who challenges the conventional view is another psychiatrist, Dr. Immanuel Velikovsky, who at one time practised in Tel Aviv. Dr. Velikovsky's reconstruction of Egyptian chronology covers a 1200year span from the time of the Exodus to the conquest by Alexander the Great in 332 BC. This fascinating and scholarly work will eventually be completed in four volumes: the first, published in 1952 and entitled "Ages in Chaos covered the earlier part of this span, and "Peoples of the Sea"2 covers the last 200 years approximately, down to Alexander. Two further volumes will deal with the intervening centuries and one of them, to be entitled "Ramesses II and His Time", is due to appear " 1
References 1. The National Ambulatory Medical Care Survey; 1973 Summary, United States, May 1973April 1974, DHEW pubi no (HRA) 76-1772, Washington, US Govt Printing Office, October 1975 2. Blood Pressure of Adults by Age and Sex; United States 1960-1962, Public Health Service pubi no 1000, ser 11, no 4, Washington, US Govt Printing Office. June 1964
20 CMA JOURNAL/JANUARY 7, 1978/VOL. 118
early this year. Dr. Velikovsky's books represent a sustained effort in real-life detective work; they richly repay careful reading because he is at great pains to explain all his clues and supply all his references. His reconstruction has a strong appeal to anyone who has no axe to grind and no vested interest in maintaining the conventional chronology. Dr. Velikovsky gathers and arranges a wealth of evidence to show why the presently accepted order of the dynasties is arbitrary and wrong, and how the same events have come to be described twice in some instances, so that Egyptian history has been artificially extended anywhere from about 500 years (e.g., at the time of Tutankhamun) to nearly 800 years (at the time of Ramesses III and his predecessor). It is this period, when Nakht is said to have lived, that is painstakingly reconstructed in "Peoples of the Sea". Furthermore, the book contains a threechapter supplement that explains in detail exactly how the conventional chronology came about, and how its astronomic support - always triumphantly quoted as unassailable - is actually rooted in a fallacy. Any nonexpert who takes the trouble to grasp the intricate details set out in that supplement can hardly help but agree with Dr. Velikovsky that the conventional chronology "does not seem so stable and secure as once thought; it looks more like an aggregation of many unconnected things, each unstable by itself, piled precariously one upon the other."2 Up to now there has been a scarcity of 14C dates on objects from the New Kingdom of Egypt. Objects of organic origin are needed, of course, and some are far more suitable than others. All such ancient objects are precious, and the conventional chronology has hitherto been regarded as more accurate than 14C dating. Egyptologists are prone to suggest that in these cases the 14C method is being tested, the date of the object being already "known". It is believed widely that a number of 14C dates of Egyptian sources have been discarded if they have turned out to be a few centuries out of line. One archeologist, Professor Brew,3 has been quoted as saying: "If a 14C date supports our theories, we put it in the main text. If it does not entirely contradict them, we put it in a foot-note. And if it is completely 'out-of-date' we just drop it." Two British Museum tests (BM-642A and BM-642B), the results of which, were never officially published, yielded dates about 500 years too recent for the accepted chronology but they neatly support Dr. Velikovsky's theory; they were conducted on reed and palm nut kernels from Tutankhamun's tomb. Chips of wood from
Indomethacin and aplastic anemia To the editor: In their letter entitled "Fatal aplastic anemia following indomethacin ingestion" (Can Med Assoc J 117: 118, 1977) Drs. E. Menkes and G.J. Kutas report a case of aplastic anemia following 3 days' standarddosage indomethacin therapy. They failed to consider the possible role of the patient's past drug therapy in this adverse effect. In the case described the patient was treated previously for rheumatoid arthritis with an unstated number of enteric-coated tablets of acetylsalicylic acid and had received a 10-month course of sodium aurothiomalate (total dose, 435 mg). Gold salts have been reported to be one of the agents most frequently associated with drug-induced aplastic anemia.' In their review, Swanson and Cook2 tabulated 80 reports of gold salt-induced aplastic anemia. They noted that aplastic anemia secondary to gold salt therapy may occur 3 days to 6 months after the cessation of treatment. As reported in the literature (C.A. Shearer, W.A. Parker: unpublished data, 1977), symptoms of aplastic anemia occur in over 50% of patients within the first 7 weeks after the final injection. The onset may be quite sudden and without warning,3 and may occur despite monthly blood counts (including platelet counts).4 Menkes and Kutas state that for their patient gold injections were discontinued 6 weeks prior to the onset of symptoms. Therefore, I believe that gold salt therapy should be considered a possible etiologic factor in inducing aplastic anemia in their patient. Fourteen cases of acetylsalicylic acid-induced aplastic anemia have been reported.2 In view of this low incidence, despite their widespread use, salicylates are less likely than gold salts to have caused aplastic anemia in this patient. The authors state that "there have been three reports of deaths due to progressive aplastic anemia with onset 3 to 10 days after the institution of therapy with indomethacin in the usual therapeutic doses." This statement may be misleading. Firstly, from a cursory look at this statement one might infer
that there have been three reports of aplastic anemia following 3 to 10 days of indomethacin therapy. These would appear to resemble the case presented by Menkes and Kutas. However, the patient in the report by Frederick and Tanaka5 was treated with indomethacin, 75 mg/d for 1 month, 1 year prior to admission for aplastic anemia. The patient later received indomethacin for 3 to 4 days and presented with symptoms of lethargy and weakness 2 weeks post-therapy, and with bruisability and petechiae 5 weeks post-therapy. Therefore, this case report does not conform to the criteria of onset 3 to 10 days after therapy was begun. Secondly, the authors cite a review1 of drug-induced aplastic anemia to justify the previously quoted statement. This review states only that indomethacin has been implicated in causing aplastic anemia; no information is provided to indicate dose, duration or time of onset of symptoms. The report by Menkes and Kutas highlights one of the major problems of iatrogenic blood dyscrasias - that is, the positive identification of the etiologic agent. The possibility exists that gold salts or, less likely, acetylsalicylic acid therapy, rather than indomethacin was responsible for this fatal adverse effect. The situation is further complicated in that approximately 50% of cases of aplastic anemia are idiopathic.1 CAMERON A. SHEARER, PHARM D Assistant professor College of pharmacy Dalhousie University Halifax, MS
References 1. WILLIAMS DM, LYNCH RE, CARTWRIGHT GE: Drug-induced aplastic anemia. Semin Hemato!
10: 195, 1973 2. SWANSON M, COOK R: Drugs, Chemicals and Blood Dvscrasias, Hamilton, Drug Jntelligence PubI, 1977, pp 126, 466 3. KAY AGL: Myelotoxicity of gold. Br Med I 1: 1266, 1976 4. Gold for rheumatoid arthritis (E). Br Med I 1: 471, 1971 5. FREDRICK GR, TANAKA KR: Indomethacin and aplastic anemia (C). N Engi I Med 279: 1291, 1968
What do family physicians see in practice? To the editor: I am surprised at the conclusions reached by Dr. A.M. Warrington and his colleagues in their article on this subject (Can Med Assoc J 117: 354, 1977) and also by the methodology they used in their study. The purpose of the investigation was to determine what Canadian physicians see in general practice. There is no way in which a self-selected group of seven physicians in a middle-income area of one city can be representative of all physicians. To make suggestions for training based on this biased sample seems inappropriate.
18 CMA JOURNAL/JANUARY 7, 1978/VOL. 118
(amoxicillin) AMOXIL. (amoxicillin). -. A new generation broad-spectrum penicillin. INDICATIONS: Infections due to susceptible strains of the following microorganisms: Gram-negative-H. influenzae, E. coli, R mirabilis and Ngonorrhoeae. Gram-positive-Streptococci, Dpneumoniae and penicillin-sensitive staphylococci. In emergency cases where the causative organism is not yet identified. therapy may be initiated with AMOXIL on the basis of clinical judgment while awaiting the results of bacteriologic studies. DOSAGE AND ADMINISTRATION: Infections of the ear, nose and throat due to streptococci, pneumococci, and penicillin-sensitive staphylococci; infections of the upper respiratory tract due to H. influenzae; in ections of the genitourinary tract due to E. coli, R mirabilis, and S. faecalis; infections of the skin and soft tissues due to streptococci, penicillin-sensitive staphyloc.occi and E. coil: Usual Dose: Adults-250 mg every 8 hours. Children-25 mg/kg/day in divided doses every 8 hours. This dosage should not exceed the recommended adult dosage. In severe infections or infections caused by less sensitive organisms: 500 mg every 8 hours for adults, and 50 mg/kg/day in divided doses every 8 hours for children. Infections of the lower respiratory tract due to streptococci, pneumococci, penicillin-sensitive staphylococci and H. influenzae: Usual Dose: Adults-SQO mg every 8 hours. Children-SO mg/kg/day in divided doses every 8 hours. This dosage should not exceed the recommended adult dosage. Urethritis due to N. gonorrhoeae: 3 g as a single oral dose. Patients with gonorrhea, with a suspected lesion of syphilis, should have darkfield examinations before receiving AMOXIL, and monthly serologic tests for a minimum of four months. For chronic urinary tract infections, frequent bacteriologic and clinical appraisals are necessary. Smaller doses than those recommended above should not be used. Stubborn infections may require several weeks' treatment, sometimes at higher doses than recommended above. Concurrent bacteriologic sensitivity monitoring is recommended. Continued clinical and/or bacteriologic follow-up for several months after cessation of therapy may be required. Treatment should continue for 48 to 72 hours beyond the time patient becomes asymptomatic or bacterial eradication is obtained. At least 10 days' treatment is recommended for infections caused by beta- hemolytic streptococci to prevent acute rheumatic fever or glomerulonephritis. CONTRAINDICATION: In patients with a history of allergy to the penicillins or the cephalosporins. PRECAUTIONS: Periodic assessment of renal, hepatic, and hematopoietic function should be made during prolonged AMOXIL therapy. AMOXIL is excreted mostly by the kidney. The dosage administered to patients with renal impairment should be reduced proportionately to the degree of loss of renal function. The possibility of superinfections with mycotic or bacterial organisms should be kept in mind during therapy. If superinfections occur (usually involving Aerobacter, Pseudomonas or Candida), the drug should be discontinued and aproriatethera instituted. ADVERSE R EAC. S.As with other penicillins, presumably the most common untoward reactions will be related to sensitivity phenomena, similar to those observed with ampicillin. They are more likely to occur in individuals who have previously demonstrated hypersensitivity to penicillins and in those with a history of allergy, asthma, hay fever or urticaria. (See Product Monograph which is available on request).SUPPLI ED: AMOXIL-250 Capsules (250 mg amoxicillin) in bottles of 100 and 500. AMOXIL-500 Capsules (500 mg amoxicillin) in bottles of 100.AMOXIL.l2sSuspension(125mg amoxicillin per 5 ml) in bottles of 75, 100 and 150 ml. AMOXIL-250 Suspension (250 mg amoxicillin per 5 ml) in bottles of 75, 100 and 150 ml. AMOXIL Pediatric Drops (50 mg amoxicillin per ml) in bottles of 15 ml. AYERST LABORATORIES Division of Ayerst, McKenna & Harrison Limited Montreal, Canada Made in Canada by arrangement with Reg'd BEECHAM, iNC.
I hope physicians are trained to cope with all the problems the patients have, not just the problems the physicians recognize. The Canadian study refers to the high level of recognition by physicians of hypertension in patients in the Virginia study; it comments on the similarities, not on the differences between the two investigations. I doubt whether people in Canada are significantly different from those in the United States. The Virginia.. study involved more physicians than 'the Canadian one and its results are similar in most respects to those of the national ambulatory care study of the US National Center for Health Statistics.1 The national ambulatory care study found the distribution of problems seen to be similar but not identical to that found in surveys of the US population. These surveys examined probability samples of the US public to verify the prevalence of common conditions such as hypertension, diabetes, coronary artery disease, gout and rheumatoid disease.24 Hypertension is the most common chronic disease in the US; its prevalence is between 15% and 18% .5,6 Coronary artery disease is the most common cause of morbidity and death. Diabetes affects 2% or more of the population. Similar studies show the prevalence of conditions in the general population to be greater than that recognized by family practitioners. One would expect persons with chronic disease to constitute a higher percentage of the physician's practice than of the general population. Conditions of "soft addiction", such as obesity, alcoholism and smoking are very common in the general population, although the last two were not recognized as problems in these studies. The article by Warrington and colleagues suggests to me the failure on the part of the physicians sampled to recognize common conditions and emotional problems in their patients. All chronic diseases have associated emotional problems that need special psychosocial skills and attitudes. Or perhaps, as I hope is true, they failed to code them. This is borne out by the article on the treatment of hypertension in a family practice by K.V. Rudnick and associates in a subsequent issue of the Journal (117: 492, 1977). C.M.G. BUTTERY, MD, MPH Associate professor Department of family medicine Eastern Virginia Medical School Norfolk, Va
3. Blood Pressure of Adults by Race and Area; United States 1960-1964, Public Health Service publ no 1000, ser 11, no 5, Washington, US Govt Printing Office, July 1964 4. Hypertension and Hypertensive Heart Disease in Adults; United States 1960-1962, Public Health Service pubi no 1000, ser 11, no 13, Washington, US Govt Printing Office, May 1966 5. Blood Pressure of Persons 6-74 Years of Age in the United States, advance data from vital and health statistics of the National Center for Health Statistics, no 1, Hyattsville, Md, NCHS, Oct 18, 1976 6. Hypertension; United States, 1974, advance data from vital and health statistics of the National Center for Health Statistics, no 2, Hyattsville, Md, NCHS, Nov. 8, 1976
Autopsy of an Egyptian mummy (Nakht-ROM I) To the editor: It was interesting to learn about the contributions of so many disciplines to the elaborate autopsy of the mummy of Nakht (ROM I), and about the use of advanced technologies to extract the greatest amount of information (Can Med Assoc J 117: 461, 1977). Some presumably highpriced equipment was used and no expense was spared to do a thorough job, even if the various experts' services were donated. It therefore seems a great pity that one extremely valuable means of research either was not reported or was omitted, namely carbon-14 dating of the body or the cloth wrappings. As little as 50 g of the body, and even less of the wrappings (maybe 20 g), would have had to be sacrificed. The article by N.B. Millet on the archeologic background (page 462) claims accurate dating of Nakht, but the only thing that seems certain is that this boy-weaver lived in the XXth Dynasty during the reign of the predecessor of Ramesses III. Conventional Egyptian chronology has long placed the start of the XXth Dynasty at about 1200 BC, but this is now being challenged strongly. As a matter of fact, the first person to put a date on Ramesses III's accession was J.C. Prichard, a Scottish psychiatrist, who, in 1819, stated that it was 1147 BC; that was before anybody had succeeded in deciphering a Single hieroglyph. The person who challenges the conventional view is another psychiatrist, Dr. Immanuel Velikovsky, who at one time practised in Tel Aviv. Dr. Velikovsky's reconstruction of Egyptian chronology covers a 1200year span from the time of the Exodus to the conquest by Alexander the Great in 332 BC. This fascinating and scholarly work will eventually be completed in four volumes: the first, published in 1952 and entitled "Ages in Chaos covered the earlier part of this span, and "Peoples of the Sea"2 covers the last 200 years approximately, down to Alexander. Two further volumes will deal with the intervening centuries and one of them, to be entitled "Ramesses II and His Time", is due to appear " 1
References 1. The National Ambulatory Medical Care Survey; 1973 Summary, United States, May 1973April 1974, DHEW pubi no (HRA) 76-1772, Washington, US Govt Printing Office, October 1975 2. Blood Pressure of Adults by Age and Sex; United States 1960-1962, Public Health Service pubi no 1000, ser 11, no 4, Washington, US Govt Printing Office. June 1964
20 CMA JOURNAL/JANUARY 7, 1978/VOL. 118
early this year. Dr. Velikovsky's books represent a sustained effort in real-life detective work; they richly repay careful reading because he is at great pains to explain all his clues and supply all his references. His reconstruction has a strong appeal to anyone who has no axe to grind and no vested interest in maintaining the conventional chronology. Dr. Velikovsky gathers and arranges a wealth of evidence to show why the presently accepted order of the dynasties is arbitrary and wrong, and how the same events have come to be described twice in some instances, so that Egyptian history has been artificially extended anywhere from about 500 years (e.g., at the time of Tutankhamun) to nearly 800 years (at the time of Ramesses III and his predecessor). It is this period, when Nakht is said to have lived, that is painstakingly reconstructed in "Peoples of the Sea". Furthermore, the book contains a threechapter supplement that explains in detail exactly how the conventional chronology came about, and how its astronomic support - always triumphantly quoted as unassailable - is actually rooted in a fallacy. Any nonexpert who takes the trouble to grasp the intricate details set out in that supplement can hardly help but agree with Dr. Velikovsky that the conventional chronology "does not seem so stable and secure as once thought; it looks more like an aggregation of many unconnected things, each unstable by itself, piled precariously one upon the other."2 Up to now there has been a scarcity of 14C dates on objects from the New Kingdom of Egypt. Objects of organic origin are needed, of course, and some are far more suitable than others. All such ancient objects are precious, and the conventional chronology has hitherto been regarded as more accurate than 14C dating. Egyptologists are prone to suggest that in these cases the 14C method is being tested, the date of the object being already "known". It is believed widely that a number of 14C dates of Egyptian sources have been discarded if they have turned out to be a few centuries out of line. One archeologist, Professor Brew,3 has been quoted as saying: "If a 14C date supports our theories, we put it in the main text. If it does not entirely contradict them, we put it in a foot-note. And if it is completely 'out-of-date' we just drop it." Two British Museum tests (BM-642A and BM-642B), the results of which, were never officially published, yielded dates about 500 years too recent for the accepted chronology but they neatly support Dr. Velikovsky's theory; they were conducted on reed and palm nut kernels from Tutankhamun's tomb. Chips of wood from
