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asymptomatic patients independent <strong>of</strong> the presence <strong>of</strong> atopy or the treatment modality.<br />

Urinary EDN levels in the asthmatics correlated to lung function, and in the subgroup <strong>of</strong> 15<br />

children re-examined two months after commencement <strong>of</strong> treatment, the reduction <strong>of</strong> EDN<br />

also correlated with the changes in lung function (Lugosi, Halmerbauer et al. 1997). While no<br />

correlation was found between urinary EDN values and lung function in two other studies <strong>of</strong><br />

155 and 39 children, there was a similar reduction <strong>of</strong> EDN three months after commencing<br />

IHCS treatment (Krisdansson, Strannegard et al. 1996; Labbe, Aublet-Cuvelier et al. 2001).<br />

Circadian variations <strong>of</strong> the eosinophil proteins in urine samples have been demonstrated with<br />

high early morning and nocturnal peaks compared to lower levels in the afternoon in both<br />

asthmatic and non-atopic, non-asthmatic groups <strong>of</strong> children (Storm van's Gravesande, Mattes<br />

et al. 1999; Wolthers and Heuck 2003).<br />

A more explored area using these samples has been in measuring the levels <strong>of</strong> the leukotriene<br />

goup <strong>of</strong> proteins, particularly in urine samples. <strong>The</strong>se proteins were shown to increase early<br />

in adult asthmatic groups following an airway challenge (Westcott, Smith et al. 1991; Kumlin,<br />

Dahlen et al. 1992; O'Sullivan, Roquet et al. 1998; Bancalari, Conti et al. L999) with peak<br />

excretion occurring at two hours (Kumlin and Dahlen 2000; Mai, Bottcher et al. 2005). <strong>The</strong><br />

results were more variable when assessing whether levels remained elevated during the late<br />

asthmatic response - not seen in one study (Manning, Rokach et al. 1990) but documented in<br />

two others (O'Sullivan, Roquet et al. 1998; Bancalari, Conti et al. 1999). LT& was high in<br />

184 adults presenting with moderate to severe acute asthma and reduced two weeks later in<br />

the 146 followed up during recovery (Green, Malice et al. 2OO4). Compared to control<br />

subjects, there was an increase in the LTEI level in asthmatics with nocturnal asthma<br />

exacerbations but not in asthmatics without, although the numbers in each group were less<br />

than ten (Bellia, Bonanno et al. 1996). Patients with asthma did excrete more LT& over a24<br />

hour period than normal subjects, again with less than ten subjects in each group (Asano,<br />

Lilly et al. 1995). In 40 severe asthmatics, 25 mild to moderate asthmatics and 20 non-<br />

asthmatic controls, there was a gradation LTE4 levels despite treatment with high dose IHCS<br />

in the severe group (Vachier, Kumlin et al. 2003). LTE4 in urine was higher in 35 atopic<br />

asthmatic than32 non-atopic children with RSV bronchiolitis and 23 controls (Oh, Shin et al.<br />

200s).<br />

Other studies have been less positive about the correlations between inflammatory markers<br />

measured in blood and urine samples and asthmatic disease. In adults, no correlation between<br />

clinical status, functional status and serum ECP was seen during five months in asthmatics<br />

either admitted for acute asthma or who were seasonally sensitised to birch and tree pollens<br />

42

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