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Relevant bibliographies by topics / Asthma – Chemotherapy

Academic literature on the topic 'Asthma – Chemotherapy'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 January 2023

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Journal articles on the topic "Asthma – Chemotherapy"

1

FALLIERS, C. "Cancer chemotherapy: Hormonal changes and recurring asthma." Journal of Allergy and Clinical Immunology 87, no. 3 (March 1991): 747–48. http://dx.doi.org/10.1016/0091-6749(91)90398-8.

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Palmieri, C., R. Gillmore, A. Menzies-Gow, S. Fishpool, D. Robinson, R. Shaw, and R. C. Coombes. "Resolution of late-onset asthma following high-dose chemotherapy." Bone Marrow Transplantation 32, no. 8 (October 2003): 847–48. http://dx.doi.org/10.1038/sj.bmt.1704268.

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Anak, Sema, Nermin Guler, and Ebru Tugrul Saribeyoglu. "POSSIBLE CURATIVE EFFECT OF INTENSIVE CHEMOTHERAPY ON ASTHMA IN CHILDREN." Pediatric Hematology and Oncology 18, no. 6 (January 2001): 421–22. http://dx.doi.org/10.1080/088800101316922065.

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Protasov, A. D., M. P. Kostinov, A. V. Zhestkov, D. O. Gorbachev, A. M. Kostinov, M. E. Elner, and T. A. Kozina. "Changes in Sputum Microbiocenosis and Clinical Pattern Under Different Vaccination Protocols for Pneumococcal Infection in Patients with Bronchial Asthma." Global Journal of Respiratory Care 8 (December 28, 2022): 18–27. http://dx.doi.org/10.12974/2312-5470.2022.08.05.

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Bronchial asthma is a serious public health issue. It is important to reduce the frequency of attacks for BA patients. Vaccination for pneumococcal infection is an important complementary tool that can improve the clinical pattern of bronchial asthma. The study involved 102 patients with bronchial asthma, who were monitored over 4 years. The patients were divided into 4 groups based on the vaccination scheme used for pneumococcal infection: PCV13, PPV23, PPV23/PCV13, PCV13/PPV23. Sequential vaccination with pneumococcal conjugate and polysaccharide vaccines leads to a decrease in the isolation of pneumococcus from sputum in BA patients, which has a pronounced positive effect on the clinical pattern of this disease, namely, it leads to a decrease in the frequency of attacks, the requirement for courses of antibacterial chemotherapy and hospitalizations, and therefore this vaccination protocol should be included in the standards of BA patient management.

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Jones, PD, RL Henry, L. Francis, and PG Gibson. "Chemotherapy reduces the prevalence of asthma symptoms in children with cancer: Implications for the role of airway inflammation in asthma." Journal of Paediatrics and Child Health 35, no. 3 (June 1999): 269–71. http://dx.doi.org/10.1046/j.1440-1754.1999.00358.x.

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Falliers, Constantine J. "Relapse and Repeated Remission of Asthma After Cancer Chemotherapy and Secondary Hormonal Changes." Journal of Asthma 28, no. 5 (January 1991): 381–87. http://dx.doi.org/10.3109/02770909109089465.

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Walters, E. Haydn, Julia AE Walters, and Richard Wood-Baker. "Anti-IgE and chemotherapy: a critical appraisal of treatment options for severe asthma." Expert Opinion on Pharmacotherapy 8, no. 5 (March 22, 2007): 585–92. http://dx.doi.org/10.1517/14656566.8.5.585.

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Tintinger, Gregory R., Charles Feldman, Annette J. Theron, and Ronald Anderson. "Montelukast: More than a Cysteinyl Leukotriene Receptor Antagonist?" Scientific World JOURNAL 10 (2010): 2403–13. http://dx.doi.org/10.1100/tsw.2010.229.

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The prototype cysteinyl leukotriene receptor antagonist, montelukast, is generally considered to have a niche application in the therapy of exercise- and aspirin-induced asthma. It is also used as add-on therapy in patients whose asthma is poorly controlled with inhaled corticosteroid monotherapy, or with the combination of a long-acting β(2)-agonist and an inhaled corticosteroid. Recently, however, montelukast has been reported to possess secondary anti-inflammatory properties, apparently unrelated to conventional antagonism of cysteinyl leukotriene receptors. These novel activities enable montelukast to target eosinophils, monocytes, and, in particular, the corticosteroid-insensitive neutrophil, suggesting that this agent may have a broader spectrum of anti-inflammatory activities than originally thought. If so, montelukast is potentially useful in the chemotherapy of intermittent asthma, chronic obstructive pulmonary disease, cystic fibrosis, and viral bronchiolitis, which, to a large extent, involve airway epithelial cell/neutrophil interactions. The primary objective of this mini-review is to present evidence for the cysteinyl leukotrien–independent mechanisms of action of montelukast and their potential clinical relevance.

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Bitik, B., M. Aydin, G. Sahin Dalgic, D. Kaskari, and A. E. Yucel. "AB0464 THE ROLE OF CYCLOPHOSPHAMIDE CHEMOTHERAPY IN THE TREATMENT OF EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1530.2–1531. http://dx.doi.org/10.1136/annrheumdis-2020-eular.6481.

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Background:Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare type of ANCA associated Vasculitis (AAVs). Cyclophosphamide (CYC) is generally recommended for the induction of remission in life/organ threatening AAVs in combination with glucocorticoids. However, due to its rarity, randomized controlled trials regarding the efficacy of treatment modalities in EGPA are hard to perform. Therefore, the level of evidence for the use of CYC in the treatment of EGPA is lower when compared to other AAVs (1).Objectives:The aim of this study is to investigate common therapeutic agents used for the treatment of patients with EGPA.Methods:Medical records of patients who were followed-up with the diagnosis of EGPA between 2007-2020, in rheumatology clinics of Ankara and Adana Hospitals of Başkent University, were analyzed retrospectively. Treatment outcomes were assessed.Results:Records of 11 patients (six females) were analyzed. The median age was 47 (19-77) years. The median follow-up time of the patients was 24 (9-156) months. Six patients were diagnosed with asthma. The median time between the diagnosis of asthma and EGPA was 4.5 (1-3) years. Five patients had tissue biopsies. Biopsy locations were terminal ileum, lung, myocardium and nerve. The most common forms of involvement were asthma, eosinophilic pneumonia and / or nodule, cardiovascular involvement, mononoritis multiplex, vasculitic skin rash, arthritis and bowel involvement, respectively. P-ANCA was positive in 8 patients. Three patients had myocarditis and cardiomyopathy, and two patients had isolated valve problems. The median BVAS value at the time of diagnosis and the third month of treatment was 17 (6-27) and 4 (2-7), respectively.Nine patients used oral 1mg/ kg methylprednisolone (MP) and 500mg CYC every two weeks as an induction therapy. The cumulative median CYC dose was 4.5 g (1.5-8). Neither of the patients developed CYC related side effects. MP was tapered to 2 mg in five patients, and was quited in two patients. Azathioprine (AZA) was used in remission treatment following CYC therapy. Rituximab (RTX) therapy 1 g twice, 2 weeks apart was initiated in two patients due to unresponsiveness to CYC. While RTX was effective in one patient, newly developed renal involvement was detected after the third cycle of RTX therapy in other patient. Two patients had pregnancy plan therefore they used AZA plus MP as induction. A patient had mycophenolate mofetil plus MP due to AZA allergy. All patients are currently in remission except one patient.Conclusion:In seven out of 11 EGPA patients, long-term remission was achieved with CYC treatment. CYC appears to be an effective and inexpensive method of first-line treatment for organ threatening EGPA.References:[1]Yates M, Watts RA, Bajema IM, et al. EULAR/ERA-EDTA recommendations for the management of ANCA-associated vasculitis. Ann Rheum Dis. 2016 Sep;75(9):1583-94.Disclosure of Interests:None declared

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Zhu, Xiaorui. "Clinical Effect of Auricular Point Sticking in Patients with Lung Cancer Receiving Chemotherapy." Proceedings of Anticancer Research 5, no. 6 (November 30, 2021): 73–77. http://dx.doi.org/10.26689/par.v5i6.2810.

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Objective: To discuss and analyze the clinical effect of auricular point sticking in lung cancer chemotherapy. Methods: Sixty-two patients with lung cancer treated with chemotherapy in Suqian Traditional Chinese Medicine Hospital of Jiangxi Province were selected for case evaluation and analysis. The time span of the research was from June 2020 to June 2021. The patients were divided into two groups: a study group (n = 31) and a control group (n = 31) based on their medical record numbers. All the patients were treated with conventional western medicine before and after chemotherapy to prevent adverse reactions; however, the patients in the study group were also treated with auricular point sticking in addition to the former. The relevant indexes of the two groups were compared. Results: The incidence of adverse reactions was significantly lower in the study group compared to the control group (P < 0.05); the rate of symptomatic relief of the patients in the study group was higher than that of the control group (P < 0.05); the stress response indexes toward chemotherapy of the study group were better than those of the control group (P < 0.05). Conclusion: Auricular point sticking for patients with lung cancer who are receiving chemotherapy can reduce the incidence of adverse reactions, alleviate clinical symptoms, such as chest distress, asthma, and poor appetite, significantly alleviate stress response caused by chemotherapy, as well as promote the treatment effect; thus, it is worthy of promotion.

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Dissertations / Theses on the topic "Asthma – Chemotherapy"

1

王衛慶 and Wei-qing Wang. "Prevention therapy on bone loss in asthmatic patients on high dose inhaled steroids." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31214691.

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Herbert, Cristan Medical Sciences Faculty of Medicine UNSW. "Effects of glucocorticoid and phosphodiesterase-4 inhibitor therapy in a mouse model of chronic asthma." 2007. http://handle.unsw.edu.au/1959.4/40535.

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Asthma is a chronic inflammatory disease of the airways. Using a murine model which replicates many characteristic features of human asthma, this study evaluated the effects of treatment with anti-inflammatory drugs on the lesions of chronic asthma, and investigated potential underlying molecular mechanisms. Treatment with dexamethasone, a glucocorticoid, was compared with roflumilast, a novel phosphodiesterase-4 (PDE4) inhibitor. BALB/c mice sensitised to ovalbumin were challenged with a low mass concentration of aerosolised antigen for 30 min/day, 3 days/week for 6 weeks. In weeks 5 and 6, groups of animals were treated with either dexamethasone or roflumilast. Assessment included changes in acute-on-chronic inflammation, structural remodelling of the airways and airway hyper-responsiveness to a bronchoconstrictor stimulus. These were correlated with the expression of pro-inflammatory cytokines and growth factors. Compared to vehicle-treated control animals, dexamethasone- and roflumilast-treated mice exhibited reduced accumulation of intra-epithelial eosinophils and chronic inflammatory cells, including CD3+ T-lymphocytes in the airways. Similarly, both drugs inhibited subepithelial fibrosis and airway epithelial thickening, although only dexamethasone inhibited goblet cell hyperplasia/metaplasia. Airway hyper-reactivity was not diminished by either drug. Both treatments suppressed production of Th2 cytokines by ovalbumin-restimulated peribronchial lymph node cells. In selectively dissected airway tissue from vehicletreated animals, increased expression of mRNA for several pro-inflammatory cytokines (TNF-α, GM-CSF, IL-6) and cytokines characteristic of Th1 (IFN-γ), Th2 (IL-5, IL-13)and Th17 (IL-17A) cells was demonstrated using real-time PCR. Enhanced expression of growth factors (TGF-β1 and FGF-2) was also demonstrated in airway epithelium isolated by laser capture microdissection. Interestingly, whereas treatment with dexamethasone significantly inhibited expression of mRNA for all of the inflammationrelated cytokines examined, roflumilast inhibited only IL-17A, TNF-α, GM-CSF and IL-6. Both drugs inhibited mRNA expression of growth factors by epithelial cells. Because roflumilast was as effective as dexamethasone in suppressing inflammation and most changes of remodelling, the selective suppression of IL-17A, TNF-α, GM-CSF and IL-6 suggests that these mediators, or the cells that produce them, may have critical roles in pathogenesis. Furthermore, they may be particularly appropriate therapeutic targets in chronic asthma.

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"Costimulatory molecules, chemokines and transcription factors, and immunomodulatory effect of Chinese medicine in asthma." Thesis, 2006. http://library.cuhk.edu.hk/record=b6074269.

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Lun Samantha Wei Man.
"August 2006."
Thesis (Ph.D.)--Chinese University of Hong Kong, 2006.
Includes bibliographical references (p. 181-206).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.

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4

Irusen, Elvis Malcolm. "Glucocorticosteroid receptor characteristics of peripheral blood mononuclear cells in oral steroid dependent asthma : utilization of an in vitro model of steroid resistant asthma to investigate mechanisms of resistance and functional consequences of altered receptor affinity." Thesis, 2007. http://hdl.handle.net/10413/2527.

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Background: Although glucocorticoids are the most effective treatment for asthma, some patients show a poor response. In such patients with steroid resistant asthma, this has been ascribed to altered glucocorticoid receptor (GR) ligand-binding affinity induced by IL-2 combined with IL-4 or IL-13 alone- all of which can also modulate glucocorticoid function in vitro. Objective: We sought to assess the ligand-binding affinity in a distinct group of oral steroid-dependent asthmatic subjects and examine the mechanisms by which IL-2 and IL-4 (or IL-13) modify the ligand-binding affinity of the GR. Methods: Using dexamethasone-binding assays, we examined PBMCs ex vivo from healthy subjects, subjects with controlled asthma, and oral steroiddependent subjects with severe asthma. In addition, IL-2 and IL-4 were used to alter GR affinity in vitro. We used mediators or inhibitors of signal transduction to investigate the mechanisms of resistance. We also determined cytokine production of PBMC's by means of ELISA. Results: GR ligand-binding affinity was significantly reduced in the nucleus but not in the cytoplasm of oral steroid-dependent asthmatic subjects compared with that seen in steroid-sensitive and healthy subjects (dissociation constant, 41.37 ± 17.83 vs. 25.36 ± 2.63 nmol/L vs. 9.40 ± 4.01 nmol/L, respectively [p<.05 for both in comparison to normals] ). This difference in ligand-binding affinity could be mimicked by IL-2 and IL-4 co-treatment and was blocked by the p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580. PBMC's rendered resistant in vitro demonstrated lower IL-10 and increased GM-CSF production following LPS or PMA & PHA stimulation compared to cells with normal GR affinity. Resistant cells also showed reduced dexamethasone repression of LPSstimulated IL-10 release. These effects were also reversed by SB203580. Inhibition of the ERK MAPK pathway by PD098059 (10 mol/L), phosphoinositol 3 kinase by wortmannin (5 nmol/L) or treatment with IL-10 (10 ng/mL) failed to modulate the effect of IL-2 and IL-4 on receptor affinity. Ro318220 (10 nmol/L), a specific protein kinase C inhibitor and theophylline, similarly, had no effect on affinity. Conclusion: GR ligand binding affinity is tiered; compared to normal subjects; steroid responsive asthmatics have a mild reduction in ligand binding whereas oral steroid dependent asthmatics have greater reductions. When mononuclear cells are rendered resistant in vitro, cytokine production (low IL-10 and high GM-CSF) favours a pro-inflammatory state. Our data do not support the ERK MAPK, phosphoinositol 3 kinase, protein kinase C pathways in steroid resistance. Treatment with IL-10 and theophylline also failed to modulate the effect of IL-2 and IL-4 on receptor affinity. However, P38 MAPK inhibitors may have potential in reversing glucocorticoid insensitivity and re-establishing the beneficial effects of glucocorticoids in patients with severe asthma.
Thesis (Ph.D.)-University of KwaZulu-Natal, Durban, 2007.

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Books on the topic "Asthma – Chemotherapy"

1

Li, James T. C., 1953-, ed. Pharmacotherapy of asthma. New York: Taylor & Francis, 2006.

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B, Kay A., ed. Asthma: Clinical pharmacology and therapeutic progress. Oxford: Blackwell Scientific, 1986.

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Romain, Pauwels, and O'Byrne Paul M. 1951-, eds. Beta₂-agonists in asthma treatment. New York: Dekker, 1997.

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1946-, Martin Richard J., and Kraft Monica, eds. Combination therapy for asthma and chronic obstructive pulmonary disease. New York: Marcel Dekker, 2000.

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International, Conference on Asthma (5th 1997 Ischia Italy). Asthma and allergic diseases: Physiology, immunopharmacology, and treatment : fifth international symposium. San Diego: Academic Press, 1998.

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New drugs and targets for asthma and COPD. Basel: Karger, 2010.

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Weersink, Els J. M. The natural variability in asthma: Two therapeutic approaches. [Netherlands]: E. Weersink, 1997.

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1944-, Costello J. F., and Mann Ronald D. 1928-, eds. Beta agonists in the treatment of asthma: The proceedings. Carnforth, Lancs, UK: Parthenon Pub. Group, 1992.

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Sven-Erik, Dahlen, and Lee T. H, eds. Five-lipoxygenase products in asthma. New York: M. Dekker, 1998.

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Richard, Beasley, and Pearce Neil, eds. The Role of beta receptor agonist therapy in asthma mortality. Boca Raton: CRC Press, 1993.

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Book chapters on the topic "Asthma – Chemotherapy"

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Tam, Schuman. "Chemotherapy and Biologic Drug Allergy." In Allergy and Asthma, 1–21. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-58726-4_24-1.

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Tam, Schuman. "Chemotherapy and Biologic Drug Allergy." In Allergy and Asthma, 519–38. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-05147-1_24.

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Hamoud, Hesham. "Non-GCs Drug-Induced Osteoporosis." In Biomechanical and Mechanobiological Analysis of Bone Mineral Density [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108296.

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Medications that cause osteoporosis are numerous and common. While helping to correct one problem, they may be putting you at greater risk of having osteoporosis. A variety of drugs may cause bone loss by lowering sex steroid levels (e.g., aromatase inhibitors used in breast cancer and GnRH agonists used in prostate cancer), interfering with vitamin D levels (liver-inducing antiepileptic drugs), or directly affecting bone cells (chemotherapy, phenytoin, or thiazolidinediones) which divert mesenchymal stem cells from osteoblastogenesis to adipocytogenesis, consequently, an imbalance occurs between bone formation and resorption, as well as between soft organic matrix and hard inorganic matrix. Besides effects on the mineralized matrix, interactions with collagen and other nonmineralized matrix components can decrease bone biomechanical competence without affecting bone mineral density (BMD). Here is a quick narrative for a number of disease medications that can cause osteoporosis if taken for long periods without a preventive program of minerals and vitamins. Rheumatoid arthritis, inflammatory bowel disease, asthma, acid reflux, thyroid dysfunctions, seizures, endometriosis, aromatase inhibitors, hypertension, contraceptive Depo-Provera, antidepressant (SSRIs, SNRIs), glitazones for type 2 DM treatment.

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Conference papers on the topic "Asthma – Chemotherapy"

1

Patel, Sagar S., Ramesh Natarajan, and Rebecca L. Heise. "Mechanotransduction of Primary Cilia in Lung Adenocarcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80435.

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Lung cancer causes more than 1 million deaths worldwide annually [1]. In a recent study by the American Cancer Society in 2011, more than 221,000 new cases of lung cancers were reported [2]. Out of these, the mortality rate was found in roughly 70% of the cases [2]. Lung cancer is divided into two major categories: small cell and non-small cell. In the United States, non-small cell lung cancer accounts for 85% of all lung cancers and is considered the most common type of lung cancer [2]. It is usually resistant to chemotherapy, therefore making it extremely difficult to treat [3]. Furthermore adenocarcinomas, a type of non-small cell lung cancer, occur towards the periphery of the lungs and are the most common type accounting for 40–45% of all lung cancer cases [3]. Epithelial cells in the healthy lungs undergo stresses during inhalation and expiration of normal breathing. In addition to the forces of normal breathing, lung cancer cells may also experience abnormal mechanical forces due to pre-existing lung diseases such as asthma, bronchitis and chronic obstructive pulmonary disease or other tumor associated structural changes. These conditions can significantly alter the structure of the lungs and cell phenotype [4]. The change in the structure of the lungs affects the mechanical environment of the cells. Changes in extracellular (ECM) stiffness, cell stretch, and shear stress influence tumorigenesis and metastasis [5]. One mechanism through which the cells sense and respond to the cellular mechanical environment is through the primary cilia [6–7]. Primary cilia are non-motile, solitary structures formed from the cellular microtubules and protrude out of each cell. They have also been shown to play an important role in facilitating common cancer signaling pathways such as Sonic Hedgehog and Wnt/β-catenin signaling [8–9]. The objective of this study was to test the hypothesis that lung cancer cells respond to mechanical stimuli with the formation of primary cilia that are necessary for 3 hallmarks of tumor progression: proliferation, epithelial mesenchymal-transition, and migration.

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Kim, HJ, WC Noh, SJ Nam, B.-w. Park, ES Lee, SA Im, YS Jung, et al. "Abstract P4-14-04: Time course changes in serum FSH, estradiol, and menstruation restoration in premenopausal patients with breast cancer taking adjuvant tamoxifen after completing chemotherapy: A report from the ASTRRA study." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p4-14-04.

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Kim, HJ, SH Ahn, SJ Nam, SH Park, JS Ro, SA Im, YS Jung, and WC Noh. "Abstract P5-12-08: Time course of changes in serum FSH, serum estradiol, and menstruation in premenopausal patients with breast cancer taking tamoxifen after completing chemotherapy: A report from the ASTRRA study." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p5-12-08.

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