Introduction: There is currently no strategy for identifying chronic obstructive pulmonary disease (COPD) patients whose pulmonary function could benefit from inhaled corticosteroids. We investigated whether a 28-day regime of inhaled corticosteroids improved pulmonary function test results among COPD patients with a fractional exhaled nitric oxide concentration > 35 parts per billion. Methods: This single-centre one-arm pre–post trial included COPD patients with a fractional exhaled nitric oxide concentration > 35 parts per billion treated at our institution from September 2018 to August 2019. Patients were administered budesonide (200 μg, 8 puffs daily) for 28 days. The primary outcome measure was the difference between the forced expiratory volume in 1 s (FEV1) at baseline and after 28 days of inhaled corticosteroid treatment. Secondary outcomes included differences in COPD Assessment Test scores, %FEV1, and that between the percent forced vital capacity (%FVC) at baseline and after 28 days of treatment. Results: Twenty patients completed the 28-day inhaled corticosteroid regime. The mean difference in FEV1 between day 1 and day 28 was 340 mL (95% confidence interval: −100 to 770 mL; p = 0.122). The mean differences in secondary outcomes were: %FVC, −0.16% (95% confidence interval [CI]: −2.84 to 2.53%; p = 0.905); %FEV1, 1.63% (95%CI: −4.56 to 7.81%; p = 0.589); COPD Assessment Test score, −2.50 (95%CI: −5.72 to 0.72; p = 0.121). Conclusion: The 28-day course of inhaled corticosteroids yielded no significant difference in FEV1 for COPD patients with a fractional exhaled nitric oxide concentration > 35 parts per billion. Trial registration: University Hospital Medical Information Network Center, UMIN000034005. Registered 3 September 2018. https://upload.umin.ac.jp/cgi-open-bin/ctr/ctr_view.cgi?recptno=R000038557

Irvine-Gass syndrome, is one of the most common causes of painless decrease in vision following even uneventful cataract surgery. It usually responds well to medical therapy, but, there are no widely acceptedconsensus on the efficacy of various therapeutic options for the treatment of Irvine-Gass syndrome. The patient presenting in this case report, has systemic hypertension and chronic obstructive pulmonary disease and he use oral anti-hypertension medication and inhaler steroid. He diagnosed as Irvine-Gass syndrome due to presence of decrease in visual acuity and macular edema with hyporeflective cystic intraretinal spaces in optical coherence tomography (OCT) since4th weekcontrol visitfollowing uneventful cataract surgery. After the responsiveness of several medications including topical steroid and non-steroidal anti-inflammatory drugs and intravitreal injection of anti-vascular endothelial growth factor (anti-VEGF), intravitreal sustained-release dexamethasone implant was applied. The visual acuity improved to 0.00 logMAR at 1st month after intravitreal dexamethasone therapy and consecutive OCT images showed complete resolution of macular edema with a normalization of the foveal profile.The visual acuity and foveal architecture remained stable in 2-year follow-up period and additional treatment was not needed. To the best of our knowledge, this is the first reportthatmentions the increment of visual acuity after a single dexamethasone implant, even though it did not response anti-VEGF combined with topical steroid and non-steroidal anti-inflammatory drugs. 

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death and its prevalence and incidence is also related to smoking behavior [1]. COPD is still a chronic inflammatory and progressive disease caused by multifactorial agents including environmental pollutants [2]. Besides that, it is emerging that endogenous epigenetic factors induced by lifestyle and environment [3] could play a role in the etiopathogenesis of the disease [4]. In the last years, several authors suggested that low vitamin D levels seem to be related with the increase of COPD manifestations [5]. Moreover, a multicentre, double-blind, randomised controlled trial documented that vitamin D supplementation protects against moderate or severe exacerbation of the disease, but not by upper respiratory infections [6]. However, low levels of vitamin D can be extended to many other diseases, including multiple sclerosis, diabetes, colon rectal cancer, headache or drug use [7-11]. Moreover, it is also important to remember that Vitamin D deficiency is common in high latitude regions, such as northern Europe, New Zealand, northern USA, and Canada where weaker ultraviolet B rays is not able to produce enough vitamin D. Finally, methodological factors (using low sensitivity methods) could contribute to misleading evaluation of circulating vitamin D levels. In any case, here we shall remind that vitamin D has a fundamental role in immunity [12]. In particular, it has been reported that vitamin D is able to shift the pro-inflammatory T-helper cell 1 to anti-inflammatory T-helper cell 2 [13]. Therefore, benefits of vitamin D supplementation in chronic diseases which directly or indirectly affect immune system are obvious. Today, the burden of COPD in never smokers is higher than previously believed. Therefore, more research is needed to unravel the characteristics of non-smokers COPD [1]. Notably, vitamin D levels are reported to be significantly lower in smoker’ssubjects than in non-smokers ones [14]. Therefore, low plasma vitamin D levels in COPD seems to be more a causality than a correlation.

Blood plays an important role in oxygen absorption and its transfer to organs and tissues in vertebrates, as well as in a number of invertebrate species. Numerous interactions between cellular and non-cellular blood components constantly occur. A special role in these interactions belongs to erythrocytes and leukocytes, between which oxygen is constantly exchanged and activated, which we showed directly in whole blood. Blood is a liquid tissue, which is a complex cooperative system and has many inherent functions and the most important one is the ability to maintain the homeostasis of the body. Our experience has shown that despite its high optical density, undiluted blood of humans and animals can be a source of radiation due to the transformation of the energy of electron-excited (EEE) states and secondary processes occurring in the whole blood system. Parameters of this radiation - ultra-weak photons emission (UWPE) from blood - depend upon its physiological properties and reflect the physiological state of a donor. Analysis of UWPE from non-diluted blood is a simple and sensitive method that allows to monitor the course of treatment of a patient. In spite of high opacity of non-diluted blood it may be a strong source of UWPE both in the presence and absence of UWPE enhancers. Analysis of patterns of UWPE from blood reveals its highly non-linear, stable non-equilibrium and cooperative properties. Characteristic of a living system.

Spontaneous pneumomediastinum (SPM) is a rare condition, more commonly seen in patients with history of asthma, chronic obstructive pulmonary disease, infections, or drug users. Today, we face one novel virus that has cause an outbreak of acute respiratory illness, affecting over a million individuals worldwide. New knowledge is been gained of the virus and possible complications are been seen. Following, we present the case of a 71-year-old man with diagnosis of COVID-19 pneumonia complicated with spontaneous pneumomediastinum.

As we know that, Asthma and chronic obstructive pulmonary diseases are well characterized diseases, they can co-exist as asthma-COPD overlap (ACO). The co-existence of asthma-chronic obstructive pulmonary disease overlap (ACO) in chronic obstructive pulmonary disease (COPD) patients is often unrecognized. In patients with a primary diagnosis of COPD or Asthma, the identification of ACO has got implication for better prognosis and treatment. Such patients experience frequent exacerbations, poor quality of life, rapid decline in lung function and high mortality than COPD or Asthma alone. Inhalational steroids provide significant alleviation of symptoms in such patients and some studies suggest that the most severe patients may respond to biological agents indicated for severe asthma. Patients who have asthma with a COPD component tend to present with severe hypoxia because of Irreversible/fixed airway obstruction and impairment of the alveolar diffusion capacity by emphysematous changes. In contrast, patients with COPD who have an asthma component not only have exertional dyspnoea but also develop paroxysmal wheezing or dyspnoea at night or in the early morning. The criteria to diagnose asthma-COPD overlap (ACO) include positive bronchodilator response, sputum eosinophilia or previous diagnosis of asthma, high IgE and/or history of atopy. There is scarcity of literature available in country like India. We highlight the importance of identification of Asthma COPD overlap as different phenotype from COPD or asthma alone as it is challenging to diagnose ACO in India. We report 3 cases having both the features of asthma and COPD, later diagnosed with Asthma-COPD overlap.

As per report of WHO [1] (World Health Organization), air pollution (ambient/outdoor and household/indoor air pollution) kills an estimated seven million people worldwide every year largely as a result of increased mortality from stroke, heart disease, chronic obstructive pulmonary disease, lung cancer and acute respiratory infections. Data of WHO shows that 9 out of 10 people breathe air containing high levels of pollutants. World Health Organization is working with countries to monitor air pollution and improve air quality. From smog hanging over cities to smoke inside the home, air pollution poses a major threat to health and climate. More than 80% of people living in urban areas and around 91% of the world’s population live in places where air quality levels exceed WHO limits, with developing and under-developed countries suffering from the highest exposures, both indoors and outdoors [1]. While outdoor air pollution comes from the motor vehicles, burning of fossil fuels and other industrialization activities, indoor air pollution is the result of tobacco smoke and burning fuel for cooking & heating. Furniture and construction materials also emit such pollutants. Both outdoor and indoor air pollution are harmful to the human health.

The European Society of Cardiology (ESC) and the European Society of Hypertension (ESH) jointly developed a series of hypertension guidelines in the years 2003, 207 and 2013. The most recent guidelines were issued by the two societies in August this year (2018) and were published in the European Heart Journal. The new guidelines are printed in more than 90 pages and cover almost all aspects of hypertension based on extensive review of literature giving highest priority to data from randomized controlled trials and well conducted meta-analysis. In important areas where there is inadequate or no evidence, guidelines authors resort to expert opinion. The text was developed over approximately 24 months and was reviewed by representatives of ESC and ESH national hypertension societies. Although it is less than five years since the last hypertension European guidelines in 2013, the recent 2018 guidelines show important differences in diagnosis and treatment strategies with the addition of new sections and recommendations on management of hypertensive emergencies, hypertension in women and pregnancy, different ethnic groups, chronic obstructive pulmonary disease, cancer therapies, peri-operative management, sexual dysfunction and perioperative management.

Introduction: Acute kidney injury (AKI) is one of the complications associated with severe COVID-19 infection, and it can present in up to 20% to 40% of the cases; of these, approximately 20% will require renal replacement therapy (RRT). Objective: To establish clinical and laboratory characteristics in a group of patients from Colombia with COVID-19 infection and AKI that received intermittent and prolonged RRT with the GENIUS® 90 technology in between March and July 2020. Design: Cross-sectional study. Results: 78.9% of participants were men and 21.1% were women. The main comorbidities were the following: Hypertension (65.3%), diabetes mellitus (38.9%), obesity (26.3%), cancer (5.3%), Chronic obstructive pulmonary disease (11.6%), cardiovascular disease (23.2%), active smoking (11.6%). 33.7% had chronic kidney disease (CKD) in the average serum creatinine on admission was 4.4 mg/dl. The following inflammatory markers were elevated: C-reactive protein (CRP), d-dimer and ferritin (20.3 mg/dl, 931mcg/l and 1174 ng/ml, respectively). 63.5% of patients underwent sustained low-efficiency dialysis (SLED) (6 to 12 hours) and the rest of the patients (36.35%) underwent conventional hemodialysis (less than 4 hours). The mortality of the total patient sample was 36.9%, lower in patients with CKD than in patients with no previous renal disease history (18.7% and 40.1%, respectively). Conclusion: Renal complications are frequent in patients with severe COVID-19. The development of AKI could be an isolated prognostic marker associated with an increase in mortality in patients with COVID-19, and one of the options is intermittent and prolonged RRT with the GENIUS® 90 system.

Background: Changes in lung structures persist in stable Chronic Obstructive Pulmonary Disease (COPD), but their correlation with the clinical picture remains unclear. The purpose of this study was to assess the stable COPD picture via the relationship between exhaled breath condensate (EBC) particle concentration and the Saint George Respiratory Questionnaire (SGRQ), COPD Assessment Test (CAT), and six-minute walking test (6 MWT). Methods: 12 stable COPD and 12 healthy subjects participated in the study. The EBC was collected with Rtube and analyzed using the Accusizer FxNano. Particle concentration was measured and correlated with the findings of the tools used to assess the health status and functional profile of COPD. The results’ analysis was performed with the Spearman’s test and the Mann-Whitney U - test.Results: The COPD group presented a worse picture of health status and functional profile compared to the healthy group. Correlations were observed between components of the SGRQ and CAT. The two groups presented similar levels of EBC particle concentrations, but the number of small particles was higher in COPD subjects. A correlation of the EBC particle concentration with the activity and total score of the SGRQ was only observed in the healthy group. Conclusion: The total particle number was similar in the COPD and healthy groups. A few correlations between the EBC particles and tools used were also observed. The use of EBC particle concentration to monitor COPD status cannot be claimed with confidence because of the small sample size. Further research is necessary, particularly in large-scale groups.

Objective: To investigate the mechanism of MCP-1 and TGF-β regulation by TAK242 in COPD rats. Methods: Thirty-six SD rats were randomly divided into normal, COPD control, and TAK242 groups. The normal group was freely fed, and the other groups used the method of fumigation plus lipopolysaccharide tracheal drip to establish an experimental animal model of COPD. After successful modeling, each experimental group received 0.9% NaCl solution and corresponding drugs by intraperitoneal injection for 7 d. After drug administration, lung function was examined; pathological changes in lung tissue were observed by light microscopy with hematoxylin-eosin staining; mRNA expression of MCP-1 and TGF-β was detected by q-PCR; and protein expression of MCP-1 and TGF-β in lung tissue was detected by Western blot and IHC, TGF-β protein expression in rat lung tissue. Results: Compared with the normal group, rats in the COPD control group showed signs and symptoms of COPD, decreased lung function, and increased expression of MCP-1 and TGF-β. The TAK242 group showed decreased expression of MCP-1 and TGF-β compared to the COPD control group. Conclusion: MCP-1, and TGF-β played a crucial role in the early stage of COPD fibrosis. TAK242 could ameliorate airway inflammation and inhibit the progression of COPD lung fibrosis in pre-existing rats in COPD model rats.