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ANÆMIA IN AFRICANS IN UGANDA
105
cassation of benemid w" confirmed by
the
phenol-
excretion test, and in some patients this test was also done before and during the administration of benemid. In this regard it may be of interest that the 3 patients (nos. 5, 6, and 9) with the most uniformly maintained-as distinct from the highest -blood levels are those showing the most significant depressionof phenolsulphonephthalein excretion under the influence of benemid. The actual blood levels obtained are satisfactory throughout. From the results it seems fair to suggest that, with really adequate dosage-equivalent by weight - to the doses employed with the newer antibiotics-and possibly with the help of benemid, procaine penicillin given by mouth may be no less effective and reliable, in penicillin-sensitive infections, than these newer antibiotics ; and that this is at any rate worthy of therapeutic trial.’
sulphonephthalein (phenol-red)
-
’
_
indebted to Dr. ]3eyer of Messrs. Sharp & Dohme for supplies of benemid, and to Dr. H. M. Walker, of Glaxo Laboratories Ltd., for supplies of proeaine We
Ltd.,
are
Philadelphia,
’
penicillin.
Medical Medical School. School,
W. Dundee.
WALKER, WALKER
R. B. HUNTER.
ANÆMIA IN AFRICANS IN UGANDA SiR,-Certain points in the paper by Dr. Trowell and (Oct. 27) seem to me to require
clarification.
amplification
there does not seem to be anything " mysabout the rise of mean corpuscular volume (M.c.v.) in hookworm anaemia. Lehmannshowed clearly that the rise of M.c.v. on giving iron in such cases caused a.reticulocyte response which continued while the worms were still in situ. The M.c.v. rise was due to the rapid change in the cell population, the old microcytic cells being replaced by the young macrocytic cells. Further, he showed that in other anaemias where there was blood
-
Firstly,
terious
"
destruction-e.g., malaria-reticulocytosis was accompanied by macrocytosis, which disappeared with the end of the reticulocytosis. Unfortunately, the question of reticulocytosis was not discussed in the paper by Holmes and Gee2 quoted by Trowell. It does seem possible for patients with light hookworm loads and-an’adequate iron intake to have a slight anaemia which is mildly macrocytic. Foy and Kondi (personal communication) find larger reticulocytes with hookworm anaemia in Africans than those seen in Europeans. Lehmannhas pointed out the lack of apparent ripening of these immature (precoctic) cells and has suggested that this is connected with a lack of tyrosine. This precoctic blood picture is in other anaemias besides hookworm. It should be anaemia is probably far the commonest cause of severe anaemia in Uganda, at Mulago anaemia is usually polymorphic in aetiology. Hookworm infection, malaria, and nutritional status are often concerned in the same patient. I personally have had cases of hookworm anaemia in malnourished patients whose iron deficienev was restored but who made no further progress to recovery from a level of about 9 g. Hb per 100 ml. until the return of the serum-protein to normal, after which the Hb reached normal level on diet alone. This of course is not by any means an original observation. Whether the anaemia was macrocytic at this stage I did not investigate. I agree with Trowell that factors such as pteroylglutamic acid, liver, and vitamin B12 do not influence the macrocytic aspects of anaemia seen in Uganda. It should be pointed out that them despite diligent although we have not encountered search, Foy and Kondi 3 find in Kenya anaemias which seen
emphasised that, while hookworm
are
(1)megaloblastic normocytic, (2) normocytic
normo-
1. Lehmann, H. Lancet, 1949, i, 90. 2. Holmes, E. G., Gee, F. L. E. Afr. med. J. 1951, 28, 297. 3. Foy, H., Kondi, A. Trans. R. Soc. trop. Med. 1950, 43, 635.
chromic (but with
giant".&bgr;tab cells in the marrow}, or (3) megaloblastic macrocytic. All these anaemias respond to Marmite,’ liver, and pteroylglutamic acid. One case of megaloblastic macrocytic anaemia apparently responded to penicillin.4 How common they are is not clear. I would support Trowell’s contention that the unqualified use of the term" macrocytic" often implies an aetiology which is not explicit in the meaning of the word. I suspect that there really may be no real contradiction between those who contend that a macrocytosis as seen ’
-
in the local African anaemia is the result of internal or external blood-loss, and those who contend that this is due to diet. The two would seem to be interrelated, particularly if the tyrosine contention is correct. This also may explain why it appears that an anaemia with infection appears to be macrocytic in an African but not in Europeans. Certainly such a macrocytosis is not nutritional in the sense of deficiency of a specific factor. Mulago Hospital, Kampala, Uganda.
P. P W. H W HUTTON.
COALMINERS’ PNEUMOCONIOSIS SIR,—It appears to me that Dr. Meiklejohn (Dec. 29) has based his conclusions on, inter alia, two assumptions -namely (1) that certification of a miner by the Pneumoconiosis Medical Board can be relied upon as evidence for the existence of the disease in a particular case, and (2) that clinical plus radiological examination (by experienced observers, presumably) can be relied upon to confirm or exclude the presence of pneumoconios’s. Personal experience, which -is, however, confined to the eastern end of the South Wales coalfield, makes -me doubt whether we are entitled to take these two assnmptions for granted. I have seen it happen quite frequently that a miner has been examined by, say, the massradiography unit and advised that " evidence of dust disease was seen in his chest film," and shortly afterwards the medical board has refused certification. Again, I can recollect a quite considerable number of cases where the medical board issued certificates during the miner’s lifetime and yet I was unable to find any dust disease at necropsy-which negative findings were presently confirmed by the board. If my doubts are shared by other workers, who have probably more experience in these matters, it would appear that a new approach to the problems of dust disease is called for, based not so much on doubtful anatomical diagnosis as on much more reliable assessment This would, incidentally, of functional impairment. remove the very real danger of producing iatrogenic anxiety neurosis in workmen who find themselves confronted with a veritable maze of conflicting opinions
and
regulations. K. TRIGER.
Abertillery, Mon. LONGER LIFE
SIR,—Dr. Morris (Dec. 22) questions Dr. Crofts’s argument (Nov. 10) that weight reduction in obese persons leads to lower mortality. May I draw attention to the interesting evidence recently published by the Metropolitan Life Insurance Company.Among approximately 50,000 overweight men and women certain policy-holders, subsequent to the issue of substandard insurance, lost enough weight to qualify them for a lower premium, and in many cases for standard insurance. Of men limited to substandard insurance because originally they were moderately overweight, the mortality subsequent to their change of rating was 113% of the standard compared with 142% for all men moderately overweight. Weight reduction may not postpone the onset of a pathological process, but it may postpone disease, and it 4. Foy, H., Kondi, A., Hargreaves, A. Brit. med. J. 1951, i, 380. 5. Statistical Bulletin, Metropolitan Life Insurance Company, New York. October, 1951.
cassation of benemid w" confirmed by
the
phenol-
excretion test, and in some patients this test was also done before and during the administration of benemid. In this regard it may be of interest that the 3 patients (nos. 5, 6, and 9) with the most uniformly maintained-as distinct from the highest -blood levels are those showing the most significant depressionof phenolsulphonephthalein excretion under the influence of benemid. The actual blood levels obtained are satisfactory throughout. From the results it seems fair to suggest that, with really adequate dosage-equivalent by weight - to the doses employed with the newer antibiotics-and possibly with the help of benemid, procaine penicillin given by mouth may be no less effective and reliable, in penicillin-sensitive infections, than these newer antibiotics ; and that this is at any rate worthy of therapeutic trial.’
sulphonephthalein (phenol-red)
-
’
_
indebted to Dr. ]3eyer of Messrs. Sharp & Dohme for supplies of benemid, and to Dr. H. M. Walker, of Glaxo Laboratories Ltd., for supplies of proeaine We
Ltd.,
are
Philadelphia,
’
penicillin.
Medical Medical School. School,
W. Dundee.
WALKER, WALKER
R. B. HUNTER.
ANÆMIA IN AFRICANS IN UGANDA SiR,-Certain points in the paper by Dr. Trowell and (Oct. 27) seem to me to require
clarification.
amplification
there does not seem to be anything " mysabout the rise of mean corpuscular volume (M.c.v.) in hookworm anaemia. Lehmannshowed clearly that the rise of M.c.v. on giving iron in such cases caused a.reticulocyte response which continued while the worms were still in situ. The M.c.v. rise was due to the rapid change in the cell population, the old microcytic cells being replaced by the young macrocytic cells. Further, he showed that in other anaemias where there was blood
-
Firstly,
terious
"
destruction-e.g., malaria-reticulocytosis was accompanied by macrocytosis, which disappeared with the end of the reticulocytosis. Unfortunately, the question of reticulocytosis was not discussed in the paper by Holmes and Gee2 quoted by Trowell. It does seem possible for patients with light hookworm loads and-an’adequate iron intake to have a slight anaemia which is mildly macrocytic. Foy and Kondi (personal communication) find larger reticulocytes with hookworm anaemia in Africans than those seen in Europeans. Lehmannhas pointed out the lack of apparent ripening of these immature (precoctic) cells and has suggested that this is connected with a lack of tyrosine. This precoctic blood picture is in other anaemias besides hookworm. It should be anaemia is probably far the commonest cause of severe anaemia in Uganda, at Mulago anaemia is usually polymorphic in aetiology. Hookworm infection, malaria, and nutritional status are often concerned in the same patient. I personally have had cases of hookworm anaemia in malnourished patients whose iron deficienev was restored but who made no further progress to recovery from a level of about 9 g. Hb per 100 ml. until the return of the serum-protein to normal, after which the Hb reached normal level on diet alone. This of course is not by any means an original observation. Whether the anaemia was macrocytic at this stage I did not investigate. I agree with Trowell that factors such as pteroylglutamic acid, liver, and vitamin B12 do not influence the macrocytic aspects of anaemia seen in Uganda. It should be pointed out that them despite diligent although we have not encountered search, Foy and Kondi 3 find in Kenya anaemias which seen
emphasised that, while hookworm
are
(1)megaloblastic normocytic, (2) normocytic
normo-
1. Lehmann, H. Lancet, 1949, i, 90. 2. Holmes, E. G., Gee, F. L. E. Afr. med. J. 1951, 28, 297. 3. Foy, H., Kondi, A. Trans. R. Soc. trop. Med. 1950, 43, 635.
chromic (but with
giant".&bgr;tab cells in the marrow}, or (3) megaloblastic macrocytic. All these anaemias respond to Marmite,’ liver, and pteroylglutamic acid. One case of megaloblastic macrocytic anaemia apparently responded to penicillin.4 How common they are is not clear. I would support Trowell’s contention that the unqualified use of the term" macrocytic" often implies an aetiology which is not explicit in the meaning of the word. I suspect that there really may be no real contradiction between those who contend that a macrocytosis as seen ’
-
in the local African anaemia is the result of internal or external blood-loss, and those who contend that this is due to diet. The two would seem to be interrelated, particularly if the tyrosine contention is correct. This also may explain why it appears that an anaemia with infection appears to be macrocytic in an African but not in Europeans. Certainly such a macrocytosis is not nutritional in the sense of deficiency of a specific factor. Mulago Hospital, Kampala, Uganda.
P. P W. H W HUTTON.
COALMINERS’ PNEUMOCONIOSIS SIR,—It appears to me that Dr. Meiklejohn (Dec. 29) has based his conclusions on, inter alia, two assumptions -namely (1) that certification of a miner by the Pneumoconiosis Medical Board can be relied upon as evidence for the existence of the disease in a particular case, and (2) that clinical plus radiological examination (by experienced observers, presumably) can be relied upon to confirm or exclude the presence of pneumoconios’s. Personal experience, which -is, however, confined to the eastern end of the South Wales coalfield, makes -me doubt whether we are entitled to take these two assnmptions for granted. I have seen it happen quite frequently that a miner has been examined by, say, the massradiography unit and advised that " evidence of dust disease was seen in his chest film," and shortly afterwards the medical board has refused certification. Again, I can recollect a quite considerable number of cases where the medical board issued certificates during the miner’s lifetime and yet I was unable to find any dust disease at necropsy-which negative findings were presently confirmed by the board. If my doubts are shared by other workers, who have probably more experience in these matters, it would appear that a new approach to the problems of dust disease is called for, based not so much on doubtful anatomical diagnosis as on much more reliable assessment This would, incidentally, of functional impairment. remove the very real danger of producing iatrogenic anxiety neurosis in workmen who find themselves confronted with a veritable maze of conflicting opinions
and
regulations. K. TRIGER.
Abertillery, Mon. LONGER LIFE
SIR,—Dr. Morris (Dec. 22) questions Dr. Crofts’s argument (Nov. 10) that weight reduction in obese persons leads to lower mortality. May I draw attention to the interesting evidence recently published by the Metropolitan Life Insurance Company.Among approximately 50,000 overweight men and women certain policy-holders, subsequent to the issue of substandard insurance, lost enough weight to qualify them for a lower premium, and in many cases for standard insurance. Of men limited to substandard insurance because originally they were moderately overweight, the mortality subsequent to their change of rating was 113% of the standard compared with 142% for all men moderately overweight. Weight reduction may not postpone the onset of a pathological process, but it may postpone disease, and it 4. Foy, H., Kondi, A., Hargreaves, A. Brit. med. J. 1951, i, 380. 5. Statistical Bulletin, Metropolitan Life Insurance Company, New York. October, 1951.