- Email: [email protected]
Hepatitis E virus infection
CORRESPONDENCE
Urinary incontinence and the rhabdosphincter
3
4
Sir—Hannes Strasser and colleagues (Sept 11, p 918)1 report on an agedependent decrease of striated muscle cells in the rhabdosphincter and suggest this is the main reason for the increased rate of urinary incontinence in the elderly. We doubt whether this conclusion can be drawn from the study undertaken. First, the patients investigated were reported to be healthy individuals, which implicates that their continence status was normal. Thus, the lower density of striated rhabdosphincter muscle fibres seen with older age may reflect a physiological rather than a pathological condition—ie, urinary incontinence and morphological changes of the rhabdosphincter were not associated in these individuals. Second, alterations of the rhabdosphincter may not be the main reason for urinary incontinence in the elderly at all. A compromised nervous control of rhabdosphincter function is another attractive explanation. Older people have a greater likelihood to be affected by neurological diseases resulting in impaired urinary storage—such as cerebrovascular disease2 and dementia.3 Because these diseases tend to induce detrusor hyper-reflexia,4 they might further promote urinary incontinence. This could reflect the clinical observation reported by Strasser and colleagues that 30% of older people living at home and even 50% of the elderly living in nursing homes are incontinent. Besides this, urinary infection and irritative lower urinary tract symptoms5 are more prevalent in the elderly and may jeopardise continence, irrespective of rhabdosphincter function. Although the results presented by Strasser and colleagues are intriguing, correlation with clinical findings is necessary to confirm the density of the muscle cells in the rhabdosphincter as the key element of urinary continence. *C Goessl, K Miller Department of Urology, Klinikum Benjamin Franklin, Free University of Berlin, D-12200 Berlin, Germany (e-mail: [email protected]) 1
2
Strasser H, Tiefenthaler M, Steinlechner M, Bartsch G, Konwalinka G. Urinary incontinence in the elderly and agedependent apoptosis of rhabdosphincter cells. Lancet 1999; 354: 918–19. Arena MG, Di Rosa AE, Arcudi L, et al. Voiding disorders in patients with cerebrovascular disease. Funct Neurol 1992; 7: 47–49.
578
5
Skelly J, Flint AJ. Urinary incontinence associated with dementia. J Am Geriatr Soc 1995; 43: 286–94. Hebjorn S, Andersen JT, Walter S, Mouritzen Dam A. Detrusor hyperreflexia. A survey on its etiology and treatment. Scand J Urol Nephrol 1976; 10: 103–09. Madersbacher S, Pycha A, Klingler CH, Schatzl G, Marberger M. The International Prostate Symptom score in both sexes: a urodynamics-based comparison. Neurourol Urodyn 1999; 18: 173–82.
Thus, we agree with Scharschmidt5 that the “pace of HEV research is hectic”, but unlike Skidmore, we believe that progress has been impressive. *Robert H Purcell, Suzanne U Emerson *Hepatitis Viruses Section and Molecular Hepatitis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-0740, USA 1
Hepatitis E virus infection Sir—We agree with Susan Skidmore (Sept 25, p 1049)1 that the seroepidemiology of hepatitis E virus (HEV) infection in the rural riverine ecology of southeast Asia is strikingly different from that of another enterically transmitted hepatitis virus, hepatitis A virus. However, similar epidemiological characteristics of HEV infection have been identified in urban and non-riverine ecologies elsewhere. Also, much higher prevalences of antiHEV antibodies, in children as well as in adults, have been reported in other studies, suggesting that the epidemiology of HEV infection is more complex than Skidmore implies. However, the apparent high prevalence of anti-HEV antibodies is dependent on the serological test used, and many tests, including the two most frequently used commercial diagnostic tests, do not have the best sensitivity for seroepidemiological studies.2 Therefore, comparisons are difficult unless the same test is used. The zoonotic spread of HEV in developing countries was originally suggested on the basis of reports of HEV infection of rats, swine, and other animals in central Asia. The finding that most swine and rats tested in the USA were infected with HEV-like agents suggests that zoonotic spread of HEV can also occur in more developed countries. In fact, serologically-related HEV strains recovered from human beings and swine in the USA have crossed species barriers.3 Immunoprophylaxis against HEV infection has progressed rapidly. Both passive and active immunoprophylaxis have been shown under experimental conditions.4 Macaques immunised with recombinant capsid protein are protected against hepatitis E after massive intravenous challenge with the same or a different genotype of HEV.4 Based on these results, SmithKline Beecham Biologicals (Rixensart, Belgium) sponsored the preparation of such a vaccine for assessment in human beings. The vaccine was safe and immunogenic in volunteers and is ready for tests of efficacy.
2
3
4
5
Skidmore SJ. Factors in spread of hepatitis E. Lancet 1999; 354: 1049–50. Mast EE, Alter MJ, Holland PV, et al. Evaluation of assays for antibody to hepatitis E virus by a serum panel. Hepatitis E Virus Antibody Serum Panel Evaluation Group. Hepatology 1998; 27: 857–61. Kabrane-Lazizi Y, Fine JB, Elm J, et al. Evidence for widespread infection of wild rats with hepatitis E virus in the United States. Am J Trop Med Hyg 1999; 61: 331–35. Tsarev SA, Tsareva TS, Emerson SU, et al. Recombinant vaccine against hepatitis E: dose response and protection against heterologous challenge. Vaccine 1997; 15: 1834–38. Scharschmidt BF. Hepatitis E: a virus in waiting. Lancet 1995; 346: 519–20.
Pneumococcal vaccine and the elderly Sir—Your Dec 11 editorial1 makes a good case for the global benefits of pneumococcal vaccination and the need for consensus in the industrialised world. It is worth contrasting UK policy with that of the USA, where a key National Health Objective for 2000 is to increase pneumococcal vaccination of the elderly (over 65 years) to 60% or more.2 There is no such objective in the UK. Vaccination is recommended only for those with chronic cardiac, respiratory, or renal disease, diabetes, hyposplenism, chronic liver disease, and immunodeficiency. Uptake of these groups is only 4% in the UK, although this can rise to 33% during general practice campaigns.3 In the USA, where there is an explicit goal for vaccine uptake, 45% of people aged over 65 years receive pneumococcal vaccine. The elderly are 12 times as likely as younger patients to be admitted to hospital with pneumonia.4 The commonest pathogen remains Streptococcus pneumonia, with bacteraemia affecting 20% of patients and carrying a 25–30% mortality. At least six case-control and cohort studies show that the vaccine has a 50–80% efficacy in preventing pneumococcal bacteraemia, not pneumonia per se, in those over age 65 years, with or without other risk factors.5 The vaccine is cheap
THE LANCET • Vol 355 • February 12, 2000
Urinary incontinence and the rhabdosphincter
3
4
Sir—Hannes Strasser and colleagues (Sept 11, p 918)1 report on an agedependent decrease of striated muscle cells in the rhabdosphincter and suggest this is the main reason for the increased rate of urinary incontinence in the elderly. We doubt whether this conclusion can be drawn from the study undertaken. First, the patients investigated were reported to be healthy individuals, which implicates that their continence status was normal. Thus, the lower density of striated rhabdosphincter muscle fibres seen with older age may reflect a physiological rather than a pathological condition—ie, urinary incontinence and morphological changes of the rhabdosphincter were not associated in these individuals. Second, alterations of the rhabdosphincter may not be the main reason for urinary incontinence in the elderly at all. A compromised nervous control of rhabdosphincter function is another attractive explanation. Older people have a greater likelihood to be affected by neurological diseases resulting in impaired urinary storage—such as cerebrovascular disease2 and dementia.3 Because these diseases tend to induce detrusor hyper-reflexia,4 they might further promote urinary incontinence. This could reflect the clinical observation reported by Strasser and colleagues that 30% of older people living at home and even 50% of the elderly living in nursing homes are incontinent. Besides this, urinary infection and irritative lower urinary tract symptoms5 are more prevalent in the elderly and may jeopardise continence, irrespective of rhabdosphincter function. Although the results presented by Strasser and colleagues are intriguing, correlation with clinical findings is necessary to confirm the density of the muscle cells in the rhabdosphincter as the key element of urinary continence. *C Goessl, K Miller Department of Urology, Klinikum Benjamin Franklin, Free University of Berlin, D-12200 Berlin, Germany (e-mail: [email protected]) 1
2
Strasser H, Tiefenthaler M, Steinlechner M, Bartsch G, Konwalinka G. Urinary incontinence in the elderly and agedependent apoptosis of rhabdosphincter cells. Lancet 1999; 354: 918–19. Arena MG, Di Rosa AE, Arcudi L, et al. Voiding disorders in patients with cerebrovascular disease. Funct Neurol 1992; 7: 47–49.
578
5
Skelly J, Flint AJ. Urinary incontinence associated with dementia. J Am Geriatr Soc 1995; 43: 286–94. Hebjorn S, Andersen JT, Walter S, Mouritzen Dam A. Detrusor hyperreflexia. A survey on its etiology and treatment. Scand J Urol Nephrol 1976; 10: 103–09. Madersbacher S, Pycha A, Klingler CH, Schatzl G, Marberger M. The International Prostate Symptom score in both sexes: a urodynamics-based comparison. Neurourol Urodyn 1999; 18: 173–82.
Thus, we agree with Scharschmidt5 that the “pace of HEV research is hectic”, but unlike Skidmore, we believe that progress has been impressive. *Robert H Purcell, Suzanne U Emerson *Hepatitis Viruses Section and Molecular Hepatitis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-0740, USA 1
Hepatitis E virus infection Sir—We agree with Susan Skidmore (Sept 25, p 1049)1 that the seroepidemiology of hepatitis E virus (HEV) infection in the rural riverine ecology of southeast Asia is strikingly different from that of another enterically transmitted hepatitis virus, hepatitis A virus. However, similar epidemiological characteristics of HEV infection have been identified in urban and non-riverine ecologies elsewhere. Also, much higher prevalences of antiHEV antibodies, in children as well as in adults, have been reported in other studies, suggesting that the epidemiology of HEV infection is more complex than Skidmore implies. However, the apparent high prevalence of anti-HEV antibodies is dependent on the serological test used, and many tests, including the two most frequently used commercial diagnostic tests, do not have the best sensitivity for seroepidemiological studies.2 Therefore, comparisons are difficult unless the same test is used. The zoonotic spread of HEV in developing countries was originally suggested on the basis of reports of HEV infection of rats, swine, and other animals in central Asia. The finding that most swine and rats tested in the USA were infected with HEV-like agents suggests that zoonotic spread of HEV can also occur in more developed countries. In fact, serologically-related HEV strains recovered from human beings and swine in the USA have crossed species barriers.3 Immunoprophylaxis against HEV infection has progressed rapidly. Both passive and active immunoprophylaxis have been shown under experimental conditions.4 Macaques immunised with recombinant capsid protein are protected against hepatitis E after massive intravenous challenge with the same or a different genotype of HEV.4 Based on these results, SmithKline Beecham Biologicals (Rixensart, Belgium) sponsored the preparation of such a vaccine for assessment in human beings. The vaccine was safe and immunogenic in volunteers and is ready for tests of efficacy.
2
3
4
5
Skidmore SJ. Factors in spread of hepatitis E. Lancet 1999; 354: 1049–50. Mast EE, Alter MJ, Holland PV, et al. Evaluation of assays for antibody to hepatitis E virus by a serum panel. Hepatitis E Virus Antibody Serum Panel Evaluation Group. Hepatology 1998; 27: 857–61. Kabrane-Lazizi Y, Fine JB, Elm J, et al. Evidence for widespread infection of wild rats with hepatitis E virus in the United States. Am J Trop Med Hyg 1999; 61: 331–35. Tsarev SA, Tsareva TS, Emerson SU, et al. Recombinant vaccine against hepatitis E: dose response and protection against heterologous challenge. Vaccine 1997; 15: 1834–38. Scharschmidt BF. Hepatitis E: a virus in waiting. Lancet 1995; 346: 519–20.
Pneumococcal vaccine and the elderly Sir—Your Dec 11 editorial1 makes a good case for the global benefits of pneumococcal vaccination and the need for consensus in the industrialised world. It is worth contrasting UK policy with that of the USA, where a key National Health Objective for 2000 is to increase pneumococcal vaccination of the elderly (over 65 years) to 60% or more.2 There is no such objective in the UK. Vaccination is recommended only for those with chronic cardiac, respiratory, or renal disease, diabetes, hyposplenism, chronic liver disease, and immunodeficiency. Uptake of these groups is only 4% in the UK, although this can rise to 33% during general practice campaigns.3 In the USA, where there is an explicit goal for vaccine uptake, 45% of people aged over 65 years receive pneumococcal vaccine. The elderly are 12 times as likely as younger patients to be admitted to hospital with pneumonia.4 The commonest pathogen remains Streptococcus pneumonia, with bacteraemia affecting 20% of patients and carrying a 25–30% mortality. At least six case-control and cohort studies show that the vaccine has a 50–80% efficacy in preventing pneumococcal bacteraemia, not pneumonia per se, in those over age 65 years, with or without other risk factors.5 The vaccine is cheap
THE LANCET • Vol 355 • February 12, 2000