12 research outputs found

    Histogram of latest VBLL during the entire study period as a percentage of pre-chelation VBLL per child.

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    <p>As the role of repeated courses on combined overall change cannot be extracted, change includes effect of all courses (e.g., 5-d and CaNa<sub>2</sub>EDTA courses). This does not represent the end of treatment in most cases, but rather an interim measure at the end of the study period.</p

    Flow chart of children commencing chelation in period analysed, with inclusion and exclusion in analysis and death outcomes.

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    <p>Lead was attributed as the primary cause of death where there was a high (>100 µg/dl) VBLL within 10 d before death, where there was no other obvious cause, and where lead toxicity could not be excluded as a cause. Lead was attributed as a contributory cause where a serious comorbidity was present (measles, bronchopneumonia, malaria, septicaemia, or severe malnutrition) but with a recent VBLL> 90 µg/dl. Deaths were categorized as “no clear role of lead” where there was another obvious cause (e.g., fell into an open well, anaemic heart failure, or measles) and no recent VBLL> 65 µg/dl. Reasons for not including in the study cohort were not finishing the chelation course (through defaulting or death before end of course) or no VBLL recorded at end of course. *All died during first treatment course. †Two died during first treatment course.</p

    Mixed model of ECP using nested random effects for a 19-d (7 d TDS + 12 d BD) DMSA chelation course (<i>n = </i>2,285 in unadjusted analysis; <i>n = </i>2,262 in adjusted analysis limited to patients with data on all covariates).

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    <p>A positive value of ECP indicates an increase in VBLL; a negative value of ECP indicates a decrease in VBLL. DOT by clinic staff; non-DOT doses administered by caretaker.</p><p>*Total patients in unadjusted analyses<i> = </i>2,285. Final model (<i>n = </i>2,262) excludes those with missing data (1%).</p>†<p>Adjusted for all other variables shown in the table.</p>‡<p>An end-course VBLL was accepted if up to 2 d before and up to 10 d after last dose of DMSA.</p><p>Mixed model of ECP using nested random effects for a 19-d (7 d TDS + 12 d BD) DMSA chelation course (<i>n = </i>2,285 in unadjusted analysis; <i>n = </i>2,262 in adjusted analysis limited to patients with data on all covariates).</p

    Mixed model of VBLL rebound following a course of chelation (nested random effects; <i>n = </i>2,444).

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    <p>VBLL rebound is VBLL at the next test after the end of a 19-d course as a percentage of end-course VBLL.</p><p>Mixed model of VBLL rebound following a course of chelation (nested random effects; <i>n = </i>2,444).</p

    Association of dose regimen and dose administration method with geometric mean ECP (expressed as percent).

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    <p>Data are ECP (95% CI). See <a href="http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.1001739#pmed.1001739-t004" target="_blank">Table 4</a> for number of courses per cell.</p><p>Association of dose regimen and dose administration method with geometric mean ECP (expressed as percent).</p

    Number of courses by dose regimen and administration regimen.

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    <p>Data are <i>n</i> (percent of regimen). Categories differentiate full DOT (here meaning entire course was taken in hospital) compared with various combinations of partial DOT when a child was discharged mid-course to receive the remainder of the course in the community, either with daily or alternate-day DOT of one of the day's doses and the remainder administered by the caretaker at home.</p>†<p>Courses in this row included in model in <a href="http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.1001739#pmed.1001739-t006" target="_blank">Table 6</a>.</p><p>Number of courses by dose regimen and administration regimen.</p
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