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Jonathan J Deeks, Senior Medical Statistician Centre for Statistics in Medicine, Old Road Campus, Headington, Oxford OX3 7LF
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The figures for mortality in columns 2-5 of Table 1 are the average annual mortality rates during each time period. The label for these columns was unintentionally deleted during final revision of the manuscript. Competing interests: None declared |
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Fotios C Papadopoulos, MD Department of Hygiene and Epidemiology, Athens University Medical School,75 M.Asias Str-11527,GREECE, Constantine Frangakis, Constantine Lyketsos
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Hawton et al.(1) report that suicide deaths from paracetamol and salicylates in the UK were reduced by 22% in the year after new legislation on 16 September 1998, a reduction that persisted in the next two years. The legislation limited the size of packs of analgesics (paracetamol, salicylates and their compounds) sold over the counter, and was aimed at reducing household stocks of these medications and the respective overdose danger from these supplies. We are concerned that suicidal people who act impulsively and cannot have access to a lethal dose of analgesics, might turn to other methods in order to commit suicide. In order to test this hypothesis, yearly data on suicide mortality (E950-E959 codes in ICD9 and X60-X84 in ICD10) for England and Wales and for years 1996-2001 were downloaded from the website of the Office for National Statistics (http://www.statistics.gov.uk) We compared suicide deaths, total and by method of suicide, during the 3 year period 1999-2001, after the legislation enforcement, with suicide deaths during the 3 year period before the legislation (1996- 1998), using Poisson regression. 1998 was considered a pre-legislation year, since the law was introduced in mid-September. Total suicide deaths did not differ before and after the law was introduced, with 10468 deaths in 1996-1998 vs. 10433 deaths in 1999-2001 (p=0.803). Suicides by poisoning (E950) declined (2319 deaths in 1996-1998 vs. 2190 deaths in 1999-2001, p=0.053), while suicides by hanging (E953) increased (4363 deaths in 1996-1998 vs. 5067 deaths in 1999-2001, p<0.001) after 1998. Suicides by other means did not change after 1998, except for a significant decrease in suicides by “other gases and vapours” (E952) (1909 deaths in 1996-1998 vs. 1190 deaths in 1999-2001, p<0.001). (2,3,4,5) The latter is likely related to 1993 legislation introducing catalytic coverters in motor vehicles. (6) Legislation such as the one limiting the size of packs of analgesics may well have prevented accidental poisonings and frivolous suicide attempts that aim to draw attention. This is well documented by Hawton et al, with a 30% decrease in the number of people admitted to liver units because of paracetamol induced hepatotoxicity. (1) However, as the data above suggest, people who are seriously suicidal may be less likely to benefit from such legislation, as they might turn to other, probably more violent, methods of completing suicide. (6) References 1.Hawton K, Simkin S, Deeks J, Cooper J, Johnston A, Waters K, Arundel M, Bernal W, Gunson B, Hudson M, Suri D, Simpson K. UK legislation on analgesic packs: before and after study of long term effect on poisonings. BMJ. 2004 Oct 29 [Epub ahead of print] 2.Office for National Statistics. Series DH4 No 24 Mortality statistics: cause. London: ONS, 2001. 3.Office for National Statistics. Series DH2 No 26 Mortality statistics: cause. London: ONS, 2000. 4.Office for National Statistics. Series DH2 No 27 Mortality statistics: cause. London: ONS, 2001. 5.Office for National Statistics. Series DH2 No 28 Mortality statistics: cause. London: ONS, 2002. 6.Amos T, Appleby L, Kiernan K. Changes in rates of suicide by car exhaust asphyxiation in England and Wales. Psychol Med. 2001 Jul;31(5):935 -9. Competing interests: None declared |
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Nigel I Jowett, Consultant in Cardiovascular Medicine Withybush General Hospital, Pembrokehire, SA61 2PZ WALES
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Hawton et al[1] have endorsed Government legislation limiting pack size of analgesics introduced in 1998. They demonstrate a persisting reduction of suicide deaths from paracetamol and salicylates, and conclude “a further reduction in pack sizes of paracetamol and salicylates would be unlikely to inconvenience users and could have beneficial effects in preventing deaths from self poisoning”. This is unsupported by their paper. Paracetamol 2-4 g daily is recommended first line treatment for degenerative arthritis[2]. For sufferers who do not wish to bother their GP for prescriptions, this necessitates twice weekly visits to drug outlets, and further restriction would increase this to alternate days. Our elderly arthritic patients may like to comment on this being no inconvenience. More importantly, there is no evidence that paracetamol restriction has reduced overall mortality from self-poisoning, as other agents have not been considered. Our report in 2001[3] showed that with paracetamol restriction, self-poisoners were choosing alternative drugs (predominantly antidepressants, anti-psychotics and sedatives), and drug “cocktails” were more common, often increasing risk because of individual drug toxicity and interactions. Paracetamol restriction had no effect on either case numbers or bed occupancy, and actually increased the use of coronary care beds because of the potential cardiac toxicity of many poisons. The effects of this selective legislation was entirely predicatble[4], and may have taken pressure of our liver units, but has simply displaced activity to acute medical and high dependency units. The Media have also misunderstood this paper, and reported that “smaller pack sizes had slashed rates of suicides involving overdoses”[5]. However, figures from the Office of National Statistics on suicides before and after paracetamol restriction have not shown any significant decline in deaths due to poisonings[6]. Such selective information on the effects of analgesia restriction will provide the public and our legislators with a blinkered approach to an unsolved problem and continuing major drain on NHS resources. The Government should understand this, and perhaps turn its attention to the over-prescription of anti-depressant, anti-psychotic and sedative drugs, before placing any further inconvenience to those with chronic pain who have used paracetamol responsibly and safely. REFERENCES 1. Hawton K, Simkin S, Deeks J et al. UK legislation on analgesic packs: before and after study of long-term effects on poisonings. BMJ 2004;329:1076-9. 2. Eccles M, Freemantle N, Mason J. North of England evidence based guidelines; summary guidance for non-steroidal anti-inflammatory drugs versus basic analgesia in treating pain of degenerative arthritis. BMJ 1998; 3:526-30. 3. Thomas M & Jowett NI. Restriction has not reduced admissions with self-poisoning. BMJ 2001; 322:554. 4. Jowett NI. Restriction to 16g will not prevent overdose and is unhelpful for patients with chronic disease. BMJ 1998; 317:1657. 5. BBC News 28th October 2004. http://news.bbc.co.uk/go/pr/fr/- /hi/health/3961339.stm 6. Office of National Statistics Series DH2 No: 24-28; 200-2002. http://www.statistics.gov.uk Competing interests: Regular user of paracetamol |
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Reginald Michael Sherratt, Consultant Neurophysiology LU4 0DZ
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The data are welcome and interesting. With respect to aspirin, should not a more wide ranging cost benefit analysis be done before making further restrictions (packs of 16 suggested)? Proper users of these over the counter medicines have been substantially inconvenienced by the restrictions on quantity per purchase, and by the price increases which occurred when the pack sizes were drastically reduced. To frustrate impulsive overdoses, the general population have had a cost which the authors did not attemot to assess. This should be done before a further change is espoused! Competing interests: None declared |
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Rajesh.S. Aruna, Specialist Registrar Parkview Clinic, 60 Queensbridge Road,Moseley, Birmingham - B13 8QE, Dr.G.S.Rajesh, Dr.A.White
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Dear Sir, It was interesting to read the study by Hawton et al. (1) that has demonstrated a sustained decrease in suicidal deaths due to paracetamol overdoses, liver unit admissions and liver transplantations during the three years after the legislation. Some of the results are in agreement with a study (2) that we had conducted to assess the local impact of the legislation, in the Selly Oak hospital a large teaching hospital in Birmingham. We had examined the number of paracetamol related admissions, paracetamol related liver unit admissions, and paracetamol related deaths in March – August prior to (1998), just after (1999) and four years after (2002) the legislation. Our study showed that the number of clients presenting to hospital fell significantly (164,108,119 resp.) during these periods (P<0.05). There was a similar significant decrease in the number of liver unit admissions (30, 20,25). However during these periods the number of paracetamol related deaths as recorded by the Birmingham Coroner’s Office did not decline (60,61,81) Analysis of data regarding self-poisoning presentations in Hawton et al’s study (1) shows an interesting trend. In their study the initial decrease has not been sustained over the years with numbers actually increasing over the study period. This clearly shows that even though there has been a reduction in the severity of the consequences of paracetamol overdoses, patients continue to use paracetamol as an agent in overdoses with the associated adverse consequences. Availability is a key factor in these over doses (3) and therefore measures to reduce availability such as further reductions in pack sizes are to be welcomed. The increase in Ibuprofen overdoses is a cause for concern even though it hasn’t affected the death rate. This may be an indication that patients are switching to other drugs for overdoses. This study has not examined the trends in use of other toxic agents such as co-proxamol, antidepressants and sedatives that are potentially dangerous. Further studies and careful analysis of long term trends are essential in order to detect changes in the use of these drugs in overdoses and clinicians need to be cautious about prescribing large amounts of these medication. References. 1.Hawton K, Simkin S, Deeks J, Cooper J, Johnston A, Waters K, Arundel M, Bernal W, Gunson B, Hudson M, Suri D, Simpson K. UK legislation on analgesic packs: before and after study of long term effect on poisonings. BMJ. 2004.Oct 29. 2. Langford NJ, Aruna RS, Mutimer D, AC White, Ferner RE.Impact of pack size legislation on paracetamol (Acetaminophen) poisoning in the West Midlands. Abstracts of the EAPCCT international congress.Journal of Toxicology and Clinical Toxicology .2003.Vol 41-4 .419-420. 3.Hawton K, Ware C, Mistry H, Hewitt J, Kingsbury S, Roberts D, et al. Why patients choose paracetamol for self poisoning and their knowledge of its dangers. BMJ 1995; 310: 164. Competing interests: None declared |
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James N Hardy, GP Principal Bethnal Green Health Centre, 60 Florida Street, London E2 6LL
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Editor The paper by Hawton et al has rightly demonstrated a decline in successful paracetamol suicides (1). Unfortunately the official statistics show no decline in real terms in the suicide rate and merely underline what we already know – that the there are powerful societal forces influencing individual behaviour. If we wish to see a real decline in the suicide rate we would do well to address the central themes of Durkheim’s seminal work, Le Suicide, published at the end of 19th century in which he argued that the more the individual was a part of the whole, the less likely was that individual to kill himself. Where there is disintegration there is suicidal ideation and where there is suicidal ideation there are plentiful exit strategies. Jim Hardy (1)Keith Hawton, Sue Simkin, Jonathan Deeks, Jayne Cooper, Amy Johnston, Keith Waters, Morag Arundel, William Bernal, Bridget Gunson, Mark Hudson, Deepak Suri, and Kenneth Simpson UK legislation on analgesic packs: before and after study of long term effect on poisonings BMJ 2004;329:1076 Competing interests: None declared |
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Adrian S. Blaj, Psychiatrist London, England
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In what circumstances exit strategies are considered politically correct? Why a threat to kill someone is a criminal offence and the threat of killing oneself is not? Is suicide an act of courage or an act of cowardice? Competing interests: None declared |
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D Nicholas Bateman, Consultant Clinical Toxicologist Royal Infirmary of Edinburgh EH16 4SA, Dermot Gorman, Marion Bain, Jamie HC Inglis, David Murphy
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Dear Sir
Hawton and colleagues (1) have
published a detailed examination of the effects of the legislation on pack size
in the UK on a variety of aspects of paracetamol poisoning epidemiology. Apart from a small amount of material
originating from the Liver Transplant Unit in Edinburgh, their conclusions are
wholly based on English and Welsh data. Examining morbidity and mortality from
paracetamol poisoning is complex, since the most important end point, death, is
evaluated independently by Coroners in England and Wales, and Procurators
Fiscal in Scotland. There is no single authority making the judgement on
causation in any UK country. The
toxicology of paracetamol is well understood, and the mode of death from paracetamol
itself is due to hepatic failure, clinically manifesting between 48 and 72
hours after drug ingestion. In the
context of paracetamol overdose alone, therefore, it is highly unusual for
patients to die outside hospital, because they present with the symptoms and
signs of hepatic failure in this time frame.
It is our experience that paracetamol is associated with death in a far larger number of cases than are
actually due to the drug itself. To
further describe this we have explored the patterns of mortality between 1995 and 2003 in Scotland
for deaths involving paracetamol. The data analysed covered all deaths where
paracetamol (or a combination product that includes paracetamol) was recorded
on the death certificate, or the supplementary return from departments of
forensic pathology sent to the General Register Office for Scotland (GROS) (Table). We examined the data by dividing the cause
of death into four separate categories. These are patients in whom the death
certificate documents: i) paracetamol ± ethanol
alone; ii) paracetamol in combination with other drugs; iii) co-proxamol
(including death where dextropropoxyphene or its metabolites detected). In addition we separately evaluated for each
of these categories deaths reported to occur in-hospital, where it is far more
likely that paracetamol itself is likely to blame, and deaths reported outside
hospital, where it is less likely that paracetamol is the primary agent
responsible. Thus for paracetamol ± ethanol alone 183 of the 242 deaths (76%) occurring in
Scotland over the nine year period occurred inside hospital. For all other categories mortality outside
hospital exceeded that in-hospital, the ratio being 4.2:1 for co-proxamol
(412 outside hospital, 99 inside hospital); 2.9:1 for paracetamol and
other drugs (131 outside hospital, 45
inside hospital). Data
on in-hospital mortality involving paracetamol in this series will include the
Edinburgh liver unit material previously published by Hawton, but we are unable
to ascertain exactly which cases match. Nevertheless it is clear from the table
that in-hospital mortality with paracetamol ± ethanol did not decrease following 1999, although it did
fall in 1999 itself. Although numbers
are small, and there is a year-to-year fluctuation, for which we have no
obvious explanation, there is no consistent effect on mortality either overall
involving paracetamol, or in the subgroup of interest over this period.
Analysis of the proportion of all poisoning cases associated with paracetamol
where death was in-hospital was examined using multiple regression to test for
the effect of a possible step change in September 1998. This suggested no such effect (P=0.98, 95% CI for step
change in percentage -15% to +18%).
Also when deaths from paracetamol ± ethanol and all
other paracetamol associated deaths for 1995-97 and 1999-2003 were examined by
Chi square the results were also not significant, Chi square = 0.65, p = 0.42
suggesting no difference pre and post restriction. Overdose
rates in Scotland have traditionally been higher than the rest of the UK, and
these data, which show no sustained effect on mortality rates in Scotland
following the restrictions on paracetamol, throw doubts on the major conclusion
of Hawton’s group in respect to Scotland, as has been previously suggested
(2,3). We suggest that further work is
required to explore the nature of the apparent differences between England,
Wales and Scotland. These data
additionally also demonstrate the impact of co-proxamol on mortality in Scotland,
and add further weight to calls for its withdrawal from general prescription. References: 1.
Hawton
K, Simkin S, Deeks J et al. UK legislation on analgesic packs: before and after
study of long term effect on poisonings. BMJ
2004;329:1076. 2. Sheen CL, Dillon JF, Bateman DN et
al. Paracetamol related deaths in Scotland, 1994-2000. Br J Clin Pharmacol 2002;54:430-432. 3. Newsome PN, Bathgate AJ, Henderson
NL, MacGilchrist AJ, Plevris JN, Masterton G, Garden OJ, Lee A, Hayes PL,
Simpson KJ. Referral patterns and social deprivation in paracetamol-induced
liver injury in Scotland. Lancet 2001;358:1612-3. Acknowledgement: We gratefully acknowledge the
assistance of Graham Jackson, General Register Office for Scotland, who
provided the mortality data. Rob Elton kindly assisted with statistical advice. Table 1 Deaths
in which reference to paracetamol is made on death certificates, 1995-2003.
Deaths are shown as “out of hospital” and “in-hospital” for 3 categories:
paracetamol ± ethanol alone; paracetamol + other drugs; co-proxamol (alone or in
combination).
Authors DN Bateman NPIS Edinburgh, Scottish Poisons
Information Bureau, Royal Infirmary of Edinburgh, Edinburgh, EH16 4SA Director and Consultant Physician DR Gorman NHS Lothian,
148 The Pleasance, Edinburgh, EH8 9RS Consultant in Public Health Medicine M Bain NHS Scotland,
Information & Statistics Division, Gyle Square, 1 South Gyle Crescent,
Edinburgh, EH12 9EB Medical Director JHC Inglis NHS
Health Scotland, The Priory , Canaan Lane, Edinburgh EH10 4SG D Murphy NHS Scotland,
Information & Statistics Division, Gyle Square, 1 South Gyle Crescent,
Edinburgh, EH12 9EB Senior Information Analyst Correspondence
to: nick.bateman{at}luht.scot.nhs.uk
Competing interests: None declared |
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Peter Morrell, Hon Research Associate, History of Medicine Staffordshire University, UK
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When Jim Hardy says, "if we wish to see a real decline in the suicide rate we would do well to address the central themes of Durkheim’s seminal work, Le Suicide, published at the end of 19th century," [1] while that may well be so, the central themes of that work are probably more subtle than it seems on face value. Certainly, Durkheim "argued that the more the individual was a part of the whole, the less likely was that individual to kill himself," [1] in the sense that Durkheim's work quite centrally concerned itself with exploring social cohesion and social alienation, with the social norms and the behaviour of those who broke them...such as in his interest in deviance and marginality, criminality and religion. In this respect, it might be better to say that Durkheim regarded suicide to often flow from, and be preceded by, a deep sense of alienation from the host culture, from the human herd. At least that gives a predictive value of which people he felt were more prone to suicide than others. "In every case, Durkheim observed, suicide increases in those months, days of the week and hours of the day when social life is most active, and decreases when collective activity declines...Durkheim thus suggested that suicide is the consequence of the intensity of social life." [2] For Durkheim, this observation suggested that it is some aspect of socialisation that upsets those disposed towards suicide... However, to then say "where there is disintegration there is suicidal ideation and where there is suicidal ideation there are plentiful exit strategies," [1] might actually be an oversimplification of Durkheim's views. Much depends what you mean by disintegration or whether a better word might be dislocation. Certainly Durkheim felt that it is social dislocation that gives rise to what Dr Hardy terms 'suicidal ideation.' Basically, Durkheim's view is of what he termed anomic suicide, the suicide of the outcasts, the unloved, the socially excluded, those rejected by the human herd. It is these in whom he took a special interest as they illustrated for him important aspects of social processes. He was not really interested in all the other forms of suicide and thus Durkheim cannot be satisfactorily invoked to explain these other forms of suicide. Even so, according to Durkheim, no decline of suicide rates is going to be possible as long as some people feel alienated. As Durkheim took the view that alienation, like his view of crime and deviance, is a natural phenomenon for some sections of society, even in a very healthy society, then clearly he accepted that suicide was natural, normal and to a large extent as unavoidable as crime and deviance. That being so, it is hard to find support from Durkheim for the suggestion that Dr Hardy makes here: "if we wish to see a real decline in the suicide rate we would do well to address the central themes of Durkheim’s seminal work, Le Suicide." [1] How can one do that? Durkheim concludes it is normal...stalemate? Another problem is that Durkheim believed that suicide had economic causes in poverty, for example, and that when a country's fortunes sank low then suicides tended to increase. This can in my opinion be explained in part by the tightening impact poverty has on the social norms, which become more severely applied, especially on anyone who is perceived as a 'social deviant.' The resulting search for scapegoats often finds them in the usual suspects--all types of social deviants, including the mentally ill, homosexuals, prostitutes, drifters and racial minorities, etc. In this socio-economic and Durkheimian scenario suicide rates therefore increase because of an overzealous expulsion of deviants from the human herd and the resulting enhancement of their sense of alienation. Further to this, with unforgiving figures like George Bush around, Dr Hardy will have his work cut out attempting to reintegrate alienated persons in order to achieve his stated objective. Not only would an amused Durkheim regard that as a Sisyphean task but would likely predict it as limited, brief and temporary even in the modest confines of Dr Hardy's own medical practice. The problem is that people become alienated either because they are genuinely odd or because they seem that way to others and fail to socialise successfully. It is precisely such people who, Durkheim would argue, eventually reach the conclusion that dying is a better option than staying alive. Some are outcasted by the human herd, while others outcast themselves from it. Further, the implication that alienation is the root of suicide, as Durkheim suggested, also reveals that the sound identity of those of us who prefer living, for example, comes in large measure from successful socialisation and a good sense of self and society. This formed part of his theoretical views of the nature of social cohesion. Alternatively, we must not forget that many 'alienated' people do not attempt suicide, and have no prospect of ever doing so because they have found a way to be buoyant and happy embedded in unorthodox lifestyles outside the mainstream from which or within which they receive continuous affirmation that they are good people and that life is therefore sweet. These confirm Durkheim's sociology, rather than invalidate it; only those who do not find such positive affirmation for living will feel tempted by the prospect of suicide. I am sure that Durkheim would have argued that a person who has a massively diminished sense of self-worth, whose sense of self is degraded and who much of the time feels 'invisible' to the point of not mattering to anyone in this world if they live or die, is only a very small step from the physicial act of self-extinction. Suicide thus becomes portrayed as merely the physicial culmination of an already pervasive sense of mental annihilation already apparent and of being an unloved outcast whose existence does not even matter, who can make, and will make, no lasting impression upon this world. Such a person, in Durkheim's view, is indeeed filled with what Dr Hardy called "suicidal ideation." Such a person is an example of Durkheim's anomic suicide. "Suicide thus varies inversely with the degree of integration of the religious, domestic, and political groups of which the individual forms a part; in short, as a society weakens or "disintegrates," the individual depends less on the group, depends more upon himself, and recognizes no rules of conduct beyond those based upon private interests. Durkheim called this state f "excessive individualism" egoism, and the special type of self-inflicted death it produces egoistic suicide." [2] "Durkheim argues that there is an inverse association between social integration and suicide rates." [3] Some of the most notable suicides have clearly been people who somehow felt alienated and isolated, outcasts from the human herd. They include Isobel Barnett (1980), Richard Brautigan (1984), Hart Crane (1932), Ernest Hemingway (1961), Terence Donovan (1996), Justin Fashanu (1998), Tony Hancock (1968), Arthur Koestler (1983), Marilyn Monroe (1962), Sylvia Plath (1963), Mark Rothko (1970), Harold Shipman, (2004), Vincent van Gogh (1890), Stephen Ward (1963) and Virginia Woolf (1941). Sources [1] James N Hardy, The mode of suicide is ever-changing, BMJ e- letter, 23 November 2004 http://bmj.bmjjournals.com/cgi/eletters/329/7474/1076#86642 [2] Robert Alun Jones, Emile Durkheim: An Introduction to Four Major Works. Beverly Hills, CA: Sage Publications, Inc., 1986. pp.82-114 http://www.relst.uiuc.edu/durkheim/Summaries/suicide.html [3] Robert M. Fernquist, Education, Race/Ethnicity, Age, Sex, and Suicide: Individual-level data in the United States, 1991-19941, Central Missouri State University http://www.uiowa.edu/~grpproc/crisp/crisp.6.18.htm Competing interests: None declared |
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Rajendra P Deolankar, Assistant Director National Institute of Virology, Pune 411 001, India
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Legislation restricting pack sizes of analgesics (paracetamol, salicylates, and their compounds) sold over the counter in the United Kingdom has been beneficial. It is suggested that a further reduction in pack sizes could prevent more deaths [1]. Developing countries need to follow these steps. Hepatotoxicity has occurred with recommended dosages of these drugs in children from developing countries. Fever is a common symptom of childhood illness and antipyretics are prescribed commonly. Fever itself that can be treated using antipyretics is not harmful but rather beneficial in enhancing the host response to infection. Despite this, it is believed that antipyretic treatment improves febrile children's comfort and behavior and given in therapeutic doses in febrile children with viral or bacterial infections or with malaria [2]. It is known that virus and aspirin work together to cause Reye’s syndrome [3]. Hepatotoxicity might knock down the liver function of Calcidiol synthesis. It is suggested that kidney and liver vitamin D event might precede encephalitis [4]. Smallest dose of acetaminophen could damage kidney, liver and pancreas [5]. Renal failure may happen due to diethylene glycol in paracetamol elixir [6]. In vitro antiviral effects of NSAIDs [7] could be misleading for patient treatment. Oseltamivir, a non-NSAID, is associated with Sudden Death during Sleep in influenza-related encephalopathy [8,9]. Several other drugs could act in similar manner [10]. Vitamin D deficiency have probable role in infectious diseases [11] and could be rectified. DHEA treatment is suggested as an answer to the West Nile Encephalitis [12]. Calcitriol (1,25-dihydroxyvitamin D) is suggested for emergency encephalitis treatment in the normal VDR patients [13]. Tepid sponging also helps during fever [14]. Study of disease causal chain of infectious diseases is a practical method to identify several targets for prevention and treatment of infectious diseases [15]. Summarily, drug that may appear otherwise safe could work fatally with virus or infection. Data needs to be collected for studying the association of drugs with infectious diseases and formulating Do’s and Don’ts during fever, particularly pediatric cases, in developing countries and in viral fevers. References: 1. Hawton K, Simkin S, Deeks J, Cooper J, Johnston A, Waters K, Arundel M, Bernal W, Gunson B, Hudson M, Suri D, Simpson K. UK legislation on analgesic packs: before and after study of long term effect on poisonings. BMJ. 2004 Nov 6;329(7474):1076.[Full Text] 2. Russell FM, Shann F, Curtis N, Mulholland K. Evidence on the use of paracetamol in febrile children. Bull World Health Organ. 2003;81(5):367-72.[Full Text] 3. Glasgow JF, Middleton B. Reye syndrome--insights on causation and prognosis. Arch Dis Child. 2001 Nov;85(5):351-3.[Full Text] 4. Deolankar RP. Kidney and liver vitamin D event might precede encephalitis. BMJ Rapid Response. 1 April 2005. [Full Text] 5. Mofenson HC, Caraccio TR, Nawaz H, Steckler G. Acetaminophen induced pancreatitis. J Toxicol Clin Toxicol. 1991;29(2):223-30.[Medline] 6. Hanif M, Mobarak MR, Ronan A, Rahman D, Donovan JJ Jr, Bennish ML. Fatal renal failure caused by diethylene glycol in paracetamol elixir: the Bangladesh epidemic. BMJ. 1995 Jul 8;311(6997):88-91.[Full Text] 7. Chen CJ, Raung SL, Kuo MD, Wang YM. Suppression of Japanese encephalitis virus infection by non-steroidal anti-inflammatory drugs. J Gen Virol. 2002 Aug;83(Pt 8):1897-905.[Full Text] 8. Hama R. Confirmed Influenza A and Sudden Death during Sleep after Taking Oseltamivir. BMJ Rapid Response. 4 Apr 2005.[Full Text] 9. Hama R. New type of influenza-related encephalopathy or new adverse drug reaction? BMJ Rapid Response. 27 Feb 2005. [Full Text] 10. Deolankar RP. Virus related encephalitis and adverse drug reactions. BMJ Rapid Response. 1 Apr 2005.[Full Text] 11. Deolankar RP. Vitamin D deficiency have probable role in infectious diseases. BMJ Rapid Response. 1 April 2005.[Full Text] 12. Howard JM. DHEA may be an answer to West Nile Virus. BMJ Rapid Response 18 April 2003. [Full Text] 13. Deolankar RP. Calcitriol (1,25-dihydroxyvitamin D) for emergency encephalitis treatment in the normal VDR patients. BMJ Rapid Response. 31 March 2005. [Full Text] 14. Luxemburger C, van Vugt M, Slight T, Price RN, Chongsuphajaisiddhi T, Chanthavanich P, et al. Early vomiting of mefloquine in children with malaria is not modified by the timing of antipyretic treatment. Transactions of the Royal Society of Tropical Medicine and Hygiene 1998;92:562-3.[Medline] 15. Deolankar RP. Epidemiology, Risk Events and Risk Factors of Japanese Encephalitis. BMJ Rapid Response. 12 April 2005 [Full Text]
Competing interests: None declared |
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Leonard C Hawkins, Specialist in Poisons Information Guy's & St Thomas' Poisons Unit, Guy's & St Thomas' NHS Foundation Trust, London, UK
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The authors state that the legislation reduced the previously unrestricted sale limit for pharmacies to a maximum of 32 tablets and for other retail outlets from 24 to 16 tablets. The legislation [1,2] restricts pack size of GSL (general sale)paracetamol and aspirin to 16 tablets or less per pack and P (pharmacy only) preparations to 32 tablets or less per pack; however, it does not restrict the number of packets (or number of tablets) that may be supplied in a single purchase. Therefore, it is incorrect to state that a retailer is not adhering to the legislation if they sell more than 16 tablets in a single purchase of GSL paracetamol or aspirin. However, the MHRA strongly discourages multiple sales and the majority of retailers voluntarily restrict sales of paracetamol by, for example, using till bars. However, these restrictions are voluntary and retailers are under no legal or legislative obligation to restrict the amount of paracetamol they can sell in a single purchase (this applies up to a maximum of 100 tablets, at which point a medicine becomes subject to prescription control). 1. Statutory Instrument 1997 No. 2045. The Medicines (Sale or Supply) (Miscellaneous Provisions) Amendment (No. 2) Regulations 1997. 2. Statutory Instrument 1997 No. 2044. The Prescription Only Medicines (Human Use) Amendment Order 1997. Competing interests: None declared |
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