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<title>Archives of Disease in Childhood Miscellanea</title>
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<title>Archives of Disease in Childhood</title>
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<title><![CDATA[Submandibular sialolithiasis in a child]]></title>
<link>http://adc.bmj.com/cgi/content/short/98/6/407?rss=1</link>
<description><![CDATA[ <p>A 14-year-old boy presented with a 6-year history of intermittent right submandibular swelling. It arose with no specific trigger but was associated with pain on swallowing. It usually lasted several hours before spontaneously subsiding. There was no pyrexia, sore throat, tuberculosis contact or foreign travel.</p> <p>On examination the lump measured 3<FONT FACE="arial,helvetica">x</FONT>3&nbsp;cm, was non-tender, firm, mobile, non-fluctuant, with normal overlying skin. The patient thrived along the 25th and 50th centiles for height and weight respectively. No lymphadenopathy, pallor or petechiae was noted. All systemic examinations were normal.</p> <p>Laboratory findings, chest x-ray and neck ultrasound scan were normal. A presumed diagnosis of reactive submandibular lymphadenitis was made but the swelling was resistant to antibiotics. Subsequent bimanual palpation revealed a stone in the right submandibular gland. This was confirmed on neck x-ray (<cross-ref type="fig" refid="ARCHDISCHILD2012303491F1">figure 1</cross-ref>) and was removed surgically.</p> <p>Sialolithiasis in children comprises only 3% of all cases.<cross-ref type="bib" refid="R1">1</cross-ref> The...]]></description>
<dc:creator><![CDATA[Liu, N. M., Rawal, J.]]></dc:creator>
<dc:date>2013-05-09T02:05:40-07:00</dc:date>
<dc:identifier>info:doi/10.1136/archdischild-2012-303491</dc:identifier>
<dc:identifier>hwp:master-id:archdischild;archdischild-2012-303491</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Submandibular sialolithiasis in a child]]></dc:title>
<prism:publicationDate>2013-06-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>98</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>407</prism:startingPage>
<prism:endingPage>407</prism:endingPage>
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<item rdf:about="http://adc.bmj.com/cgi/content/short/98/6/418?rss=1">
<title><![CDATA[Idiopathic intracranial hypertension associated with iron-deficiency anaemia]]></title>
<link>http://adc.bmj.com/cgi/content/short/98/6/418?rss=1</link>
<description><![CDATA[ <sec> <p>A 12-year-old Nigerian girl presented to the Emergency Department with headache, dizziness and diplopia. She had a history of menorrhagia. Mild dyspnoea, tachycardia, left sixth cranial nerve palsy and papilloedema (<cross-ref type="fig" refid="ARCHDISCHILD2012303543F1">figures 1</cross-ref> and <cross-ref type="fig" refid="ARCHDISCHILD2012303543F2">2</cross-ref>) were noted. Body mass index was normal. Full blood count revealed haemoglobin of 4.8&nbsp;g/dl. The red cells were hypochromic and mircocytic. A CT scan of the brain with venous contrast was normal. A lumbar puncture showed opening and closing pressures of 35 and 33.5&nbsp;cm H<SUB>2</SUB>O, respectively. The diagnosis of idiopathic intracranial hypertension secondary to iron-deficiency anaemia was made. Treatment of the anaemia (transfusion and iron supplements) resulted in resolution of symptoms and signs. Although stroke and cerebral venous sinus thrombosis are well-recognised complications of anaemia,<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> idiopathic intracranial hypertension has also been described in association with iron-deficiency anaemia<cross-ref type="bib" refid="R3">3&ndash;5</cross-ref><cross-ref type="bib" refid="R4"></cross-ref><cross-ref type="bib" refid="R5"></cross-ref> and usually...]]></description>
<dc:creator><![CDATA[Forman, E. B., O'Byrne, J. J., Capra, L., McElnea, E., King, M. D.]]></dc:creator>
<dc:date>2013-05-09T02:05:40-07:00</dc:date>
<dc:identifier>info:doi/10.1136/archdischild-2012-303543</dc:identifier>
<dc:identifier>hwp:master-id:archdischild;archdischild-2012-303543</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Idiopathic intracranial hypertension associated with iron-deficiency anaemia]]></dc:title>
<prism:publicationDate>2013-06-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>98</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>418</prism:startingPage>
<prism:endingPage>418</prism:endingPage>
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<title><![CDATA[Supernumerary intrathoracic rib]]></title>
<link>http://adc.bmj.com/cgi/content/short/98/6/441?rss=1</link>
<description><![CDATA[ <p>An 8-year-old afebrile boy presented with a 10-day history of runny nose and coughing, with no history of lung or other systemic disease and no sign of respiratory distress, tachypnoea or tachycardia. Chest radiography revealed that anterior portion of the right third rib was oriented caudally and ended mid-thorax (<cross-ref type="fig" refid="ARCHDISCHILD2012303550F1">figure 1</cross-ref>). A thick band extended from the anterior edge of the third rib to the anterior portion of the sixth rib, causing retraction of the attached pleura. Unenhanced helical thorax CT demonstrated inward and downward sloping of the distal end of the right third rib (<cross-ref type="fig" refid="ARCHDISCHILD2012303550F2">figures 2</cross-ref> and <cross-ref type="fig" refid="ARCHDISCHILD2012303550F3">3</cross-ref>). A thick band extended from the medial end of the third rib and attached to the diaphragm, which was pulled superiorly.</p> <p>These findings were consistent with a supernumerary intrathoracic rib, a rare congenital anomaly arising from abnormal segmentation of adjacent sclerotomes.<cross-ref type="bib" refid="R1">1</cross-ref> Since...]]></description>
<dc:creator><![CDATA[Kayiran, S. M., Gumus, T., Kayiran, P. G., Gurakan, B.]]></dc:creator>
<dc:date>2013-05-09T02:05:40-07:00</dc:date>
<dc:identifier>info:doi/10.1136/archdischild-2012-303550</dc:identifier>
<dc:identifier>hwp:master-id:archdischild;archdischild-2012-303550</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Supernumerary intrathoracic rib]]></dc:title>
<prism:publicationDate>2013-06-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>98</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>441</prism:startingPage>
<prism:endingPage>441</prism:endingPage>
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<title><![CDATA[Antibiotics in severe acute malnutrition]]></title>
<link>http://adc.bmj.com/cgi/content/short/98/6/448?rss=1</link>
<description><![CDATA[ <sec id="s1"> <p>Children with severe acute malnutrition may be infected and the routine addition of antibiotics to nutritional treatment has been recommended although there have been no clinical trials and there is observational evidence that giving antibiotics may be unnecessary or even harmful. Now, a trial in rural Malawi (Indi Trehan and colleagues, <I>New England Journal of Medicine</I> 2013;368:425&ndash;35) has shown antibiotics are beneficial.</p> <p>At 18 rural feeding clinics a total of 2767 children aged 6&ndash;59 months with uncomplicated severe acute malnutrition were randomised to three groups: amoxicillin suspension 80&ndash;90&nbsp;mg per kg daily in two divided doses, cefdinir suspension 14&nbsp;mg per kg in two divided doses, or placebo twice daily. All children received ready-to-use therapeutic food and were treated as outpatients. Recovery (no oedema and weight for height z score &ndash;2 or higher) occurred in 88.7% (amoxicillin), 90.9% (cefdinir), and 85.1% (placebo). The risk of treatment failure with placebo...]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2013-05-09T02:05:40-07:00</dc:date>
<dc:identifier>info:doi/10.1136/archdischild-2013-304020</dc:identifier>
<dc:identifier>hwp:master-id:archdischild;archdischild-2013-304020</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Antibiotics in severe acute malnutrition]]></dc:title>
<prism:publicationDate>2013-06-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>98</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>448</prism:startingPage>
<prism:endingPage>448</prism:endingPage>
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<title><![CDATA[Fetal macrosomia in developing countries]]></title>
<link>http://adc.bmj.com/cgi/content/short/98/6/461?rss=1</link>
<description><![CDATA[ <sec id="s1"> <p>The prevalence of fetal macrosomia in developed countries has increased by some 15&ndash;25% in recent decades, an increase largely attributed to increasing maternal obesity and diabetes. Risk factors for macrosomia include male fetal sex, high parity, maternal age, and height, post-term pregnancy, and pre-gestational or gestational diabetes. Neonatal and obstetric complications include perinatal asphyxia and death, shoulder dystocia, increased risk of caesarean section, prolonged labour, maternal haemorrhage, and perineal trauma. Data about macrosomia for hospital deliveries in 23 developing countries in Africa and Latin America (2004&ndash;05) and Asia (2007&ndash;08) have been obtained from the WHOs Global Survey on Maternal and Perinatal health (Ai Koyanagi and colleagues. <I>Lancet</I> 2013;381:476&ndash;83; See also Comment, ibid: 435&ndash;6). For this study, macrosomia was defined as a birthweight &gt;90<sup>th</sup> percentile for country-specific birthweights. (It has previously been defined by birthweight: &gt;4000&nbsp;g or (in the USA) &gt;4500g. A total of 276436 singleton livebirths or...]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2013-05-09T02:05:40-07:00</dc:date>
<dc:identifier>info:doi/10.1136/archdischild-2013-304021</dc:identifier>
<dc:identifier>hwp:master-id:archdischild;archdischild-2013-304021</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Fetal macrosomia in developing countries]]></dc:title>
<prism:publicationDate>2013-06-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>98</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>461</prism:startingPage>
<prism:endingPage>461</prism:endingPage>
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<title><![CDATA[A digital picture is worth a thousand words in a different dialect: improving adherence to antiretroviral medication]]></title>
<link>http://adc.bmj.com/cgi/content/short/98/6/467?rss=1</link>
<description><![CDATA[ <sec id="s1"> <p>A 4-year-old HIV-positive girl who had recently migrated from Kenya presented with chronic otitis media and poor growth. Her viral load was 139&nbsp;000&nbsp;copies/ml with CD4 lymphocytes 1050<FONT FACE="arial,helvetica">x</FONT>10<sup>9</sup>/ml (15%). After resistance testing and education through a Swahili interpreter, she started abacavir 150&nbsp;mg am/300&nbsp;mg pm, lamivudine 75&nbsp;mg am/150&nbsp;mg pm and lopinavir/ritonavir 100/25 three tablets twice daily (with translated fact sheets and colour-coded medicine bottles). After 4&nbsp;weeks her viral load was &lt;50&nbsp;copies/ml, but 3&nbsp;months later was 189&nbsp;copies/ml. Concerned about compliance, we questioned her mother through an interpreter, who indicated she spoke an unusual dialect, but his understanding was that she was giving the medicines. The low-level viraemia persisted, and on pill counting, the pharmacist observed that she had too many tablets remaining. To enhance adherence, we designed a pictorial representation of how to give the medications, including digital photographs of her specific doses (<cross-ref type="fig" refid="ARCHDISCHILD2013304223F1">figure 1</cross-ref>). Four weeks later,...]]></description>
<dc:creator><![CDATA[Bryant, P. A., Bordun, L., Connell, T. G.]]></dc:creator>
<dc:date>2013-05-09T02:05:40-07:00</dc:date>
<dc:identifier>info:doi/10.1136/archdischild-2013-304223</dc:identifier>
<dc:identifier>hwp:master-id:archdischild;archdischild-2013-304223</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[A digital picture is worth a thousand words in a different dialect: improving adherence to antiretroviral medication]]></dc:title>
<prism:publicationDate>2013-06-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>98</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>467</prism:startingPage>
<prism:endingPage>467</prism:endingPage>
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<title><![CDATA[Highlights from the literature]]></title>
<link>http://adc.bmj.com/cgi/content/short/98/6/480?rss=1</link>
<description><![CDATA[ <sec id="s1"> <p>Diagnosing the cause of intracranial calcification may be difficult and require a high degree of paediatric neurological or paediatric neuroradiological expertise. Workers in Leeds, Manchester and Amsterdam (<I>Developmental Medicine and Child Neurology</I> 2013;<b>55</b>:46&ndash;57 see also Commentary, ibid: 7&ndash;8) have used a neuroimaging pattern recognition approach and proposed a new classification system. They analysed 244 scans (140 CT, 104 MRI) from 119 patients (mostly children but a few adults). The clinical details and scans of patients were sent to the authors because of their known interests, particularly in Aicardi-Gouti&egrave;res syndrome (AGS) and the series was therefore highly selective. A diagnosis was available for 59 patients, including 33 with AGS. No patient with prenatal viral infection such as cytomegalovirus infection was referred. The most frequent other diagnoses were cerebroretinal microangiopathy with calcification and cysts (10 patients), band-like calcification with simplified gyration and polymicrogyria (BLC-PMG) (6), and <I>COL4A1</I> mutation related...]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2013-05-09T02:05:40-07:00</dc:date>
<dc:identifier>info:doi/10.1136/archdischild-2013-304216</dc:identifier>
<dc:identifier>hwp:master-id:archdischild;archdischild-2013-304216</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Highlights from the literature]]></dc:title>
<prism:publicationDate>2013-06-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>98</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>480</prism:startingPage>
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