Unmasking the Silent Threat: Periodontal Health's Impact on COPD Severity and Hospitalization.

OBJECTIVE: This study investigated the relationship between chronic obstructive pulmonary disease (COPD) and periodontitis, focusing on how periodontal health impacts COPD airflow limitation, exacerbations, and hospitalization. BACKGROUND: Periodontitis, a multifactorial inflammatory disease, is characterized by destruction of tooth-supporting structures, while COPD is a global pulmonary disorder with high mortality. METHODS: A total of 199 COPD patients aged over 40 years underwent lung function tests (spirometry), 6 min walk test, and St George's Respiratory Questionnaire-COPD (SGRQ-C) to assess lung health. Periodontal indices such as probing depth (PD), clinical attachment loss (CAL), and plaque index (PI) were assessed. RESULTS: We found a significant negative correlation between periodontal disease severity and lung function (lower FEV1, FVC, and FEV1/FVC ratio) after adjusting for smoking. Likewise, periodontal parameters (PPD, PI, and CAL) exhibited negative correlations with lung function. These periodontal indices were independently associated with airflow limitation severity, exacerbations frequency, and prior-year hospitalization. Linear regression indicated that each unit increase in PPD, PI, and CAL corresponded to estimated increases in GOLD airflow limitation grading (0.288, 0.718, and 0.193, respectively) and number of exacerbations (0.115, 0.041, and 0.109, respectively). In logistic regression, PPD, PI, and CAL adjusted odds ratios (ORs) were estimated to increase by 1.29 (95%CI: 1.03-1.62), 3.04 (95%CI: 1.28-7.2), and 1.26 (95%CI: 1.06-1.49), respectively, for hospitalization in previous year. CONCLUSION: Periodontitis is associated with COPD airflow limitation, exacerbation, and hospitalization, with PI being the most clinically relevant periodontal factor. Dentists and physicians should monitor and increase awareness among COPD patients to maintain oral hygiene for prevention of periodontal diseases and mitigate its effect on COPD progression.

Effects of Ambient Air Pollutants on Hospital Admissions among Children Due to Asthma and Wheezing-Associated Lower Respiratory Infections in Mysore, India: A Time Series Study.

Air pollutants are known to trigger asthma and wheezing-associated lower respiratory infections in children, but evidence regarding their effect on hospital admissions in India is limited. We conducted a time-series study over a period of five years to assess the role of ambient air pollutants in daily asthma-related hospital admissions in children in Mysore, India. Daily asthma and wheeze (associated with lower respiratory infections) admissions were modelled using a generalised additive model (GAM) to examine the non-linear effects and generalised linear models (GLM) for linear effects, if any. Models were adjusted by day of the week and lag days, with smooth terms for time, maximum temperature, and relative humidity, and they were stratified by sex and age group. Of the 362 children admitted, more than 50% were boys, and the mean age was 5.34 years (±4.66). The GAMs showed non-linear associations between NO2, PM2.5, and NH3. For example, a 10 µgm-3 (or 10%) increase in NO2 increased admissions by 2.42. These non-linear effects were more pronounced in boys. A linear effect was detected for PM10 with a relative risk (95% CI) of 1.028, 1.013, and 1.043 with admission. Further research is needed to explore whether these findings can be replicated in different cities in India. Air pollution needs to be controlled, and policies that focus on lower cut-off levels for vulnerable populations are necessary.

Hematological Parameters for Predicting Mortality in Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

(1) Introduction: COPD is a common and serious condition affecting a significant proportion of the population globally. Patients often suffer from exacerbations which lead to the worsening of their health status and respiratory function, and can often lead to death. Quick and cheap investigations are required that are capable of predicting mortality in patients with acute exacerbations that can be applied in low resource settings. (2) Materials and methods: This was a retrospective study carried out using hospital records of patients admitted for AECOPD from 1 January 2017 to 30 November 2022. Chi-square test (for sex) and Student's t-test were used to look for significant associations. Receiver Operating Characteristics (ROC) curves were plotted and Area Under Curve (AUC) values were calculated for various hematological parameters. Youden's J was used to identify the ideal cut-off with optimal sensitivity and specificity. Multivariate Cox regression was used to identify independent hematological predictors of mortality. Kaplan-Meir survival plots for neutrophil lymphocyte ratio (NLR) with the optimal cut-off were plotted. (3) Results: Amongst the 500 patients, 42 died while 458 survived, giving a mortality rate of 8.4%. NLR had the strongest association with mortality. The cut-off for various parameters were: NLR 14.83 (AUC 0.73), total leukocyte count (TLC) 13,640 cells/mm3 (AUC 0.60), absolute neutrophil count (ANC) 12,556 cells/mm3 (AUC 0.62), derived NLR (dNLR) 9.989 (AUC 0.73), hemoglobin 11.8 mg/dL (AUC 0.59), packed cell volume (PCV) 36.6% (AUC 0.60), and platelet lymphocyte ratio (PLR) 451.32 (AUC 0.55). (4) Conclusions: In patients with acute exacerbation of COPD, NLR was strongly associated with mortality, followed by dNLR. Cox regression identified NLR as an independent predictor of mortality.

Circulatory Serum Krebs von Den Lungen-6 and Surfactant Protein-D Concentrations Predict Interstitial Lung Disease Progression and Mortality.

There is a need for biomarkers to predict outcomes, including mortality, in interstitial lung disease (ILD). Krebs von den Lungen-6 (KL-6) and surfactant protein D (SP-D) are associated with lung damage and fibrosis in all ILDs and are related to important clinical outcomes. Though these two biomarkers have been associated with ILD outcomes, there are no studies that have evaluated their predictive potential in combination. This study aims to determine whether KL-6 and SP-D are linked to poor disease outcomes and mortality. Additionally, we plan to examine whether changes in KL-6 and SP-D concentrations correspond with changes in lung function and whether serial measurements improve their predictive potential to identify disease progression and mortality. Forty-four patients with ILD participated in a prospective 6-month longitudinal observational study. ILD patients who succumbed had the highest KL-6 levels (3990.4 U/mL (3490.0-4467.6)) and highest SP-D levels (256.1 ng/mL (217.9-260.0)), followed by those who deteriorated: KL-6 levels 1357.0 U/mL (822.6-1543.4) and SP-D levels 191.2 ng/mL (152.8-210.5). The generalized linear model (GLM) analysis demonstrated that changes in forced vital capacity (FVC), diffusing capacity of lungs for carbon monoxide (DLCO), forced expiratory volume in 1 s (FEV1), and partial pressure of arterial oxygen (PaO2) were correlated to changes in KL6 (p = 0.016, 0.014, 0.027, 0.047) and SP-D (p = 0.008, 0.012, 0.046, 0.020), respectively. KL-6 (odds ratio (OR): 2.87 (1.06-7.79)) and SPD (OR: 1.76 (1.05-2.97)) were independent predictors of disease progression, and KL-6 (hazard ratio (HR): 3.70 (1.46-9.41)) and SPD (HR: 2.58 (1.01-6.59)) were independent predictors of death by Cox regression analysis. Combined biomarkers (KL6 + SPD + CT + FVC) had the strongest ability to predict disease progression (AUC: 0.797) and death (AUC: 0.961), on ROC analysis. Elevated KL-6 and SPD levels are vital biomarkers for predicting the severity, progression, and outcomes of ILD. High baseline levels or an increase in levels over a six-month follow-up despite treatment indicate a poor prognosis. Combining KL6 and SPD with conventional measures yields a more potent prognostic indicator. Clinical studies are needed to test additional interventions, and future research will determine if this combined biomarker benefits different ethnicities globally.

Association between ADAM33 Single-Nucleotide Polymorphisms and Treatment Response to Inhaled Corticosteroids and a Long-Acting Beta-Agonist in Asthma.

ADAM33 has been linked to airway structural changes in patients with asthma, leading to airway hyperresponsiveness, narrowing, and ultimately poor treatment responsiveness. This study aimed to evaluate the genetic association of ADAM33 SNPs with asthma, disease severity, and treatment responsiveness to ICS+LABA in the South Indian population. In this case-control study (486 controls and 503 cases), we performed genotyping using MassArray for six SNPs of ADAM33, namely rs2280091, rs2787094, rs3918396, rs67044, rs2853209, and rs3918392. We studied the association with asthma and treatment responsiveness to ICS+LABA, using genotype, allele frequency distribution, and haplotype analysis. A significant clinical finding of the study was that certain patients in the disease severity group (moderate and mild) showed poor or no improvement after a three-month follow-up of regular ICS+LABA therapy. Of the studied ADAM33 SNPs, rs2853209 showed an association with asthma. The further analysis of asthma patients according to disease severity suggested an association between moderate disease and the minor allele "T" for rs2853209. The homozygous minor allele of SNP rs2787094 was found to be associated with poorer lung function and the least lung-function improvement after three months of ICS+LABA therapy. The haplotype analysis of six SNPs showed a significant association between the rs2853209 and rs3918396 blocks and asthma. ADAM33 gene polymorphism has clinical relevance in terms of disease association and response to treatment. SNP rs2853209 seemed most relevant to asthma, and SNP rs2787094 could be a genetic marker for predicting response to ICS+LABA therapy in the study population.

The Assessment of Serum Fibronectin Levels as a Potential Biomarker for the Severity of Drug-Sensitive Pulmonary Tuberculosis: A Pilot Study.

BACKGROUND: Tuberculosis (TB) is a global health burden caused by Mycobacterium tuberculosis (Mtb) infection. Fibronectin (Fn) facilitates Mtb attachment to host cells. We studied the Fn levels in smear-positive TB patients to assess its correlation with disease severity based on sputum smears and chest X-rays. METHODS: Newly detected consecutive sputum AFB-positive pulmonary TB patients (n = 78) and healthy control subjects (n = 11) were included. The mycobacterial load in the sputum smear was assessed by IUATLD classification, ranging from 0 to 3. The severity of pulmonary involvement was assessed radiologically in terms of both the number of zones involved (0-6) and as localized (up to 2 zones), moderate (3-4 zones), or extensive (5-6 zones). The serum human fibronectin levels were measured by using a commercially available enzyme-linked immunosorbent assay (ELISA) kit (Catalogue No: CK-bio-11486, Shanghai Coon Koon Biotech Co., Ltd., Shanghai, China). RESULTS: The PTB patients showed lower Fn levels (102.4 ± 26.7) compared with the controls (108.8 ± 6.8), but they were not statistically significant. Higher AFB smear grades had lower Fn levels. The chest X-ray zones involved were inversely correlated with Fn levels. The Fn levels, adjusted for age and gender, decreased with increased mycobacterial load and the number of chest radiograph zones affected. A Fn level <109.39 g/mL predicted greater TB severity (sensitivity of 67.57% and specificity of 90.38%), while a level <99.32 pg/mL predicted severity based on the chest radiology (sensitivity of 84.21% and specificity of 100%). CONCLUSIONS: The Fn levels are lower in tuberculosis patients and are negatively correlated with severity based on sputum mycobacterial load and chest radiographs. The Fn levels may serve as a potential biomarker for assessing TB severity, which could have implications for early diagnosis and treatment monitoring.

Trends in the Bacterial Prevalence and Antibiotic Resistance Patterns in the Acute Exacerbation of Chronic Obstructive Pulmonary Disease in Hospitalized Patients in South India.

Exacerbation due to antimicrobial-drug-resistant bacteria among chronic obstructive pulmonary disease (AECOPD) patients contributes to mortality and morbidity. We examined the prevalence of the bacterial organisms and trends in drug resistance in AECOPD. In this retrospective study, between January 2016 to December 2020, among 3027 AECOPD patients, 432 (14.3%) had bacteria isolated. The regression and generalized estimating equations (GEE) were used for trends in the resistance patterns over five years, adjusting for age, gender, and comorbidities. Klebsiella pneumoniae (32.4%), Pseudomonas aeruginosa (17.8%), Acinetobacter baumannii (14.4%), Escherichia coli (10.4%), and Staphylococcus aureus (2.5%) were common. We observed high levels of drug resistance in AECOPD patients admitted to ICU (87.8%) and non-ICU (86.5%). A Cox proportional hazard analysis, observed infection with Acinetobacter baumannii and female sex as independent predictors of mortality. Acinetobacter baumannii had 2.64 (95% confidence interval (CI): 1.08−6.43) higher odds of death, compared to Klebsiella pneumoniae. Females had 2.89 (95% CI: 1.47−5.70) higher odds of death, compared to males. A high proportion of bacterial AECOPD was due to drug-resistant bacteria. An increasing trend in drug resistance was observed among females.

Association of Serum Albumin and Copeptin with Early Clinical Deterioration and Instability in Community-Acquired Pneumonia.

Background: There is a paucity of data on biomarkers for the early deterioration and clinical instability of patients in community-acquired pneumonia (CAP), as treatment failure occurs in the first seven days in 90% of patients. Aim: To evaluate serum albumin and copeptin with CURB-65, PSI scoring and ATS/IDSA minor criteria for the prediction of early mortality or ICU-admission (7 days) and clinical instability after 72 h. Methods: In 100 consecutive hospitalized adult CAP patients, PSI-scores, CURB-65 scores, ATS/IDSA 2007 minor criteria, copeptin and albumin on admission were evaluated. Univariate and multivariate Cox regression analysis was performed to assess independent risk factors for early combined mortality or ICU admission. Predictive powers of albumin and copeptin were tested with ROC curves and ICU-free survival probability was tested using Kaplan−Meier analysis. Results: Albumin was lower and copeptin higher in patients with short-term adverse outcomes (p < 0.05). Cox regression analysis showed that albumin [HR (95% CI): 0.41 (0.18−0.94, p = 0.034)] and copeptin [HR (95% CI): 1.94 (1.03−3.67, p = 0.042)] were independent risk factors for early combined mortality or ICU admission (7 days). The Kaplan−Meier analysis observed that high copeptin (>27.12 ng/mL) and low albumin levels (<2.85 g/dL) had a lower (p < 0.001) survival probability. The diagnostic accuracy of albumin was better than copeptin. The inclusion of albumin and copeptin into ATS/IDSA minor criteria significantly improved their predictive power. Conclusions: Both biomarkers serum albumin and copeptin can predict early deterioration and clinical instability in hospitalized CAP patients and increase the prognostic power of the traditional clinical scoring systems.

Willingness to Accept the COVID-19 Vaccine and Related Factors among Indian Adults: A Cross-Sectional Study.

To achieve herd immunity to a disease, a large portion of the population needs to be vaccinated, which is possible only when there is broad acceptance of the vaccine within the community. Thus, policymakers need to understand how the general public will perceive the vaccine. This study focused on the degree of COVID-19 vaccine hesitancy and refusal and explored sociodemographic correlations that influence vaccine hesitancy and refusal. A cross-sectional online survey was conducted among the adult population of India. The survey consisted of basic demographic questions and questions from the Vaccination Attitudes Examination (VAX) Scale. Multinomial logistical regression was used to identify correlates of vaccine hesitancy and refusal. Of the 1582 people in the study, 9% refused to become vaccinated and 30.8% were hesitant. We found that both hesitancy and refusal predictors were nearly identical (lower socioeconomic status, female gender, and older age groups), except for three groups (subjects aged 45−64 years, those with approximate income <10,000 INR/month, and those residing in rural households) that showed slightly higher odds of vaccine hesitancy than refusal. We need to address the underlying sociodemographic determinants and formulate public awareness programs to address specific subgroups that are at higher risk of rejecting the vaccine and convert those who are undecided or hesitant into those willing to accept the vaccine.

Circulating Secretoglobin Family 1A Member 1 (SCGB1A1) Levels as a Marker of Biomass Smoke Induced Chronic Obstructive Pulmonary Disease.

Secretoglobin family 1A member 1 (SCGB1A1) alternatively known as club cell protein 16 is a protective pneumo-protein. Decreased serum levels of SCGB1A1 have been associated with tobacco smoke induced chronic obstructive pulmonary disease (TS-COPD). Exposure to biomass smoke (BMS) is an important COPD risk factor among women in low and lower-middle income countries. Therefore, in a cross-sectional study (n = 50/group; total 200 subjects) we assessed serum SCGB1A1 levels in BMS-COPD subjects (11 male, 39 female) compared to TS-COPD (all male) along with TS-CONTROL (asymptomatic smokers, all male) and healthy controls (29 male, 21 female) in an Indian population. Normal and chronic bronchitis like bronchial mucosa models developed at the air-liquid interface using human primary bronchial epithelial cells (3 donors, and three replicates per donor) were exposed to cigarette smoke condensate (CSC; 0.25, 0.5, and 1%) to assess SCGB1A1 transcript expression and protein secretion. Significantly (p < 0.0001) decreased serum SCGB1A1 concentrations (median, interquartile range, ng/mL) were detected in both BMS-COPD (1.6; 1.3-2.4) and TS-COPD (1.8; 1.4-2.5) subjects compared to TS-CONTROL (3.3; 2.9-3.5) and healthy controls (5.1; 4.5-7.2). The levels of SCGB1A1 were positively correlated (r = 0.7-0.8; p < 0.0001) with forced expiratory volume in 1 s, forced vital capacity, their ratios, and exercise capacity. The findings are also consistent within the BMS-COPD sub-group as well. Significantly (p < 0.03) decreased SCGB1A1 concentrations were detected with severity of COPD, dyspnea, quality of life, and mortality indicators. In vitro studies demonstrated significantly (p < 0.05) decreased SCGB1A1 transcript and/or protein levels following CSC exposure. Circulating SCGB1A1 levels may therefore also be considered as a potent marker of BMS-COPD and warrant studies in larger independent cohorts.

Putative Systemic Biomarkers of Biomass Smoke-Induced Chronic Obstructive Pulmonary Disease among Women in a Rural South Indian Population.

RATIONALE: Exposure to biomass smoke (BMS) has been implicated in chronic obstructive pulmonary disease (COPD). About 3 billion people worldwide use biomass fuel for cooking and heating. Women in rural communities of low- and lower-middle-income countries are disproportionately exposed to massive amounts of BMS during active cooking hours (4-6 h/day). Therefore, BMS exposure is considered as a risk factor for COPD in the same order of magnitude as tobacco smoke. In rural India, due to cultural reasons, women are the primary cook of the family and are mostly nonsmokers. Thus, BMS-induced COPD is predominant among rural Indian women. However, BMS-COPD remains a relatively unexplored health problem globally. Therefore, we investigated the serum chemokine and cytokine signatures of BMS-COPD and tobacco smoke-induced COPD (TS-COPD) patients compared to their control in a rural South Indian population for this field study. METHODS: Concentrations of 40 serum chemokines and cytokines were measured using a multiplexed immunoassay. The study cohort consisted of BMS-COPD (female; n = 29) and BMS-exposed subjects without COPD (BMS-CONTROL; female; n = 24). For comparison, data from TS-COPD patients (male, n = 23) and tobacco smokers without COPD (TS-CONTROL; male, n = 22) were investigated. Subjects were matched for age, sex, and biomass exposure. Tobacco consumption was slightly higher in TS-COPD subjects compared to TS-CONTROL. BMS-exposed and TS-exposed subjects (currently exposed) were from the same locality with similar dwelling habits and socioeconomic status. A validated structured questionnaire-based survey and spirometry was performed. An additional control group with no tobacco and BMS exposure (TS-BMS-CONTROL; n = 15) was included. Statistical significance was set at p ≤ 0.01. RESULTS: Serum median concentrations (pg/ml) of CCL15 [8799.35; 5977.22], CCL27 [1409.14; 1024.99], and CXCL13 [37.14; 26.03] were significantly higher in BMS-CONTROL compared to BMS-COPD subjects. Nine analytes exhibited higher concentrations in TS-CONTROL compared to TS-COPD subjects. Comparison of chemokine and cytokine concentrations among BMS-COPD versus TS-COPD and BMS-CONTROL versus TS-CONTROL subjects also revealed distinct molecular signatures. CONCLUSION: Our data identifies CCL27 and CXCL13 as putative, plausibly homeostatic/protective biomarkers for BMS-COPD within the investigated population that warrants validation in larger and multiple cohorts. The findings further indicate exposure-specific systemic response of chemokines and cytokines.