- Email: [email protected]
VACCINE PROTECTION AGAINST THE NEONATAL HBsAg CARRIER STATE
168
complicit. Certainly, it is only the health professions who are in position to stress the benefits of protection against the disease.
a
As with a clinical treatment, it is the indications for its use that are of primary importance. The indisputable indications for measles prophylaxis are represented by those levels of morbidity and mortality ascertained in the two major national surveysl,2 cited in your editorial. They are levels which should be unacceptable today, and which have led to the advocacy of strenuous efforts to improve vaccine uptake and, very possibly, to eradicate the disease. 3-6 We support this view, and are grateful for your editorial contribution on the subject. Department of Community Medicine, Coventry Health Authority, Coventry CV1 2GQ
J. D. MIDDLETON G. T. POLLOCK
prostaglandin effect, since potent conventional cyclo-oxygenase inhibitors, including indomethacin 1-3 and flurbiprofen,4are at best ineffective in this disease. Indeed, non-steroidal anti-inflammatory drugs seem to be harmful in some patients with ulcerative colitis,1,3-5 as well as in subjects with previously normal colons. These observations support the possibility that, as in the upper gastrointestinal tract,prostaglandins may be protective to the mucosa of the large bowel; the evidence is difficult to reconcile with the proposal that enhanced prostaglandin formation makes a major contribution to relapse in ulcerative colitis. If smoking does prove to be a beneficial activity in ulcerative colitis, the explanation is likely to be more complex than McGarry suggests: its elucidation may shed valuable light on the pathogenesis of the disease. Newham General London E13 8RU
VACCINE PROTECTION AGAINST THE NEONATAL HBsAg CARRIER STATE
SiR,—Dr Beasley and colleagues (Nov 12, p 1099) have demonstrated a high degree of protection (94%) against the
perinatally transmitted HBsAg carrier state with combined hepatitis B immunoglobulin and hepatitis B vaccine prophylaxis. However, their explanation for the persistence of HBs antigenaemia in 9 (6%) of the 159 infants receiving prophylaxis is not satisfactory. Of these 9 infants 4 had been HBsAg positive even before the vaccination and were suspected to have been infected in utero. This mode of transmission seems unlikely since the absence of anti-HBc IgM in all babies born to HBV carrier mothers strongly argues against transplacental transmission of hepatitis B virus. The 5 (3’2%) other infants who acquired a carrier state had been HBsAg negative before vaccination and anti-HBs did not develop after vaccination. A similar percentage of healthy adults also fail to develop anti-HBs after vaccination.This is because B lymphocytes from chronic HBV carriers have a specific inability to synthesise anti-HBs.3A similar mechanism may be operating in babies and healthy adults who do not acquire anti-HBs after HB vaccination. This group of non-responders may therefore need to be vaccinated with an adjuvant; in mice anti-idiotype antibodies injected before HBsAg enhance the anti-HBs immune response.44 D. N. REDDY J. B. DILAWARI
D. S. RAMPTON
CHRONIC ALCOHOLISM AND HYPERTENSION a
SiR,-Heavy drinking of alcohol is thought to be accompanied by dose-dependent increase in blood pressure.7 Saunders et al8 found
that alcohol-induced hypertension fell to normal after detoxification. However, it has also been suggested that alcohol may be responsible for as much as 25-30% of "essential" hypertension.9The question is-does excessive alcohol intake cause permanent high blood pressure? To address that question twenty male chronic alcoholics aged 32-51 (mean 41 yr) were studied 9-75 days (mean 38) after stopping drinking. They had been admitted to an institution for alcoholics. None had taken any drug known to
SR, Brash AR, Conolly ME, Lennard-Jones JE. Studies of prostaglandins and sulphasalazine in ulcerative colitis. Prostaglandins Med 1981; 6: 165-82. 2. Gilat T, Ratan J, Rosen P, Peled Y Prostaglandins and ulcerative colitis Gastroenterology 1979; 77: 1083. 3. Campieri M, Lanfranchi GA, Bazzochi G, et al. Prostaglandins, indomethacin and ulcerative colitis Gastroenterology 1980; 78: 193. 4. Rampton DS, Sladen GE. Prostaglandin synthesis inhibitors in ulcerative colitis flurbiprofen compared with conventional treatment. Prostaglandins 1981, 21: 1. Gould
417-25. 5.
6 7
Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh- 160012, India
Hospital,
8 9.
Rampton DS,
Sladen GE.
Relapse of ulcerative proctocolitis during
treatment
with
non-steroidal anti-inflammatory drugs Postgrad Med J 1981, 57: 297-99. Robert A Cytoprotection by prostaglandins. Gastroenterology 1979, 77: 761-67. Klatsky AL, Friedman GD, Siegelaub AB, Gérard MJ Alcohol consumption and blood pressure N Engl J Med 1977, 296: 1194-200. Saunders JB, Beevers DG, Paton A Alcohol-induced hypertension. Lancet 1981, ii 653-56. Mathews JD. Alcohol use, hypertension and coronary heart disease Clin Sci Mol Med 1976; 51: 661s-63s
SMOKING AND ULCERATIVE COLITIS
SIR,-Dr McGarry (Dec 24/31, p 1498) reiterates earlier proposals that active ulcerative colitis is caused by overproduction of prostaglandins by the gut and suggests that the apparent association of the disease with non-smoking is due to the inhibitory effect of smoking on prostaglandin synthesis. Although trials of nicotine in ulcerative colitis may well be worthwhile, any benefit established is unlikely to be mediated simply by an anti1. Miller CL 2.
3. 4. 5. 6. 7
J 1: 1253 Severity of notified measles Br Med 1978; A report to the Medical Research Council by the Measles Vaccines Committee. Br Med J 1966, i: 441 Editorial. Measles and Indians. Br Med J 1982; 285: 1762-63 Anon Commun Dis Rep (January to March, 1983) Measles control: are community physicians concerned? Commun Med 1983, 5: 264-67. WHO Measles surveillance. Feasibility of measles elimination in Europe Wkly Epidemiol Rev 1983, 58: 229-30. Hopkins DR, Hmman AR, Koplan JP, Lane JM. The case for global measles eradication. Lancet 1982, i 1396-98. Goudeau A, Lesage G, Denis F, Chiron JP, Yvonnet B, Barin F, Coursaget P, Diop Mar I. Lack of anti-HBc IgM in neonates with HBsAg carrier mothers argues against transplacental transmission of hepatitis B virus infection. Lancet 1983, n: 1103-04.
8
09
10.
Szumuness W, Stevens CE, Harley EJ, Zang EA, Alter HJ, Taylor PE, Devera A, Chen GTS, Keller A. Hepatitis B vaccine in medical staff of hemodialysis units: Efficacy and subtype cross protection N Engl J Med 1982, 307: 1481-86 Dusheike GM, Hoofnagle JH, Cooksley WG, James SP, Jones EA. Synthesis of antibodies to hepatitis B virus by cultured lymphocytes from chronic hepatitis B surface antigen carrier. J Clin Invest 1983, 71: 1104-13. Kennedy RC, Alder-Storthz K, Hankel RD, Sanchez Y, Melnick JL, Drecoman GR. Immune response to hepatitis B surface antigen: Enhancement by prior injection of antibodies to idiotype. Science 1983, 223: 853-55.
B
1
p<—— Blood pressure
tilting
test.
2
3
4
Tilting 60°
(BP) and heart
rate
5
6
7
-1-(HR) after
8
Supine rest
(B)
9
10 Min
--i and
during
complicit. Certainly, it is only the health professions who are in position to stress the benefits of protection against the disease.
a
As with a clinical treatment, it is the indications for its use that are of primary importance. The indisputable indications for measles prophylaxis are represented by those levels of morbidity and mortality ascertained in the two major national surveysl,2 cited in your editorial. They are levels which should be unacceptable today, and which have led to the advocacy of strenuous efforts to improve vaccine uptake and, very possibly, to eradicate the disease. 3-6 We support this view, and are grateful for your editorial contribution on the subject. Department of Community Medicine, Coventry Health Authority, Coventry CV1 2GQ
J. D. MIDDLETON G. T. POLLOCK
prostaglandin effect, since potent conventional cyclo-oxygenase inhibitors, including indomethacin 1-3 and flurbiprofen,4are at best ineffective in this disease. Indeed, non-steroidal anti-inflammatory drugs seem to be harmful in some patients with ulcerative colitis,1,3-5 as well as in subjects with previously normal colons. These observations support the possibility that, as in the upper gastrointestinal tract,prostaglandins may be protective to the mucosa of the large bowel; the evidence is difficult to reconcile with the proposal that enhanced prostaglandin formation makes a major contribution to relapse in ulcerative colitis. If smoking does prove to be a beneficial activity in ulcerative colitis, the explanation is likely to be more complex than McGarry suggests: its elucidation may shed valuable light on the pathogenesis of the disease. Newham General London E13 8RU
VACCINE PROTECTION AGAINST THE NEONATAL HBsAg CARRIER STATE
SiR,—Dr Beasley and colleagues (Nov 12, p 1099) have demonstrated a high degree of protection (94%) against the
perinatally transmitted HBsAg carrier state with combined hepatitis B immunoglobulin and hepatitis B vaccine prophylaxis. However, their explanation for the persistence of HBs antigenaemia in 9 (6%) of the 159 infants receiving prophylaxis is not satisfactory. Of these 9 infants 4 had been HBsAg positive even before the vaccination and were suspected to have been infected in utero. This mode of transmission seems unlikely since the absence of anti-HBc IgM in all babies born to HBV carrier mothers strongly argues against transplacental transmission of hepatitis B virus. The 5 (3’2%) other infants who acquired a carrier state had been HBsAg negative before vaccination and anti-HBs did not develop after vaccination. A similar percentage of healthy adults also fail to develop anti-HBs after vaccination.This is because B lymphocytes from chronic HBV carriers have a specific inability to synthesise anti-HBs.3A similar mechanism may be operating in babies and healthy adults who do not acquire anti-HBs after HB vaccination. This group of non-responders may therefore need to be vaccinated with an adjuvant; in mice anti-idiotype antibodies injected before HBsAg enhance the anti-HBs immune response.44 D. N. REDDY J. B. DILAWARI
D. S. RAMPTON
CHRONIC ALCOHOLISM AND HYPERTENSION a
SiR,-Heavy drinking of alcohol is thought to be accompanied by dose-dependent increase in blood pressure.7 Saunders et al8 found
that alcohol-induced hypertension fell to normal after detoxification. However, it has also been suggested that alcohol may be responsible for as much as 25-30% of "essential" hypertension.9The question is-does excessive alcohol intake cause permanent high blood pressure? To address that question twenty male chronic alcoholics aged 32-51 (mean 41 yr) were studied 9-75 days (mean 38) after stopping drinking. They had been admitted to an institution for alcoholics. None had taken any drug known to
SR, Brash AR, Conolly ME, Lennard-Jones JE. Studies of prostaglandins and sulphasalazine in ulcerative colitis. Prostaglandins Med 1981; 6: 165-82. 2. Gilat T, Ratan J, Rosen P, Peled Y Prostaglandins and ulcerative colitis Gastroenterology 1979; 77: 1083. 3. Campieri M, Lanfranchi GA, Bazzochi G, et al. Prostaglandins, indomethacin and ulcerative colitis Gastroenterology 1980; 78: 193. 4. Rampton DS, Sladen GE. Prostaglandin synthesis inhibitors in ulcerative colitis flurbiprofen compared with conventional treatment. Prostaglandins 1981, 21: 1. Gould
417-25. 5.
6 7
Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh- 160012, India
Hospital,
8 9.
Rampton DS,
Sladen GE.
Relapse of ulcerative proctocolitis during
treatment
with
non-steroidal anti-inflammatory drugs Postgrad Med J 1981, 57: 297-99. Robert A Cytoprotection by prostaglandins. Gastroenterology 1979, 77: 761-67. Klatsky AL, Friedman GD, Siegelaub AB, Gérard MJ Alcohol consumption and blood pressure N Engl J Med 1977, 296: 1194-200. Saunders JB, Beevers DG, Paton A Alcohol-induced hypertension. Lancet 1981, ii 653-56. Mathews JD. Alcohol use, hypertension and coronary heart disease Clin Sci Mol Med 1976; 51: 661s-63s
SMOKING AND ULCERATIVE COLITIS
SIR,-Dr McGarry (Dec 24/31, p 1498) reiterates earlier proposals that active ulcerative colitis is caused by overproduction of prostaglandins by the gut and suggests that the apparent association of the disease with non-smoking is due to the inhibitory effect of smoking on prostaglandin synthesis. Although trials of nicotine in ulcerative colitis may well be worthwhile, any benefit established is unlikely to be mediated simply by an anti1. Miller CL 2.
3. 4. 5. 6. 7
J 1: 1253 Severity of notified measles Br Med 1978; A report to the Medical Research Council by the Measles Vaccines Committee. Br Med J 1966, i: 441 Editorial. Measles and Indians. Br Med J 1982; 285: 1762-63 Anon Commun Dis Rep (January to March, 1983) Measles control: are community physicians concerned? Commun Med 1983, 5: 264-67. WHO Measles surveillance. Feasibility of measles elimination in Europe Wkly Epidemiol Rev 1983, 58: 229-30. Hopkins DR, Hmman AR, Koplan JP, Lane JM. The case for global measles eradication. Lancet 1982, i 1396-98. Goudeau A, Lesage G, Denis F, Chiron JP, Yvonnet B, Barin F, Coursaget P, Diop Mar I. Lack of anti-HBc IgM in neonates with HBsAg carrier mothers argues against transplacental transmission of hepatitis B virus infection. Lancet 1983, n: 1103-04.
8
09
10.
Szumuness W, Stevens CE, Harley EJ, Zang EA, Alter HJ, Taylor PE, Devera A, Chen GTS, Keller A. Hepatitis B vaccine in medical staff of hemodialysis units: Efficacy and subtype cross protection N Engl J Med 1982, 307: 1481-86 Dusheike GM, Hoofnagle JH, Cooksley WG, James SP, Jones EA. Synthesis of antibodies to hepatitis B virus by cultured lymphocytes from chronic hepatitis B surface antigen carrier. J Clin Invest 1983, 71: 1104-13. Kennedy RC, Alder-Storthz K, Hankel RD, Sanchez Y, Melnick JL, Drecoman GR. Immune response to hepatitis B surface antigen: Enhancement by prior injection of antibodies to idiotype. Science 1983, 223: 853-55.
B
1
p<—— Blood pressure
tilting
test.
2
3
4
Tilting 60°
(BP) and heart
rate
5
6
7
-1-(HR) after
8
Supine rest
(B)
9
10 Min
--i and
during