Course Of Chronic Lung Disease Research Articles

Relationship between vitamin D sufficiency and interferon-γ levels in children with chronic lung diseases

Introduction. The role and mechanism of the effect of vitamin D on the course of chronic lung diseases in children are not yet fully understood. In particular, there are not enough studies on the effect of vitamin D status on the production of interferon-γ (IFN-γ) in children with cystic fibrosis and bronchial asthma.Aim. To analyse the changes in IFN-γ levels in children with cystic fibrosis and bronchial asthma according to the serum 25(OH)D level before and during cholecalciferol supplementation.Materials and methods. A total of 114 children (aged from 3 months to 18 years old) were examined, including 51 (44.7%) children with bronchial asthma, 34 (29.8%) children with cystic fibrosis, and 29 (25.5%) children of the control group. If hypovitaminosis D was diagnosed, the children received a three-month cholecalciferol course at doses in accordance with the recommendations of the national consensus - Cystic Fibrosis: Definition, Diagnostic Criteria, Therapy and the national program - Vitamin D Deficiency in Children and Adolescents of the Russian Federation: Current Approaches to Management. The 25(OH)D and IFN-γ levels were twice determined in all children.Results. Median 25(OH)D levels in patients with cystic fibrosis and bronchial asthma did not reach the level of healthy children either before or after supplementation with cholecalciferol drugs at the recommended doses. Vitamin D intake resulted in a decrease in IFN-γ levels in healthy children from 3.07 [2.29; 4.81] pg/ml to 2.18 [1.74; 3.45] pg/ml (p < 0.05), whereas such changes were not detected in the paediatric patients with cystic fibrosis and bronchial asthma in the general population. However, after supplementation with cholecalciferol, the IFN-γ level was significantly higher in patients with cystic fibrosis and bronchial asthma - 2.86 [2.13; 3.86] pg/ml and 3.11 [0.89; 5.0] pg/ml, respectively, than in healthy children - 2.18 [1.74; 3.45] pg/ml (p < 0.05). A statistically significant decrease in IFN-γ level was observed in girls with cystic fibrosis and in healthy girls after supplementation with cholecalciferol, whereas no significant changes in IFN-γ levels were detected in the groups of boys.Conclusion. Modulation of IFN-γ levels appears to be one of the mechanisms of immunotropic effect of vitamin D on the course of chronic inflammation of infectious (cystic fibrosis) and allergic (bronchial asthma) etiology in children.

The upper digestive tract pathology effect on the course of chronic lung diseases

Aim was to study the prevalence of gastrointestinal tract pathology and the state of intestinal biocenosis among bronchial asthma patients.Materials and methods: 93 patients with asthma in the exacerbation stage who had diseases of the gastrointestinal tract were examined. Instrumental, immunological, bacterial studies of the respiratory and digestive organs were carried out.The results of our study indicate a relationship between the development of bronchial asthma and gastrointestinal pathology due to negative environmental effects, stress, glucocorticosteroid therapy, changes in general and local protective reactions against a background of a chronic disease involving organ barriers with an autoimmune pathogenesis mechanism in the pathological process.

Perinatal Nutritional and Metabolic Pathways: Early Origins of Chronic Lung Diseases.

Lung development is not completed at birth, but expands beyond infancy, rendering the lung highly susceptible to injury. Exposure to various influences during a critical window of organ growth can interfere with the finely-tuned process of development and induce pathological processes with aberrant alveolarization and long-term structural and functional sequelae. This concept of developmental origins of chronic disease has been coined as perinatal programming. Some adverse perinatal factors, including prematurity along with respiratory support, are well-recognized to induce bronchopulmonary dysplasia (BPD), a neonatal chronic lung disease that is characterized by arrest of alveolar and microvascular formation as well as lung matrix remodeling. While the pathogenesis of various experimental models focus on oxygen toxicity, mechanical ventilation and inflammation, the role of nutrition before and after birth remain poorly investigated. There is accumulating clinical and experimental evidence that intrauterine growth restriction (IUGR) as a consequence of limited nutritive supply due to placental insufficiency or maternal malnutrition is a major risk factor for BPD and impaired lung function later in life. In contrast, a surplus of nutrition with perinatal maternal obesity, accelerated postnatal weight gain and early childhood obesity is associated with wheezing and adverse clinical course of chronic lung diseases, such as asthma. While the link between perinatal nutrition and lung health has been described, the underlying mechanisms remain poorly understood. There are initial data showing that inflammatory and nutrient sensing processes are involved in programming of alveolarization, pulmonary angiogenesis, and composition of extracellular matrix. Here, we provide a comprehensive overview of the current knowledge regarding the impact of perinatal metabolism and nutrition on the lung and beyond the cardiopulmonary system as well as possible mechanisms determining the individual susceptibility to CLD early in life. We aim to emphasize the importance of unraveling the mechanisms of perinatal metabolic programming to develop novel preventive and therapeutic avenues.

Multifocal Pseudotumorous Form of Neuroparacoccidioidomycosis in an Immunocompetent Patient: A Clinicopathological Review Based on a Case Report

AbstractNeuroparacoccidiodimycosis (NPDM) is an uncommon granulomatous disease, which more frequently affects immunocompromised male patients over 30 years of age in the course of chronic lung disease. Paracoccidioides brasiliensis (PB) is an endemic fungus in Brazil, and grows as thick-walled yeast (with round to oval bodies) measuring 10 µm to 60 µm in diameter. Neuroparacoccidiodimycosi may develop many years after transmission and/or primary lung involvement. The authors describe a case of NPDM affecting a male patient, 52 years of age, farmer, heavy smoker, with clinical complaint of headache, asthenia, seizures, and prostration in the previous nine months. Upon physical examination, the patient presented regular general condition, without other relevant physical alterations. Computed tomography (CT) showed multiple bilateral pulmonary nodules associated to enlargement of the mediastinal lymph node. Magnetic resonance imaging (MRI) and CT scans of the central nervous system showed six heterogeneous nodular lesions compromising the frontal and parietal lobes, the largest one measuring 3.8 × 3.2 × 3.2 cm. The hypothesis of a neoplastic process compromising the lung and brain was considered. A biopsy of the mediastinal lymph node showed epithelioid granulomas, which exhibited round, thin-walled fungal structures in Grocott silver stain. The stereotactic biopsy of the frontal lesion was constituted by necrotic tissue admixed with some round to oval, thin-walled fungi measuring 10 µm to 60 µm, compatible with PB (identified on Grocott silver stain/confirmed in culture). The diagnosis of NPDM was then established. The employed therapeutic regimen was intravenous amphotericin B, itraconazole, and sulfamethoxazole-trimetropin. After ninety days of clinical follow-up, no episodes of seizures/neurological deficits were identified, and a marked decrease in the number and size of the lung and brain lesions were found.

Течение хронических заболеваний легких у детей в призме полиморфизма FokI гена VDR

Течение хронических заболеваний легких у детей в призме полиморфизма FokI гена VDR

Особенности течения хронических заболеваний легких у детей на современном этапе

Особенности течения хронических заболеваний легких у детей на современном этапе

Global Considerations in Human Immunodeficiency Virus-Associated Respiratory Disease

Respiratory tract infection, particularly tuberculosis, is a major cause of mortality among human immunodeficiency virus (HIV)-infected individuals. Antiretroviral therapy (ART) has resulted in a dramatic increase in survival, although coverage of HIV treatment remains low in many parts of the world. There is a concurrent growing burden of chronic noninfectious respiratory disease as a result of increased survival. Many risk factors associated with the development of respiratory disease, such as cigarette smoking and intravenous drug use, are overrepresented among people living with HIV. In addition, there is emerging evidence that HIV infection may directly cause or accelerate the course of chronic lung disease. This review summarizes the clinical spectrum and epidemiology of respiratory tract infections and noninfectious pulmonary pathologies, and factors that explain the global variation in HIV-associated respiratory disease. The potential for enhancing diagnoses of noninfective chronic conditions through the use of clinical algorithms is discussed. We also consider issues in assessment and management of HIV-related respiratory disease in view of the increasing global scale up of ART.

Does RSV Infection Alter the Course of Chronic Lung Disease in Prematurely Born Infants?

Very premature birth frequently results in chronic respiratory morbidity, particularly if complicated by the development of chronic lung disease, bronchopulmonary dysplasia (BPD). Affected infants may remain oxygen dependent for many months and require hospital readmission in the first two years after birth. Troublesome, recurrent respiratory symptoms requiring treatment are common. The worst affected may remain symptomatic with evidence of airways obstruction even as adults. Infant who are born prematurely and develop BPD are at increased risk of severe respiratory syncytial virus (RSV) infection. RSV infection in prematurely born infants is associated with excess chronic respiratory morbidity, as evidenced by greater frequency of respiratory symptoms, lung function abnormalities and healthcare utilisation. There is some evidence to suggest that prematurely born infants, as those born at term, may be predisposed to symptomatic RSV lower respiratory tract infections by pre-morbid abnormal lung function. Longitudinal studies assessing lung function before and after RSV infection are required to determine whether RSV infection does alter the course of chronic lung disease in prematurely born infants.

Czynnik Wzrostu śródbłonka Naczyniowego—Struktura, Funkcje oraz rola w Zapaleniu Oskrzeli i Przebiegu Klinicznym Astmy

Vascular endothelial growth factor (VEGF) is produced by a wide range of cells and plays an important role in normal and pathological angiogenesis. The formation of the vascular system is essential for inflammatory process in airways, especially in the course of chronic lung diseases - for example bronchial asthma. Increased level of VEGF in serum and induced sputum has been demonstrated in patients with stable asthma, as well as during the exacerbation of this disease. VEGF end VEGF-receptor's expressions is closely correlated with neovascularization and seems to be an important predictor of the lung's remodeling. Due to direct causative relationship between inflammatory process and angiogenesis in airways, it was suggested, that inhibiting VEGF's activity would have an anti-inflammatory effect on airways. In this article the potential role of vascular endothelial growth factor in airways inflammation, remodeling and the clinical course of bronchial asthma is presented.

Chronic Obstructive Lung Diseases and Risk of Non-small Cell Lung Cancer in Women

The link between lung cancer and chronic obstructive lung diseases (COPD) has not been well studied in women even though lung cancer and COPD account for significant and growing morbidity and mortality among women. We evaluated the relationship between COPD and non-small cell lung cancer in a population-based case-control study of women and constructed a time course of chronic lung diseases in relation to onset of lung cancer. Five hundred sixty-two women aged 18 to 74, diagnosed with non-small cell lung cancer and 564 population-based controls matched on race and age participated. Multivariable unconditional logistic regression models were used to estimate risk associated with a history of COPD, chronic bronchitis, or emphysema. Lung cancer risk increased significantly for white women with a history of COPD (odds ratios [OR] = 1.85; 95% confidence intervals [CI]: 1.21-2.81), but this was not seen in African American women. Risk associated with a history of chronic bronchitis was strongest when diagnosed at age 25 or earlier (OR = 2.35, 95% CI: 1.17-4.72); emphysema diagnosed within 9 years of lung cancer was also associated with substantial risk (OR = 6.36, 95% CI: 2.36-17.13). Race, pack-years of smoking, exposure to environmental tobacco smoke as an adult, childhood asthma, and exposure to asbestos were associated with a history of COPD among lung cancer cases. In women, COPD is associated with risk of lung cancer differentially by race. Untangling whether COPD is in the causal pathway or simply shares risk factors will require future studies to focus on specific COPD features, while exploring underlying genetic susceptibility to these diseases.

Postnatal steroids and chronic lung disease in the newborn.

Chronic lung disease (CLD) represents a condition of persistent inflammation within the airways which may have its origin either in utero or after birth. Corticosteroids, because of their anti- inflammatory actions, have been used to modify the course of CLD. There have been almost 40 randomised controlled trials of postnatal dexamethasone and 12 of inhaled steroids. Systematic reviews of randomised controlled trials of postnatal steroids (either systemic or inhaled) for CLD in the Cochrane Library were evaluated as a guide to clinical practice. Results are presented as relative risks (RR), numbers needed to treat (NNT) or harm (NNH) each with 95% confidence intervals (CI). Postnatal dexamethasone reduces the incidence of CLD and facilitates earlier extubation but with early treatment there are serious long-term neurological adverse effects. Inhaled steroids used early (<2 wk) reduce the need for later dexamethasone (RR 0.78; 0.62-0.99 and NNT 11; 6-125). Inhaled steroids used late (>2 wk) increase the chances of extubation (RR 0.38; 0.20-0.72 and NNT 3; 2-6) and improve ventilator settings and lung mechanics. There appear to be no serious adverse effects of inhaled steroids but comparative studies suggest that dexamethasone acts more rapidly. Postnatal dexamethasone at currently recommended doses should be avoided. Lower dose dexamethasone or inhaled steroids might be indicated for ill, ventilator-dependent infants with CLD after the age of 2 weeks. More trials of inhaled steroids should be undertaken and these should include long-term follow-up.

Predicting chronic lung disease in very low birthweight infants: comparison of 3 scores.

To evaluate 3 scores in their ability to predict Chronic Lung Disease (CLD) in very low birthweight (VLBW) infants. The records of 188 VLBWs admitted to neonatal intensive care within two years were retrospectively reviewed. Two mortality scores -the CRIB (clinical risk index for babies) score and the Berlin admission score- and one morbidity score developed to predict CLD (Sinkin score) were assigned to each infant. Areas (AUC) under receiver operating characteristic (ROC) curves were used for comparison. The Sinkin score and the Berlin admission score had AUCs of 89.0 and 85.8% to predict CLD ("alive in oxygen at 28 days of life"). The AUCs were 87.7 and 81.2%, respectively, using the CLD definition "alive in oxygen at 36 weeks gestational age", the CRIB had an AUC of 77.0%. To enroll patients in trials aimed at early interference with the course of CLD, the Berlin admission score or the Sinkin score could be used.

Postnatal undernutrition slows development of bronchiolar epithelium in rats.

The lung's small conducting airways are sites of dysfunction early in the course of chronic lung diseases that are prevalent in humans; furthermore, there is evidence that aspects of childhood environment may adversely influence small airway function in adulthood. Because there is considerable early postnatal morphological maturation of the bronchiolar epithelium in rats, these considerations led to the present study in which we assessed the effect of early postnatal undernutrition in rats on the anatomic development of the bronchiolar epithelium. We found undernutrition, produced by increasing rat litter size shortly after birth, led to delayed development of the mitochondria and rough endoplasmic reticulum of bronchiolar Clara cells. Of particular interest, underfeeding resulted in considerably diminished mitosis by Clara cells, decreased nuclear numerical density of bronchiolar ciliated cells, evidence of diminished conversion of Clara cells to ciliated cells, and an abnormal cellular composition of the small airway epithelium that persisted well beyond the period of underfeeding. We conclude that early neonatal events can have long-term effects on the bronchiolar epithelium.

Chronic lung disease in the territory of Papula and New Guinea--an epidemiological study.

SummaryA preliminary epidemiological survey of natives in the Eastern and Western Highlands of the Territory of Papua and New Guinea shows that chronic lung disease is common.The disease is more frequently seen in natives aged over 30 years, appears to be restrictive in the early stages but to produce obstruction as well in the later stages, and appears to lead to cor pulmonale. The cause is not known, but repeated infections appear to be an important factor.A definitive epidemiological study is planned to investigate the incidence, nature, cause and course of chronic lung disease and to define its relationship to cor pulmonale. The plan of this study is outlined.