1141 BETA-THALASSÆMIC TRAIT AND RHEUMATOID ARTHRITIS
SIR,-One approach
to
the
epidemiology
of rheumatoid
arthritis (R.A.) could be the possible relationship between the high incidence of malaria or other parasitic infections, thalasssmic trait, and glucose-6-phosphate-dehydrogenase (G.-6-P.D.) deficiency and the prevalence of R.A. in some populations, such as African and Sardinian people.1,2 In many parts of tropical Africa a large proportion of the population show a number of immunological changes related to the prevalence of malaria or other parasitic infections.3 In the same areas, diseases of the immune group, such as R.A. are uncommon, and their clinical picture and4 course seem to be modified by environmental factors. 1, 3, Apart from anæmia,5 thalasssemic trait is a symptom-free state in most subjects; but the &bgr;-thalassaEmic carrier’s biology is still not fully understdod. A
R.A. When small number of patients are being investigated, the association may be fortuitous. However, this finding, if confirmed, may be relevant to a better understanding of some biological aspects of thalasssmia and R.A.
of
The way in which the thalasssemic trait could interfere with the appearance of R.A. remains a matter for speculation. Particularly, there is no study of the immunological reactivity of the heterozygous j3-thalassasmic subjects, and we do not know whether the increased prevalence of j3thalassæmic carriers with R.A. may be related to a genetically determined susceptibility or to the action of some environmental factors which may alter host susceptibility and facilitate R.A. development. Cattedra di Reumatologia, Università di Siena, Italy. Divisione di
Reumatologia, Arcispedale S. Anna, Ferrara, Italy.
ROBERTO MARCOLONGO. FRANCESCO TROTTA MASSIMO SCARAMELLI.
THALASSÆMIA TRAIT AND RHEUMATOID ARTHRITIS
EXERCISE, SPORT, AND SUDDEN DEATH SIR; The comments of Dr Carruthers and his colleagues on safe sport (Feb. 22, p. 447) are appreciated.
i
of the
possible association between this condition diseases might verify the protective or the facilitating role that thalassaemia may exert towards certain diseases.6 It has been reported, for example, that individuals
study and
some
with
&bgr;-thalassæmic trait and/or G.-6-P.D. deficiency are resistant to malaria, tuberculosis, and essential hypertension, and more susceptible to gastroduodenal
more
ulcers and liver cirrhosis than non-thalassasmic persons. 6,7 We were interested in the prevalence of R.A. in heterozygous &bgr;-thalassæmic subjects. We studied the incidence of &bgr;-thalassæmic trait in 146 patients (age 31-72) consecutively admitted to hospital for R.A. and compared it with that of the control population of the Ferrara and Rovigo areas, where the prevalence of thalassaemia is high. The results are given in the accompanying table. We found a significant increase of thalasseemia in the rheumatoid series. The frequency of &bgr;-thalassæmic trait reached 19-8% among patients with R.A. compared with 13.4% and 11-3% in the random population of the same areas, and was 1.5 times greater than the expected prevalence-rate of 13-1%. The clinical, serological, and radiological features did not differ between the two groups of R.A. patients (with and without thalassaemic trait); the male/female ratio was 1/368 in non-thalasssemic patients, and 1/1-63 in the rheumatoid subjects with thalassaemic trait. A similar finding was observed in Nigeria.1 On the basis of these results it is possible to suggest a relationship between p-thalassaemic heterozygous subjects and R.A., even if the onset, course, and clinical picture of the rheumatoid disease did not appear to be modified by this haematological feature. Considerable caution is needed before drawing the conclusion that thalassoeniic trait may have some facilitating effect in the development 1. 2. 3. 4. 5.
Greenwood, B. M. Ann. rheum. Dis. 1969, 28, 488. Marcolongo, R. Reumatismo, 1971, 23, 241. Greenwood, B. M. Lancet, 1968, ii, 380. Greenwood, B. M., Herrick, E. M. Br. med. J. 1970, i, 71. Castaldi, G., Zavagli, G., Ambrose, G., Dallapiccola, B., Trotta, F. ibid. 1974, i, 518. 6. Baserga, A. Prog. Medico, 1972, 28, 413. 7. Tannoia, N., Ciaravella, N., Putignano, A., Bini, L. Policl. Sez. Prat. 1968, 75, 241.
The purpose of my article was certainly not to deter the inert majority from taking part in supervised gymnasium training programmes but rather to help identify those sportsmen prone to sudden death. The precautions taken by Dr Carruthers and others to prevent the development of arrhythmias during supervised training appear to be simple and safe. However, should we not distinguish between supervised training sessions in a laboratory or gymnasium, and sporting activity as usually understood ? It is not really very practical for rugby players to monitor their pulse-rates, or to avoid isometric exertion, or to start up at very low workloads. My article was dealing with sportsmen and not with those undergoing controlled exercise in controlled conditions, and extrapolation from the one situation to the other may not be warranted. Particularly important differences may be the denial of symptoms1 to which aggressive sportsmen seem particularly prone,2 and the competitive element in most sports. In attempting to understand the complex interrelation between exercise and the heart, it may be helpful to consider the following ways in which exercise could influence the susceptibility of the individual to ischsemic heartdisease. First, exercise could influence the blood cholesterol and/or triglyceride values. Dr Carruthers and his colleagues found decreased serum-cholesterol after an exercise programme, and Dr Oakley’s (March 8, p. 584) executives took greater pleasure from diving into the cold water at dawn because their blood-cholesterol levels were falling. (Incidentally, what about their blood-pressures ?) These studies agree with the earlier report of Mann et al.,3 who found a small drop in the serum-cholesterol in exercising American men. Nevertheless, other evidence argues an effect of exercise on serum-cholesterol. Two against series on coronary patients actually report an increased serum-cholesterol after exercise. 4,5 Neither Morris6 nor Truswell and Mann could establish a relation between activity levels and serum-cholesterol, although the latter Nixon, P. G. F., Bethell, H. J. N. Am. J. Cardiol. 1974, 33, 446. Opie, L. H. Lancet, Feb. 1, 1975, p. 263. Mann, G. V., Garrett, H. L., Farhi, A., Murray, H., Billings, F. T. Am. J. Med. 1969, 46, 12. 4. Allard, C., Alteresco, M., Ferguson, R. J., Chaniotis, L., Choquette, G., Skinner, J. Can. med. Ass. J. 1973, 109, 194. 5. Ferguson, R. J., Petitclerc, R., Choquette, G., Chaniotis, L., Gauthier, P., Huot, R., Allard, C., Jankowski, L., Campeau, L. Am. J. Cardiol. 1974, 34, 764. 6. Morris, J. N., Chave, S. P. W., Adam, C., Sirey, C. Lancet, 1973, i,
1. 2. 3.
333. 7.
Truswell, A. S., Mann, J. I. Atherosclerosis, 1972, 16, 15.
SIR,-One approach
to
the
epidemiology
of rheumatoid
arthritis (R.A.) could be the possible relationship between the high incidence of malaria or other parasitic infections, thalasssmic trait, and glucose-6-phosphate-dehydrogenase (G.-6-P.D.) deficiency and the prevalence of R.A. in some populations, such as African and Sardinian people.1,2 In many parts of tropical Africa a large proportion of the population show a number of immunological changes related to the prevalence of malaria or other parasitic infections.3 In the same areas, diseases of the immune group, such as R.A. are uncommon, and their clinical picture and4 course seem to be modified by environmental factors. 1, 3, Apart from anæmia,5 thalasssemic trait is a symptom-free state in most subjects; but the &bgr;-thalassaEmic carrier’s biology is still not fully understdod. A
R.A. When small number of patients are being investigated, the association may be fortuitous. However, this finding, if confirmed, may be relevant to a better understanding of some biological aspects of thalasssmia and R.A.
of
The way in which the thalasssemic trait could interfere with the appearance of R.A. remains a matter for speculation. Particularly, there is no study of the immunological reactivity of the heterozygous j3-thalassasmic subjects, and we do not know whether the increased prevalence of j3thalassæmic carriers with R.A. may be related to a genetically determined susceptibility or to the action of some environmental factors which may alter host susceptibility and facilitate R.A. development. Cattedra di Reumatologia, Università di Siena, Italy. Divisione di
Reumatologia, Arcispedale S. Anna, Ferrara, Italy.
ROBERTO MARCOLONGO. FRANCESCO TROTTA MASSIMO SCARAMELLI.
THALASSÆMIA TRAIT AND RHEUMATOID ARTHRITIS
EXERCISE, SPORT, AND SUDDEN DEATH SIR; The comments of Dr Carruthers and his colleagues on safe sport (Feb. 22, p. 447) are appreciated.
i
of the
possible association between this condition diseases might verify the protective or the facilitating role that thalassaemia may exert towards certain diseases.6 It has been reported, for example, that individuals
study and
some
with
&bgr;-thalassæmic trait and/or G.-6-P.D. deficiency are resistant to malaria, tuberculosis, and essential hypertension, and more susceptible to gastroduodenal
more
ulcers and liver cirrhosis than non-thalassasmic persons. 6,7 We were interested in the prevalence of R.A. in heterozygous &bgr;-thalassæmic subjects. We studied the incidence of &bgr;-thalassæmic trait in 146 patients (age 31-72) consecutively admitted to hospital for R.A. and compared it with that of the control population of the Ferrara and Rovigo areas, where the prevalence of thalassaemia is high. The results are given in the accompanying table. We found a significant increase of thalasseemia in the rheumatoid series. The frequency of &bgr;-thalassæmic trait reached 19-8% among patients with R.A. compared with 13.4% and 11-3% in the random population of the same areas, and was 1.5 times greater than the expected prevalence-rate of 13-1%. The clinical, serological, and radiological features did not differ between the two groups of R.A. patients (with and without thalassaemic trait); the male/female ratio was 1/368 in non-thalasssemic patients, and 1/1-63 in the rheumatoid subjects with thalassaemic trait. A similar finding was observed in Nigeria.1 On the basis of these results it is possible to suggest a relationship between p-thalassaemic heterozygous subjects and R.A., even if the onset, course, and clinical picture of the rheumatoid disease did not appear to be modified by this haematological feature. Considerable caution is needed before drawing the conclusion that thalassoeniic trait may have some facilitating effect in the development 1. 2. 3. 4. 5.
Greenwood, B. M. Ann. rheum. Dis. 1969, 28, 488. Marcolongo, R. Reumatismo, 1971, 23, 241. Greenwood, B. M. Lancet, 1968, ii, 380. Greenwood, B. M., Herrick, E. M. Br. med. J. 1970, i, 71. Castaldi, G., Zavagli, G., Ambrose, G., Dallapiccola, B., Trotta, F. ibid. 1974, i, 518. 6. Baserga, A. Prog. Medico, 1972, 28, 413. 7. Tannoia, N., Ciaravella, N., Putignano, A., Bini, L. Policl. Sez. Prat. 1968, 75, 241.
The purpose of my article was certainly not to deter the inert majority from taking part in supervised gymnasium training programmes but rather to help identify those sportsmen prone to sudden death. The precautions taken by Dr Carruthers and others to prevent the development of arrhythmias during supervised training appear to be simple and safe. However, should we not distinguish between supervised training sessions in a laboratory or gymnasium, and sporting activity as usually understood ? It is not really very practical for rugby players to monitor their pulse-rates, or to avoid isometric exertion, or to start up at very low workloads. My article was dealing with sportsmen and not with those undergoing controlled exercise in controlled conditions, and extrapolation from the one situation to the other may not be warranted. Particularly important differences may be the denial of symptoms1 to which aggressive sportsmen seem particularly prone,2 and the competitive element in most sports. In attempting to understand the complex interrelation between exercise and the heart, it may be helpful to consider the following ways in which exercise could influence the susceptibility of the individual to ischsemic heartdisease. First, exercise could influence the blood cholesterol and/or triglyceride values. Dr Carruthers and his colleagues found decreased serum-cholesterol after an exercise programme, and Dr Oakley’s (March 8, p. 584) executives took greater pleasure from diving into the cold water at dawn because their blood-cholesterol levels were falling. (Incidentally, what about their blood-pressures ?) These studies agree with the earlier report of Mann et al.,3 who found a small drop in the serum-cholesterol in exercising American men. Nevertheless, other evidence argues an effect of exercise on serum-cholesterol. Two against series on coronary patients actually report an increased serum-cholesterol after exercise. 4,5 Neither Morris6 nor Truswell and Mann could establish a relation between activity levels and serum-cholesterol, although the latter Nixon, P. G. F., Bethell, H. J. N. Am. J. Cardiol. 1974, 33, 446. Opie, L. H. Lancet, Feb. 1, 1975, p. 263. Mann, G. V., Garrett, H. L., Farhi, A., Murray, H., Billings, F. T. Am. J. Med. 1969, 46, 12. 4. Allard, C., Alteresco, M., Ferguson, R. J., Chaniotis, L., Choquette, G., Skinner, J. Can. med. Ass. J. 1973, 109, 194. 5. Ferguson, R. J., Petitclerc, R., Choquette, G., Chaniotis, L., Gauthier, P., Huot, R., Allard, C., Jankowski, L., Campeau, L. Am. J. Cardiol. 1974, 34, 764. 6. Morris, J. N., Chave, S. P. W., Adam, C., Sirey, C. Lancet, 1973, i,
1. 2. 3.
333. 7.
Truswell, A. S., Mann, J. I. Atherosclerosis, 1972, 16, 15.
