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Parthasarathi Bhattacharyya

Bio: Parthasarathi Bhattacharyya is an academic researcher from R. G. Kar Medical College and Hospital. The author has contributed to research in topics: Medicine & COPD. The author has an hindex of 10, co-authored 44 publications receiving 261 citations.


Papers
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Journal ArticleDOI
TL;DR: The proposed multichannel asthma detection method, where the presence of wheeze in lung sound is not a necessary requirement, outperforms commonly used lung sound classification methods in this field and provides significant relative improvement.

43 citations

Journal ArticleDOI
TL;DR: The energy metabolites, cholesterol and fatty acids correlated significantly with the immunological mediators, suggesting existence of a possible link between the inflammatory status of these patients and impaired metabolism.
Abstract: Asthma-COPD overlap (ACO) refers to a group of poorly studied and characterised patients reporting with disease presentations of both asthma and COPD, thereby making both diagnosis and treatment challenging for the clinicians. They exhibit a higher burden in terms of both mortality and morbidity in comparison to patients with only asthma or COPD. The pathophysiology of the disease and its existence as a unique disease entity remains unclear. The present study aims to determine whether ACO has a distinct metabolic and immunological mediator profile in comparison to asthma and COPD. Global metabolomic profiling using two different groups of patients [discovery (D) and validation (V)] were conducted. Serum samples obtained from moderate and severe asthma [n = 34(D); n = 32(V)], moderate and severe COPD [n = 30(D); 32(V)], ACO patients [n = 35(D); 40(V)] and healthy controls [n = 33(D)] were characterized using gas chromatography mass spectrometry (GC-MS). Multiplexed analysis of 25 immunological markers (IFN-γ (interferon gamma), TNF-α (tumor necrosis factor alpha), IL-12p70 (interleukin 12p70), IL-2, IL-4, IL-5, IL-13, IL-10, IL-1α, IL-1β, TGF-β (transforming growth factor), IL-6, IL-17E, IL-21, IL-23, eotaxin, GM-CSF (granulocyte macrophage-colony stimulating factor), IFN-α (interferon alpha), IL-18, NGAL (neutrophil gelatinase-associated lipocalin), periostin, TSLP (thymic stromal lymphopoietin), MCP-1 (monocyte chemoattractant protein- 1), YKL-40 (chitinase 3 like 1) and IL-8) was also performed in the discovery cohort. Eleven metabolites [serine, threonine, ethanolamine, glucose, cholesterol, 2-palmitoylglycerol, stearic acid, lactic acid, linoleic acid, D-mannose and succinic acid] were found to be significantly altered in ACO as compared with asthma and COPD. The levels and expression trends were successfully validated in a fresh cohort of subjects. Thirteen immunological mediators including TNFα, IL-1β, IL-17E, GM-CSF, IL-18, NGAL, IL-5, IL-10, MCP-1, YKL-40, IFN-γ, IL-6 and TGF-β showed distinct expression patterns in ACO. These markers and metabolites exhibited significant correlation with each other and also with lung function parameters. The energy metabolites, cholesterol and fatty acids correlated significantly with the immunological mediators, suggesting existence of a possible link between the inflammatory status of these patients and impaired metabolism. The present findings could be possibly extended to better define the ACO diagnostic criteria, management and tailoring therapies exclusively for the disease.

35 citations

Journal ArticleDOI
TL;DR: The findings suggest that ACO has an enhanced energy and metabolic burden associated with it as compared to asthma and COPD.
Abstract: Asthma-chronic obstructive pulmonary disease (COPD) overlap, termed as ACO, is a complex heterogeneous disease without any clear diagnostic or therapeutic guidelines. The pathophysiology of the disease, its characteristic features, and existence as a unique disease entity remains unclear. Individuals with ACO have a faster lung function decline, more frequent exacerbations, and worse quality of life than those with COPD or asthma alone. The present study aims to determine whether ACO has a distinct metabolic profile in comparison to asthma and COPD. Two different groups of patients were recruited as discovery (D) and validation (V) cohorts. Serum samples obtained from moderate and severe asthma patients diagnosed as per GINA guidelines [n = 34(D); n = 32(V)], moderate and severe COPD cases identified by GOLD guidelines [n = 30(D); 32(V)], ACO patients diagnosed by joint GOLD and GINA guidelines [n = 35(D); 40(V)] and healthy controls [n = 33(D)] were characterized using nuclear magnetic resonance (NMR) spectrometry. Multivariate and univariate analysis indicated that 12 metabolites [lipid, isoleucine, N-acetylglycoproteins (NAG), valine, glutamate, citric acid, glucose, l-leucine, lysine, asparagine, phenylalanine and histidine] were dysregulated in ACO patients when compared with both asthma and COPD. These metabolites were further validated in a fresh cohort of patients, which again exhibited a similar expression pattern. Our findings suggest that ACO has an enhanced energy and metabolic burden associated with it as compared to asthma and COPD. It is anticipated that our results will stimulate researchers to further explore ACO and unravel the pathophysiological complexities associated with the disease.

26 citations

Journal ArticleDOI
TL;DR: Frequency of osteoporosis and osteopenia was found to be very high (73%) in the population of advanced COPD, which suggest a need for further in-depth study regarding the issue.
Abstract: Background: Reduction of bone mineral density (BMD) is a known and established phenomenon in chronic obstructive pulmonary disease (COPD). However, there have been no data regarding osteoporosis/osteopenia in COPD patients in India. Aim: To look for the degree and frequency of osteoporosis/osteopenia in our OPD patients being diagnosed as COPD. Materials and Methods: Thirty-seven randomly selected patients with COPD were assessed for BMD with commercially available ultrasound bone densitometer (HOLOGIC SAHARA) in a pulmonary OPD. Some cofactors for reduced BMD were also noted. Results: Out of the 37 COPD (all belonging to the GOLD III/IV category) patients studied, the BMD was found to be normal in 10 (27%) patients, while 27 (73%) patients were found to have osteopenia/osteoporosis [19 (51.35%) and 8 (21.62%) patients having osteopenia and osteoporosis, respectively]. Conclusion: Frequency of osteoporosis and osteopenia was found to be very high (73%) in our population of advanced COPD. The data suggest a need for further in-depth study regarding the issue.

25 citations

Journal ArticleDOI
TL;DR: Bronchoscopically punctured transbronchial decompression of emphysematous bullae can be an effective therapeutic option and warrants further investigation.
Abstract: Bullae are common accompaniments of chronic obstructive pulmonary disease especially emphysema. They contribute to increased lung volume and worsen the mechanical disadvantage of the inspiratory muscles by increasing the residual volume (RV) and RV/total lung capacity ratio. Thus effective decompression of a large bulla or bullae is thus important to improve the lung function of affected patients and also to provide symptomatic relief. Surgery and thoracoscopy are two commonly performed procedures used to treat bullae. Although bronchoscopic lung volume reduction has been successfully accomplished for emphysema, isolated decompression of bullae bronchoscopically has not been tried to date. A large emphysematous bulla in the left lower lobe of a surgically unfit patient was bronchoscopically punctured with a transbronchial aspiration needle; the position of the needle inside the bulla was confirmed and the air from the bulla was aspirated slowly to allow collapse. Finally, some autologous blood was instilled into the bulla before the needle was withdrawn. The patient had immediate and sustained symptomatic relief with significant improvement in lung function. Bronchoscopic transbronchial decompression of emphysematous bullae can be an effective therapeutic option and warrants further investigation.

24 citations


Cited by
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Journal Article
TL;DR: In the article the authors describe changes in airways wall in asthmatic patients and their clinical consequences.
Abstract: Asthma is a chronic inflammatory disease of the airways in which many cell types play a role. These cells are involved in the regulation of the airways inflammation and initiate the process of remodelling by the release of cytokines and growth factors. In the article the authors describe changes in airways wall in asthmatic patients and their clinical consequences.

441 citations

Journal ArticleDOI
TL;DR: The epidemiologic and mechanistic studies indicate that COPD is associated with a high frequency of coronary artery disease, congestive heart failure and cardiac arrhythmias, independent of shared risk factors.

169 citations

Journal ArticleDOI
TL;DR: Immunomodulatory therapies targeting MMPs in preclinical and clinical trials are potential adjuncts to TB treatment and Strategies targeting patients with cavitary TB have the potential to improve cure rates and reduce disease transmission.
Abstract: Tuberculosis (TB), a chronic infectious disease of global importance, is facing the emergence of drug-resistant strains with few new drugs to treat the infection. Pulmonary cavitation, the hallmark of established disease, is associated with very high bacillary burden. Cavitation may lead to delayed sputum culture conversion, emergence of drug resistance, and transmission of the infection. The host immunological reaction to Mycobacterium tuberculosis is implicated in driving the development of TB cavities. TB is characterized by a matrix-degrading phenotype in which the activity of proteolytic matrix metalloproteinases (MMPs) is relatively unopposed by the specific tissue inhibitors of metalloproteinases. Proteases, in particular MMPs, secreted from monocyte-derived cells, neutrophils, and stromal cells, are involved in both cell recruitment and tissue damage and may cause cavitation. MMP activity is augmented by proinflammatory chemokines and cytokines, is tightly regulated by complex signaling paths, and...

161 citations

Journal ArticleDOI
TL;DR: The fibrosis in IPF is increasingly understood to be the result of a fibroproliferative and aberrant wound healing cascade, and the development of therapeutic targets has shifted in accord with this paradigm change.
Abstract: Idiopathic pulmonary fibrosis (IPF) is a progressively fibrotic interstitial lung disease that is associated with a median survival of 2-3 years from initial diagnosis. To date, there is no treatment approved for IPF in the United States, and only one pharmacological agent has been approved outside of the United States. Nevertheless, research over the past 10 years has provided us with a wealth of information on its histopathology, diagnostic work-up, and a greater understanding of its pathophysiology. Specifically, IPF is no longer thought to be a predominantly pro-inflammatory disorder. Rather, the fibrosis in IPF is increasingly understood to be the result of a fibroproliferative and aberrant wound healing cascade. The development of therapeutic targets has shifted in accord with this paradigm change. This review highlights the current understanding of IPF, and the recent as well as novel therapeutics being explored in clinical trials for the treatment of this devastating disease.

143 citations