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H.A.A. IN DRUG ADDICTS
433 and Lind in 1965,3 and have added nothing new, except for some odd conclusions. The sentence that " a hiatus hernia apparently has no effect on the gastro-esophageal sphincter competencehas no adequate data to support it, because they do not give the natural history of a sphincter after it has been displaced. They use high pressures and
sphincter strength as synonymous. There is no evidence for this in their paper nor anywhere else as yet. A dis4 crepancy arises because, in 1966, Harris stated that " certainly one cannot reliably equate pressure recorded from the lower esophageal sphincter to its clinically assessed competence ". In group C no details of manometry are given to confirm whether patients with symptoms had a hernia or not, so the statement that reflux can occur without a hernia depends entirely on radiology. I disagree with their final statement that the rationale for surgical repair must be questioned. This is all right for an excathedra statement, but there are again no data in their paper to support this generalisation. Experimental evidence suggests that the gastro-oesophageal junction functions best when it is returned to the diaphragm,5 which is the basis of most repairs even though some may add a flap-valve mechanism. I hope that editors will continue to give space to articles on cesophageal motility, because some of us are genuinely attempting to quantitate changes and correlate them with clinical symptoms, so that patients can be treated more effectively. One must not believe everything that is published nor should one develop a negative attitude to these efforts. Your editorial supports controlled trials of investigation techniques and surgical treatment, as I have always done.6 Surgical Unit, London Hospital, El 1BB.
R. J. EARLAM.
H.A.A. IN DRUG ADDICTS
SiR,—The great majority of addicted intravenous drug share injection equipment with other addicts, and are therefore repeatedly exposed to serum hepatitis infection.’-9 In some surveys up to a third of the interviewed drug addicts gave a past history of icteric viral hepatitis. Assuming a 1/2 ratio for icteric to anicteric cases, this would mean that practically all of them had been exposed to infection. The relatively low prevalence (2-4%) of the s.H. (Australia) antigen in drug addicts without clinical hepatitis reported by workers in the U.S.10-11 and Sweden 12 probably reflects both the insensitivity of the screening techniques employed and the fact that only a small proportion of those exposed become persistent carriers of the antigen. In light of the above, nearly all drug addicts might be expected to show detectable amounts of anti-s.H. antibody by the hsemagglutination assay.13 This assay has been found to be highly specific, and about 2000 times more sensitive than the immunoelectro-osmophoresis method (unpublished data). We have lately retested 340 sera drawn from addicts without signs of viral hepatitis admitted to an institution for drug withdrawal. The study sample has been described users
3.
Lind, J. F., Burns, C. M., MacDougall, J.
T. Archs Surg.
1965, 91,
233.
4. 5. 6.
Harris, L. D. Gastroenterology, 1966, 50, 708. Earlam, R. J., Ellis, F. H., Jr. Archs Surg. 1967, 95, 585. Earlam, R. J., Ellis, F. H., Jr. Surg. Clins N. Am. 1967, 47, 313. 7. Schafer, I. A., Mosley, J. W. Ann. intern. Med. 1958, 49, 1162. 8. Levine, R. A., Payne, M. A. ibid. 1960, 53, 164. 9. Rosenstein, B. J. J. Am. med. Ass. 1967, 199, 698. 10. Cherubin, C. E., Hargrove, R. L., Prince, A. M. Am. J. Epid. 1970, 91, 510. 11. Sutnick, A. I., Cerda, J. J., Toskes, P. P., London, W. T., Blumberg, B. S. Archs intern. Med. 1971, 127, 939. 12. Nordenfelt, E. Vox Sang. 1970, 19, 371. 13. Vyas, G. N., Shulman, N. R. Science, 1970, 170, 332.
PREVALENCE OF ANTI-S.H. Hrr-1viAGGLLTTIMATD4G ANTIBODY
1 ’4)
(TITRES
IN RELATION TO CERTAIN CHARACTERISTICS
elsewhere.lO The prevalence of the s.H.-antigen carrier state in the tested sample was 1-5% by the immunodiffusion technique and 1-7% by the haemagglutination-inhibition technique. We found that only 56% of the antigennegative addicts showed detectable amounts of haemagglutinating antibody. In 19% the titre ranged between 1/4 and 1/16, in 25% between 1/32 and 1/128, and in only 12% was it 1/256 or higher. By comparison, in another high-risk group-mentally retarded patients of similar age in an institution (both with and without mongolism)-detectable levels of antibody were present in up to 90%. No significant differences in antibody prevalence were found between males and females, Whites and Blacks, or those with normal and abnormal glutamic-pyruvic transaminase (S.G.P.T.) levels (see table). Age seemed to be the only factor associated with prevalence; drug addicts aged 40 or more had antibody significantly more frequently than those under 20 years of age (P < 0-02). The relatively low prevalence of haemagglutmating antibody in this population could be explained by two
years
hypotheses: 1. In some individuals who develop an immune response the antibody may subsequently disappear or decrease to a level that is not detectable by the haemagglutina-
tion 2.
test.
Serum-hepatitis infections may be caused by more than one type of virus; addicts in whom antibody is
detectable may have been exposed to a virus with an antigenic specificity that differs from that of the antigen employed in the haemagglutination assay. The first hypothesis seems unlikely. As previously mentioned,drug addicts are repeatedly exposed to infection, and in cases of secondary immune response the antibody appears to persist for long periods of time.14 Long persistence of antibody in cases of repeated exposure is also indicated by the increase in antibody prevalence with advancing age that we have observed in mentally retarded patients, some African populations, drug addicts, and closed institutions-with increasing duration of institutionalisation (unpublished data). Studies concerning the antigenic composition of serumhepatitis virus(es) and its subspecificities, now in progress in many laboratories, will determine the validity of the second hypothesis. Laboratory of Virology, New York Blood Center, WOLF SZMUNESS 310 E. 67th Street, ALFRED M. PRINCE. New York, N.Y. 10021, U.S.A. 14. Greenberg, H. B., Gocke, D. J. J. infect. Dis. 1971, 123, 356. not
sphincter strength as synonymous. There is no evidence for this in their paper nor anywhere else as yet. A dis4 crepancy arises because, in 1966, Harris stated that " certainly one cannot reliably equate pressure recorded from the lower esophageal sphincter to its clinically assessed competence ". In group C no details of manometry are given to confirm whether patients with symptoms had a hernia or not, so the statement that reflux can occur without a hernia depends entirely on radiology. I disagree with their final statement that the rationale for surgical repair must be questioned. This is all right for an excathedra statement, but there are again no data in their paper to support this generalisation. Experimental evidence suggests that the gastro-oesophageal junction functions best when it is returned to the diaphragm,5 which is the basis of most repairs even though some may add a flap-valve mechanism. I hope that editors will continue to give space to articles on cesophageal motility, because some of us are genuinely attempting to quantitate changes and correlate them with clinical symptoms, so that patients can be treated more effectively. One must not believe everything that is published nor should one develop a negative attitude to these efforts. Your editorial supports controlled trials of investigation techniques and surgical treatment, as I have always done.6 Surgical Unit, London Hospital, El 1BB.
R. J. EARLAM.
H.A.A. IN DRUG ADDICTS
SiR,—The great majority of addicted intravenous drug share injection equipment with other addicts, and are therefore repeatedly exposed to serum hepatitis infection.’-9 In some surveys up to a third of the interviewed drug addicts gave a past history of icteric viral hepatitis. Assuming a 1/2 ratio for icteric to anicteric cases, this would mean that practically all of them had been exposed to infection. The relatively low prevalence (2-4%) of the s.H. (Australia) antigen in drug addicts without clinical hepatitis reported by workers in the U.S.10-11 and Sweden 12 probably reflects both the insensitivity of the screening techniques employed and the fact that only a small proportion of those exposed become persistent carriers of the antigen. In light of the above, nearly all drug addicts might be expected to show detectable amounts of anti-s.H. antibody by the hsemagglutination assay.13 This assay has been found to be highly specific, and about 2000 times more sensitive than the immunoelectro-osmophoresis method (unpublished data). We have lately retested 340 sera drawn from addicts without signs of viral hepatitis admitted to an institution for drug withdrawal. The study sample has been described users
3.
Lind, J. F., Burns, C. M., MacDougall, J.
T. Archs Surg.
1965, 91,
233.
4. 5. 6.
Harris, L. D. Gastroenterology, 1966, 50, 708. Earlam, R. J., Ellis, F. H., Jr. Archs Surg. 1967, 95, 585. Earlam, R. J., Ellis, F. H., Jr. Surg. Clins N. Am. 1967, 47, 313. 7. Schafer, I. A., Mosley, J. W. Ann. intern. Med. 1958, 49, 1162. 8. Levine, R. A., Payne, M. A. ibid. 1960, 53, 164. 9. Rosenstein, B. J. J. Am. med. Ass. 1967, 199, 698. 10. Cherubin, C. E., Hargrove, R. L., Prince, A. M. Am. J. Epid. 1970, 91, 510. 11. Sutnick, A. I., Cerda, J. J., Toskes, P. P., London, W. T., Blumberg, B. S. Archs intern. Med. 1971, 127, 939. 12. Nordenfelt, E. Vox Sang. 1970, 19, 371. 13. Vyas, G. N., Shulman, N. R. Science, 1970, 170, 332.
PREVALENCE OF ANTI-S.H. Hrr-1viAGGLLTTIMATD4G ANTIBODY
1 ’4)
(TITRES
IN RELATION TO CERTAIN CHARACTERISTICS
elsewhere.lO The prevalence of the s.H.-antigen carrier state in the tested sample was 1-5% by the immunodiffusion technique and 1-7% by the haemagglutination-inhibition technique. We found that only 56% of the antigennegative addicts showed detectable amounts of haemagglutinating antibody. In 19% the titre ranged between 1/4 and 1/16, in 25% between 1/32 and 1/128, and in only 12% was it 1/256 or higher. By comparison, in another high-risk group-mentally retarded patients of similar age in an institution (both with and without mongolism)-detectable levels of antibody were present in up to 90%. No significant differences in antibody prevalence were found between males and females, Whites and Blacks, or those with normal and abnormal glutamic-pyruvic transaminase (S.G.P.T.) levels (see table). Age seemed to be the only factor associated with prevalence; drug addicts aged 40 or more had antibody significantly more frequently than those under 20 years of age (P < 0-02). The relatively low prevalence of haemagglutmating antibody in this population could be explained by two
years
hypotheses: 1. In some individuals who develop an immune response the antibody may subsequently disappear or decrease to a level that is not detectable by the haemagglutina-
tion 2.
test.
Serum-hepatitis infections may be caused by more than one type of virus; addicts in whom antibody is
detectable may have been exposed to a virus with an antigenic specificity that differs from that of the antigen employed in the haemagglutination assay. The first hypothesis seems unlikely. As previously mentioned,drug addicts are repeatedly exposed to infection, and in cases of secondary immune response the antibody appears to persist for long periods of time.14 Long persistence of antibody in cases of repeated exposure is also indicated by the increase in antibody prevalence with advancing age that we have observed in mentally retarded patients, some African populations, drug addicts, and closed institutions-with increasing duration of institutionalisation (unpublished data). Studies concerning the antigenic composition of serumhepatitis virus(es) and its subspecificities, now in progress in many laboratories, will determine the validity of the second hypothesis. Laboratory of Virology, New York Blood Center, WOLF SZMUNESS 310 E. 67th Street, ALFRED M. PRINCE. New York, N.Y. 10021, U.S.A. 14. Greenberg, H. B., Gocke, D. J. J. infect. Dis. 1971, 123, 356. not