GUM CHEWING AT CRICKET

GUM CHEWING AT CRICKET

326 clearance for this study, and Dr K. Gibson (I.C.I.) for and to Dr B. Furr (I.C.I.) for P.G.I2 antiserum. Department of Pharmacology, Imperial Che...

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326 clearance for this study, and Dr K. Gibson (I.C.I.) for and to Dr B. Furr (I.C.I.) for P.G.I2 antiserum.

Department of Pharmacology, Imperial Chemical Industries, Macclesfield, Cheshire

Department of Surgery, Manchester Royal Infirmary

SERUM-CHOLESTEROL AFTER NATURAL MEASLES

synthetic P.G.I,

M. JOHNSON H. E. HARRISON A. T. RAFTERY J. B. ELDER

EFFECT OF MEASLES AND MEASLES VACCINE ON

SERUM-CHOLESTEROL

observed between the initial cholesterol values or changes in cholesterol values and measles antibody responses. After 8 and 10 months the relative increase of serum-cholesterol was still recorded in two children. After natural measles infection the mean serum-cholesterol was low in the specimens collected 1-7 days after the onset of were

SIR,—Dr Mathews and Dr Feery reported! that immunisation with influenza vaccine seemed to be followed by an increase in serum-total-cholesterol and by a decrease in H.D.L.-cholesterol. They suggested that immunisation with viral antigens or natural virus infections might contribute to variation in lipid levels. We have measured serum-total-cholesterol in 97 children (average age 2 years) before and 6 weeks after measles vaccination (’Rimevax’, R.I.T., Belgium) and in serial serum samples of 27 measles patients (average age 4 years). Children were fed ad libitum. Antibody titres were assayed by haemagglutination inhibition2 and serum-cholesterol was measured with the method of Leppanen.3 Samples from the same child were measured in the same series. The mean serum-cholesterol before and after the vaccination were 5.9+1.2 (S.D.) mmo1/1 and 5.8+1.0 mmo1/1, respectively. No sign of heavy hypertriglyceridsemia was detected in serum after standing overnight at 4°C. As indicated in the figure five children showed exceptionally high relative increase (40%) of serum-cholesterol after vaccination, although the absolute values remained within normal limits. No correlations 1. 2.

Mathews, J. D., Feery, B. J. Lancet, 1978, ii, 1212. Panelius, M., Salmi, A., Halonen, P. E., Kivalo, E., Rinne, U. K., Penttinen, K. Acta neurol. scand. 1973, 49, 85. 3. Leppänen, V. Scand. J. clin. Lab. Invest. 1956, 8, 201.

symptoms (see table). Cholesterol levels were about 40% higher in the specimens collected 8-19 days after the onset of the disease and remained at this normal level during the observation period of more than 3 months. Our data show that natural measles decreases serum-cholesterol values in the acute phase of the disease. This accords with the observations of Lees et al.,4 who showed that experimental infection with sandfly virus infection decreased serum-cholesterol values for at least 10 days. Whether the same kind of decrease of cholesterol level occurs also after measles vaccination and, possibly, after other virus vaccinations needs to be clarified. Our observations support the view presented by Mathews and Feery that natural virus infection or immunisation with viral antigen induces changes in serumlioid levels in man. Departments of Internal Medicine, Pædiatrics and Virology, University of Turku, 20520 Turku 52, Finland

J. VIIKARI O. RUUSKANEN T. SALMI P. HALONEN

GUM CHEWING AT CRICKET

SIR,-The Observer of Jan. 28 reported details of the injury the Australian batsman Darling on the first day of the fifth match in Adelaide. Darling was hit under the heart by an ordinary ball from Willis, collapsed, choked on his chewinggum, and somehow swallowed his tongue. When the crisis of choking was over, the injury to Darling was found not to be serious. Over the past two to three summers whilst watching firstclass cricket, I have noticed an increasing number of players chewing. On the second day of the Trent Bridge test match, at the beginning of the New Zealand innings, an urgent signal was sent to the England dressing-room, and eventually the twelfth man brought out a packet of chewing-gum which was quickly distributed among several players. During the two New Zealand innings, most England players were chewing and some replenished their gum, returning the tell-tale silver paper to their pockets. Subsequent inquiry revealed that chewing gum whilst playing first-class cricket is a common habit. Chewing-gum, inspired whilst playing cricket or other sports, may become lodged in one of the bronchi and cause wheezing or infection. If it gets stuck in the trachea, asphyxia and sudden death may ensue. The cricketer will be at greatest risk when he takes a sudden inspiration-as when hit in the abdomen or chest whilst batting (as in Darling’s case) or when reaching for a high catch. I am unaware of any catastrophe resulting from the use of gum by cricketers, but it is fortunate that skilled attention was immediately available for Darling-it will not be at most cricket matches. It would be prudent for cricketers to abandon this

to

test

Relative serum-cholesterol and measles-antibody titres in 97 children 6 weeks after measles vaccination. Serum-cholesterol is expressed as % of value before vaccination.

4. Lees, R. S., Fisser, R.

21, 825.

H., Beisel, W. R., Bartelioni, P. J. Metabolism, 1972,

327

apparently widespread habit, and we must hope that youngsters will not follow the dangerous example now being set by English and Australian test cricketers. The controversy over short-pitched bowling and the risk of injury to batsmen goes on, while in gum chewing we have a real danger to cricketers that could easily be eliminated. University Department of Surgery, General Hospital,

Nottingham NG1

6HA

J. B. BOURKE

X-ASSOCIATED IMMUNOCOMPETENCE The Lancet on hepatitis B virus have revealed a marked predominance of males affected by membranous nephropathy (M.N.)’ and hepatocarcinoma (H.C.j.2 A third article indicates a possible influence of H.B.v. on the sex ratio.3 Despite there being a male:female ratio of greater than 4:1 for M.N. and H.c., the possibility that the male predominance of these disorders could be due to X-associated immunodeficiency to H.B.v. was not considered.!.2 9 of the 11 Japanese patients with M.N.’ were males and all were positive for HB surface antigen (HBJ whereas none had anti-HB, in serum. 6 of the 11 mothers of the children were positive for REs and one had anti-HBs’ It seems to me that this male predominance of M.N. could be associated with inferior immunocompetence to H.B.v. of males as compared to females. Immunodeficiency could be partly responsible for the predominance of males with H.B.v. and associated M.N. and H.c. J. L. Sullivan and I have recently reviewed evidence (to be published elsewhere) which demonstrates immunological bases for superior immunocompetence and survival of females. Males experience more frequent and severe illness and higher mortality from many common infectious and neoplastic disorders than do females. This superior immunocompetence probably compensates for the immunosuppression which accompanies pregnancy.4 Females have higher serum-IgM concentrations, superior ability to form antibodies to infectious agents, and experience lower incidence of viral and bacteriological infectious diseases. Similarly, females have a lower incidence of most malignancies. Defective immune responses in males could account for their being frequent carriers of viruses such as H.B.v. Heptatitis B carrier states occur three times more frequently in males than in females.5 In contrast, antibody to HBs develops approximately three times more often in females than in males.6 Drew et al.7 have postulated cross-reactivity between H.B.v. and a human male-determined tissue antigen as being responsible for the sex ratio. They have suggested that males, being self-tolerant, possess weaker immune defences against H.B.v., resulting in disproportionate losses of male infants. Possibly, another factor to be evaluated is the apparent lack of immunocompetence of males to H.B.v. caused by mutant X-linked recessive immunoregulatory genes or weaker immune responsiveness than females from differences in hormonal milieu. Our study of cirrhosis and H.c. at Boston City Hospital during 1917-68 had revealed a striking male predominance which was associated with cirrhosis and chronic alcoholism.8 After having personally observed numerous alcoholic vagrants drinking in Boston, we had speculated that H.B.v. could have acted synergistically with alcoholism to provoke cirrhosis and H.c. The study performed by Trichopoulos et al. has revealed

SIR,—Recent articles in

(H.B.v.)

a high prevalence of active or past H.B.v. infections in 80 Greek patients with H.c., and 86% of the patients were males. They found active infection with H.B.v. as detected by the presence of HB, or anti-HB core antigen, but anti-HBs was lacking. Despite the lack of anti-BHs Trichopoulos et al. did not speculate that immunodeficiency to H.B.v. could have been a major factor in the emergence of H.c. Considerable effort has been directed toward finding human oncogenic viruses, but with little success.9 Our studies of the X-linked lymphoproliferative syndrome and immune deficiency to Epstein-Barr virus with fatal infectious mononucleosis or malignant lymphoma in males is a model for viral induced oncogenesis. 10 Supporting evidence stems from acquired immunodeficiency in transplant recipients as being a factor in the frequent occurrence of opportunistic lymphomas in this population." It seems plausible that the predominance of males with H.B.v. and hepatocarcinoma could be due to immunoincompetence which is based on mutant X-linked recessive immunoregulatory genes, differences in hormonal

milieu, or acquired immunodeficiency. University of Massachusetts Medical Center

Worcester, Massachusetts 01605, U.S.A

DAVID T. PURTILO

PREGNANCY, BREAST-CANCER RISK, AND MATERNAL-FETAL GENETICS

SIR,-In reviewing the epidemiological evidence linking pregnancy and breast-cancer risk I believe the data suggest that pregnancy has a biphasic effect on subsequent breastcancer risk-an adverse effect in the short run and a beneficial effect in the long run. The biological explanation for this may lie in the immunological similarity between fetal and malignant cells, described by Castro et al. and others. The epidemiological evidence linking pregnancy to breastcancer risk is extensive and controversial. A comprehensive review of the evidence is not possible here. In general, single women2 have higher rates of breast cancer than do married women, and this is thought to be a beneficial after-effect of pregnancy.3 There is a small but, I believe, biologically important exception to this pattern. The rates of breast cancer in single and married women cross each other about 35 or 40 years of age. This was first reported by Deelman4and later by Lilienfeld.2 From the mid-20’s, when breast-cancer rates begin to rise, until about 35 or 40 years of age, married women have a higher rate of breast cancer than single women. Single women have higher rates from 35 or 40 on. The table presents data from the New York Cancer Registry and shows the proportion of single women among breast-cancer cases and nonbreast-cancer cases, by age-group. There is a deficit of single women among the breast-cancer cases until 40 years of age, and a slight excess thereafter. This is consistent with the crossover shown previously by Deelman and Lilienfeld. If one accepts that the basic reason for the different rates between married and single women is some effect from pregnancy, then it is not unreasonable to suggest that pregnancy can increase the risk of breast cancer for a short and limited period of time. A second piece of epidemiological evidence suggesting that pregnancy promotes before it protects involves the sex of the first offspring among breast-cancer patients. Juret et al.5 reported that breast-cancer patients whose first child was a son

1. Tekekoshi, Y.,

Shida, N., Saheki, Y., Tanaka, M., Satake, Y., Matsumoto, S. Lancet, 1978, ii, 1065. 2. Trichopoulos, D., Gerety, R. J., Sparos, L., Tabor, E., Xirouchaki, E., Munoz, N., Linsell, C. A. ibid. 1978, ii, 1211. 3. Lancet, 1978, ii, 1241. 4. Purtilo, D. T., Hallgren, H. M., Yunis, E. J. ibid. 1972, i, 767. 5. Goodman, M., and others. Pediatrics, 1971, 48, 907. 6. London, W. T., Drew, J. S. Proc. natn. Acad. Sci. U.S.A. 1977, 74, 2561. 7. Drew, J. S., London, W. T., Lustbader, E. D., Hesser, J. E., Blumberg, B. S.Science, 1978, 201, 687. 8. Purtilo, D. T., Gottleib, L. S. Cancer, 1973, 32, 458.

9. Klein, P. A., Smith, R. T. Ann. Rev. Med. 1977, 28, 311. 10. Purtilo, D. T., and others. New Engl. J. Med 1977, 297, 1077. 11. Penn, I. Transplant. Proc. 1977, 9, 1133. 1. Castro, J. E., Lance, E. M., Medawar, P. B., and others. Nature, 1973, 243, 225. 2. Lilienfeld, A. M. Cancer Res.

1963, 23, 1503.

3. MacMahon, B., Cole, P., Brown, J. J. Natn. Cancer Inst. 1973, 4. Deelman, H. T. Z. Krebsforsch. 1920, 17, 164. 5. Juret, P., and others. Lancet, 1978, i, 415.

30, 21.