Lower Airway Disease Research Articles

Titanium dioxide nanoparticles exaggerate respiratory syncytial virus-induced airway epithelial barrier dysfunction.

Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infections in children worldwide. While most develop a mild, self-limiting illness, some develop severe acute lower respiratory infection and persistent airway disease. Exposure to ambient particulate matter has been linked to asthma, bronchitis, and viral infection in multiple epidemiological studies. We hypothesized that coexposure to nanoparticles worsens RSV-induced airway epithelial barrier dysfunction. Bronchial epithelial cells were incubated with titanium dioxide nanoparticles (TiO2-NP) or a combination of TiO2-NP and RSV. Structure and function of epithelial cell barrier were analyzed. Viral titer and the role of reactive oxygen species (ROS) generation were evaluated. In vivo, mice were intranasally incubated with TiO2-NP, RSV, or a combination. Lungs and bronchoalveolar lavage (BAL) fluid were harvested for analysis of airway inflammation and apical junctional complex (AJC) disruption. RSV-induced AJC disruption was amplified by TiO2-NP. Nanoparticle exposure increased viral infection in epithelial cells. TiO2-NP induced generation of ROS, and pretreatment with antioxidant, N-acetylcysteine, reversed said barrier dysfunction. In vivo, RSV-induced injury and AJC disruption were augmented in the lungs of mice given TiO2-NP. Airway inflammation was exacerbated, as evidenced by increased white blood cell infiltration into the BAL, along with exaggeration of peribronchial inflammation and AJC disruption. These data demonstrate that TiO2-NP exposure exacerbates RSV-induced AJC dysfunction and increases inflammation by mechanisms involving generation of ROS. Further studies are required to determine whether NP exposure plays a role in the health disparities of asthma and other lung diseases, and why some children experience more severe airway disease with RSV infection.

Hyaluronic acid for the treatment of airway diseases in children: Little evidence for few indications.

Hyaluronic acid (HA) is major physiological component of the extracellular matrix, which, in its high molecular weight form (HMW-HA) has anti-inflammatory properties. The diffusion of many different medical devices for inhalation therapy containing HA has led to an increase in their prescription, also in children. Here, we systematically review the published evidence on the efficacy and safety of HA for the treatment of upper and lower airway diseases in childhood. Relevant published studies (randomized controlled trials) for the efficacy of HA inhalation in children with upper airways diseases, asthma, cystic fibrosis (CF), and non-CF bronchiectasis were searched in Pubmed, Scopus, and Web of Knowledge databases by combining the adequate Medical Subject Headings terms and keywords, with no limit for the year of publication. We identified seven relevant publications for upper airways diseases, one for asthma, and five for CF, while we found no clinical trial including children with non-CF bronchiectasis. Meta-analysis was not conducted due to the heterogeneity of the included studies. The evidence of HA efficacy in the treatment of the upper and lower airways is still limited in children. Available data suggest that inhaled HMW-HA could be useful in the treatment of recurrent upper respiratory infections and chronic or recurrent inflammation of the middle ear and adenoids as well as of the lower airways in cystic fibrosis in association with hypertonic saline solution. Studies on larger populations and on the different formulations and nebulization methods, especially in pediatric age, are urgently needed.

New variants in NLRP3 inflammasome genes increase risk for asthma and Blomia tropicalis-induced allergy in a Brazilian population

Atopic asthma is a chronic lung disease of lower airways caused mainly due to action of T-helper (Th) 2 type cytokines, eosinophilic inflammation, mucus hypersecretion and airway remodelling. Interleukin (IL)-33 increases type 2 immunity polarization in airway playing critical role in eosinophilic asthma. On the other hand, NLRP3 inflammasome activation results in the release of caspase-1 (Casp-1) which, in its turn, promotes IL-33 inactivation. Recent studies have shown associations between NLRP3 variants and inflammatory diseases. However, no study with genes in NLRP3 inflammassome route has been conducted so far with asthma and atopy in any population to date. Blood samples were collected from 1246 asthmatic and non-asthmatic children. Associations were tested for single nucleotide polymorphism (SNP)s in NLRP3 and CASP1 with asthma and markers of atopy and in cultures stimulated with Blomia tropicalis (Bt) mite crude extract. The T allele of rs4925648 (NLRP3) was associated with increased asthma risk (OR 1.50, P = 0.005). In addition, the T allele of rs12130711 polymorphism, whithin the same gene, acted as a protector factor for asthma (OR 0.78, P = 0.038). On the other hand, the C allele of rs4378247 NLRP3 variant was associated with lower levels of IL-13 production when peripheral blood cells were stimulated with Bt (OR 0.39, P = 4E-04). In addition, the greater the number of risk alleles in IL33/NLRP3/CASP1 route the greater was the risk for asthma. The T allele of rs7925706 CASP1 variant was also associated with increased risk for asthma (OR 1.47, P = 0.008). In addition, this same allele increased the eosinophil counts in blood (mm3) in asthmatic individuals compared with non-asthmatic (P = 0.0004). These results suggest that NLRP3 and CASP1 polymorphisms may be associated with susceptibility for asthma and markers of atopy in our population.

Volumetric assessment of paranasal sinus opacification on computed tomography can be automated using a convolutional neural network.

Computed tomography (CT) plays a key role in evaluation of paranasal sinus inflammation, but improved, and standardized, objective assessment is needed. Computerized volumetric analysis has benefits over visual scoring, but typically relies on manual image segmentation, which is difficult and time-consuming, limiting practical applicability. We hypothesized that a convolutional neural network (CNN) algorithm could perform automatic, volumetric segmentation of the paranasal sinuses on CT, enabling efficient, objective measurement of sinus opacification. In this study we performed initial clinical testing of a CNN for fully automatic quantitation of paranasal sinus opacification in the diagnostic workup of patients with chronic upper and lower airway disease. Sinus CT scans were collected on 690 patients who underwent imaging as part of multidisciplinary clinical workup at a tertiary care respiratory hospital between April 2016 and November 2017. A CNN was trained to perform automatic segmentation using a subset of CTs (n = 180) that were segmented manually. A nonoverlapping set (n = 510) was used for testing. CNN opacification scores were compared with Lund-MacKay (LM) visual scores, pulmonary function test results, and other clinical variables using Spearman correlation and linear regression. CNN scores were correlated with LM scores (rho = 0.82, p < 0.001) and with forced expiratory volume in 1 second (FEV1 ) percent predicted (rho = -0.21, p < 0.001), FEV1 /forced vital capacity ratio (rho = -0.27, p < 0.001), immunoglobulin E (rho = 0.20, p < 0.001), eosinophil count (rho = 0.28, p < 0.001), and exhaled nitric oxide (rho = 0.40, p < 0.001). Segmentation of the paranasal sinuses on CT can be automated using a CNN, providing truly objective, volumetric quantitation of sinonasal inflammation.

Bronchial wall thickening is associated with severity of chronic rhinosinusitis.

Though the relationship between chronic rhinosinusitis (CRS) and lower airway diseases is well recognized, the impact of CRS on bronchial wall structure has not been elucidated. Here, we evaluated the bronchial wall structure of CRS patients with or without diagnosed airway diseases by three-dimensional computed tomography (3D-CT). Subjects who underwent both chest CT and sinus CT within a year were recruited from consecutive medical records. CRS was defined as a Lund-Mackay score (LMS) of over 5 points. Airway dimensions were measured using validated software. Standard blood tests and pulmonary function tests were performed, and their correlation with airway thickness was examined. One-hundred-seventy-two patients were recruited (93 CRS subjects and 79 non-CRS subjects). The bronchial walls of CRS subjects were significantly thicker than those of non-CRS subjects. CRS and asthma were related to bronchial wall thickening by multivariate linear regression analysis adjusted for age, smoking status, and chest symptoms. In addition, LMS was significantly correlated with bronchial wall thickening. Airway walls in CRS subjects were thicker than those in non-CRS subjects and associated with the severity of CRS. These data indicate strong relationship between upper and lower airways regardless of chest symptoms or diagnosed airway diseases.

Proximal reflux: biochemical mediators, markers, therapeutic targets, and clinical correlations.

Airway reflux is implicated in the pathophysiology of a wide range of adult and pediatric upper and lower airway diseases. However, the diagnosis of proximal reflux-associated disease remains challenging due to evolving clinical criteria and institutional and regional variances in diagnostic practices. Evidence suggests that nonacidic contents of reflux may serve as both pathologic mediators of and biomarkers for reflux in the upper airway. Furthermore, they offer potential pharmaceutical and surgical intervention targets and are the focus of novel clinical diagnostic tools currently under investigation.

The Effects of Rare SERPINA1 Variants on Lung Function and Emphysema in SPIROMICS.

Rationale: The role of PI (protease inhibitor) type Z heterozygotes and additional rare variant genotypes in the gene encoding alpha-1 antitrypsin, SERPINA1 (serpin peptidase inhibitor, clade A, member 1), in determining chronic obstructive pulmonary disease risk and severity is controversial.Objectives: To comprehensively evaluate the effects of rare SERPINA1 variants on lung function and emphysema phenotypes in subjects with significant tobacco smoke exposure using deep gene resequencing and alpha-1 antitrypsin concentrations.Methods: DNA samples from 1,693 non-Hispanic white individuals, 385 African Americans, and 90 Hispanics with ≥20 pack-years smoking were resequenced for the identification of rare variants (allele frequency < 0.05) in 16.9 kB of SERPINA1.Measurements and Main Results: White PI Z heterozygotes confirmed by sequencing (MZ; n = 74) had lower post-bronchodilator FEV1 (P = 0.007), FEV1/FVC (P = 0.003), and greater computed tomography-based emphysema (P = 0.02) compared with 1,411 white individuals without PI Z, S, or additional rare variants denoted as VR. PI Z-containing compound heterozygotes (ZS/ZVR; n = 7) had lower FEV1/FVC (P = 0.02) and forced expiratory flow, midexpiratory phase (P = 0.009). Nineteen white heterozygotes for five non-S/Z coding variants associated with lower alpha-1 antitrypsin had greater computed tomography-based emphysema compared with those without rare variants. In African Americans, a 5' untranslated region insertion (rs568223361) was associated with lower alpha-1 antitrypsin and functional small airway disease (P = 0.007).Conclusions: In this integrative deep sequencing study of SERPINA1 with alpha-1 antitrypsin concentrations in a heavy smoker and chronic obstructive pulmonary disease cohort, we confirmed the effects of PI Z heterozygote and compound heterozygote genotypes. We demonstrate the cumulative effects of multiple SERPINA1 variants on alpha-1 antitrypsin deficiency, lung function, and emphysema, thus significantly increasing the frequency of SERPINA1 variation associated with respiratory disease in at-risk smokers.

Potentially lethal cystic fibrosis gene variant in the orangutan.

A syndrome of chronic upper and lower airway disease leading to increased morbidity and mortality occurs primarily in captive orangutans. Similarities in symptoms to the inherited human respiratory disease, cystic fibrosis, led us to hypothesize that orangutan respiratory disease is a result of variants in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene. We identified the nonsense variant, c.484A>T (p.Lys162X), in heterozygosity in an unaffected orangutan. Analysis of the pedigree of this orangutan confirmed that both his sire and deceased fetus also harbored the c.484A>T allele. An expression minigene harboring c.484A>T produced no full-length CFTR protein in HEK293 cells. Finally, the c.484A>T CFTR messenger RNA abundance was severely reduced in primary nasal epithelial cells of the orangutan indicating that c.484A>T (p.Lys162X) is potentially lethal. Genetic screening of the captive orangutan population could be used to prevent transmission of this potentially lethal variant, and thus aid in the conservation of this critically endangered species.

Identification of Novel Genes and Biological Pathways That Overlap in Infectious and Nonallergic Diseases of the Upper and Lower Airways Using Network Analyses.

Previous genetic studies on susceptibility to otitis media and airway infections have focused on immune pathways acting within the local mucosal epithelium, and outside of allergic rhinitis and asthma, limited studies exist on the overlaps at the gene, pathway or network level between the upper and lower airways. In this report, we compared [1] pathways identified from network analysis using genes derived from published genome-wide family-based and association studies for otitis media, sinusitis, and lung phenotypes, to [2] pathways identified using differentially expressed genes from RNA-sequence data from lower airway, sinus, and middle ear tissues, in particular cholesteatoma tissue compared to middle ear mucosa. For otitis media, a large number of genes (n = 1,806) were identified as differentially expressed between cholesteatoma and middle ear mucosa, which in turn led to the identification of 68 pathways that are enriched in cholesteatoma. Two differentially expressed genes CR1 and SAA1 overlap in middle ear, sinus, and lower airway samples and are potentially novel genes for otitis media susceptibility. In addition, 56 genes were differentially expressed in both tissues from the middle ear and either sinus or lower airways. Pathways that are common in upper and lower airway diseases, whether from published DNA studies or from our RNA-sequencing analyses, include chromatin organization/remodeling, endocytosis, immune system process, protein folding, and viral process. Taken together, our findings from genetic susceptibility and differential tissue expression studies support the hypothesis that the unified airway theory wherein the upper and lower respiratory tracts act as an integrated unit also applies to infectious and nonallergic airway epithelial disease. Our results may be used as reference for identification of genes or pathways that are relevant to upper and lower airways, whether common across sites, or unique to each disease.

The Roadmap From Allergic Rhinitis to Asthma

Upper and lower airways display some common characteristic described as a holistic model. Because rhinitis may proceed asthma, it is imperative to understand the mechanisms and risk factors responsible for the progression from rhinitis to asthma. Subclinical lower airway abnormalities have been observed in patients with rhinitis without asthma. Recent evidence indicates that these patients may have an increased risk of developing asthma. Environmental and genetic factors can contribute to enhance this possibility. The treatments of rhinitis have also been shown to be beneficial to the lower airway, and therefore potentially modify the natural evolution of the atopic march. Lower airway disease is a good predictor for the roadmap from rhinitis to asthma. The shared genetic link and environmental factors could be essential for this progression. Albeit treatment of rhinitis has a beneficial effect on lower airway defects, their role to prevent the progression to asthma remains yet to be confirmed.

Epithelial dysfunction in chronic respiratory diseases, a shared endotype?

Epithelial barrier defects are being appreciated in various inflammatory disorders; however, causal underlying mechanisms are lacking. In this review, we describe the disruption of the airway epithelium with regard to upper and lower airway diseases, the role of epigenetic alterations underlying this process, and potential novel ways of interfering with dysfunctional epithelial barriers as a novel therapeutic approach. A defective epithelial barrier, impaired innate defence mechanisms or hampered epithelial cell renewal are found in upper and lower airway diseases. Barrier dysfunction might facilitate the entrance of foreign substances, initiating and facilitating the onset of disease. Latest data provided novel insights for possible involvement of epigenetic alterations induced by inflammation or other unknown mechanisms as a potential mechanism responsible for epithelial defects. Additionally, these mechanisms might precede disease development, and represent a novel therapeutic approach for restoring epithelial defects. A better understanding of the role of epigenetics in driving and maintaining epithelial defects in various inflammatory diseases, using state-of-the-art biology tools will be crucial in designing novel therapies to protect or reconstitute a defective airway epithelial barrier.

Eupatilin downregulates phorbol 12-myristate 13-acetate-induced MUC5AC expression via inhibition of p38/ERK/JNK MAPKs signal pathway in human airway epithelial cells.

Chronic inflammatory airway diseases, such as chronic rhinosinusitis, chronic obstructive pulmonary disease, and asthma, are associated with excessive mucus production. Hence, the regulation of mucus production is important for the treatment of upper and lower airway diseases. Eupatilin is a pharmacologically active ingredient obtained from Artemisia asiatica Nakai (Asteraceae) and exerts potent anti-inflammatory, anti-allergic, and anti-tumor activities. In the present study, we investigated the effect of eupatilin on phorbol 12-myristate 13-acetate (PMA)-induced MUC5AC and MUC5B expression in human airway epithelial cells. We found that eupatilin treatment significantly inhibited PMA-induced mucus secretion in PAS staining. In addition, qRT-PCR results showed that eupatilin dose-dependently decreased the mRNA expression of MUC5AC in human airway epithelial cells. Western blot and immunofluorescence assay also showed that PMA-induced protein expression of MUC5AC was inhibited by eupatilin treatment. Finally, we investigated MAPKs activity after stimulation with PMA using western blot analysis in human airway epithelial cells. The results showed that eupatilin downregulated the levels of phosphorylated p38, ERK, and JNK. In summary, the anti-inflammatory activities of eupatilin, characterized as the suppression of MUC5AC expression and secretion in human airway epithelial cells, were found to be associated with the inhibition of p38/ERK/JNK MAPKs signaling pathway of MUC5AC secretion.

Upper and Lower Airways Diseases in Childhood

: In the last decade, extensive research has provided consistent advances in molecular biology and “omics” science (genomics, metabolomics, proteomics, and transcriptomics), which have led to the detailed characterization of the etiology, pathophysiological mechanisms, and subtypes of many diseases. Based on these developments, the concept of precision medicine was established. : About a quarter of medical consultations related to primary care in children involves respiratory problems. About 10% of the cases are asthma, while the other most important respiratory diseases includes bronchiolitis, acute bronchitis and respiratory infections. Today, beyond the most common respiratory pathology, it is appropriate to discuss what are the novelties in the management of more complex, frequent and infrequent, pathologies because they are those in which it is possible to implement the concept of precision medicine.

Wet Cough and Nasal Symptoms in Children: Can We Do Better?

The causes of chronic cough in children are mainly dependent on the setting and age of the child. Protracted bacterial bronchitis is a frequent cause of morbidity in childhood, and antibiotic treatment is beneficial. Prompt recognition and early treatment is important both to prevent inappropriate use of asthma medications and also progression to bronchiectasis, but the diagnosis should not be made uncritically, because chronic wet cough is not necessarily due to lower airway disease. Upper Airway Cough Syndrome (UACS) is considered by some to cause chronic cough in childhood. Underlying UACS are many common conditions, including allergic rhinitis, adenoiditis and rhinosinusitis. Diagnosis relies on a combination of clinical criteria that are relatively sensitive but non-specific. The role of nasal endoscopy in children with chronic cough and signs suggesting UACS is unclear. Nasal saline solution irrigation is commonly used in UACS, but most studies have methodological biases, and efficacy data are scanty. Randomized controlled trials are urgently required. However, if saline washes, rather than oral antibiotics, can effectively treat some children with wet cough associated with upper airway conditions, antibiotic resistance could potentially be reduced. There is a need to further study wet cough and not to assume it to be equivalent to lower airway infection in all children.

Exercise Induced Laryngeal Obstruction in Humans and Equines. A Comparative Review.

Dynamic obstructions of the larynx are a set of disorders that occur during exercise in equines and humans. There are a number of similarities in presentation, diagnosis, pathophysiology and treatment. Both equines and humans present with exercise intolerance secondary to dyspnea. During laryngoscopy at rest, the larynx appears to function normally. Abnormalities are only revealed during laryngoscopy at exercise, seemingly triggered by increased ventilatory demands, and quickly resolve after cessation of exercise. Lower airway disease (asthma being the most prevalent condition), cardiac disease and lack of fitness are the major differentials in both species. Laryngoscopic examination during exercise should be performed from rest to peak exertion to allow for a comprehensive diagnosis, including where the airway collapse begins, and thereafter how it progresses. Dynamic disorders with most visual similarity between humans and equines are: aryepiglottic fold collapse (both species); equine dynamic laryngeal collapse (DLC) relative to some forms of human combined supraglottic/glottic collapse; and epiglottic retroversion (both species). Quantitative grading techniques, such as airway pressure measurement, that have proven effective in veterinary research are currently being piloted in human studies. Conditions that appear visually similar are treated in comparable ways. The similarities of anatomy and certain types of dynamic collapse would suggest that the equine larynx provides a good model for human upper respiratory tract obstruction during exercise. Thus, close collaboration between veterinarians and medical personal may lead to further advancements in understanding pathophysiologic processes, and enhance the development of improved diagnostic tests and treatments that will benefit both species.

Altered Middle Ear Microbiome in Children With Chronic Otitis Media With Effusion and Respiratory Illnesses.

Chronic otitis media with effusion (COME) is a common childhood disease characterized by an accumulation of fluid behind the eardrum. COME often requires surgical intervention and can also lead to significant hearing loss and subsequent learning disabilities. Recent characterization of the middle ear fluid (MEF) microbiome in pediatric patients has led to an improved understanding of the microbiota present in the middle ear during COME. However, it is not currently known how the MEF microbiome might vary due to other conditions, particularly respiratory disorders. Here, we apply an amplicon sequence variant (ASV) pipeline to MEF 16S rRNA high-throughput sequencing data from 50 children with COME (ages 3–176 months) undergoing tube placement. We achieve a more detailed taxonomic resolution than previously reported, including species and genus level resolution. Additionally, we provide the first report of the functional roles of the MEF microbiome and demonstrate that despite high taxonomic diversity, the functional capacity of the MEF microbiome remains uniform between patients. Furthermore, we analyze microbiome differences between children with COME with and without a history of lower airway disease (i.e., asthma or bronchiolitis). The MEF microbiome was less diverse in participants with lower airway disease than in patients without, and phylogenetic β-diversity (weighted UniFrac) was significantly different based on lower airway disease status. Differential abundance between patients with lower airway disease and those without was observed for the genera Haemophilus, Moraxella, Staphylococcus, Alloiococcus, and Turicella. These findings support previous suggestions of a link between COME and respiratory illnesses and emphasize the need for future study of the middle ear and respiratory tract microbiomes in diseases such as asthma and bronchiolitis.

Comparison of signalment, clinical, laboratory and radiographic parameters in cats with feline asthma and chronic bronchitis.

Feline asthma (FA) and feline chronic bronchitis (CB) are common respiratory conditions in cats, frequently referred to as 'feline lower airway disease'. However, the aetiologies of both inflammatory airway diseases are probably different. Little is known about the differences in signalment, clinical signs, laboratory abnormalities and radiographic features between cats with these two airway diseases. The aim of the study was to investigate whether certain parameters can help in differentiating between both diseases, as distinguished by airway cytology. Seventy-three cats with FA and 24 cats with CB were included in the retrospective study. Inclusion criteria were compatible clinical signs and a cytological evaluation of bronchoalveolar lavage fluid indicating either FA (eosinophilic inflammation) or CB (neutrophilic inflammation) without cytological or microbiological evidence of bacterial infection. Parameters of signalment, physical examination, haematology and thoracic radiographs of both disease groups were compared statistically (P <0.05). The median age of cats with FA was 6 years, and was 7.5 years in cats with CB (P = 0.640). The most commonly reported clinical signs in both groups were a cough (95% FA/96% CB; P = 1.000), pathological pulmonary auscultatory sounds (82% FA/79% CB; P = 0.766) and dyspnoea (73% FA/79% CB; P = 0.601). Abnormal radiographic lung patterns were detected in 94% of cats with FA and 91% with CB (P = 0.629), respectively. Blood eosinophilia was significantly more common in cats with FA (40%) compared with CB (27%) (P = 0.026). The study indicates that a differentiation of FA and CB by means of signalment, a single clinical sign, and haematological and radiographic findings is not possible.

Identifying Clinical and Research Priorities in Sickle Cell Lung Disease. An Official American Thoracic Society Workshop Report.

Background: Pulmonary complications of sickle cell disease (SCD) are diverse and encompass acute and chronic disease. The understanding of the natural history of pulmonary complications of SCD is limited, no specific therapies exist, and these complications are a primary cause of morbidity and mortality.Methods: We gathered a multidisciplinary group of pediatric and adult hematologists, pulmonologists, and emergency medicine physicians with expertise in SCD-related lung disease along with an SCD patient advocate for an American Thoracic Society–sponsored workshop to review the literature and identify key unanswered clinical and research questions. Participants were divided into four subcommittees on the basis of expertise: 1) acute chest syndrome, 2) lower airways disease and pulmonary function, 3) sleep-disordered breathing and hypoxia, and 4) pulmonary vascular complications of SCD. Before the workshop, a comprehensive literature review of each subtopic was conducted. Clinically important questions were developed after literature review and were finalized by group discussion and consensus.Results: Current knowledge is based on small, predominantly observational studies, few multicenter longitudinal studies, and even fewer high-quality interventional trials specifically targeting the pulmonary complications of SCD. Each subcommittee identified the three or four most important unanswered questions in their topic area for researchers to direct the next steps of clinical investigation.Conclusions: Important and clinically relevant questions regarding sickle cell lung disease remain unanswered. High-quality, multicenter, longitudinal studies and randomized clinical trials designed and implemented by teams of multidisciplinary clinician-investigators are needed to improve the care of individuals with SCD.

Demographic and clinical profile of chronic rhinosinusitis patients in a rural based tertiary hospital

&lt;p class="abstract"&gt;&lt;strong&gt;Background:&lt;/strong&gt; Chronic rhinosinusitis (CRS) is one of the most common health problems which incurs significant medical costs and has severe impact on lower airway diseases and general health of the patient. The aim of this study was to describe the demographic and clinical profile of chronic rhinosinusitis patients.&lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Methods:&lt;/strong&gt; In this study 94 patients were included. After taking a brief history, their clinical symptoms were assessed using SNSG test (sino nasal symptom grading test). The findings were further confirmed by diagnostic nasal endoscopy. &lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Results:&lt;/strong&gt; We found that maximum number of patients were in the age group of 18-27 years with a slight male preponderance. Also rural population had more cases of CRS with nasal discharge being the commonest complaint at the time of presentation. After diagnostic nasal endoscopy (DNE) it was found that ethmoidal polyps are more common in CRS patients however more number of CRS patients presented without polyps.&lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Conclusions:&lt;/strong&gt; We conclude that chronic rhinosinusitis manifests more in male and rural population with nasal discharge and ethomoidal polyps being the most common presentation. The subjective assessment of clinical symptoms could be done by SNSG test; however it further requires detailed studies.&lt;/p&gt;&lt;p class="abstract"&gt; &lt;/p&gt;

Feline asthma and heartworm disease: Clinical features, diagnostics and therapeutics.

For feline practitioners, the cat with a cough or respiratory distress and thoracic radiographs with a bronchial or bronchointerstitial pattern suggests lower airway disease. Two important differentials, allergic asthma and heartworm disease (HWD), have many overlapping clinicopathologic features, but also clear and important differences in terms of cause and disease progression, treatment and prognosis. Notably, asthma is readily treatable and HWD is preventable. Feline HWD comprises two clinical syndromes: the comparatively recently described heartworm-associated respiratory disease (HARD) and adult HWD. The former is much more common; very few cats with HARD develop adult HWD. In HARD, following death of immature worms, pulmonary lesions may improve over time ('self-cure'). Lesions of adult HWD also improve over time as long as reinfection does not occur; however, with death of adult heartworms, mortality is high, and the prognosis is guarded. In asthma, morbidity is relatively high, but mortality is low, with an overall good to excellent prognosis. Feline asthma is encountered worldwide. In the authors' impression, feline HWD is often under-recognized. The aim of this review is to assist clinicians in differentiating feline asthma from feline HWD; as such, the emphasis is on distinguishing clinical features, as well as on diagnostics, therapy and prognosis. In differentiating these conditions, clinicians can attempt the goal of properly managing these diseases and can best educate owners on prognosis. For both feline asthma and feline HWD, the authors have drawn on the available peer-reviewed literature studies involving experimental models as well as spontaneous disease.