252
Managing hypertension
in the
elderly
SiR,—The STOP-Hypertension trial (Nov 23, p 1281) compared four different once-daily medications for hypertension (atenolol, hydrochlorothiazide plus amiloride, metoprolol, and pindolol) with matching placebos, but in the report the results of the active treatments are lumped together. We are not even told how many patients received each treatment. Did the active treatments differ in their therapeutic or in their unwanted effects? I would certainly expect differences in the adverse effect profiles. And why was
this information omitted?
9 Park Crescent, London N3 2NL, UK
ANDREW HERXHEIMER
** This letter has been shown to Dr Dahlof and colleagues, whose reply follows.-ED. L. SIR,-A clearly stated aim in the STOP study was to evaluate "active treatment" versus placebo. An analysis of the effects of each of the four active regimens separately on hard end-points was never intended. It would be scientifically inappropriate to make such a post-hoc subgroup analysis, a procedure that regrettably is not uncommon in studies of this kind. The fact that 68% of all patients on active therapy were on combined treatment with one of the three
P-blockers
and the diuretic does not increase
our
urge to do the
subgroup analysis proposed. Department of Medicine, University of Gothenburg, Ostra Hospital, S-146 85 Gothenberg, Sweden, Health Sciences Centre, University of Lund, Dalby, and Department of Medicine, University Hospital, Umeå
B. DAHLÖF L. H. LINDHOLM L. HANSSON B. SCHERSTÉN T. EKBOM P. O. WESTER
SiR,—Your editorial commenting on the SHEP and STOPHypertension trials (Nov 23, p 1299) concludes that previous concerns about treating elderly hypertensive patients are unwarranted. But there is a new risk in treating older hypertensive patients which needs attention. Brandt et aP recently reported a group of old patients with severe systemic hypertension who were found to have hypertrophic cardiomyopathy with left-ventricular outflow obstruction (demonstrated by an isoproterenol test). Recognition of this group is clinically important because use of afterload-reducing agents, such as arterial vasodilators and angiotensin-converting-enzyme inhibitors or/and preloadreducing agents such as diuretics and nitrates, both of which may aggravate left-ventricular outflow obstruction of the dynamic variety, will be harmful. The frequency with which this group is met in clinical practice needs further study. Department of Medicine, George Washington University, Washington, DC 20037, USA 1. Brandt
TSUNG O. CHENG
CM, Boulenc JM, Carriere T, Verdun A, Imbs JL Myocardiopathie du ventncule gauche
hypertrophique avec syndrome d’obstruction dynamique chez l’adulte hypertendu. Presse Méd 1991; 20: 1923-26.
contact, the immediate environment, or some other route does not affect the validity of the notion of separation of a potential source of infection from those at risk of acquisition of that infection. For 4 years our policy has been geographical separation of colonised and non-colonised patients in our CF clinic of over 100 adults, both as inpatients and outpatients, through the use of separate wards and clinics. Despite these measures, in 1991 we noted 5 new cases of Ps cepacia infection. Ribotyping of the organisms isolated from these 5 patients revealed that 3 have strains that are indistinguishable. These 3 patients had had no contact with each other within the hospital environment or with patients known to be colonised with Ps cepacia. However, inquiry into their social contacts outside the hospital environment has revealed episodes of contact between these 3 patients and other CF individuals whose microbiological status is not known to us. We believe that this provides further evidence of the possibility of person-to-person transmission of Ps cepacia among the CF community outside the hospital environment.s We now advise our patients that, although the level of risk remains to be defmed, there may be transmission of Ps cepacia through social as well as hospital contact and that social contact should be kept to a minimum. We suggest that until Ps cepacia can be shown not to be infectious, and that it does not lead to accelerated deterioration or premature death in some patients, then we should err on the side of safety. There are clearly important issues arising from such advice which can only be addressed in consultation with individual patients. The adoption of this advice has been very difficult for some patients, their families, and members of the CF team. However, we have been heartened by their response to open discussion of these difficulties. We thank Dr Ty Pitt for
ribotype analysis of Ps cepacia strains.
I, Corey M, et al. Pseudomonas cepacia infection in cystic fibrosis: an emerging problem. J Pediatr 1984, 104: 206-10. 2. Simmonds EJ, Conway SP, Ghoneim ATM, Ross H, Littlewood JM. Ps cepacia. a new pathogen in patients with cystic fibrosis referred to a large centre m the United Kingdom Arch Dis Child 1990; 65: 874-77. 3. Gilligan PH. Microbiology of airways disease in patients with cystic fibrosis. Clin 1. Isles A, Maclusky
Microbiol Rev 1991; 4: 35-51. 4. Tablan OC, Martone WJ, Doershuk CF, et al. Colonisation of the respiratory tract with Ps cepacia in cystic fibrosis: risk factors and outcomes. Chest 1987; 91: 527-32 5. LiPuma JJ, Dasen SE, Nielson DW, Stem RC, Stull TL. Person-to-person transmission of Ps cepacia between patients with cystic fibrosis. Lancet 1990; 336: 1094-96. 6. Rabkin CS, Jarvis WR, Anderson RL, et al. Ps cepacia typing systems: collaborative study to assess their potential in epidemiological investigations. Rev Infect Dis 1989, 11: 600-07 7. Gilligan PH, Gage PA, Bradshaw LM, Schidlow DV, Decicco BT. Isolation medium for the recovery of Ps cepacia from the respiratory secretions of patients with cystic fibrosis. J Clin Microbiol 1985, 22: 5-8. 8 Thomassen MJ, Demko CA, Klinger JD, Stem RC. Ps cepacia colonisation amongst patients with cystic fibrosis: a new opportunist. Am Rev Respir Dis 1985; 131: 791-96.
Childhood leukaemia
Pseudomonas cepacia infection in cystic fibrosis SiR,—Dr Nelson and colleagues (Dec 14, p 1525) report success in isolating Pseudomonas cepacia from the immediate environment of two colonised cystic fibrosis (CF) patients in hospital. They rightly point out the importance of the use of selective media and comment that their results confirm the potential for indirect transmission of Ps cepacia between patients. They do not, however, reach any firm conclusions about some aspects of the management of colonised patients either from their own work or from the publications that they cited Our experience and that of others’-4,8 is that acquisition of Ps cepacia for some patients with CF heralds the onset of increased morbidity and unexpected early death. Although the precise mode of transmission remains unknown, evidence suggests that colonised patients are a potential source for transmission to non-colonised patients. Whether transmission is via droplet spread, physical
D. L. SMITH E. G. SMITH L. B. GUMERY D. E. STABLEFORTH
Adult Cystic Fibrosis Unit and Department of Microbiology, East Birmingham Hospital, Birmingham B9 5ST, UK
on
Greek Islands
SIR,—Ur Petridou and colleagues (Nov 9, p 1204) raise when
an
interesting possibility they imply that mass tourism may involve the type of population mixing that is conducive to an increase of childhood leukaemia, as found in rural new towns in Britain and in keeping with my hypothesis.’ However, those towns experienced increases only in the first decade of their existence, after which there was no excess. Still more limited in time was the increase of childhood leukaemia recorded near large military encampments in England and Wales early in the period of post-war national military service.2 Petridou and colleagues were able to study leukaemia mortality on Greek islands only in a period starting in 1976--ie, about 15 years after the start of large-scale tourism there. Since no excess of childhood leukaemia was observed in new towns in the corresponding period, it is incorrect to state that the Greek results "do not seem compatible with" my hypothesis. Petridou and colleagues acknowledge that the population mixing involved in tourism may not be comparable with that in British new
Managing hypertension
in the
elderly
SiR,—The STOP-Hypertension trial (Nov 23, p 1281) compared four different once-daily medications for hypertension (atenolol, hydrochlorothiazide plus amiloride, metoprolol, and pindolol) with matching placebos, but in the report the results of the active treatments are lumped together. We are not even told how many patients received each treatment. Did the active treatments differ in their therapeutic or in their unwanted effects? I would certainly expect differences in the adverse effect profiles. And why was
this information omitted?
9 Park Crescent, London N3 2NL, UK
ANDREW HERXHEIMER
** This letter has been shown to Dr Dahlof and colleagues, whose reply follows.-ED. L. SIR,-A clearly stated aim in the STOP study was to evaluate "active treatment" versus placebo. An analysis of the effects of each of the four active regimens separately on hard end-points was never intended. It would be scientifically inappropriate to make such a post-hoc subgroup analysis, a procedure that regrettably is not uncommon in studies of this kind. The fact that 68% of all patients on active therapy were on combined treatment with one of the three
P-blockers
and the diuretic does not increase
our
urge to do the
subgroup analysis proposed. Department of Medicine, University of Gothenburg, Ostra Hospital, S-146 85 Gothenberg, Sweden, Health Sciences Centre, University of Lund, Dalby, and Department of Medicine, University Hospital, Umeå
B. DAHLÖF L. H. LINDHOLM L. HANSSON B. SCHERSTÉN T. EKBOM P. O. WESTER
SiR,—Your editorial commenting on the SHEP and STOPHypertension trials (Nov 23, p 1299) concludes that previous concerns about treating elderly hypertensive patients are unwarranted. But there is a new risk in treating older hypertensive patients which needs attention. Brandt et aP recently reported a group of old patients with severe systemic hypertension who were found to have hypertrophic cardiomyopathy with left-ventricular outflow obstruction (demonstrated by an isoproterenol test). Recognition of this group is clinically important because use of afterload-reducing agents, such as arterial vasodilators and angiotensin-converting-enzyme inhibitors or/and preloadreducing agents such as diuretics and nitrates, both of which may aggravate left-ventricular outflow obstruction of the dynamic variety, will be harmful. The frequency with which this group is met in clinical practice needs further study. Department of Medicine, George Washington University, Washington, DC 20037, USA 1. Brandt
TSUNG O. CHENG
CM, Boulenc JM, Carriere T, Verdun A, Imbs JL Myocardiopathie du ventncule gauche
hypertrophique avec syndrome d’obstruction dynamique chez l’adulte hypertendu. Presse Méd 1991; 20: 1923-26.
contact, the immediate environment, or some other route does not affect the validity of the notion of separation of a potential source of infection from those at risk of acquisition of that infection. For 4 years our policy has been geographical separation of colonised and non-colonised patients in our CF clinic of over 100 adults, both as inpatients and outpatients, through the use of separate wards and clinics. Despite these measures, in 1991 we noted 5 new cases of Ps cepacia infection. Ribotyping of the organisms isolated from these 5 patients revealed that 3 have strains that are indistinguishable. These 3 patients had had no contact with each other within the hospital environment or with patients known to be colonised with Ps cepacia. However, inquiry into their social contacts outside the hospital environment has revealed episodes of contact between these 3 patients and other CF individuals whose microbiological status is not known to us. We believe that this provides further evidence of the possibility of person-to-person transmission of Ps cepacia among the CF community outside the hospital environment.s We now advise our patients that, although the level of risk remains to be defmed, there may be transmission of Ps cepacia through social as well as hospital contact and that social contact should be kept to a minimum. We suggest that until Ps cepacia can be shown not to be infectious, and that it does not lead to accelerated deterioration or premature death in some patients, then we should err on the side of safety. There are clearly important issues arising from such advice which can only be addressed in consultation with individual patients. The adoption of this advice has been very difficult for some patients, their families, and members of the CF team. However, we have been heartened by their response to open discussion of these difficulties. We thank Dr Ty Pitt for
ribotype analysis of Ps cepacia strains.
I, Corey M, et al. Pseudomonas cepacia infection in cystic fibrosis: an emerging problem. J Pediatr 1984, 104: 206-10. 2. Simmonds EJ, Conway SP, Ghoneim ATM, Ross H, Littlewood JM. Ps cepacia. a new pathogen in patients with cystic fibrosis referred to a large centre m the United Kingdom Arch Dis Child 1990; 65: 874-77. 3. Gilligan PH. Microbiology of airways disease in patients with cystic fibrosis. Clin 1. Isles A, Maclusky
Microbiol Rev 1991; 4: 35-51. 4. Tablan OC, Martone WJ, Doershuk CF, et al. Colonisation of the respiratory tract with Ps cepacia in cystic fibrosis: risk factors and outcomes. Chest 1987; 91: 527-32 5. LiPuma JJ, Dasen SE, Nielson DW, Stem RC, Stull TL. Person-to-person transmission of Ps cepacia between patients with cystic fibrosis. Lancet 1990; 336: 1094-96. 6. Rabkin CS, Jarvis WR, Anderson RL, et al. Ps cepacia typing systems: collaborative study to assess their potential in epidemiological investigations. Rev Infect Dis 1989, 11: 600-07 7. Gilligan PH, Gage PA, Bradshaw LM, Schidlow DV, Decicco BT. Isolation medium for the recovery of Ps cepacia from the respiratory secretions of patients with cystic fibrosis. J Clin Microbiol 1985, 22: 5-8. 8 Thomassen MJ, Demko CA, Klinger JD, Stem RC. Ps cepacia colonisation amongst patients with cystic fibrosis: a new opportunist. Am Rev Respir Dis 1985; 131: 791-96.
Childhood leukaemia
Pseudomonas cepacia infection in cystic fibrosis SiR,—Dr Nelson and colleagues (Dec 14, p 1525) report success in isolating Pseudomonas cepacia from the immediate environment of two colonised cystic fibrosis (CF) patients in hospital. They rightly point out the importance of the use of selective media and comment that their results confirm the potential for indirect transmission of Ps cepacia between patients. They do not, however, reach any firm conclusions about some aspects of the management of colonised patients either from their own work or from the publications that they cited Our experience and that of others’-4,8 is that acquisition of Ps cepacia for some patients with CF heralds the onset of increased morbidity and unexpected early death. Although the precise mode of transmission remains unknown, evidence suggests that colonised patients are a potential source for transmission to non-colonised patients. Whether transmission is via droplet spread, physical
D. L. SMITH E. G. SMITH L. B. GUMERY D. E. STABLEFORTH
Adult Cystic Fibrosis Unit and Department of Microbiology, East Birmingham Hospital, Birmingham B9 5ST, UK
on
Greek Islands
SIR,—Ur Petridou and colleagues (Nov 9, p 1204) raise when
an
interesting possibility they imply that mass tourism may involve the type of population mixing that is conducive to an increase of childhood leukaemia, as found in rural new towns in Britain and in keeping with my hypothesis.’ However, those towns experienced increases only in the first decade of their existence, after which there was no excess. Still more limited in time was the increase of childhood leukaemia recorded near large military encampments in England and Wales early in the period of post-war national military service.2 Petridou and colleagues were able to study leukaemia mortality on Greek islands only in a period starting in 1976--ie, about 15 years after the start of large-scale tourism there. Since no excess of childhood leukaemia was observed in new towns in the corresponding period, it is incorrect to state that the Greek results "do not seem compatible with" my hypothesis. Petridou and colleagues acknowledge that the population mixing involved in tourism may not be comparable with that in British new
