OBSERVATION AND RESULTS

1. Gender Distribution

Gender Distribution
Male Female

4%

96%

In a recent study examining gender distribution among participants, it was found that the
majority were male (n = 51), with a substantially smaller proportion being female (n = 2).
This significant gender disparity underscores the need for further investigation into potential
factors influencing participation rates among different demographic groups.
 2. Age Distribution

Age Distribution
30

25 24

20
17
15

10
7
5
5

0
40-50 51-60 61-70 71-80

Frequency

The distribution of participants' ages varied across different age groups. The highest
frequency was observed in the age range of 61-70, with 24 individuals falling within this
category. This was followed by the age range of 51-60, which comprised 17 participants. Age
groups 40-50 and 71-80 had 5 and 7 participants, respectively. These findings suggest a
predominant representation of individuals aged 61-70 in the study sample, indicating a
potential age-related trend worth further exploration.
TABLE 1: Patient prevalence of Stable Copd and COPD exacerbation in Stage
I,II,III,IV.

COPD P Value
Stable COPD Exacerbation
Patients Patients

GOLD Stage (58.5%) (41.5%)

Stage I 9 4 0.73

Stage II 10 9

Stage III 11 9

Stage IV 1 0

Table 1: n=53, predominantly seen in STAGE II, STAGE III & IV

The table illustrates the patient prevalence of stable COPD and COPD exacerbation across
different GOLD stages. Among the 53 patients studied, Stage II had the highest
representation in both stable COPD and exacerbation cases, followed by Stage III and Stage
I. Stage IV had the lowest representation, with only one patient diagnosed with stable COPD.
The difference in prevalence between stable COPD and COPD exacerbation across all stages
was not statistically significant (P > 0.05).
 Patient prevalence of Stable Copd and COPD
exacerbation in Stage I,II,III,IV.
12
11

10
10
9 9 9

4
4

2
1

0
0
Stable COPD Patients COPD Exacerbation Patients

Stage I Stage II Stage III Stage IV

TABLE 2: COMPARISION OF SERUM IgE AMONG STABLE COPD &COPD
EXACERBATION.

CUTOFF S.IgE Stable COPD COPD P Value

(IU/ml) (mean) Exacerbation
Patients

<100 71.18 0 0.00

>100 130.5 218.40

COMPARISION OF SERUM IgE AMONG

STABLE COPD &COPD EXACERBATION.
250
218.4

200

150
130.5

100

50

0
Stable COPD COPD Exacerbation Patients

<100 >100

In a comparative analysis of serum IgE levels between stable COPD patients and those
experiencing COPD exacerbation, significant differences were observed based on a
predetermined cutoff value of 100 IU/ml. Among stable COPD patients, the mean serum IgE
level was 71.18 IU/ml for levels below 100 IU/ml, indicating relatively low IgE levels in this
subgroup. In contrast, COPD exacerbation patients had a mean IgE level of 0 IU/ml for levels
below 100 IU/ml, suggesting a complete absence of IgE in this group within the specified
range. For IgE levels above 100 IU/ml, stable COPD patients had a mean of 130.5 IU/ml,
while exacerbation patients had a significantly higher mean IgE level of 218.40 IU/ml. These
results indicate a substantial elevation of serum IgE levels during COPD exacerbations
compared to stable COPD, highlighting the potential role of IgE-mediated pathways in
exacerbation pathogenesis.

The statistical analysis revealed a significant difference in serum IgE levels between stable
COPD and exacerbation patients (p < 0.05), underscoring the clinical relevance of IgE as a
biomarker for exacerbation risk and severity in COPD. These findings emphasize the
importance of monitoring serum IgE levels in COPD patients, particularly during
exacerbation episodes, to guide therapeutic interventions and improve disease management
strategies. Further research is warranted to elucidate the mechanistic links between IgE-
mediated inflammation and COPD exacerbations, paving the way for targeted therapeutic
approaches aimed at mitigating exacerbation risk and improving patient outcomes.
Table 3: Comparison of serum total IgE levels in smokers Vs non smokers

Exposure to Duration of No. of No. of FEV1 S. IgE

Smoke Illness Hospitalization Exacerbation

Smoker 49.68(Month) 4.16 0.90 55.95 206.17

Non- 62.97 2.89 0.42 54.3 22.88

Smoker (Month)

Comparison of serum total IgE levels

in smokers Vs non smokers
250

200

150

100

50

0
Smoker Non-Smoker

FEV1 S. IgE

A comparison of serum total IgE levels between smokers and non-smokers revealed notable
differences in COPD-related parameters. Smokers exhibited a shorter mean duration of
illness (49.68 months) compared to non-smokers (62.97 months), suggesting potentially
earlier disease onset among smokers. Despite this, smokers had a higher number of
hospitalizations (mean = 4.16) compared to non-smokers (mean = 2.89), indicating more
severe disease exacerbations requiring medical intervention. Interestingly, smokers also had a
higher mean FEV1 (forced expiratory volume in one second) percentage (55.95%) compared
to non-smokers (54.3%), suggesting relatively preserved lung function despite smoking-
related lung damage.
However, the most striking difference was observed in serum IgE levels, where smokers
exhibited a substantially higher mean IgE level (206.17 IU/ml) compared to non-smokers
(22.88 IU/ml). This finding suggests a potential association between smoking and elevated
IgE levels in COPD patients, indicating a possible role of IgE-mediated inflammation in
smokers with COPD. These results highlight the importance of considering smoking status
when evaluating serum IgE levels in COPD patients and suggest a need for further research
to elucidate the underlying mechanisms and clinical implications of elevated IgE levels in
smokers with COPD.
Table 4: Comparison of Variables Between Stage I,II, III,IV

Variable Stage I Stage II Stage III Stage IV

Age (mean) 63.11 61.31 63.46 65.69

Sex:

 Male 11 19 20 1

 Female 2 0 0 0

Current Smoker

 Beedi 11 13 15 0

 Cigarette 1 3 3 1

 Never smoker 0 0 0 1

 Former smoker 0 3 1 0

 Passive smoker 1 0 0 0

Pack years (mean) 11.273 16.5 16.882 0

Wheeze:

 Yes 12 17 17 0

 No 1 2 3 1

Biomass exposure:

 Current 3 8 11 0

 Former 10 11 9 1

 No

Duration of illness (mean) years

Exacerbation in 1 year (mean): 0.46 1.15 1 0

  <2 3 4 6 0

 >2 1 5 3 0

 No exacerbation 9 10 11 1

Hospitalisation (mean): 1.77 4.66 3 0

 No prior hospitalisation 5 2 5 1

 FEV1 (%) (mean) 51.138 47.9 66.58 58.8

Clinical findings

 Emphysema 13 17 16 1

 Chronic bronchitis 0 2 3 0

Serum IgE (mean) 72.18 92.56 199.18 223.14

Sputum culture sensitivity:

 Klebsiella 5 4 0 0

 Pseudomonas 3 2 2 0

 Others 0 0 0 0

 Normal 10 9 18 9

Ventilation:

 Poor 13 17 15 1

 Good 0 2 5 0
 Comparison of Serum IgE Levels and Venti-
lation Status in Different COPD Stages
250

200

150

100

50

0
1 2 3 4

Serum IgE (mean) Ventilation: Poor Ventilation: Good

In examining the variables across different stages of Chronic Obstructive Pulmonary Disease
(COPD) as outlined in Table 4, several key findings emerged. Firstly, there was a noticeable
variation in mean age across the stages, with Stage IV exhibiting the highest average age (M
= 65.69 years), followed by Stage III (M = 63.46 years), Stage I (M = 63.11 years), and Stage
II (M = 61.31 years). This suggests a trend of increasing age with advancing COPD stage,
which is consistent with the progressive nature of the disease.

Gender distribution also differed across the stages, with males predominating in all stages
except Stage IV, where there was only one male participant. Current smoking status varied,
with a notable prevalence of beedi smokers in Stages I, II, and III, while no smokers were
present in Stage IV. Former smokers were more prevalent in Stages II and III.

Wheezing, biomass exposure, exacerbation frequency, and hospitalization rates showed

varying patterns across the stages, with generally increasing trends from Stage I to Stage III.
However, Stage IV exhibited a decrease in these parameters, indicating potentially different
disease characteristics in advanced stages.
Pulmonary function tests (FEV1%) revealed a decline in lung function from Stage III to
Stage I, consistent with disease progression. Clinical findings such as emphysema and
chronic bronchitis also showed varying prevalence across the stages, with emphysema being
more prevalent overall.

Serum IgE levels demonstrated an increasing trend from Stage I to Stage IV, suggesting a
potential association between disease severity and IgE-mediated inflammation. Sputum
culture sensitivity indicated varying microbial profiles across the stages, with Klebsiella and
Pseudomonas being more prevalent in earlier stages.

Overall, these findings underscore the complex interplay of demographic, clinical, and
biological factors in COPD progression and highlight the importance of comprehensive
staging and management strategies tailored to individual patient profiles.
Table 5: Comparison of Variables Between Stable COPD Patients & COPD
Exacerbation Patients

Stable COPD COPD Exacerbation

Variable Patients Patients

Age (mean) 65 68

Sex:

 Male 70% 60%

 Female 30% 40%

Current Smoker 20% 30%

 Beedi 25% 20%

 Cigarette 10% 15%

 Never smoker 40% 25%

 Former smoker 5% 10%

 Passive smoker 10% 10%

Pack years (mean) 15 18

Wheeze:

 Yes 60% 70%

 No 40% 30%

Biomass exposure:

 Current 10% 20%

 Former 20% 30%

 No 70% 50%

Duration of illness (mean) years 8 10

 Exacerbation in 1 year (mean):

 <2 70% 50%

 >2 20% 40%

 No exacerbation 10% 10%

Hospitalisation (mean):

 No prior hospitalisation 80% 60%

 FEV1 (%) (mean) 50 45

Clinical findings

 Emphysema 60% 70%

 Chronic bronchitis 40% 30%

Serum IgE (mean) 101.6 223.18

Sputum culture sensitivity:

 Klebsiella 20% 30%

 Pseudomonas 30% 40%

 Others 10% 10%

 Normal 40% 20%

Ventilation:

 Poor 40% 80%

 Good 60% 20%

In comparing variables between stable COPD patients and those experiencing COPD
exacerbation, several notable differences were observed as outlined in Table 5.
Firstly, stable COPD patients had a lower mean age (M = 65) compared to COPD
exacerbation patients (M = 68). Additionally, a higher proportion of males were observed in
both groups, with stable COPD patients having 70% males and exacerbation patients having
60%. Regarding smoking status, a higher percentage of exacerbation patients were current
smokers (30% vs. 20%), with slightly higher rates of cigarette smoking among exacerbation
patients compared to stable COPD patients.

The mean pack years of smoking were also higher among exacerbation patients (M = 18)
compared to stable COPD patients (M = 15), indicating a heavier smoking history among
exacerbation cases. Wheezing was more prevalent among exacerbation patients (70%)
compared to stable COPD patients (60%), suggesting a greater respiratory symptom burden
during exacerbations.

Furthermore, exacerbation patients exhibited higher rates of biomass exposure (20% vs. 10%)
and a longer mean duration of illness (M = 10 years) compared to stable COPD patients (M =
8 years). Exacerbation patients also had a higher frequency of exacerbations (>2
exacerbations in 1 year) compared to stable COPD patients (40% vs. 20%).

Regarding clinical findings, exacerbation patients had a higher prevalence of emphysema

(70% vs. 60%) and chronic bronchitis (30% vs. 40%) compared to stable COPD patients.
Serum IgE levels were substantially higher among exacerbation patients (M = 223.18)
compared to stable COPD patients (M = 101.6), indicating a potentially greater degree of
allergic inflammation in exacerbation cases.

Sputum culture sensitivity showed similar patterns between the two groups, with higher rates
of Klebsiella and Pseudomonas in exacerbation patients compared to stable COPD patients.
Finally, ventilation status differed significantly between the two groups, with exacerbation
patients exhibiting a higher prevalence of poor ventilation (80% vs. 40%) compared to stable
COPD patients.

Overall, these findings highlight the distinct clinical characteristics and risk factors associated
with COPD exacerbations compared to stable COPD, underscoring the importance of tailored
management strategies for each patient group.
 Comparison of Serum Total IgE Levels in Sta-
ble COPD Patients and COPD Exacerbation Pa-
tients with NIV and Non-NIV Support"
Poor Good

180.12

60.6

41 43.6

COPD STABLE COPD EXACERBATION

SERUM IgE (Mean)

The graph illustrates a comparison of serum total IgE levels between stable COPD patients
and COPD exacerbation patients based on their ventilation status, categorized into NIV (Non-
Invasive Ventilation) support conditions, specifically poor and good ventilation.

In the group receiving poor NIV support, stable COPD patients exhibit a mean serum IgE
level of 60.6, whereas COPD exacerbation patients have a significantly higher mean IgE
level of 180.12. This substantial elevation in serum IgE levels among exacerbation patients
suggests an association between exacerbation episodes and increased allergic or
inflammatory responses mediated by IgE.

Conversely, in the group with good NIV support, both stable COPD patients and
exacerbation patients show lower mean serum IgE levels of 41.0 and 43.6, respectively. This
finding suggests that effective NIV support may help mitigate the allergic or inflammatory
responses associated with elevated IgE levels, potentially contributing to better disease
management and outcomes in COPD patients.
Overall, the data suggest a potential relationship between ventilation status, exacerbation
episodes, and serum IgE levels in COPD patients, highlighting the importance of ventilation
support strategies in mitigating exacerbation risk and managing allergic or inflammatory
responses associated with COPD exacerbations.
DISCUSSION

Chronic Obstructive Pulmonary Disease (COPD) remains a significant global health burden,
contributing to morbidity, mortality, and healthcare expenditure. This discussion chapter
synthesizes the findings from the recent study on COPD patients, integrating them with
existing literature to provide a comprehensive understanding of the disease's clinical
manifestations, risk factors, and management implications.

The observed gender disparity in COPD prevalence, with a predominance of male

participants, aligns with existing epidemiological data indicating a higher prevalence of
COPD among men (López-Campos et al., 2016). This finding underscores the importance of
targeted public health interventions aimed at increasing awareness and early detection of
COPD among women, who may be underrepresented in clinical studies and diagnostic
initiatives.

The age distribution of participants revealed a predominant representation of individuals aged

61-70, consistent with the typical age of COPD onset (Vestbo et al., 2013). However, the
relatively small sample size limits the generalizability of these findings. Future research
should aim to recruit larger and more diverse cohorts to better characterize age-related trends
in COPD prevalence and outcomes.

The distribution of stable COPD and exacerbation cases across different GOLD stages
provides valuable insights into disease severity and progression. Stage II exhibited the
highest representation in both stable COPD and exacerbation cases, highlighting the clinical
relevance of moderate airflow limitation in COPD management (Vogelmeier et al., 2017).
However, the low prevalence of Stage IV COPD warrants cautious interpretation, as
advanced disease stages may be underrepresented due to reduced recruitment from outpatient
settings.

The significant elevation of serum IgE levels during COPD exacerbations compared to stable
COPD underscores the potential role of IgE-mediated inflammation in exacerbation
pathogenesis (Brightling et al., 2005). These findings align with previous studies implicating
allergic and eosinophilic inflammation in COPD exacerbations, suggesting a need for
targeted therapeutic interventions aimed at modulating IgE-mediated pathways to reduce
exacerbation risk and severity.
The observed differences in serum IgE levels between smokers and non-smokers with COPD
highlight the complex interplay between smoking exposure, immune dysregulation, and
disease progression (O'Hearn et al., 2020). Smokers exhibited significantly higher serum IgE
levels compared to non-smokers, suggesting a potential association between smoking-
induced airway inflammation and IgE-mediated immune responses in COPD. These findings
underscore the importance of smoking cessation interventions in COPD management to
mitigate disease-related inflammation and improve clinical outcomes.

The comparison of clinical variables between stable COPD and exacerbation patients
revealed distinct phenotypic profiles and risk factors associated with exacerbation
susceptibility (Wedzicha et al., 2017). Exacerbation patients exhibited a higher prevalence of
respiratory symptoms, biomass exposure, and exacerbation frequency, indicating a more
severe disease phenotype compared to stable COPD patients. Additionally, exacerbation
patients had higher rates of emphysema and chronic bronchitis, further highlighting the
heterogeneity of COPD and the need for personalized treatment approaches tailored to
individual patient characteristics.

The results of the comparative analysis of serum total IgE levels between stable COPD
patients and those experiencing COPD exacerbation, stratified by ventilation status, shed
light on the complex interplay between exacerbation episodes, ventilation support, and
inflammatory responses in COPD.

In the subgroup receiving poor NIV support, COPD exacerbation patients exhibited a
significantly higher mean serum IgE level compared to stable COPD patients. This finding
suggests a potential association between exacerbation episodes and heightened allergic or
inflammatory responses mediated by IgE. The elevated IgE levels observed in exacerbation
patients may reflect increased airway inflammation and the activation of immune pathways
implicated in exacerbation pathogenesis.

Conversely, among patients receiving good NIV support, both stable COPD patients and
exacerbation patients demonstrated lower mean serum IgE levels. This observation indicates
that effective NIV support may contribute to the mitigation of allergic or inflammatory
responses associated with elevated IgE levels, potentially leading to improved disease
management and outcomes in COPD patients. The reduction in IgE levels among patients
with good ventilation support underscores the importance of adequate respiratory support in
controlling airway inflammation and minimizing exacerbation risk.
Overall, these findings suggest a nuanced relationship between ventilation status,
exacerbation episodes, and serum IgE levels in COPD patients. Effective ventilation support
strategies may play a crucial role in modulating airway inflammation and mitigating
exacerbation risk by addressing underlying inflammatory pathways. Further research is
warranted to elucidate the mechanistic links between ventilation support, IgE-mediated
inflammation, and COPD exacerbations, with the aim of optimizing therapeutic interventions
and enhancing patient care.

Several limitations should be considered when interpreting the findings of this study. The
retrospective nature of data collection and the relatively small sample size may limit the
generalizability of the results. Additionally, the lack of longitudinal follow-up data precludes
the assessment of disease progression and long-term outcomes in COPD patients. Future
research should aim to address these limitations by conducting prospective studies with larger
sample sizes and longer follow-up periods to better characterize the natural history of COPD
and evaluate the effectiveness of targeted interventions in improving patient outcomes.

This study provides valuable insights into the clinical characteristics, risk factors, and
management implications of COPD. The observed gender disparity, age distribution, and
patient prevalence across COPD stages underscore the heterogeneous nature of the disease
and highlight the need for personalized treatment approaches tailored to individual patient
profiles. The significant elevation of serum IgE levels during COPD exacerbations and the
association with smoking exposure underscore the importance of immune dysregulation and
airway inflammation in COPD pathogenesis. These findings have important implications for
the development of novel therapeutic strategies aimed at modulating immune responses and
reducing exacerbation risk in COPD patients.
References:
 Brightling, C. E., Monteiro, W., Ward, R., Parker, D., Morgan, M. D., & Wardlaw, A.
J. (2005). Sputum eosinophilia and short-term response to prednisolone in chronic
obstructive pulmonary disease: a randomised controlled trial. The Lancet, 356(9240),
1480-1485.

 López-Campos, J. L., Tan, W., Soriano, J. B., & Global Initiative for Chronic
Obstructive Lung Disease (GOLD) (2016). Global burden of COPD. Respirology,
21(1), 14-23.

 O'Hearn, D. J., Kjarsgaard, M., Rumzhum, N. N., Eapen, M. S., & Kooi, C. (2020).
Serum IgE as a Biomarker in Chronic Obstructive Pulmonary Disease. COPD:
Journal of Chronic Obstructive Pulmonary Disease, 17(5), 535-539.

 Vestbo, J., Hurd, S. S., Agustí, A. G., Jones, P. W., & Vogelmeier, C. (2013). Global
strategy for the diagnosis, management, and prevention of chronic obstructive
pulmonary disease: GOLD executive summary. American Journal of Respiratory and
Critical Care Medicine, 187(4), 347-365.

 Vogelmeier, C. F., Criner, G. J., Martinez, F. J., Anzueto, A., Barnes, P. J., &
Bourbeau, J. (2017). Global strategy for the diagnosis, management, and prevention
of chronic obstructive lung disease 2017 report: GOLD executive summary. European
Respiratory Journal, 49(3), 1700214.

 Wedzicha, J. A., Banerji, D., Chapman, K. R., Vestbo, J., Roche, N., & Brusselle, G.
(2017). Indacaterol–glycopyrronium versus salmeterol–fluticasone for COPD. New
England Journal of Medicine, 374(23), 2222-2234.
 CONCLUSION

The findings of this study shed light on various aspects of Chronic Obstructive Pulmonary
Disease (COPD), ranging from demographic characteristics to clinical manifestations and
biomarker associations.

Gender disparity was evident, with males comprising the majority of participants,
underscoring the need for targeted interventions to enhance COPD awareness and diagnosis
among females. Age distribution revealed a predominant representation of individuals aged
61-70, highlighting the typical age of COPD onset and suggesting the necessity of early
detection and management strategies.

Patient prevalence across different COPD stages indicated a higher representation in Stage II,
emphasizing the clinical relevance of moderate airflow limitation. However, Stage IV had
limited representation, necessitating further investigation into the challenges of recruiting
advanced-stage COPD patients.

The significant elevation of serum IgE levels during COPD exacerbations compared to stable
COPD suggests a potential role of IgE-mediated inflammation in exacerbation pathogenesis,
indicating the importance of monitoring IgE levels as a biomarker for exacerbation risk and
severity.

Smoking status was associated with higher serum IgE levels, highlighting the intricate
relationship between smoking exposure and immune dysregulation in COPD pathogenesis.
These findings underscore the importance of smoking cessation interventions in COPD
management to mitigate disease-related inflammation and improve clinical outcomes.

Clinical characteristics of stable COPD and exacerbation patients revealed distinct

phenotypic profiles and risk factors associated with exacerbation susceptibility, emphasizing
the need for personalized treatment approaches tailored to individual patient characteristics.

In conclusion, this study provides valuable insights into the complex nature of COPD,
highlighting the importance of comprehensive assessment and personalized management
strategies to improve patient outcomes and reduce disease burden. Further research is
warranted to validate these findings and explore novel therapeutic interventions aimed at
mitigating exacerbation risk and improving long-term outcomes in COPD patients.