In this current study it was report

In this current study it was reported that there is a highly
significant difference in the level of IL-1B between the three
groups. The level of (IL-1Beta) was related to the stage of
the disease as there was a significant increase in (IL-1Beta)
level with increasing severity of COPD; very severe COPD
cases have a higher level of (IL-1Beta) than severe and moderate
cases, (IL-1Beta) was also raised in severe cases than moderate
cases and the difference between them was highly
statistically significant (p < 0.01) (Table 7).
This is matched with [1], who reported that COPD results
from airway inflammation involving multiple inflammatory
mediators and tissue damage.
This could be explained by the nature of COPD as a complex
chronic inflammatory disease of the lungs involving several
types of inflammatory cells and a variety of
inflammatory mediators. Although primarily affecting the
lungs, the chronic inflammatory process of COPD does have
systemic repercussions [2].
This result is in agreement with [16], who found that there is
a significantly high level of IL-1b in serum of the COPD
patients as compared to the healthy controls. A few studies
previously undertaken have also reported a rise in IL-1b in
COPD cases.
Also this result is in agreement with [17], who reported that
in the control group, the IL-1b level was 2.11 ± 0.16 pg/ml
(range: 0.39–2.97 pg/ml), which was significantly lower than
COPD patients (3.14 ± 0.07, range: 2.8–4.59 pg/ml, p < 0.05).
Sapey et al. [16], proved that there are increased levels of
circulating cytokines and acute phase reactants have been seen
in the peripheral circulation of patients suffering from COPD,
especially during exacerbations. They also proved that IL-1b
plays a critical role in COPD where it was found to correlate
significantly with FEV1 suggesting its role in clinical aspects
of disease severity.
All these results are in agreement with [9], who concluded
that modulation of various inflammatory mediators may help
in combating the clinical outcome of COPD and may have
therapeutic implications whereas determination of serum IL-
1b levels may help in differentiating COPD from other respiratory
disorders such as asthma.
On the contrary, this result disagreed with [15], who proved
that IL-1b may be related to pathophysiology in COPD,
although there were no significant differences in IL-1b concentrations
between their groups (Table 10).
In this current work it was found that there is a highly significant
correlation between IL-1B and COPD severity in
groups I and II (Table 11 and 12).
This result matched with [11], who found that IL-1b expression
in COPD neutrophils correlates with disease severity. This
result is also in agreement with [16], when studying the demonstration
of IL-1B and TNF levels in serum and sputum, he
found that IL-1B plays a critical role in COPD where it was
found to correlate significantly with FEV1 suggesting its role
in clinical aspects of disease severity

ผลลัพธ์ (ไทย) 1:

In this current study it was reported that there is a highlysignificant difference in the level of IL-1B between the threegroups. The level of (IL-1Beta) was related to the stage ofthe disease as there was a significant increase in (IL-1Beta)level with increasing severity of COPD; very severe COPDcases have a higher level of (IL-1Beta) than severe and moderatecases, (IL-1Beta) was also raised in severe cases than moderatecases and the difference between them was highlystatistically significant (p < 0.01) (Table 7).This is matched with [1], who reported that COPD resultsfrom airway inflammation involving multiple inflammatorymediators and tissue damage.This could be explained by the nature of COPD as a complexchronic inflammatory disease of the lungs involving severaltypes of inflammatory cells and a variety ofinflammatory mediators. Although primarily affecting thelungs, the chronic inflammatory process of COPD does havesystemic repercussions [2].This result is in agreement with [16], who found that there isa significantly high level of IL-1b in serum of the COPDpatients as compared to the healthy controls. A few studiespreviously undertaken have also reported a rise in IL-1b inCOPD cases.Also this result is in agreement with [17], who reported thatin the control group, the IL-1b level was 2.11 ± 0.16 pg/ml(range: 0.39–2.97 pg/ml), which was significantly lower thanCOPD patients (3.14 ± 0.07, range: 2.8–4.59 pg/ml, p < 0.05).Sapey et al. [16], proved that there are increased levels ofcirculating cytokines and acute phase reactants have been seenin the peripheral circulation of patients suffering from COPD,especially during exacerbations. They also proved that IL-1bplays a critical role in COPD where it was found to correlatesignificantly with FEV1 suggesting its role in clinical aspectsof disease severity.All these results are in agreement with [9], who concludedthat modulation of various inflammatory mediators may helpin combating the clinical outcome of COPD and may havetherapeutic implications whereas determination of serum IL-1b levels may help in differentiating COPD from other respiratorydisorders such as asthma.On the contrary, this result disagreed with [15], who provedthat IL-1b may be related to pathophysiology in COPD,although there were no significant differences in IL-1b concentrationsbetween their groups (Table 10).In this current work it was found that there is a highly significantcorrelation between IL-1B and COPD severity ingroups I and II (Table 11 and 12).This result matched with [11], who found that IL-1b expressionin COPD neutrophils correlates with disease severity. Thisresult is also in agreement with [16], when studying the demonstrationof IL-1B and TNF levels in serum and sputum, hefound that IL-1B plays a critical role in COPD where it wasfound to correlate significantly with FEV1 suggesting its roleในลักษณะทางคลินิกของความรุนแรงของโรค

ผลลัพธ์ (ไทย) 3:

That's all I need to know.That's all I need to know.That's all I need to know.That's all I need to know.That's all I need to know.That's all I need to know.That's all I need to know.That's all I need to know.