Letters to the Editor
(Aust Prescr 2002;25:131-2)
Letters, which may not necessarily be published in full, should be restricted to not more than 250 words. When relevant, comment on the letter is sought from the author. Due to production schedules, it is normally not possible to publish letters received in response to material appearing in a particular issue earlier than the second or third subsequent issue.
Warfarin and antiplatelet drugs
Editor, - We read with interest the article 'Warfarin, antiplatelet drugs and their interactions' (Aust Prescr 2002;25:81-5) and were disappointed that although the authors emphasise the risks of combining warfarin with aspirin, they fail to acknowledge the proven benefits of this combination in patients with prosthetic heart valves. A recent meta-analysis1 showed that compared with anticoagulation alone, the addition of an antiplatelet drug reduced the risk of not only thromboembolic events (odds ratio 0.41, p < 0.001) but also total mortality (odds ratio 0.49, p < 0.001).The old view that the combination is dangerous is still held by many doctors and pharmacists. We certainly agree with the authors' recommendation that with the combination, low-dose aspirin should be used and the INR 'kept at the lower end of the desired target', and that patients on the combination should be carefully monitored for possible bleeding complications, including gastrointestinal blood loss. However, the evidence that adding low-dose aspirin to warfarin reduces total mortality by 50% in these patients should not be ignored and needs wide dissemination.
Con Aroney
Associate Professor of Medicine
University of Queensland
Cardiology Department
Prince Charles Hospital
Brisbane
Peter Thompson
Professor of Medicine and Public Health
University of Western Australia
Perth
Reference
1. Massel D, Little SH. Risks and benefits of adding anti-platelet
therapy to warfarin among patients with prosthetic heart valves: a meta-analysis.
J Am Coll Cardiol 2001;37:569-78.
Managing constipation in children
Editor, - It was pleasing to see the article 'Managing constipation in children' (Aust Prescr 2002;25:85-7) as it is such a common problem. It was particularly pleasing to see the prominence given to the emotional aspects.However, the article needs several comments. The first is the strong recommendation for oral bowel cleansing solutions and rectal medications. Oral cleansing solutions have significant risks in the presence of faecal impaction. Rectal medications frequently interfere with emotional management.
The article deals with stimulant aperients in the same paragraph as stool softeners. The two have very different indications. Stimulants such as senna and phenolphthalein often cause significant pain or incontinence due to increased muscle activity. Furthermore, their long-term use damages the intramural ganglion cells of the colon.
Stool softening agents are usually all that is needed for children with constipation unless there is an underlying organic cause. The vast majority of children who have no abnormality of the colon (albeit with a secondary fissure) require nothing more than stool softening. Dietary means alone are rarely enough in the first instance, but are important in long-term management. Paraffin oil, either plain or as an emulsion, is the only agent that will soften inspissated faeces. It is not absorbed so is safe to give in large doses and for prolonged periods. It takes 5-10 days to soften old hard faeces, but it will eventually do so and thereby avoid any anal manipulations or general anaesthetic to perform manual evacuation. It has a reputation for interfering with absorption of fat-soluble vitamins, but I am unable to find a reliable reference for this.
Apart from a small number of children with an organic cause or very resistant constipation, the majority of constipated children have a totally normal colon, so once sensation and motility are restored by getting rid of accumulated faeces, they will defecate quite satisfactorily if the stool is soft.
Hugh Martin
Paediatric Surgeon
The Children's Hospital at Westmead
Westmead, NSW
Editor, - The article 'Malaria prevention in the expatriate and long-term traveller' (Aust Prescr 2002;25:66-9) was good but deficient in a few areas. I am a pharmacist living in a malaria endemic area of Nigeria. By virtue of this I am aware of other ways of managing malaria as we are faced with this terrible disease for a lifetime.
In the section on the malaria standby treatment regimens, attention was not drawn to the use of dihydroartemisinine - a novel drug developed from the malaria herb Qinghaosu in China. This drug happens to be the most effective and safest antimalarial compared to the others listed in the article. It has a very fast onset of action and adverse effects that are not debilitating.
I would emphasise the life cycle of the plasmodium parasite, as the dormant hypnozoites and gametocyte forms in the liver and blood respectively contribute significantly in reinfection and transmission of the diseases. The need for a radical cure when the expatriate or traveller returns home means there is a possible role for a drug like primaquine.
In conclusion, these aspects would definitely add the cherry on the cake and make the article well balanced.
Bamgboye Olusegun Raymond
Department of Clinical Pharmacy
University of Benin
Benin City, Edo State
Nigeria
We acknowledge the comments of Bamgboye Raymond regarding our article 'Malaria prevention in the expatriate and long-term traveller'. Indeed dihydroartemisinine is used widely throughout malarial endemic countries as a safe and effective treatment for malaria. However, our paper was written for Australian health practitioners, and as this medication is not currently registered for use in Australia, it was not included.
We also agree that treatment of malaria due to Plasmodium vivax and Plasmodium ovale requires consideration of eradication of the liver hypnozoites to reduce the chance of recurrent infection in those who have left the endemic area, and are unlikely to be re-exposed in the near future. However our article deals with emergency standby treatment for those developing malaria in endemic areas. Here there is little value in treatment with drugs such as primaquine due to the likelihood of reinfection.
Sensitivity and specificity - is your test reliable?
Editor, - The recent article on sensitivity and specificity (Aust Prescr 2002;25:107) is of concern in that it implies that sensitivity and specificity are invariant when applied to a particular disease state. This is not so. We give examples below.Following occlusion of a coronary artery during myocardial infarction, cardiac troponin will be released. However, troponin is a protein and will not get into the circulation until some hours after the coronary occlusion has occurred. Thus samples collected early, say at two hours post-event, will have a poor diagnostic sensitivity for identifying myocardial infarction, while samples collected later, say at 12 hours post-infarction, will have a very high diagnostic sensitivity. These two clinical settings with very different sensitivities are not covered by the usual statement that 'cardiac troponin has a sensitivity for myocardial infarction approaching 100%'.
Consider the use of ferritin measurement to establish or exclude a diagnosis of iron-deficiency anaemia. A low ferritin concentration is considered to support the diagnosis of iron-deficiency anaemia. If samples are collected only in the general practice setting there will be very few 'false normal' results. If however, samples are collected in the acute hospital setting, where there is a relatively higher prevalence of liver disease with release of tissue ferritin, then there will be proportionately more people falsely identified as having 'normal' iron homeostasis. The apparent diagnostic sensitivity in these two populations, if compared to the best test available - bone marrow biopsy and quantitation of stored iron - would be quite different, because of the characteristics of the two populations.
Both of the examples above demonstrate that diagnostic sensitivity can vary for a particular disease state, and are one of the reasons why tests appear to perform differently in the reports in the literature. It is important to define very precisely the population that is being studied, when diagnostic sensitivity and specificity is being discussed.
Peter E. Hickman
Director of Chemical Pathology
Princess Alexandra Hospital
Woolloongabba, Qld
Julia M. Potter
Director of Chemical Pathology
Royal Brisbane Hospital
Herston, Qld
