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Journal articles on the topic 'Chronic lung disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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1

Petty, Thomas L. "Chronic lung disease." Postgraduate Medicine 86, no. 6 (November 1989): 113. http://dx.doi.org/10.1080/00325481.1989.11704476.

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2

Falcão, Mário Cícero. "Neonatal chronic lung disease." Revista do Hospital das Clínicas 54, no. 6 (December 1999): 173–74. http://dx.doi.org/10.1590/s0041-87811999000600001.

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3

Filho, Luiz Vicente F. da Silva. "Neonatal chronic lung disease." Jornal de Pediatria 74, no. 4 (July 15, 1998): 265–74. http://dx.doi.org/10.2223/jped.433.

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4

Avent, Minyon, Diana Coile, and Letha Mathai. "Neonatal Chronic Lung Disease." Journal of Pharmacy Practice 14, no. 3 (June 2001): 181–206. http://dx.doi.org/10.1106/j5vj-evx8-19ru-7e0b.

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Chronic lung disease (CLD), formerly known as bronchopulmonary dysplasia, is presently defined as the need for oxygen therapy either at 28 days of age or greater than 36 weeks postmenstrual age. Clinical signs and symptoms include tachypnea, retractions, apnea, and radiographic findings of poorly inflated lungs with reticulogranular opacities. The disease develops as a result of chronic pulmonary inflammation and continuous lung injury induced by oxygen, positive pressure ventilation, and other causes. Fifty to sixty-five percent of neonates with CLD are rehospitalized with respiratory problems, and 21% of very low birth weight neonates are diagnosed with asthma or other respiratory disorders by the age of five. These infants are at risk of adverse neurodevelopmental sequelae as they have a more complicated neonatal course. Many studies have explored various preventive therapies including α1-proteinase inhibitors, superoxide dismutase, antioxidants, and ventilatory management. Although the results from these trials are promising, further studies are needed to define which patients are most likely to benefit from preventive therapy. Two preventive treatment approaches that have shown a decrease in morbidity and an improvement in mortality are antenatal steroids and surfactant therapy. Postnatal corticosteroid therapy continues to be the mainstay of treatment for CLD, however, there are a number of detrimental side effects associated with this treatment. Due to the increased incidence in periventricular leukomalacia, early treatment of steroid therapy cannot be recommended. The optimal time to start steroid therapy appears to be after the first week of life. In addition, the lowest dose and shortest duration of treatment needs to be implemented in order to minimize potential complications. Although bronchodilators and diuretics continue to be used extensively in infants with CLD, there are surprisingly few well-controlled studies that have evaluated the clinical impact of this therapy. Further trials are needed in order to support the routine use of these therapies in CLD. Unfortunately, inhaled steroids have not shown an improvement in long-term outcomes of CLD, however, they have shown a decrease in systemic steroid usage. CLD is a complex disease with many unanswered questions. Further studies are needed to evaluate the effects of various treatment modalities with particular focus on the long-term outcomes such as oxygen and ventilator dependency as well as the incidence of CLD.
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5

Brauer, Sandra. "Chronic obstructive lung disease." Journal of Physiotherapy 59, no. 4 (December 2013): 278. http://dx.doi.org/10.1016/s1836-9553(13)70212-1.

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6

Hilman, Bettina C. "Chronic Interstitial Lung Disease." Clinical Pediatrics 37, no. 11 (November 1998): 701–2. http://dx.doi.org/10.1177/000992289803701111.

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7

Hogg, James C. "A Brief Review of Chronic Obstructive Pulmonary Disease." Canadian Respiratory Journal 19, no. 6 (2012): 381–84. http://dx.doi.org/10.1155/2012/496563.

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A recent study, based on a combination of multidetector computed tomography scanning of an intact specimen with microcomputed tomography and histological analysis of lung tissue samples, reported that the number of terminal bronchioles were reduced from approximately 44,500/lung pair in control (donor) lungs to approximately 4800/lung pair in lungs donated by individuals with very severe (Global initiative for chronic Obstructive Lung Disease stage 4) chronic obstructive pulmonary disease (COPD) treated by lung transplantation. The present short review discusses the hypothesis that a rapid rate of terminal bronchiolar destruction causes the rapid decline in lung function leading to advanced COPD. With respect to why the terminal bronchioles are targeted for destruction, the postulated mechanisms of this destruction and the possibility that new treatments are able to either prevent or reverse the underlying cause of airway obstruction in COPD are addressed.
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8

Gilpin, Sarah E., and Darcy E. Wagner. "Acellular human lung scaffolds to model lung disease and tissue regeneration." European Respiratory Review 27, no. 148 (June 6, 2018): 180021. http://dx.doi.org/10.1183/16000617.0021-2018.

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Recent advances in whole lung bioengineering have opened new doors for studying lung repair and regeneration ex vivo using acellular human derived lung tissue scaffolds. Methods to decellularise whole human lungs, lobes or resected segments from normal and diseased human lungs have been developed using both perfusion and immersion based techniques. Immersion based techniques allow laboratories without access to intact lobes the ability to generate acellular human lung scaffolds. Acellular human lung scaffolds can be further processed into small segments, thin slices or extracellular matrix extracts, to study cell behaviour such as viability, proliferation, migration and differentiation. Recent studies have offered important proof of concept of generating sufficient primary endothelial and lung epithelial cells to recellularise whole lobes that can be maintained for several days ex vivo in a bioreactor to study regeneration. In parallel, acellular human lung scaffolds have been increasingly used for studying cell–extracellular environment interactions. These studies have helped provide new insights into the role of the matrix and the extracellular environment in chronic human lung diseases such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. Acellular human lung scaffolds are a versatile new tool for studying human lung repair and regeneration ex vivo.
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9

COOPER, JOEL D. "Lung Transplantation for Chronic Obstructive Lung Disease." Annals of the New York Academy of Sciences 624, no. 1 (May 1991): 209–11. http://dx.doi.org/10.1111/j.1749-6632.1991.tb17019.x.

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10

Wu, Yifan, Evan Li, Morgan Knight, Grace Adeniyi-Ipadeola, Li-zhen Song, Alan R. Burns, Ana Clara Gazzinelli-Guimaraes, Ricardo Fujiwara, Maria Elena Bottazzi, and Jill E. Weatherhead. "Transient Ascaris suum larval migration induces intractable chronic pulmonary disease and anemia in mice." PLOS Neglected Tropical Diseases 15, no. 12 (December 16, 2021): e0010050. http://dx.doi.org/10.1371/journal.pntd.0010050.

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Ascariasis is one of the most common infections in the world and associated with significant global morbidity. Ascaris larval migration through the host’s lungs is essential for larval development but leads to an exaggerated type-2 host immune response manifesting clinically as acute allergic airway disease. However, whether Ascaris larval migration can subsequently lead to chronic lung diseases remains unknown. Here, we demonstrate that a single episode of Ascaris larval migration through the host lungs induces a chronic pulmonary syndrome of type-2 inflammatory pathology and emphysema accompanied by pulmonary hemorrhage and chronic anemia in a mouse model. Our results reveal that a single episode of Ascaris larval migration through the host lungs leads to permanent lung damage with systemic effects. Remote episodes of ascariasis may drive non-communicable lung diseases such as asthma, chronic obstructive pulmonary disease (COPD), and chronic anemia in parasite endemic regions.
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11

Burgess, Janette K., and Martin C. Harmsen. "Chronic lung diseases: entangled in extracellular matrix." European Respiratory Review 31, no. 163 (March 9, 2022): 210202. http://dx.doi.org/10.1183/16000617.0202-2021.

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The extracellular matrix (ECM) is the scaffold that provides structure and support to all organs, including the lung; however, it is also much more than this. The ECM provides biochemical and biomechanical cues to cells that reside or transit through this micro-environment, instructing their responses. The ECM structure and composition changes in chronic lung diseases; how such changes impact disease pathogenesis is not as well understood. Cells bind to the ECM through surface receptors, of which the integrin family is one of the most widely recognised. The signals that cells receive from the ECM regulate their attachment, proliferation, differentiation, inflammatory secretory profile and survival. There is extensive evidence documenting changes in the composition and amount of ECM in diseased lung tissues. However, changes in the topographical arrangement, organisation of the structural fibres and stiffness (or viscoelasticity) of the matrix in which cells are embedded have an undervalued but strong impact on cell phenotype. The ECM in diseased lungs also changes in physical and biomechanical ways that drive cellular responses. The characteristics of these environments alter cell behaviour and potentially orchestrate perpetuation of lung diseases. Future therapies should target ECM remodelling as much as the underlying culprit cells.
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12

Duan, Mubing, Waichu Li, Daniel Steinfort, Louis Irving, Gary Anderson, and Margaret Hibbs. "Delineating residential macrophage heterogeneity in lung disease (P3282)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 136.23. http://dx.doi.org/10.4049/jimmunol.190.supp.136.23.

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Abstract In healthy lungs, alveolar macrophages comprise >95% of the immune cells in the alveolar airspaces where they regulate local lung surfactant production and act as the primary sentinels of respiratory pathogens. Interestingly, increased AMΦ numbers are observed in many animal models of chronic lung diseases and also clinically in patients with COPD. Combining flow cytometry and chimeric mice studies, we observed that residential AMΦs form two distinct subpopulations (by either remaining Mac-1neg/low or turning Mac-1pos) during acute inflammation and in chronic inflammatory lung disease subsequent to SHIP-1 deletion. SHIP-1-/- mice which spontaneously develop COPD-like lung disease maintain both Mac-1neg/low and Mac-1pos AMΦ subpopulations. This additional Mac-1pos subpopulation highly expresses MMP-12 and tracks with the induction of lung disease using SHIP-1-/- chimeric mice. Altogether, our results suggest that residential AMΦ heterogeneity is a component of acute lung inflammation and chronic inflammatory lung disease. Consequently, whether residential AMΦ heterogeneity may be a novel hallmark of inflammation-driven human lung diseases has been our final area of study. Overall, our studies of both animal models and patient samples may allow us to better understand the role of AMΦ heterogeneity in lung homeostasis and disease.
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13

Griese, Matthias. "Chronic interstitial lung disease in children." European Respiratory Review 27, no. 147 (February 7, 2018): 170100. http://dx.doi.org/10.1183/16000617.0100-2017.

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Children's interstitial lung diseases (chILD) are increasingly recognised and contain many lung developmental and genetic disorders not yet identified in adult pneumology. Worldwide, several registers have been established. The Australasian Registry Network for Orphan Lung Disease (ARNOLD) has identified problems in estimating rare disease prevalence; focusing on chILD in immunocompetent patients, a period prevalence of 1.5 cases per million children and a mortality rate of 7% were determined. The chILD-EU register highlighted the workload to be covered per patient included and provided protocols for diagnosis and initial treatment, similar to the United States chILD network. Whereas case reports may be useful for young physicians to practise writing articles, cohorts of patients can catapult progress, as demonstrated by recent studies on persistent tachypnoea of infancy, hypersensitivity pneumonitis in children and interstitial lung disease related to interferonopathies from mutations in transmembrane protein 173. Translational research has linked heterozygous mutations in the ABCA3 transporter to an increased risk of interstitial lung diseases, not only in neonates, but also in older children and adults. For surfactant dysfunction disorders in infancy and early childhood, lung transplantation was reported to be as successful as in adult patients. Mutual potentiation of paediatric and adult pneumologists is mandatory in this rapidly extending field for successful future development.This brief review highlights publications in the field of paediatric interstitial lung disease as reviewed during the Clinical Year in Review session presented at the 2017 European Respiratory Society (ERS) Annual Congress in Milan, Italy. It was commissioned by the ERS and critically presents progress made as well as drawbacks.
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14

SCHICK, JAMES B., and BOYD W. GOETZMAN. "Chronic Lung Disease of Prematurity." Pediatrics 76, no. 4 (October 1, 1985): 652. http://dx.doi.org/10.1542/peds.76.4.652.

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To the Editor.— The paper by Avery et al,1 further demonstrates the potential usefulness of corticosteroids in chronic lung disease of prematurity. However, initial reports in 1974 and 1975 met with criticism for the use of potentially toxic drugs in premature infants.2,3 In 1983 we retrospectively reviewed 23 infants with chronic lung disease of prematurity who received corticosteroids and identified distinct differences between responders and nonresponders which suggested different types of lung disease.4 Our responders all showed a greater than 30% decrease in AaPo2 by day 6 and showed maximal response by ten days of therapy.
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15

Gilbert, Christopher R., Seth M. Arum, and Cecilia M. Smith. "Vitamin D Deficiency and Chronic Lung Disease." Canadian Respiratory Journal 16, no. 3 (2009): 75–80. http://dx.doi.org/10.1155/2009/829130.

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Vitamin D deficiency is increasingly being recognized as a prevalent problem in the general population. Patients with chronic lung diseases such as asthma, cystic fibrosis, chronic obstructive lung disease and interstitial pneumonia appear to be at increased risk for vitamin D deficiency for reasons that are not clear.Several studies indicate that vitamin D possesses a range of anti-inflammatory properties and may be involved in processes other than the previously believed functions of calcium and phosphate homeostasis. Various cytokines, cellular elements, oxidative stress and protease/antiprotease levels appear to affect lung fibroproliferation, remodelling and function, which may be influenced by vitamin D levels. Chronic lung diseases such as asthma and chronic obstructive lung disease have also been linked to vitamin D on a genetic basis. This immune and genetic influence of vitamin D may influence the pathogenesis of chronic lung diseases. A recent observational study notes a significant association between vitamin D deficiency and decreased pulmonary function tests in a large ambulatory population.The present review will examine the current literature regarding vitamin D deficiency, its prevalence in patients with chronic lung disease, vitamin D anti-inflammatory properties and the role of vitamin D in pulmonary function.
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16

Mendez, Jose L., Hassan F. Nadrous, Thomas E. Hartman, and Jay H. Ryu. "Chronic Nitrofurantoin-Induced Lung Disease." Mayo Clinic Proceedings 80, no. 10 (October 2005): 1298–302. http://dx.doi.org/10.4065/80.10.1298.

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17

Speer, Christian P., and Peter Groneck. "Pathogenesis of Chronic Lung Disease." Neonatology 69, no. 3 (1996): 188–89. http://dx.doi.org/10.1159/000244304.

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18

Rowley, Jessica E., and Jill R. Johnson. "Pericytes in Chronic Lung Disease." International Archives of Allergy and Immunology 164, no. 3 (2014): 178–88. http://dx.doi.org/10.1159/000365051.

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19

Moshal, K. L., and V. Novelli. "Series: Rare Chronic Lung Disease." Paediatric Respiratory Reviews 1, no. 2 (June 2000): 156–64. http://dx.doi.org/10.1053/prrv.2000.0038.

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20

POWARS, DARLEEN, JAMES A. WEIDMAN, TAMARA ODOM-MARYON, JOYCE C. NILAND, and CAGE JOHNSON. "Sickle Cell Chronic Lung Disease." Medicine 67, no. 1 (January 1988): 66–76. http://dx.doi.org/10.1097/00005792-198801000-00005.

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21

Voelkel, Norbert F., Ivor S. Douglas, and Mark Nicolls. "Angiogenesis in Chronic Lung Disease." Chest 131, no. 3 (March 2007): 874–79. http://dx.doi.org/10.1378/chest.06-2453.

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22

Trowbridge, John F. "Pneumonia and Chronic Lung Disease." Hospital Practice 28, sup2 (March 30, 1993): 20–24. http://dx.doi.org/10.1080/21548331.1993.11442942.

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23

Jeeva Sankar, M., Ramesh Agarwal, Ashok K. Deorari, and Vinod K. Paul. "Chronic lung disease in newborns." Indian Journal of Pediatrics 75, no. 4 (April 2008): 369–76. http://dx.doi.org/10.1007/s12098-008-0041-6.

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24

Holland, Walter W. "Chronic obstructive lung disease prevention." British Journal of Diseases of the Chest 82 (January 1988): 32–44. http://dx.doi.org/10.1016/0007-0971(88)90006-x.

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25

Goodell, Teresa Tarnowski. "Sexuality in Chronic Lung Disease." Nursing Clinics of North America 42, no. 4 (December 2007): 631–38. http://dx.doi.org/10.1016/j.cnur.2007.08.003.

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26

Tuder, Rubin M., Jeong H. Yun, Anil Bhunia, and Iwona Fijalkowska. "Hypoxia and chronic lung disease." Journal of Molecular Medicine 85, no. 12 (November 27, 2007): 1317–24. http://dx.doi.org/10.1007/s00109-007-0280-4.

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27

Wang, Xiaorui, Zhihou Guo, and Furong Yan. "RNA Epigenetics in Chronic Lung Diseases." Genes 13, no. 12 (December 16, 2022): 2381. http://dx.doi.org/10.3390/genes13122381.

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Chronic lung diseases are highly prevalent worldwide and cause significant mortality. Lung cancer is the end stage of many chronic lung diseases. RNA epigenetics can dynamically modulate gene expression and decide cell fate. Recently, studies have confirmed that RNA epigenetics plays a crucial role in the developing of chronic lung diseases. Further exploration of the underlying mechanisms of RNA epigenetics in chronic lung diseases, including lung cancer, may lead to a better understanding of the diseases and promote the development of new biomarkers and therapeutic strategies. This article reviews basic information on RNA modifications, including N6 methylation of adenosine (m6A), N1 methylation of adenosine (m1A), N7-methylguanosine (m7G), 5-methylcytosine (m5C), 2′O-methylation (2′-O-Me or Nm), pseudouridine (5-ribosyl uracil or Ψ), and adenosine to inosine RNA editing (A-to-I editing). We then show how they relate to different types of lung disease. This paper hopes to summarize the mechanisms of RNA modification in chronic lung disease and finds a new way to develop early diagnosis and treatment of chronic lung disease.
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28

Rogers, Robert M., Frank C. Sciurba, and Robert J. Keenan. "LUNG REDUCTION SURGERY IN CHRONIC OBSTRUCTIVE LUNG DISEASE." Medical Clinics of North America 80, no. 3 (May 1996): 623–44. http://dx.doi.org/10.1016/s0025-7125(05)70457-0.

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29

Allen, Julian L., and Howard B. Panitch. "Lung function testing: Chronic lung disease of infancy." Pediatric Pulmonology 26, S23 (2001): 138–40. http://dx.doi.org/10.1002/ppul.1950262354.

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30

Allen, Julian L., and Howard B. Panitch. "Lung function testing: Chronic lung disease of infancy." Pediatric Pulmonology 32, S23 (2001): 138–40. http://dx.doi.org/10.1002/ppul.1950322354.

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31

Cho, Soo Jung, and Heather W. Stout-Delgado. "Aging and Lung Disease." Annual Review of Physiology 82, no. 1 (February 10, 2020): 433–59. http://dx.doi.org/10.1146/annurev-physiol-021119-034610.

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People worldwide are living longer, and it is estimated that by 2050, the proportion of the world's population over 60 years of age will nearly double. Natural lung aging is associated with molecular and physiological changes that cause alterations in lung function, diminished pulmonary remodeling and regenerative capacity, and increased susceptibility to acute and chronic lung diseases. As the aging population rapidly grows, it is essential to examine how alterations in cellular function and cell-to-cell interactions of pulmonary resident cells and systemic immune cells contribute to a higher risk of increased susceptibility to infection and development of chronic diseases, such as chronic obstructive pulmonary disease and interstitial pulmonary fibrosis. This review provides an overview of physiological, structural, and cellular changes in the aging lung and immune system that facilitate the development and progression of disease.
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32

Locke, Brian W., Janet J. Lee, and Krishna M. Sundar. "OSA and Chronic Respiratory Disease: Mechanisms and Epidemiology." International Journal of Environmental Research and Public Health 19, no. 9 (April 30, 2022): 5473. http://dx.doi.org/10.3390/ijerph19095473.

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Obstructive sleep apnea (OSA) is a highly prevalent disorder that has profound implications on the outcomes of patients with chronic lung disease. The hallmark of OSA is a collapse of the oropharynx resulting in a transient reduction in airflow, large intrathoracic pressure swings, and intermittent hypoxia and hypercapnia. The subsequent cytokine-mediated inflammatory cascade, coupled with tractional lung injury, damages the lungs and may worsen several conditions, including chronic obstructive pulmonary disease, asthma, interstitial lung disease, and pulmonary hypertension. Further complicating this is the sleep fragmentation and deterioration of sleep quality that occurs because of OSA, which can compound the fatigue and physical exhaustion often experienced by patients due to their chronic lung disease. For patients with many pulmonary disorders, the available evidence suggests that the prompt recognition and treatment of sleep-disordered breathing improves their quality of life and may also alter the course of their illness. However, more robust studies are needed to truly understand this relationship and the impacts of confounding comorbidities such as obesity and gastroesophageal reflux disease. Clinicians taking care of patients with chronic pulmonary disease should screen and treat patients for OSA, given the complex bidirectional relationship OSA has with chronic lung disease.
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33

Gray, Diane M., Sandra Kwarteng Owusu, and Marieke M. van der Zalm. "Chronic lung disease in children: disease focused use of lung function." Current Opinion in Physiology 22 (August 2021): 100438. http://dx.doi.org/10.1016/j.cophys.2021.05.001.

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34

Bollenbecker, Seth, Brian Czaya, Orlando M. Gutiérrez, and Stefanie Krick. "Lung-kidney interactions and their role in chronic kidney disease-associated pulmonary diseases." American Journal of Physiology-Lung Cellular and Molecular Physiology 322, no. 5 (May 1, 2022): L625—L640. http://dx.doi.org/10.1152/ajplung.00152.2021.

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Chronic illnesses rarely present in a vacuum, devoid of other complications, and chronic kidney disease is hardly an exception. Comorbidities associated with chronic kidney disease lead to faster disease progression, expedited dialysis dependency, and a higher mortality rate. Although chronic kidney disease is most commonly accompanied by cardiovascular diseases and diabetes, there is clear cross talk between the lungs and kidneys pH balance, phosphate metabolism, and immune system regulation. Our present understanding of the exact underlying mechanisms that contribute to chronic kidney disease-related pulmonary disease is poor. This review summarizes the current research on kidney-pulmonary interorgan cross talk in the context of chronic kidney disease, highlighting various acute and chronic pulmonary diseases that lead to further complications in patient care. Treatment options for patients presenting with chronic kidney disease and lung disease are explored by assessing activated molecular pathways and the body’s compensatory response mechanisms following homeostatic imbalance. Understanding the link between the lungs and kidneys will potentially improve health outcomes for patients and guide healthcare professionals to better understand how and when to treat each of the pulmonary comorbidities that can present with chronic kidney disease.
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35

Al-Alawi, Alia, C. Frank Ryan, Julia D. Flint, and Nestor L. Müller. "Aspergillus-Related Lung Disease." Canadian Respiratory Journal 12, no. 7 (2005): 377–87. http://dx.doi.org/10.1155/2005/759070.

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Aspergillus is a ubiquitous dimorphic fungus that causes a variety of human diseases ranging in severity from trivial to life-threatening, depending on the host response. An intact host defence is important to prevent disease, but individuals with pre-existing structural lung disease, atopy, occupational exposure or impaired immunity are susceptible. Three distinctive patterns of aspergillus-related lung disease are recognized: saprophytic infestation of airways, cavities and necrotic tissue; allergic disease including extrinsic allergic alveolitis, asthma, allergic bronchopulmonary aspergillosis, bronchocentric granulomatosis and chronic eosinophilic pneumonia; and airway and tissue invasive disease -- pseudomembranous tracheobronchitis, acute bronchopneumonia, angioinvasive aspergillosis, chronic necrotizing aspergillosis and invasive pleural disease. A broad knowledge of these clinical presentations and a high index of suspicion are required to ensure timely diagnosis and treatment of the potentially lethal manifestations of aspergillus-related pulmonary disease. In the present report, the clinical, radiographic and pathological aspects of the various aspergillus-related lung diseases are briefly reviewed.
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36

Keramidas, George, Konstantinos I. Gourgoulianis, and Ourania S. Kotsiou. "Venous Thromboembolic Disease in Chronic Inflammatory Lung Diseases: Knowns and Unknowns." Journal of Clinical Medicine 10, no. 10 (May 11, 2021): 2061. http://dx.doi.org/10.3390/jcm10102061.

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Persistent inflammation within the respiratory tract underlies the pathogenesis of numerous chronic pulmonary diseases. There is evidence supporting that chronic lung diseases are associated with a higher risk of venous thromboembolism (VTE). However, the relationship between lung diseases and/or lung function with VTE is unclear. Understanding the role of chronic lung inflammation as a predisposing factor for VTE may help determine the optimal management and aid in the development of future preventative strategies. We aimed to provide an overview of the relationship between the most common chronic inflammatory lung diseases and VTE. Asthma, chronic obstructive pulmonary disease, interstitial lung diseases, or tuberculosis increase the VTE risk, especially pulmonary embolism (PE), compared to the general population. However, high suspicion is needed to diagnose a thrombotic event early as the clinical presentation inevitably overlaps with respiratory disorders. PE risk increases with disease severity and exacerbations. Hence, hospitalized patients should be considered for thromboprophylaxis administration. Conversely, all VTE patients should be asked for lung comorbidities before determining anticoagulant therapy duration, as those patients are at increased risk of recurrent PE episodes rather than DVT. Further research is needed to understand the underlying pathophysiology of in-situ thrombosis in those patients.
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37

Amudha VP, Amudha VP, Sucilathangam G. Sucilathangam G, and Velvizhi G. Velvizhi G. "Pulmonary Aspergilloma with No Previous History of Chronic Lung Disease: An Interesting Case Report." International Journal of Scientific Research 3, no. 3 (June 1, 2012): 1–2. http://dx.doi.org/10.15373/22778179/march2014/136.

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38

Yanti, Budi, Mauliza Mauliza, Debby Sofiana, and Aamir Shehzad. "Respiratory Bronchiolitis-Interstitial Lung Disease in Chronic Kidney Disease Mimicking Uremic Lung: A Case Report." Jurnal Respirasi 8, no. 2 (May 31, 2022): 87–93. http://dx.doi.org/10.20473/jr.v8-i.2.2022.87-93.

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Introduction: Uremic lung is a frequent complication of chronic kidney disease (CKD), while interstitial lung is an inflammation of the parenchyma which impairs its capacity. These two conditions manifest similar radiological features with bilateral diffuse infiltrates. Therefore, their clinical appearance and radiological lesions are often mistaken. Case: This study reported a case of a 55-year-old male patient with shortness of breath for 1 month and worsening 1 week before hospitalization. The patient had a smoking history for 30 years with severe Brinkman index, hypertension (HT), and diabetes mellitus (DM). Auscultation examination showed crackles in both lungs, while laboratory results showed anemia, leukocytosis, increased urea and creatinine levels, and radiological features of bilateral infiltrate suggesting a uremic lung. Furthermore, the ultrasonography showed bilateral chronic pyelonephritis and was diagnosed with CKD, uremic lung, pneumonia, anemia, hypoalbuminemia, mild hypokalemia, DM, and HT. The patient was treated with regular hemodialysis three times a week, and the serial chest X-ray after hemodialysis showed persistent bilateral infiltrates. An MSCT examination was also performed, and the results showed respiratory bronchiolitis-interstitial lung disease (RB-ILD). The patient was treated with antibiotic therapy, inhaled salbutamol, systemic steroids, and mucolytics. The patient was discharged from the hospital after the respiratory complaint were improved. Conclusion: In uremia patients with bilateral infiltrates resembling uremic lung and unresponsive to hemodialysis or other therapies, interstitial illness should be explored. To improve patient management, risk factors for suspected interstitial lung disease should always be examined.
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39

Wysocki, Kenneth. "Lung Disease and Genomics." AACN Advanced Critical Care 29, no. 1 (March 15, 2018): 74–83. http://dx.doi.org/10.4037/aacnacc2018378.

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Research and application of genomic medicine in lung disease during the past century has clarified our understanding and focus on specific phenotypes, helping clinicians tailor treatment for individual patients. Cystic fibrosis and lung cancer have been researched extensively; specific genotypes have been instrumental in precision medicine to treat these lung diseases. Asthma and chronic obstructive pulmonary disease are more complex and heterogeneous in their pathogenesis, genotypic profile, and phenotypic expression, making treatment more difficult with increasing disease severity. This article focuses on the evolving state of the science of precision medicine in lung cancer, chronic obstructive pulmonary disease, asthma, and cystic fibrosis. The body of knowledge in lung disease is growing related to pharmacogenomics, clinical guidelines, genome editing, and approaches to genomic health that will guide clinical treatment options, reduce risk, and promote health.
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Ghorban Movahed, Mahtab, and Ahya Abdi Ali. "A Review of The Role of The Microbiome on Immune Responses and Its Association With Cystic Fibrosis." Immunoregulation 3, no. 2 (January 1, 2021): 75–88. http://dx.doi.org/10.32598/immunoregulation.3.2.7.

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In recent years, the microbiome has been recognized as a key regulator of immune responses. Evidence suggests that changes in the microbiome can lead to chronic disease and even exacerbation of the disease. Impairment of innate immunity resulting from microbial incompatibility may worsen host susceptibility to infection and exacerbate chronic lung diseases. Specific microbes play a key role in improving immune responses and microbial incompatibility is involved in chronic lung diseases such as asthma, chronic obstructive pulmonary disease, and Cystic Fibrosis (CF). CF is an extremely complex disease that results from a gene mutation. Lack of expression of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) has late complications. Incompatibility in lung microbiota is associated with chronic lung diseases, but it is not determined whether this incompatibility can cause health problems or ineffective regulation of immune response create the disease and its progression. In the CF, due to the deficiency of the immune system, many opportunistic microorganisms, including Pseudomonas. aeruginosa or Staphylococcus aureus are colonized in the patient’s lung and due to an immunodeficiency causedby a defect in the system CFTR, lungs are unable to clear the bacteria that leads to severe pulmonary complications and respiratory and digestive problems in such patients. Therefore, in these patients, the microbiome contributes to dysfunctional immune responses and disease exacerbations. This review summarizes the impact of the microbiome on host immune responses and its relationship with CF to explore the role of the microbiome in causing CF.
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Choi, Joon Young, Jin Woo Song, and Chin Kook Rhee. "Chronic Obstructive Pulmonary Disease Combined with Interstitial Lung Disease." Tuberculosis and Respiratory Diseases 85, no. 2 (April 1, 2022): 122–36. http://dx.doi.org/10.4046/trd.2021.0141.

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Although chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) have distinct clinical features, both diseases may coexist in a patient because they share similar risk factors such as smoking, male sex, and old age. Patients with both emphysema in upper lung fields and diffuse ILD are diagnosed with combined pulmonary fibrosis and emphysema (CPFE), which causes substantial clinical deterioration. Patients with CPFE have higher mortality compared with patients who have COPD alone, but results have been inconclusive compared with patients who have idiopathic pulmonary fibrosis (IPF). Poor prognostic factors for CPFE include exacerbation, lung cancer, and pulmonary hypertension. The presence of interstitial lung abnormalities, which may be an early or mild form of ILD, is notable among patients with COPD, and is associated with poor prognosis. Various theories have been proposed regarding the pathophysiology of CPFE. Biomarker analyses have implied that this pathophysiology may be more closely associated with IPF development, rather than COPD or emphysema. Patients with CPFE should be advised to quit smoking and undergo routine lung function tests, and pulmonary rehabilitation may be helpful. Various pharmacologic agents and surgical approaches may be beneficial in patients with CPFE, but further studies are needed.
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Griffith, David E., and Gerald H. Mazurek. "Pneumonia in Chronic Obstructive Lung Disease." Infectious Disease Clinics of North America 5, no. 3 (September 1991): 467–84. http://dx.doi.org/10.1016/s0891-5520(20)30401-3.

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Kim, J. S., Y. H. Woo, O. B. Kim, S. K. Zeon, S. J. Suh, Y. J. Jeon, and K. Y. Kwon. "CT of chronic diffuse lung disease." Journal of the Korean Radiological Society 26, no. 1 (1990): 72. http://dx.doi.org/10.3348/jkrs.1990.26.1.72.

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Çataltepe, Sule, Charles Schick, and Gary A. Silverman. "Preventive Therapy for Chronic Lung Disease." Pediatrics 102, no. 2 (August 1, 1998): 438. http://dx.doi.org/10.1542/peds.102.2.438.

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Flenley, D. C. "Sleep in Chronic Obstructive Lung Disease." Clinics in Chest Medicine 6, no. 4 (December 1985): 651–61. http://dx.doi.org/10.1016/s0272-5231(21)00402-0.

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Baker, Christopher D. "Mechanical Ventilation During Chronic Lung Disease." Clinics in Perinatology 48, no. 4 (December 2021): 881–93. http://dx.doi.org/10.1016/j.clp.2021.08.004.

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Voynow, Judith A., and Meagan Shinbashi. "Neutrophil Elastase and Chronic Lung Disease." Biomolecules 11, no. 8 (July 21, 2021): 1065. http://dx.doi.org/10.3390/biom11081065.

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Neutrophil elastase (NE) is a major inflammatory protease released by neutrophils and is present in the airways of patients with cystic fibrosis (CF), chronic obstructive pulmonary disease, non-CF bronchiectasis, and bronchopulmonary dysplasia. Although NE facilitates leukocyte transmigration to the site of infection and is required for clearance of Gram-negative bacteria, it also activates inflammation when released into the airway milieu in chronic inflammatory airway diseases. NE exposure induces airway remodeling with increased mucin expression and secretion and impaired ciliary motility. NE interrupts epithelial repair by promoting cellular apoptosis and senescence and it activates inflammation directly by increasing cytokine expression and release, and indirectly by triggering extracellular trap release and exosome release, which magnify protease activity and inflammation in the airway. NE inhibits innate immune function by digesting opsonins and opsonin receptors, degrading innate immune proteins such as lactoferrin, and inhibiting macrophage phagocytosis. Importantly, NE-directed therapies have not yet been effective in preventing the pathologic sequelae of NE exposure, but new therapies are being developed that offer both direct antiprotease activity and multifunctional anti-inflammatory properties.
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Metersky, Mark L., and Antranik Mangardich. "Chronic suppurative lung disease in adults." Journal of Thoracic Disease 8, no. 9 (September 2016): E974—E978. http://dx.doi.org/10.21037/jtd.2016.09.24.

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Paiva, Maria Aparecida S. S., and Sandra M. M. Amaral. "Chronic interstitial lung disease in children." Jornal de Pediatria 83, no. 3 (June 1, 2007): 233–40. http://dx.doi.org/10.2223/jped.1635.

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Greenough, Anne. "Clinical Interventions in Chronic Lung Disease." Neonatology 69, no. 3 (1996): 197–98. http://dx.doi.org/10.1159/000244307.

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