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<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/441?rss=1">
<title><![CDATA[Elements: In this month's issue]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/441?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bannon, M.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp086</dc:identifier>
<dc:title><![CDATA[Elements: In this month's issue]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>442</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>441</prism:startingPage>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/443?rss=1">
<title><![CDATA[Tools used in the diagnosis and staging of lung cancer: what's old and what's new?]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/443?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Currie, G.P., Kennedy, A.-M., Denison, A.R.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp038</dc:identifier>
<dc:title><![CDATA[Tools used in the diagnosis and staging of lung cancer: what's old and what's new?]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>448</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>443</prism:startingPage>
<prism:section>Review</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/449?rss=1">
<title><![CDATA[Presentations and outcomes of neurosarcoidosis: a study of 54 cases]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/449?rss=1</link>
<description><![CDATA[
<p><b>Objective:</b> To report on the clinical presentations, laboratory abnormalities, treatment and outcomes in 54 patients with neurosarcoidosis (NS).</p>
<p><b>Background:</b> Sarcoidosis is an inflammatory granulomatous disease affecting multiple organ systems. Neurosarcoidosis (CNS involvement) is seen in approximately 25% of patients with systemic sarcoidosis, although it is subclinical in most of these cases. Because of its rarity, exposure of neurologists to the clinical spectrum of NS is limited to case reports or short case series.</p>
<p><b>Patients and Methods:</b> A database of 3900 patients treated at the Vanderbilt Multiple Sclerosis Clinic between 1995 and 2008 was searched for &lsquo;neurosarcoidosis&rsquo;, &lsquo;neurosarcoid&rsquo;, &lsquo;sarcoidosis&rsquo; and &lsquo;sarcoid&rsquo;. Of the 162 patient records that were retrieved, 54 patients were found to meet the criteria for definite, probable or possible neurosarcoidosis and were reviewed, including their clinical presentation, Cerebrospinal fluid (CSF) findings, Magnetic resonance imaging (MRIs), biopsy results, treatment, and where available, outcomes 4 months to 20 years after onset of the presenting illness.</p>
<p><b>Results:</b> Clinical presentations and imaging findings in NS were varied. Cranial nerve abnormalities were the most common clinical presentation and involvement of the optic nerve in particular was associated with a poor prognosis for visual recovery. Isolated involvement of lower cranial nerves had a more favorable outcome. T<SUB>2</SUB> hyperintense parenchymal lesions were the most common imaging finding followed by meningeal enhancement. Long-term treatment consisted of prednisone and/or other immunomodulators (azathioprine, methotrexate or mycophenolate mofetil).</p>
<p><b>Conclusions:</b> Unlike systemic sarcoidosis, there is difficulty in making tissue diagnosis when involvement of CNS is suspected. MRI and CSF studies are sensitive in the detection of CNS inflammation but lack specificity, making the ascertainment of neurosarcoidosis a clinical challenge. In addition the low prevalence of the disease makes clinical trials difficult and therapeutic decisions are likely to be made from careful reporting from case studies.</p>
]]></description>
<dc:creator><![CDATA[Pawate, S., Moses, H., Sriram, S.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp042</dc:identifier>
<dc:title><![CDATA[Presentations and outcomes of neurosarcoidosis: a study of 54 cases]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>460</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>449</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/461?rss=1">
<title><![CDATA[The intravenous adenosine test: a new test for the identification of bradycardia pacing indications? A pilot study in subjects with bradycardia pacing indications, vasovagal syncope and controls]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/461?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Intravenous adenosine has recently been used in the diagnosis of unexplained syncope, but there is no consensus as to the meaning of a &lsquo;positive&rsquo; test. The objective is to determine the sensitivity and specificity of intravenous adenosine testing in the diagnosis of bradycardia-pacing indications [sinus node dysfunction(SND), atrio-ventricular block (AVB) and cardio-inhibitory carotid sinus syndrome (CSS)].</p>
<p><b>Design:</b> Pilot cohort study.</p>
<p><b>Methods:</b> Patients&mdash;(i) <I>Bradycardia-pacing group</I>: Consecutive patients referred for pacing for SND, AVB and CSS; (ii) <I>Consecutive head-up tilt (HUT)-positive VVS patients</I>. Controls&mdash;(i) Simple controls (S-Con: normal examination/ECG) and (ii) Electrophysiology controls (EP-Con: consecutive subjects referred for accessory pathway ablation). Pacing referrals and EP-Con had electrophysiology studies to confirm referral diagnosis and exclude others. All subjects had bolus injection of 20 mg intravenous adenosine during continuous ECG and blood pressure monitoring (positive test: &gt;=6 s asystole, &gt;=10 s high-degree AVB post-injection). Sensitivity, specificity, safety and tolerability of the test were measured.</p>
<p><b>Results:</b> Of 264 potential participants (4 SND, 8 AVB, 7 CSS, 10 VVS, 10 EP-Con and 11 S-Con) 50 were studied. All (100%) of the bradycardia-pacing group were adenosine test-positive, as were 6 (60%) VVS. None (0%) and 3 (27%) of the EP- and S-Con groups were positive. Adenosine testing was 100% sensitive and 86% specific for bradycardia-pacing indications, and 100% specific using the diagnostically &lsquo;clean&rsquo; EP-Con results. There were no significant adverse or side effects.</p>
<p><b>Conclusions:</b> Adenosine testing reliably identified patients with definitive bradycardia-pacing indications in whom alternative diagnoses were excluded. Further work is needed to evaluate the role of this test in the diagnosis of unexplained syncope.</p>
]]></description>
<dc:creator><![CDATA[Parry, S.W., Chadwick, T., Gray, J.C., Bexton, R.S., Tynan, M., Bourke, J.P., Nath, S.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp048</dc:identifier>
<dc:title><![CDATA[The intravenous adenosine test: a new test for the identification of bradycardia pacing indications? A pilot study in subjects with bradycardia pacing indications, vasovagal syncope and controls]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>468</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>461</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/469?rss=1">
<title><![CDATA[Circulating plasma cortisol concentrations are not associated with coronary artery disease or peripheral vascular disease]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/469?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Although the prevalence of cardiovascular disease is declining, the obesity epidemic with associated metabolic syndrome may reverse this trend. Hypothalamic&ndash;pituitary&ndash;adrenal (HPA) axis activation may underlie the metabolic syndrome, but whether circulating cortisol levels predict vascular disease is less clear. A recent study reported a positive correlation between cortisol levels measured prior to coronary angiography and disease severity, but others have not demonstrated such a relationship. This may be due to different sampling conditions, reflecting basal cortisol levels, vs. responsiveness of HPA axis activity, which may have diverse influences on the pathogenesis of atherosclerosis.</p>
<p><b>Aims:</b> To determine whether basal circulating cortisol levels predict coronary artery (CAD) or peripheral vascular disease.</p>
<p><b>Methods:</b> Basal plasma cortisol levels were measured in 278 subjects with suspected CAD, who had undergone elective coronary angiography and in 76 cases and 85 controls with and without peripheral vascular disease, respectively.</p>
<p><b>Results:</b> After adjustment for potential confounding factors, circulating cortisol levels tended to be lower in those with confirmed coronary vessel disease at angiography (<I>P</I> = 0.10), and in those requiring intervention following angiography (<I>P</I> = 0.07). Lower cortisol levels also predicted those with more symptoms of angina (<I>P</I> = 0.01). Cortisol levels were no different in those with or without peripheral vascular disease.</p>
<p><b>Conclusion:</b> A single measurement of circulating cortisol is a poor predictor of vascular disease. More detailed characterization of the HPA axis is necessary to determine the role of circulating endogenous glucocorticoids and their responsiveness to stress in atherosclerosis.</p>
]]></description>
<dc:creator><![CDATA[Reynolds, R.M., Ilyas, B., Price, J.F., Fowkes, F.G.R., Newby, D.E., Webb, D.J., Walker, B.R.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp057</dc:identifier>
<dc:title><![CDATA[Circulating plasma cortisol concentrations are not associated with coronary artery disease or peripheral vascular disease]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>475</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>469</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/477?rss=1">
<title><![CDATA[Incidence and mortality of falls amongst older people in primary care in the United Kingdom]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/477?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Despite the role of primary care in the falls care pathway, there are almost no data on the extent of falls seen in general practices.</p>
<p><b>Aim:</b> To quantify the incidence and mortality of falls amongst older people in primary care in the UK.</p>
<p><b>Methods:</b> Cohort study of people aged &gt;=60 years and registered in a UK practice contributing data to The Health Improvement Network primary care database (THIN) throughout 2003&ndash;06. Analysis of crude incidence and estimation of incidence rate ratios using negative binomial regression, and survival using Cox regression. Sensitivity analysis of criteria for distinguishing discrete fall events from follow-up appointments.</p>
<p><b>Results:</b> Amongst people aged &gt;=60 years the overall crude incidence rate of recorded falls was 3.58/100 person-years (95% CI 3.56&ndash;3.61). The rate of recurrent falls was 0.67/100 person-years (95% CI 0.66&ndash;0.68). The incidence rate of recorded falls and recurrent falls was higher in older age groups, in women and least advantaged social groups. Incidence of recorded falls was constant through the time period 2003&ndash;06. Mortality for recurrent fallers was about twice that of general population controls.</p>
<p><b>Conclusions:</b> These data suggest that more than 475 000 fall events in older people are recorded in general practice each year in the UK, and are associated with increased mortality and relative deprivation. The underlying incidence rate has remained stable in recent years.</p>
]]></description>
<dc:creator><![CDATA[Gribbin, J., Hubbard, R., Smith, C., Gladman, J., Lewis, S.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp064</dc:identifier>
<dc:title><![CDATA[Incidence and mortality of falls amongst older people in primary care in the United Kingdom]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>483</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>477</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/485?rss=1">
<title><![CDATA[Delays and adverse clinical outcomes associated with unrecognized pacing indications]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/485?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> A recent UK audit showed that a significant proportion of patients who received pacemakers had pacing indications previously overlooked, leading to significant delays to pacemaker implantation.</p>
<p><b>Aim:</b> To investigate the reasons for, and morbidity associated with, overlooked pacing indications.</p>
<p><b>Design:</b> Prospective observational study in a UK regional pacing centre and its referring district hospitals.</p>
<p><b>Methods:</b> Hospital records from referring and implanting centres were reviewed for 95 consecutive patients undergoing first pacemaker implant to determine symptoms, investigations and hospitalisations occurring after documentation of a pacing indication.</p>
<p><b>Results:</b> Thirty-three of ninety-five patients (35%) had a pacing indication overlooked, which was Class I in 14 patients and Class IIa in 19. Reasons for not making a pacing referral in these patients included: failure to recognize the indication in 14, making adjustments to potentially culprit medication in 15 and requesting additional &lsquo;confirmatory&rsquo; tests in 4. Twenty-six patients (79%) with missed indications experienced adverse events after documentation of an indication, and before receiving a pacemaker: 23 had ongoing symptoms (including one cardiac arrest), three received temporary pacing wires and 18 were hospitalized with symptoms related to cardiac rhythm. Twenty-seven patients (82%) had a total of 38 additional specialist investigations after documentation of a pacing indication.</p>
<p><b>Conclusions:</b> Documentation of an indication for pacing failed to trigger referral for permanent pacing in 35% of patients. This failure led to significant delays, morbidity and use of health service resource, which may have been avoided if timely recognition of the pacing indication had prompted referral. Failure to recognize pacing indications and reassessing symptoms and repeating investigation after changes to medication, often required for the management of associated tachyarrhythmias or other medical conditions, contribute to these delays, perhaps unnecessarily.</p>
]]></description>
<dc:creator><![CDATA[Cunnington, M.S., Plummer, C.J., McComb, J.M.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp066</dc:identifier>
<dc:title><![CDATA[Delays and adverse clinical outcomes associated with unrecognized pacing indications]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>490</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>485</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/491?rss=1">
<title><![CDATA[An uncommon cause of small bowel obstruction: isolated primary granulocytic sarcoma]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/491?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kumar, B., Bommana, V., Irani, F., Kasmani, R., Mian, A., Mahajan, K.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp051</dc:identifier>
<dc:title><![CDATA[An uncommon cause of small bowel obstruction: isolated primary granulocytic sarcoma]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>493</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>491</prism:startingPage>
<prism:section>Case report</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/495?rss=1">
<title><![CDATA[Intestinal perforation in a patient with continuous ambulatory peritoneal dialysis]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/495?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Chang, F.-C., Wu, V.-C., Huang, J.-W., Hung, K.-Y., Liu, K.-L.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcn161</dc:identifier>
<dc:title><![CDATA[Intestinal perforation in a patient with continuous ambulatory peritoneal dialysis]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>496</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>495</prism:startingPage>
<prism:section>Clinical picture</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/497?rss=1">
<title><![CDATA[Epilepsy genetics: clinical beginnings and social consequences]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/497?rss=1</link>
<description><![CDATA[
<p>The approach to epilepsy care has transformed in the last 30 years, with more and better anti-epileptic medications, improved cerebral imaging and increased surgical options. Alongside this, developments in neuroscience and molecular genetics have furthered the understanding of epileptogenesis. Future developments in pharmacogenomics hold the promise of antiepileptic drugs matched to specific genotypes. Despite this rapid progress, one-third of epilepsy patients remain refractory to medication, with their seizures impacting upon day-to-day activity, social well-being, independence, economic output and quality of life. International genome collaborations, such as HapMap and the Welcome Trust Case&ndash;Control Consortium single nucleotide polymorphism (SNP) mapping project have identified common genetic variations in diseases of major public health importance. Such genetic signposts should help to identify at-risk populations with a view to producing more effective pharmaceutical treatments. Neurological disorders, despite comprising one-fifth of UK acute medical hospital admissions, are surprisingly under-represented in these projects. Epilepsy is the commonest serious neurological disorder worldwide. Although physically, psychologically, socially and financially disabling, it rarely receives deserved attention from physicians, scientists and governmental bodies. As outlined in this article, research into epilepsy genetics presents unique challenges. These help to explain why the identification of its complex genetic traits has lagged well behind other disciplines, particularly the efforts made in neuropsychiatric disorders. Clinical beginnings must underpin any genetic understanding in epilepsy. Success in identifying genetic traits in other disorders does not make the automatic case for genome-wide screening in epilepsy, but such is a desired goal. The essential clinical approach of accurately phenotyping, diagnosing and interpreting the dynamic nature of epilepsy remains fundamental to harvesting its potential translational outcomes.</p>
]]></description>
<dc:creator><![CDATA[Johnston, J.A., Rees, M.I., Smith, P.E.M.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp019</dc:identifier>
<dc:title><![CDATA[Epilepsy genetics: clinical beginnings and social consequences]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>499</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>497</prism:startingPage>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/501?rss=1">
<title><![CDATA[The internist's role in treating hypertension in hemodialysis patients]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/501?rss=1</link>
<description><![CDATA[
<p>Hypertension in hemodialysis patients is typically treated with a combination of volume removal with dialysis&ndash;&ndash;although limited by current dialysis paradigms&ndash;&ndash;and hypertension medications. Unfortunately, most patients treated in this manner remain hypertensive. This contrasts with superior results obtained in clinical studies in which salt restriction and augmented dialytic volume removal normalized blood pressure without requiring medicines. These results are consistent with the role of excess volume as the main etiology of hypertension in end-stage renal disease (ESRD). Interdialytic blood pressure is now recognized as important to patient prognosis. These measurements are frequently obtained by internists at office visits. Internists and nephrologists should address both peri-dialysis and interdialysis hypertension in a collaborative manner. This strategy should focus on, as much as reasonably possible, salt restriction and dialytic volume removal rather than hypertension medicines.</p>
]]></description>
<dc:creator><![CDATA[Hirsch, S.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp045</dc:identifier>
<dc:title><![CDATA[The internist's role in treating hypertension in hemodialysis patients]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>507</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>501</prism:startingPage>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/7/509?rss=1">
<title><![CDATA[When I use a word ... Fulsomely banning 'compendious']]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/7/509?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Aronson, J.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp014</dc:identifier>
<dc:title><![CDATA[When I use a word ... Fulsomely banning 'compendious']]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>7</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>510</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>509</prism:startingPage>
<prism:section>Coda</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/367?rss=1">
<title><![CDATA[Elements: In this month's issue]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/367?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bannon, M.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp063</dc:identifier>
<dc:title><![CDATA[Elements: In this month's issue]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>368</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>367</prism:startingPage>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/369?rss=1">
<title><![CDATA[Myocardial infarction after percutaneous coronary intervention: a meta-analysis of troponin elevation applying the new universal definition]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/369?rss=1</link>
<description><![CDATA[
<p><b>Aim:</b> Elevation of Troponin after scheduled percutaneous coronary intervention (PCI) is a recognized consequence. We sought to evaluate the prognostic significance and impact of the newly published definition of PCI-related myocardial infarction (MI) according to which any troponin elevation &gt;3 times the upper reference limit identify a peri-procedural MI.</p>
<p><b>Methods:</b> Search of BioMedCentral, CENTRAL, mRCT and PubMed (updated May 2008). Outcomes of interest were: MACE [the composite of all cause death, MI, repeat target vessel PCI (re-PCI) and coronary artery bypass grafting (CABG)]; single end points were also assessed.</p>
<p><b>Results:</b> Fifteen studies have been included totalling 7578 patients. Troponin elevation occurred in 28.7% of the procedures. The incidence of PCI-related MI according to the new definition was 14.5%. During the hospitalization, any level of raised troponin was associated with an increased risk of MACE [OR 11.29 (3.00&ndash;42.48), Number needed to harm (NNH) 5], death [OR 7.16 (1.95&ndash;26.27), NNH = 100], MI [OR 30.85 (6.05&ndash;157.38), NNH = 4] and re-PCI [OR 4.13 (1.23&ndash;13.88), NNH = 50]. Patients with PCI-related MI had an increased risk of death [OR 17.25 (2.71&ndash;109.96), NNH = 100] and re-PCI [OR 10.86 (3.2&ndash;36.94), NNH = 25]. At follow up of 18 months any troponin elevation was associated with an increased risk of MACE [OR 1.48 (1.12&ndash;1.96), NNH = 20], death [OR 2.19 (1.59&ndash;3.00), NNH = 50], MI [OR 3.29 (2.71&ndash;6.31), NNH = 33] and re-PCI [OR 1.47 (1.06&ndash;2.03), NNH = 25]. In patients with PCI-related MI the risk of MACE was further increased: OR 2.25 (1.26&ndash;4.00), NNH = 3. An increase of the troponin level below the cut-off was not associated with MACE.</p>
<p><b>Conclusion:</b> A diagnosis of MI according to the new guidelines applies to 15% of patients undergoing PCI and these patients are at high risk of further adverse events both during the hospital stay and at 18 months.</p>
]]></description>
<dc:creator><![CDATA[Testa, L., Van Gaal, W.J., Biondi Zoccai, G.G.L., Agostoni, P., Latini, R.A., Bedogni, F., Porto, I., Banning, A.P.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp005</dc:identifier>
<dc:title><![CDATA[Myocardial infarction after percutaneous coronary intervention: a meta-analysis of troponin elevation applying the new universal definition]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>378</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>369</prism:startingPage>
<prism:section>Reviews</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/379?rss=1">
<title><![CDATA[Severity assessment in community-acquired pneumonia: a review]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/379?rss=1</link>
<description><![CDATA[
<p>Severity assessment is an important early step in the management of patients presenting with community-acquired pneumonia. Various pneumonia-specific scores, generic sepsis scores and predictive biomarkers have been proposed as tools to aid clinicians in key management decisions. However, there is no uniform agreement about the optimum severity assessment tool to use. This review provides a summary of current evidence surrounding severity assessment in adult patients presenting with community-acquired pneumonia.</p>
]]></description>
<dc:creator><![CDATA[Singanayagam, A., Chalmers, J.D., Hill, A.T.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp027</dc:identifier>
<dc:title><![CDATA[Severity assessment in community-acquired pneumonia: a review]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>388</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>379</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/389?rss=1">
<title><![CDATA[Predicting mortality for patients with exacerbations of COPD and Asthma in the COPD and Asthma Outcome Study (CAOS)]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/389?rss=1</link>
<description><![CDATA[
<p><b>Introduction:</b> Decisions about the intensity of treatment for patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are influenced by predictions about survival and quality of life. Evidence suggests that these predictions are poorly calibrated and tend to be pessimistic.</p>
<p><b>Aim:</b> The aim of this study was to develop an outcome prediction model for COPD patients to support treatment decisions.</p>
<p><b>Methods:</b> A prospective multi-centre cohort study in Intensive Care Units (ICU) and Respiratory High Dependency Units (RHDU) in the UK recruited patients aged 45 years and older admitted with an exacerbation of obstructive lung disease. Data were collected on patients&rsquo; characteristics prior to ICU admission, and on their survival and quality of life after 180 days. An outcome prediction model was developed using multivariate logistic regression and bootstrapping.</p>
<p><b>Results:</b> Ninety-two ICUs (53% of those in the UK) and three RHDUs took part. A total of 832 patients were recruited. Cumulative 180-day mortality was 37.9%. Using data available at the time of admission to the units, a prognostic model was developed which had an estimated area under the receiver operating characteristic curve (&lsquo;c&rsquo;) of 74.7% after bootstrapping that was more discriminating than the clinicians (<I>P</I> = 0.033) and was well calibrated.</p>
<p><b>Discussion:</b> This study has produced an outcome prediction model with slightly better discrimination and much better calibration than the participating clinicians. It has the potential to support risk adjustment and clinical decision making about admission to intensive care.</p>
]]></description>
<dc:creator><![CDATA[Wildman, M.J., Sanderson, C., Groves, J., Reeves, B.C., Ayres, J., Harrison, D., Young, D., Rowan, K.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp036</dc:identifier>
<dc:title><![CDATA[Predicting mortality for patients with exacerbations of COPD and Asthma in the COPD and Asthma Outcome Study (CAOS)]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>399</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>389</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/401?rss=1">
<title><![CDATA[Incidence and prognosis of non-Q-wave vs. Q-wave myocardial infarction following catheter-based reperfusion therapy]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/401?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> The clinical importance of classifying myocardial infarction (MI) into non-Q-wave (NQWMI) vs. Q-wave (QWMI) subsets is controversial and might depend on the therapeutic reperfusion strategy employed. The prognostic implications of NQWMI development following primary percutaneous coronary intervention (PCI) have not been reported.</p>
<p><b>Aim:</b> To examine the incidence, determinants and prognostic implications of NQWMI vs. QWMI development following primary PCI.</p>
<p><b>Design:</b> The ACSIS Registry, a 2-month nationwide survey conducted biennially, prospectively collects data from all MI admissions in Israel.</p>
<p><b>Methods:</b> Outcomes were compared among patients managed by primary PCI who subsequently developed NQWMI vs. QWMI. Independent predictors of Q-wave development and 1-year mortality were determined by multivariate stepwise logistic regression analysis and Cox proportional hazard model, respectively.</p>
<p><b>Results:</b> Of 4537 MI patients with ST-segment elevation on admission, 1230 (27%) were treated with primary PCI. A discharge diagnosis of NQWMI was made in 259 (21.1%) patients. The baseline features and PCI strategies employed were similar among NQWMI vs. QWMI patients, though peak creatine kinase levels were higher (median 795 U/l vs. 1681 U/l, <I>P</I> = 0.0001) and severe left ventricular ejection fraction (LVEF) impairment (&lt;40%) more frequent (22.6% vs. 43.9%, <I>P</I> &lt; 0.0001), in the latter group. Mortality at 1-year was significantly lower in NQWMI vs. QWMI patients (3.9% vs. 10.8%, <I>P</I> log-rank = 0.001). By Cox proportional hazard analysis, NQWMI vs. QWMI was an independent predictor of freedom from 1-year mortality [HR = 0.34 (95% CI: 0.15&ndash;0.79), <I>P</I> = 0.01].</p>
<p><b>Discussion:</b> The diagnosis of NQWMI after primary PCI is associated with an excellent prognosis independent of established prognosticators, including LVEF.</p>
]]></description>
<dc:creator><![CDATA[Halkin, A., Fourey, D., Roth, A., Boyko, V., Behar, S.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp037</dc:identifier>
<dc:title><![CDATA[Incidence and prognosis of non-Q-wave vs. Q-wave myocardial infarction following catheter-based reperfusion therapy]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>406</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>401</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/407?rss=1">
<title><![CDATA[Clinically suspected acute pulmonary embolism: a comparison of presentation, radiological features and outcome in patients with and without PE]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/407?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Relatively little is known about prognosis in patients for whom suspected pulmonary embolism (PE) is refuted by imaging.</p>
<p><b>Aim:</b> This prospective study of suspected PE therefore compared clinico-radiological features and outcome in patients with and without PE.</p>
<p><b>Design and Methods:</b> Computed tomographic pulmonary angiography (CTPA) confirmed or refuted PE in consecutive patients. Clinical, laboratory and radiological features were recorded at baseline, and mortality at 1 year determined. Univariate and multivariate analyses identified variables associated with PE.</p>
<p><b>Results:</b> PE was diagnosed in 45 patients and refuted in 141. The PE and &lsquo;non-PE&rsquo; groups were similar with regard to extravascular radiology (though consolidation was significantly more common in the PE group [present in 24 (53%) of the PE group and 42 (30%) of the non-PE group, <I>P</I> &lt; 0.01)], comorbidities (no significant differences), and baseline characteristics (only serum D-dimer concentrations were independently associated with PE by multivariate analysis, <I>P</I> = 0.001). Right ventricular dimensions were significantly higher in the PE group, [right ventricular to left ventricular ratio was 0.98 (range 0.64&ndash;2.48) in the PE group and 0.92 (range 0.66&ndash;1.95) in the non-PE group, <I>P</I> &lt; 0.05]. In the PE group, right ventricular dimensions rose sharply when 10 or more segmental pulmonary arteries were occluded. One year all-cause mortality was 6.7% in the PE group and 13.5% in the non-PE group (no significant difference, <I>P</I> = 0.218).</p>
<p><b>Conclusion:</b> Among a cohort of patients presenting with clinically suspected PE, clinical characteristics, co-morbidities and radiological features were similar when comparing groups with CTPA-proven or CTPA-refuted PE. However RV dimensions, radiological consolidation on imaging and D-dimer levels were significantly higher in the PE group. Patients with suspected PE have a poor prognosis irrespective of whether PE is confirmed. This appears accentuated in patients without PE, a finding possibly under-recognized in clinical practice.</p>
]]></description>
<dc:creator><![CDATA[Akram, A.R., Cowell, G.W., Logan, L.J.A., Macdougall, M., Reid, J.H., Murchison, J.T., Simpson, A.J.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp041</dc:identifier>
<dc:title><![CDATA[Clinically suspected acute pulmonary embolism: a comparison of presentation, radiological features and outcome in patients with and without PE]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>414</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>407</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/415?rss=1">
<title><![CDATA[Renal quality outcomes framework and eGFR: impact on secondary care]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/415?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> The prognostic significance of impaired renal function has driven the need for its early recognition and the widespread introduction of the estimated glomerular filtration rate (eGFR) reporting, and the incorporation of Chronic Kidney Disease (CKD) in the revised Quality Outcomes Framework (QOF) of the General Medical Services (GMS) contract in the UK.</p>
<p><b>Aim:</b> To characterize the effect of these changes on referral numbers and appropriateness to a nephrology service, and the impact of a newly introduced Map of Medicine&reg;-based patient care pathway coupled to the systematic screening of all new referrals.</p>
<p><b>Methods:</b> The study was carried out within a single NHS Trust covering five primary health care Local Health Boards and a population of 560 000.</p>
<p><b>Results:</b> Introduction of eGFR reporting and CKD QOF domains was associated with a rapid 61% increase in new patient referral, and an increase in the mean age of the patients at referral from 63.0 &plusmn; 18.1 to 69.1 &plusmn; 18.5. The referrals did not correlate with the QOF reported prevalence of CKD. Systematic screening of new referrals demonstrated 36% to be either inappropriate or inadequate in terms of clinical information supplied. Introduction of the renal patient care pathway was associated with a fall in both the number of inadequate and total new referrals received. Overall 62% of all primary care practices registered with the Map of Medicine&reg; and these sent a higher proportion of appropriate referrals and were less likely to generate referrals with inadequate information. The initiative also enabled managed discharges from secondary to primary care settings, freeing up outpatient capacity.</p>
<p><b>Conclusion:</b> The study describes the impact of the introduction eGFR reporting and revision of the GMS contract with Renal QOF, on patient referrals to a nephrology service. In addition, we provide evidence that a new management pathway has helped to regulate and proactively manage the increased demand within the current resources.</p>
]]></description>
<dc:creator><![CDATA[Phillips, L.A., Donovan, K.L., Phillips, A.O.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp030</dc:identifier>
<dc:title><![CDATA[Renal quality outcomes framework and eGFR: impact on secondary care]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>423</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>415</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/425?rss=1">
<title><![CDATA[Discharging patients from the nephrology clinic to primary care--will they get appropriate monitoring of renal function?]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/425?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Chronic kidney disease (CKD) guidelines have been produced to allow affected individuals to be identified early and managed more effectively, thereby reducing cardiovascular risk and slowing the progression of CKD. The guidelines allow patients with stable early CKD, who were previously followed in nephrology clinics, to be discharged back to primary care for monitoring of their CKD.</p>
<p><b>Aim:</b> To determine if patients discharged from the nephrology clinic have appropriate monitoring of renal function in primary care according to the UK CKD guidelines, and if patients are being referred back to the clinic appropriately.</p>
<p><b>Methods:</b> All patients discharged from a weekly satellite unit general nephrology clinic over a 2-year period were identified (<I>n</I> = 160). Clinic letters, the local laboratory system and direct contact with the general practice were used to determine if the timing of tests of renal function were consistent with the UK CKD guidelines.</p>
<p><b>Results:</b> Most subjects (88%) had CKD Stages 1&ndash;3 at the time of discharge (i.e. eGFR &gt; 30 ml/min). After exclusion of patients with an incomplete management plan or insufficient time since discharge (<I>n</I> = 50), 85% of eligible patients (<I>n</I> = 110) had at least one measure of eGFR after discharge. In 65% (<I>n</I> = 84) of these patients, measurement occurred within 1 month of the correct timing according to the guidelines. Four patients were re-referred appropriately. There were no other patients who should have been re-referred due to deteriorating renal function.</p>
<p><b>Conclusion:</b> Patients with stable early CKD get appropriate monitoring of renal function after discharge from the nephrology clinic to primary care and are also referred back to the renal clinic appropriately.</p>
]]></description>
<dc:creator><![CDATA[Stevens, K.K., Woo, Y.M., Rodger, R.S.C., Geddes, C.C.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp040</dc:identifier>
<dc:title><![CDATA[Discharging patients from the nephrology clinic to primary care--will they get appropriate monitoring of renal function?]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>428</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>425</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/429?rss=1">
<title><![CDATA[A rare cause of syncope and pulmonary opacities]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/429?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pena, T., Bourbonnais, J. M., Soubani, A. O.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcn155</dc:identifier>
<dc:title><![CDATA[A rare cause of syncope and pulmonary opacities]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>430</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>429</prism:startingPage>
<prism:section>Clinical picture</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/431?rss=1">
<title><![CDATA[Chronic kidney disease--assessing the impact]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/431?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[O'Callaghan, C.A.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp043</dc:identifier>
<dc:title><![CDATA[Chronic kidney disease--assessing the impact]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>433</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>431</prism:startingPage>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/435?rss=1">
<title><![CDATA[Death railway and Weary-Dunlop Boonpong Fellowship Program]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/435?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kittisupamongkol, W.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp022</dc:identifier>
<dc:title><![CDATA[Death railway and Weary-Dunlop Boonpong Fellowship Program]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>435</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>435</prism:startingPage>
<prism:section>Correspondence</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/435-a?rss=1">
<title><![CDATA[Why the overstated beneficial effects of statins do not resolve the cholesterol controversy]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/435-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mascitelli, L., Pezzetta, F., Goldstein, M.R.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp028</dc:identifier>
<dc:title><![CDATA[Why the overstated beneficial effects of statins do not resolve the cholesterol controversy]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>436</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>435</prism:startingPage>
<prism:section>Correspondence</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/436?rss=1">
<title><![CDATA[History of the cholesterol hypothesis in Britain]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/436?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Grimes, D. S.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp029</dc:identifier>
<dc:title><![CDATA[History of the cholesterol hypothesis in Britain]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>438</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>436</prism:startingPage>
<prism:section>Correspondence</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/6/439?rss=1">
<title><![CDATA[The magic of Pi ({pi})]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/6/439?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Galton, D.]]></dc:creator>
<dc:date>2009-05-21</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp008</dc:identifier>
<dc:title><![CDATA[The magic of Pi ({pi})]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>440</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>439</prism:startingPage>
<prism:section>Coda</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/303?rss=1">
<title><![CDATA[Elements: In this month's issue]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/303?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bannon, M.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp050</dc:identifier>
<dc:title><![CDATA[Elements: In this month's issue]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>304</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>303</prism:startingPage>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/305?rss=1">
<title><![CDATA[Antioxidant treatment for heart failure: friend or foe?]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/305?rss=1</link>
<description><![CDATA[
<p>Increasing studies demonstrate a pivotal role for oxidant stress in the pathophysiology of heart failure (HF). Recent meta-analyses also reveal the potential pitfall of a mono-dimensional antioxidant approach. This review article summarizes the main biological pathways involved in oxidant stress and HF, the possible deleterious nature of certain antioxidant monotherapy and proposes potential antioxidant strategies necessary to challenge specific HF aetiology and progression.</p>
]]></description>
<dc:creator><![CDATA[Thomson, M. J., Frenneaux, M. P., Kaski, J. C.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcn160</dc:identifier>
<dc:title><![CDATA[Antioxidant treatment for heart failure: friend or foe?]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>310</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>305</prism:startingPage>
<prism:section>Review</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/311?rss=1">
<title><![CDATA[Voodoo dolls and the cancer patient: patients do trust their doctors]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/311?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> To determine oncology patients&rsquo; pattern and rationale of complementary and alternative medicine (CAM) use, and canvass their views on the relative merits of allopathic and alternative medicine.</p>
<p><b>Design:</b> Observational study of opinions from a cohort of patients using self-completion questionnaires.</p>
<p><b>Setting:</b> Oncology departments of two UK teaching hospitals.</p>
<p><b>Participants:</b> Voluntary participation of 200 oncology patients attending clinic.</p>
<p><b>Main findings:</b> Twenty-two percent of patients used CAM, with a preponderance towards younger, female patients. The commonest reasons for CAM use is to make the patient feel better and to help with their cancer. However, patients seldom believe there is more evidence for CAM or that CAM will cure them, indeed often noticing no benefits from the treatment. CAM users do not resort to complementary medicine due to dissatisfaction with their doctor but instead have considerable trust in their physicians. Only a minority believes their doctor knows about their CAM use.</p>
<p><b>Conclusion:</b> CAM use by oncology patients in the UK is less common than that reported elsewhere. Although patients try CAM in the hope that it will help with their treatment, they are realistic about its likely benefits. It uptake is not as an indication of lack of faith in doctors, yet physicians are frequently unaware of use. Therefore, the medical profession should not feel threatened by patients resorting to CAM but instead focus on understanding the reasons behind it.</p>
]]></description>
<dc:creator><![CDATA[Newsom-Davis, T., Kenny, L., Al-Shakarchi, I., George, J., Wong, E., Waxman, J.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp013</dc:identifier>
<dc:title><![CDATA[Voodoo dolls and the cancer patient: patients do trust their doctors]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>319</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>311</prism:startingPage>
<prism:section>Original papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/321?rss=1">
<title><![CDATA[Osteoarticular tuberculosis in patients with systemic lupus erythematosus]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/321?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Systemic lupus erythematosus (SLE) patients are at increased risk of developing tuberculosis (TB), particularly extrapulmonary TB (ExP-TB).</p>
<p><b>Aim:</b> The present study was undertaken to investigate whether SLE patients showed increased susceptibility to develop osteoarticular TB (OA-TB).</p>
<p><b>Design and Methods:</b> We retrospectively reviewed and compared the frequency of ExP-TB, in particular OA-TB, in patients with SLE at a tertiary hospital in South Africa, to a non-SLE control TB group seen at the same hospital.</p>
<p><b>Results:</b> TB was diagnosed 111 times in 97 (17%) of the 568 SLE patients. The relative frequency of ExP-TB in the SLE group (25.2%) was significantly lower than in the control group (38.5%) (OR = 1.9, <I>P</I> = 0.006). In contrast, OA-TB was diagnosed in the SLE group in nine (8.1%) patients (seven with peripheral arthritis and two with TB spine) compared to 54 (0.4%) in the overall control group (OR = 20.8, <I>P</I> &lt; 0.001) and 13 (0.2%) in the subgroup of known HIV positive patients in the control group (OR = 44.4, <I>P</I> &lt; 0.001). Within the SLE group, Black ethnicity (<I>P</I> = 0.003), lymphopaenia (<I>P</I> = 0.001), C3/C4 hypocomplementaemia (<I>P</I> = 0.05), corticosteroids [maximum dose (<I>P</I> = 0.002) and duration of treatment (<I>P</I> = 0.02)] and immunosuppressive agents (<I>P</I> = 0.02) were risk factors for TB. Duration of corticosteroid therapy was the only risk factor for OA-TB (<I>P</I> = 0.04).</p>
<p><b>Conclusion:</b> While the relative frequency of ExP-TB was lower in the SLE group compared to the control group, our findings suggest that SLE patients are at particular risk of developing OA-TB. Further prospective studies are needed to better understand the mechanisms that predispose SLE patients to OA-TB.</p>
]]></description>
<dc:creator><![CDATA[Hodkinson, B., Musenge, E., Tikly, M.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp015</dc:identifier>
<dc:title><![CDATA[Osteoarticular tuberculosis in patients with systemic lupus erythematosus]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>328</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>321</prism:startingPage>
<prism:section>Original Papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/329?rss=1">
<title><![CDATA[Retrospective analysis of Healthcare Resource Group coding allocation for local anaesthetic video-assisted 'medical' thoracoscopy in a UK tertiary respiratory centre]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/329?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Correct service costing is essential but may not always be done accurately.</p>
<p><b>Aim:</b> To assess the accuracy of Healthcare Resource Group (HRG) coding allocation for patients undergoing local anaesthetic video-assisted thoracoscopy (LAVAT) against predicted codes under Payment by Results (PbR).</p>
<p><b>Design:</b> Single centre retrospective study. Tertiary respiratory centre in Leicestershire.</p>
<p><b>Methods:</b> One hundred twenty-five patients undergoing LAVAT from July 2005 to July 2008. Main outcome measures: Predicted and actual revenue per LAVAT episode based on predicted and actual HRG codes allocated.</p>
<p><b>Results:</b> Among 125 patients undergoing LAVAT, the actual HRG code matched the predicted code in only 39 cases (31.2%), odds ratio (OR) 0.002, 95% confidence intervals (CIs) 0.0001&ndash;0.03, <I>P</I> &lt; 0.0001. In 51 cases (40.8%), this resulted in a median (interquartile range) excess of PbR revenue of &pound;574 (574&ndash;1366) per episode; a total estimated overspend of &pound;29 274. In 35 cases (28.0%), this resulted in a median underspend of &ndash;&pound;1093 (&ndash;1285 to &ndash;851) per episode; a total estimated underspend of &pound;38 529, with a total estimated financial error of &pound;67 529. The net median (interquartile range) difference for PbR-related revenue was &pound;0 (&ndash;89 to + 574). Factors associated with coding discrepancy were longer length of stay (OR = 2.52, 95% CIs = 1.09&ndash;5.81, <I>P</I> = 0.03) and talc pleurodesis (OR = 2.25, 95% CI = 1.01&ndash;4.99, <I>P</I> = 0.06).</p>
<p><b>Conclusions:</b> HRG coding allocation errors occur frequently. The potential financial implications of this are significant for providers and commissioners. Future strategies are required at multiple levels (NHS Trust, Primary Care Trust and Department of Health) to minimize future discrepancies and financial error.</p>
]]></description>
<dc:creator><![CDATA[Medford, A.R.L., Agrawal, S., Free, C.M., Bennett, J.A.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp016</dc:identifier>
<dc:title><![CDATA[Retrospective analysis of Healthcare Resource Group coding allocation for local anaesthetic video-assisted 'medical' thoracoscopy in a UK tertiary respiratory centre]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>333</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>329</prism:startingPage>
<prism:section>Original Papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/335?rss=1">
<title><![CDATA[Sitting and standing blood pressure measurements are not accurate for the diagnosis of orthostatic hypotension]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/335?rss=1</link>
<description><![CDATA[
<p><b>Introduction:</b> Orthostatic hypotension (OH) is associated with troublesome symptoms and increased mortality. It is treatable and deserving of accurate diagnosis. This can be time consuming. The current reference standard for its diagnosis is head-up tilt (HUT) testing with continuous beat-to-beat plethysmography. Our objective was to assess the accuracy of sit-stand testing with semi-automatic sphygmomanometry for the diagnosis of OH.</p>
<p><b>Design:</b> Retrospective test of diagnostic accuracy.</p>
<p><b>Methods:</b> This was a retrospective study performed using a database maintained by a busy syncope unit. HUT testing was performed using an automated tilt table with Finometer monitoring. A 3 min 70&deg; HUT was performed following 5 min supine. Sitting blood pressure (BP) was measured following 3 min rest. Standing BP was measured within 30 s of assuming the upright posture. The results of sit-stand testing were compared with HUT testing as a reference standard. Both tests happened within 5 min of each other and patients underwent no intervention between tests.</p>
<p><b>Results:</b> From a total of 1452 consecutive HUTs, we identified 730 with pre-test measures of sitting and standing BP. The mean age of this group was 70.57 years (SD = 15.1), 62% were female. The sensitivity of sit-stand testing was calculated as 15.5%, specificity as 89.9%, positive predictive value as 61.7%, negative predictive value as 50.2% and the likelihood ratio as 1.6. The area under the Receiver Operator Curve was 0.564.</p>
<p><b>Conclusion:</b> We have demonstrated that sit-stand testing for OH has very low diagnostic accuracy. We recommend that the more time-consuming reference standard method of diagnosis be used if the condition is suspected.</p>
]]></description>
<dc:creator><![CDATA[Cooke, J., Carew, S., O'Connor, M., Costelloe, A., Sheehy, T., Lyons, D.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp020</dc:identifier>
<dc:title><![CDATA[Sitting and standing blood pressure measurements are not accurate for the diagnosis of orthostatic hypotension]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>339</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>335</prism:startingPage>
<prism:section>Original paper</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/341?rss=1">
<title><![CDATA[Oral antioxidant supplementation does not prevent acute mountain sickness: double blind, randomized placebo-controlled trial]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/341?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Acute mountain sickness may be caused by cerebrovascular fluid leakage due to oxidative damage to the endothelium. This may be reduced by oral antioxidant supplementation.</p>
<p><b>Aim:</b> To assess the effectiveness of antioxidant supplementation for the prevention of acute mountain sickness (AMS).</p>
<p><b>Design:</b> A parallel-group double blind, randomized placebo-controlled trial.</p>
<p><b>Methods:</b> The study was conducted in a university clinical research facility and a high altitude research laboratory. Eighty-three healthy lowland volunteers ascended to 5200 m on the Apex 2 high altitude research expedition. The treatment group received a daily dose of 1 g <scp>l</scp>-ascorbic acid, 400 IU of -tocopherol acetate and 600 mg of -lipoic acid (Cultech Ltd., Wales, UK) in four divided doses. Prevalence of AMS was measured using the Lake Louise Consensus score sheet (LLS). Secondary outcomes were AMS severity measured using a novel visual analogue scale, arterial oxygen saturation and pulmonary artery systolic pressure (PASP).</p>
<p><b>Results:</b> Forty-one subjects were allocated to the antioxidant group, and 42 to the placebo group. There was no difference in AMS incidence or severity between the antioxidant and placebo groups using the LLS at any time at high altitude. At the pre-determined comparison point at Day 2 at 5200 m, 69% of the antioxidant group (25/36) and 66% of the placebo group (23/35) had AMS using the LLS criteria (<I>P</I> = 0.74). No differences were observed between the groups for PASP, oxygen saturation, presence of a pericardial effusion or AMS assessed by VAS.</p>
<p><b>Conclusion:</b> This trial found no evidence of benefit from antioxidant supplementation at high altitude.</p>
<p><b>Trial registration number</b>: NCT00664001</p>
]]></description>
<dc:creator><![CDATA[Baillie, J.K., Thompson, A.A.R., Irving, J.B., Bates, M.G.D., Sutherland, A.I., MacNee, W., Maxwell, S.R.J., Webb, D.J.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp026</dc:identifier>
<dc:title><![CDATA[Oral antioxidant supplementation does not prevent acute mountain sickness: double blind, randomized placebo-controlled trial]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>348</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>341</prism:startingPage>
<prism:section>Original Papers</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/349?rss=1">
<title><![CDATA[Expenditure and value for money: the challenge of implantable cardioverter defibrillators]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/349?rss=1</link>
<description><![CDATA[
<p>Many technology-driven interventions entail considerable financial cost, raising affordability issues. The implantable cardioverter defibrillator (ICD) is a case of an effective primary prevention intervention with high initial costs that is capable of delivering long-term population benefits. At first glance, such interventions may provoke diffidence, if not active resistance, due to the financial burdens which inevitably accompany their widespread adoption. In this article, we review the available economic tools that can help address the ICD cost issue. We think awareness of such knowledge may facilitate dialogues between physicians, administrators and policymakers, and help foster rational decision-making.</p>
]]></description>
<dc:creator><![CDATA[Boriani, G., Biffi, M., Martignani, C., Diemberger, I., Valzania, C., Bertini, M., Branzi, A.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp025</dc:identifier>
<dc:title><![CDATA[Expenditure and value for money: the challenge of implantable cardioverter defibrillators]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>356</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>349</prism:startingPage>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/357?rss=1">
<title><![CDATA[Haemodynamic changes in acute opiate withdrawal]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/357?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Stuart Reece, A.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcn151</dc:identifier>
<dc:title><![CDATA[Haemodynamic changes in acute opiate withdrawal]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>357</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>357</prism:startingPage>
<prism:section>Clinical picture</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/359?rss=1">
<title><![CDATA[Metastatic calcinosis cutis]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/359?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Chung, S.-D., Lu, C.-W., Wu, V.-c., Chen, Y.-S., Chang, K.-C., Chu, S.-H.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcn154</dc:identifier>
<dc:title><![CDATA[Metastatic calcinosis cutis]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>359</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>359</prism:startingPage>
<prism:section>Clinical picture</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/361?rss=1">
<title><![CDATA[Thyrotoxic periodic paralysis amongst the ethnic Asians living in the west--an important entity to consider in the hospital setting]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/361?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sinharay, R.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcn166</dc:identifier>
<dc:title><![CDATA[Thyrotoxic periodic paralysis amongst the ethnic Asians living in the west--an important entity to consider in the hospital setting]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>362</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>361</prism:startingPage>
<prism:section>Correspondence</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/362?rss=1">
<title><![CDATA[Microcytic anaemia can 'mask' co-existing cobalamin deficiency]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/362?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Jolobe, O.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp011</dc:identifier>
<dc:title><![CDATA[Microcytic anaemia can 'mask' co-existing cobalamin deficiency]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>363</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>362</prism:startingPage>
<prism:section>Correspondence</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/363?rss=1">
<title><![CDATA[Cappuccio response to correspondence]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/363?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Cappuccio, F. P., Lockley, S. W., Landrigan, C. P]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcp032</dc:identifier>
<dc:title><![CDATA[Cappuccio response to correspondence]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>364</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>363</prism:startingPage>
<prism:section>Correspondence</prism:section>
</item>

<item rdf:about="http://qjmed.oxfordjournals.org/cgi/content/short/102/5/365?rss=1">
<title><![CDATA[A chance meeting * The immortal medical portrait]]></title>
<link>http://qjmed.oxfordjournals.org/cgi/content/short/102/5/365?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[James, D. G., James, D. G.]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/qjmed/hcn167</dc:identifier>
<dc:title><![CDATA[A chance meeting * The immortal medical portrait]]></dc:title>
<dc:publisher>Association of Physicians</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>102</prism:volume>
<prism:endingPage>366</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>365</prism:startingPage>
<prism:section>Coda</prism:section>
</item>

</rdf:RDF>