- Email: [email protected]
VIRUS OF ENTERICALLY TRANSMITTED NON-A, NON-B HEPATITIS
819
Letters
to
VIRUS OF ENTERICALLY TRANSMITTED NON-A, NON-B HEPATITIS
the Editor
25 YEARS OF IMPLANTED INTRACARDIAC PACERS
SiR,—We disagree with Dr Lagergren’s occasional survey (March 19, p 636), which is an outdated and idiosyncratic view far removed from that generally accepted in the UK, Europe, and the USA. There is wide regional and national variation in the frequency of pacemaker implantation and there may well be instances where pacemakers are implanted inappropriately. However, best estimates of the likely required annual rate of implantation, based on disease prediction, suggest a figure of 300 per million population. To suggest that pacing is being adequately implemented in Stockholm by equation of the implant rate with that in the UK is misguided, since the expressed view of the British Cardiac Society and the British Pacing and Electrophysiology group is that pacing is, at present, being offered to only about half the patients who could benefit from it. Physicians, indoctrinated by antiquated viewssuch as those expressed by Lagergren, are not referring the appropriate patients to the specialist centres. The principal indication for cardiac pacing is symptomatic bradycardia, the aim being to abolish or prevent the symptoms. But even in the absence of symptoms, cardiac pacing is indicated in almost all cases of complete heart block and can reduce mortality.1 Pacing in the elderly is at least as rewarding as in younger patients.’ In complete heart block with normal sinus node function, dual chamber pacing is best, and confers haemodynamic advantages and improves quality of life compared with constant rate ventricular pacing.3 It also decreases the risk of pacemaker syndrome4 and may improve survival in patients with heart failure.s In atrial fibrillation or sinus node dysfunction a rate responsive pacemaker, capable of matching the pacing rate to the patient’s needs, may confer similar advantages.6,7 The development of such rate responsive systems has been the focus of considerable research in the past ten years, yet it receives not a single mention by Lagergren. Recognition of the value of physiological pacing has led to an increase in its use from 20% of all implants in 1977 to 72% in 1986 in one major centred Despite improvements in battery life, triggered pacing is still likely to lead to early depletion of the power source. The "drawback" of inhibited pacemakers alluded to has now been largely overcome by the use of programmable sensitivity and
bipolar sensing.9 We do
not
agree that the interpretation of the paced is difficult, particularly in the ventricular
electrocardiogram
suggest that pacemaker patients might benefit from the incorporation of an automatic implantable defibrillator in their pacemaker. It is important to recognise that pacing energies cannot be used to convert ventricular fibrillation to sinus rhythm.
inhibited mode. Lagergren
Cardiological Sciences, St George’s Hospital Medical School, University of London, London SW17 0RE
seems
to
C. P. LAU W. D. TOFF A. J. CAMM
1
Frye RL, Fisch C, Collins JJ, et al Guidelines for permanent cardiac pacemaker implantation, May 1984. J Am Coll Cardiol 1984; 2: 434-42 2. Amikam S, Lemer J, Roguin N, Pelet H, Riss E Long-term survival of elderly patients after pacemaker implantation. Am Heart J 1976; 91: 445-49. 3. Kruse I, Amman K, Conradson T-B, Ryden L A comparison of the acute and long-term hemodynamic effects of ventncular inhibited and atrial synchronous ventricular inhibited pacing. Circulation 1982; 65: 846-55. 4. Ausubel K, Furman S. The pacemaker syndrome. Ann Intern Med 1985; 103: 420-09 5. Alpert MA, Curtis AJ, Sanfellipo JF, et al. Comparative survival after permanent ventricular pacing and dual chamber pacing for patients with chronic high degree atrioventricular block with and without preexisting congestive heart failure. Circulation 1986; 7: 925-32. 6 Karlof I. Haemodynamic effect of atrial triggered versus fixed rate pacing at rest and during exercise in complete heart block. Acta Med Scand 1975; 197: 195-206. Rickards AF. Rate responsive pacing. In: Barold SS, ed. Modem cardiac pacing. New York Futura, 1985. 799-809. 8 Sutton R, Ingram A, Briers L, et al. Ten years of physiological cardiac pacing. PACE 1987; 10: 444. 9 Breivik K, Ohm O, Engedal H Long term companson of unipolar and bipolar pacing and sensing, using a new multiprogrammable pacemaker system. PACE 1983, 6: 7
592-600.
SiR,—The report by Dr Arankalle and colleagues (March 12, p 550) of 27 nm virus-like particles (VLPs) associated with a case of enterically transmitted non-A, non-B hepatitis (ET-NANBH) in India is reminiscent of earlier reports of 27-30 nm VLPs recovered from similar cases.l3 However, the aetiological agent of ETNANBH is significantly larger in diameter than 27 nm. Our most recent studies4.5 have clearly demonstrated a serological relation between 32-34 nm VLPs and ET-NANBH in man and in experimentally infected primates. Size measurements of diseaseassociated VLPs recovered from the acute-phase stools of ETNANBH cases in four geographically distinct regions of the world (the Soviet Union, Burma, Somalia, and Mexico), have shown that less than 2 % of all particles measured (n== 135) were 27 nm in diameter. Most VLPs (60%) were 32-34 nm (mean 32-2 nm).5 These findings are entirely consistent with the notion that the virus of ET-NANBH is not a picornavirus, and this is further supported by the observation that partly purified virus recovered from stools of cases in Somalia, Mexico, and the Soviet Union sediment at 183S.5 The latter biophysical property is a characteristic feature of calciviruses or calici-like viruses.6,7 While our recent findings and those of Arankalle et al seem to be at odds with one another, it is important to note that calciviruses, for example, have been shown to be susceptible to proteolytic degradation (during passage through the gut) from larger (32-38 nm) particles to smaller ones (27-29 run). It is at least taxonomically prudent not to confuse the 27-30 nm particle found in stools of some cases of ET-NANBH with the larger, undegraded virus that we have shown to be the probable cause of this disease. Our studies suggest that there is a continuum of ET-NANBH virus particle diameters from 27 to 37 nm and that individual case stool specimens may contain more virus of one size than another. Further studies of virus particle morphology and serology, including the possible confounding effects of proteolytic digestion on particle size and seroreactivity, should be considered. We also note that virus particle
instability, promoted perhaps by proteolytic degradation, may explain why we and others, including Arankalle et al, have encountered great difficulty in recovering intact virus particles from stools of acutely infected
patients.
Hepatitis Branch, Division of Viral Diseases, Center for Infectious Diseases, Atlanta, Georgia 30333, USA
DANIEL W. BRADLEY
Institute of Poliomyelitis and Viral Encephalitides,
Moscow, USSR
MIKHAIL S. BALAYAN
Balayan MS, Andjaparidze AG, Savinskaya SS, et al Evidence for a virus m non-A, non-B hepatitis transmitted via the fecal-oral route Intervirology 1983; 20: 23-31. 2. Kane MA, Bradley DW, Shrestha SM, et al. Epidemic non-A, non-B hepatitis in Nepal JAMA 1984; 252: 3140-45. 3. Sreenivasan MA, Arankalle VA, Sehgal A, Pavri KM. Non-A, non-B epidemic hepatitis: Visualization of virus-like particles in the stool by immune electron microscopy. J Gen Virol 1984; 65: 1005-07. 4. Bradley DW, Krawczynski K, Cook EH Jr, et al. Entencally transmitted non-A, non-B hepatitis Serial passage of disease in cynomolgus macaques and tamarins and recovery of disease-associated 27- to 34- nm viruslike particles. Proc Natl Acad 1.
Sci USA 1987; 84: 6277-81.
Bradley DW, Andjaparidze A, Cook EH Jr, et al. Aetiological agent of enterically transmitted non-A, non-B hepatitis. J Gen Virol 1988; 69 731-38. 6. Carter MJ, Madeley CR. Caliciviridae. In. Nessmut, Steven, eds. Animal virus structure. Amsterdam: Elsevier, 1987. 121-28. 7. Hillman B, Moms TJ, Kellen WR, Hoffman D, Schlegel DE An invertebrate calici-like virus: Evidence for partial virus disintegration in host excreta. J Gen Virol 1982, 60: 115-23 5.
TRIPTORELIN IN TREATMENT OF CERVICAL AND VAGINAL DYSPLASIA RELATED TO PAPILLOMAVIRUS
SiR,—Luteinising-hormone releasing hormone (LH-RH) agonists have been used to treat prostate and breast cancer and benign diseases of the prostate, breast, and uterus. In young people there is an epidemic of dysplastic lesions of the genital organs (eg,
Letters
to
VIRUS OF ENTERICALLY TRANSMITTED NON-A, NON-B HEPATITIS
the Editor
25 YEARS OF IMPLANTED INTRACARDIAC PACERS
SiR,—We disagree with Dr Lagergren’s occasional survey (March 19, p 636), which is an outdated and idiosyncratic view far removed from that generally accepted in the UK, Europe, and the USA. There is wide regional and national variation in the frequency of pacemaker implantation and there may well be instances where pacemakers are implanted inappropriately. However, best estimates of the likely required annual rate of implantation, based on disease prediction, suggest a figure of 300 per million population. To suggest that pacing is being adequately implemented in Stockholm by equation of the implant rate with that in the UK is misguided, since the expressed view of the British Cardiac Society and the British Pacing and Electrophysiology group is that pacing is, at present, being offered to only about half the patients who could benefit from it. Physicians, indoctrinated by antiquated viewssuch as those expressed by Lagergren, are not referring the appropriate patients to the specialist centres. The principal indication for cardiac pacing is symptomatic bradycardia, the aim being to abolish or prevent the symptoms. But even in the absence of symptoms, cardiac pacing is indicated in almost all cases of complete heart block and can reduce mortality.1 Pacing in the elderly is at least as rewarding as in younger patients.’ In complete heart block with normal sinus node function, dual chamber pacing is best, and confers haemodynamic advantages and improves quality of life compared with constant rate ventricular pacing.3 It also decreases the risk of pacemaker syndrome4 and may improve survival in patients with heart failure.s In atrial fibrillation or sinus node dysfunction a rate responsive pacemaker, capable of matching the pacing rate to the patient’s needs, may confer similar advantages.6,7 The development of such rate responsive systems has been the focus of considerable research in the past ten years, yet it receives not a single mention by Lagergren. Recognition of the value of physiological pacing has led to an increase in its use from 20% of all implants in 1977 to 72% in 1986 in one major centred Despite improvements in battery life, triggered pacing is still likely to lead to early depletion of the power source. The "drawback" of inhibited pacemakers alluded to has now been largely overcome by the use of programmable sensitivity and
bipolar sensing.9 We do
not
agree that the interpretation of the paced is difficult, particularly in the ventricular
electrocardiogram
suggest that pacemaker patients might benefit from the incorporation of an automatic implantable defibrillator in their pacemaker. It is important to recognise that pacing energies cannot be used to convert ventricular fibrillation to sinus rhythm.
inhibited mode. Lagergren
Cardiological Sciences, St George’s Hospital Medical School, University of London, London SW17 0RE
seems
to
C. P. LAU W. D. TOFF A. J. CAMM
1
Frye RL, Fisch C, Collins JJ, et al Guidelines for permanent cardiac pacemaker implantation, May 1984. J Am Coll Cardiol 1984; 2: 434-42 2. Amikam S, Lemer J, Roguin N, Pelet H, Riss E Long-term survival of elderly patients after pacemaker implantation. Am Heart J 1976; 91: 445-49. 3. Kruse I, Amman K, Conradson T-B, Ryden L A comparison of the acute and long-term hemodynamic effects of ventncular inhibited and atrial synchronous ventricular inhibited pacing. Circulation 1982; 65: 846-55. 4. Ausubel K, Furman S. The pacemaker syndrome. Ann Intern Med 1985; 103: 420-09 5. Alpert MA, Curtis AJ, Sanfellipo JF, et al. Comparative survival after permanent ventricular pacing and dual chamber pacing for patients with chronic high degree atrioventricular block with and without preexisting congestive heart failure. Circulation 1986; 7: 925-32. 6 Karlof I. Haemodynamic effect of atrial triggered versus fixed rate pacing at rest and during exercise in complete heart block. Acta Med Scand 1975; 197: 195-206. Rickards AF. Rate responsive pacing. In: Barold SS, ed. Modem cardiac pacing. New York Futura, 1985. 799-809. 8 Sutton R, Ingram A, Briers L, et al. Ten years of physiological cardiac pacing. PACE 1987; 10: 444. 9 Breivik K, Ohm O, Engedal H Long term companson of unipolar and bipolar pacing and sensing, using a new multiprogrammable pacemaker system. PACE 1983, 6: 7
592-600.
SiR,—The report by Dr Arankalle and colleagues (March 12, p 550) of 27 nm virus-like particles (VLPs) associated with a case of enterically transmitted non-A, non-B hepatitis (ET-NANBH) in India is reminiscent of earlier reports of 27-30 nm VLPs recovered from similar cases.l3 However, the aetiological agent of ETNANBH is significantly larger in diameter than 27 nm. Our most recent studies4.5 have clearly demonstrated a serological relation between 32-34 nm VLPs and ET-NANBH in man and in experimentally infected primates. Size measurements of diseaseassociated VLPs recovered from the acute-phase stools of ETNANBH cases in four geographically distinct regions of the world (the Soviet Union, Burma, Somalia, and Mexico), have shown that less than 2 % of all particles measured (n== 135) were 27 nm in diameter. Most VLPs (60%) were 32-34 nm (mean 32-2 nm).5 These findings are entirely consistent with the notion that the virus of ET-NANBH is not a picornavirus, and this is further supported by the observation that partly purified virus recovered from stools of cases in Somalia, Mexico, and the Soviet Union sediment at 183S.5 The latter biophysical property is a characteristic feature of calciviruses or calici-like viruses.6,7 While our recent findings and those of Arankalle et al seem to be at odds with one another, it is important to note that calciviruses, for example, have been shown to be susceptible to proteolytic degradation (during passage through the gut) from larger (32-38 nm) particles to smaller ones (27-29 run). It is at least taxonomically prudent not to confuse the 27-30 nm particle found in stools of some cases of ET-NANBH with the larger, undegraded virus that we have shown to be the probable cause of this disease. Our studies suggest that there is a continuum of ET-NANBH virus particle diameters from 27 to 37 nm and that individual case stool specimens may contain more virus of one size than another. Further studies of virus particle morphology and serology, including the possible confounding effects of proteolytic digestion on particle size and seroreactivity, should be considered. We also note that virus particle
instability, promoted perhaps by proteolytic degradation, may explain why we and others, including Arankalle et al, have encountered great difficulty in recovering intact virus particles from stools of acutely infected
patients.
Hepatitis Branch, Division of Viral Diseases, Center for Infectious Diseases, Atlanta, Georgia 30333, USA
DANIEL W. BRADLEY
Institute of Poliomyelitis and Viral Encephalitides,
Moscow, USSR
MIKHAIL S. BALAYAN
Balayan MS, Andjaparidze AG, Savinskaya SS, et al Evidence for a virus m non-A, non-B hepatitis transmitted via the fecal-oral route Intervirology 1983; 20: 23-31. 2. Kane MA, Bradley DW, Shrestha SM, et al. Epidemic non-A, non-B hepatitis in Nepal JAMA 1984; 252: 3140-45. 3. Sreenivasan MA, Arankalle VA, Sehgal A, Pavri KM. Non-A, non-B epidemic hepatitis: Visualization of virus-like particles in the stool by immune electron microscopy. J Gen Virol 1984; 65: 1005-07. 4. Bradley DW, Krawczynski K, Cook EH Jr, et al. Entencally transmitted non-A, non-B hepatitis Serial passage of disease in cynomolgus macaques and tamarins and recovery of disease-associated 27- to 34- nm viruslike particles. Proc Natl Acad 1.
Sci USA 1987; 84: 6277-81.
Bradley DW, Andjaparidze A, Cook EH Jr, et al. Aetiological agent of enterically transmitted non-A, non-B hepatitis. J Gen Virol 1988; 69 731-38. 6. Carter MJ, Madeley CR. Caliciviridae. In. Nessmut, Steven, eds. Animal virus structure. Amsterdam: Elsevier, 1987. 121-28. 7. Hillman B, Moms TJ, Kellen WR, Hoffman D, Schlegel DE An invertebrate calici-like virus: Evidence for partial virus disintegration in host excreta. J Gen Virol 1982, 60: 115-23 5.
TRIPTORELIN IN TREATMENT OF CERVICAL AND VAGINAL DYSPLASIA RELATED TO PAPILLOMAVIRUS
SiR,—Luteinising-hormone releasing hormone (LH-RH) agonists have been used to treat prostate and breast cancer and benign diseases of the prostate, breast, and uterus. In young people there is an epidemic of dysplastic lesions of the genital organs (eg,