When and how to wear medical masks to protect against coronavirus

By Dr Deepu

• Before putting on a mask, clean hands with alcohol-based hand rub or soap and water.
• Cover mouth and nose with mask and make sure there are no gaps between your face and the mask.
• Avoid touching the mask while using it; if you do, clean your hands with alcohol-based hand rub or soap and water.
• Replace the mask with a new one as soon as it is damp and do not re-use single-use masks.
• To remove the mask: remove it from behind (do not touch the front of mask); discard immediately in a closed bin; clean hands with alcohol-based hand rub or soap and water.

COVID -19 update

By Dr Deepu

WHAT IS COVID-19?

Coronaviruses (CoV) are a large family of viruses that cause illness ranging from the common cold to more serious diseases such as Severe Acute Respiratory Syndrome (SARS-CoV).

The 2019 novel coronavirus is a new strain that has not been seen in humans until now and has caused viral pneumonia. It was first linked to Wuhan’s South China Seafood City market which is a wholesale market for seafood and live animals in December 2019.

The virus has now been detected in several areas throughout China, along with countries across Asia, North and South America, Europe, Africa and Oceana.

WHAT DO THE DIFFERENT NAMES MEAN?

You may have noticed different names circulating which relate to the novel corona virus. Below we have listed some of the more common names and explained what they mean.

COVID-19- this is the name for the disease caused by the coronavirus. This is simply short for coronavirus disease 2019. The World Health Organization announced this name on the 11 February 2020.

SARS-CoV-2- severe acute respiratory syndrome-related coronavirus 2. This is the name of the virus, not the disease that results from it. The world Health Organization emphasizes that while the viruses are related, COVID-19 is different from the SARS outbreak of 2003.

Novel corona virus 2019 (nCoV-19)- this was initially used at the start of the outbreak. It refers to the virus which is a novel form of the coronavirus that was first seen in 2019.

Coronavirus- you may see or hear about the virus referred to just as the coronavirus. This is not inaccurate as it is a novel strain of a coronavirus.

SYMPTOMS

The World Health Organization (WHO) advises that the most common symptoms of COVID-19 are fever, tiredness, and dry cough. Some people may experience aches and pains, nasal congestion, runny nose, sore throat or diarrhea. These symptoms are usually mild and begin gradually.

People with pre-existing medical conditions (such as asthma and COPD) are more likely to become severely ill with the virus.

WHAT CAN I DO TO LIMIT MY RISK OF CATCHING COVID-19?

• Do not touch your mouth, nose or eyes with unwashed hands
• Try to avoid contact with people who are sick
• Cover your coughs and sneezes with a tissue and throw it in a bin and
• Wash your hands thoroughly after touching surfaces that may be contaminated

PROPER HAND WASHING TECHNIQUE

• Wet your hands under running water
• apply soap
• rub hands together vigorously for at least 20 seconds.
• make sure you apply soap to all parts of your hands including the backs, between your fingers, fingertips, around and under your nails, thumbs and wrists
• thoroughly rinse your hands under running water
• turn off the tap with a paper towel to avoid recontaminating your hands and
• dry your hands with a disposable paper towel or hand dryer (do not touch the hand dryer).

PROPER ALCOHOL GEL (HAND SANITIZER) TECHNIQUE

• Apply one to two squirts of hand sanitizer to your hands
• rub all over your hands including: the backs, between your fingers, fingertips, around and under your nails, thumbs and wrists and
• allow the hand sanitizer to dry. This takes about 20-30 seconds.

SHOULD I BE WORRIED ABOUT TRAVELLING?

Due to the changing nature of travel restrictions, please refer to the World Health Organization for updates.

As symptoms include fever and difficulty breathing, you are advised to speak with a doctor and to make them aware of your travel history if you experience these during or after travel.

Exit screening at international airports and ports in the affected areas may take place to prevent the disease from spreading.

Severe COVID-19 risk could be increased in people with COPD and smokers

By Dr Deepu

People with chronic obstructive pulmonary disease (COPD) and people who currently smoke may have higher levels of a molecule, called angiotensin converting enzyme II (ACE-2), in their lungs according to a study published in the European Respiratory Journal (ERJ).

Previous research shows that ACE-2, which sits on the surface of lung cells, is the ‘entry point’ that allows coronavirus to get into the cells of the lungs and cause an infection.

The new study also shows that levels of ACE-2 in former smokers is lower than in current smokers.

The research was led by Dr Janice Leung at the University of British Columbia and St. Paul’s Hospital, Vancouver, Canada. She said: “The data emerging from China suggested that patients with COPD were at higher risk of having worse outcomes from COVID-19. We hypothesised that this could be because the levels of ACE-2 in their airways might be increased compared to people without COPD, which could possibly make it easier for the virus to infect the airway.”

The team studied samples taken from the lungs of 21 COPD patients and 21 people who did not have COPD. They tested the samples to gauge the level of ACE-2 and compared this with other factors, such whether they were from people who never smoked, were current smokers or former smokers. Not only did they find higher levels of ACE-2 in COPD patients, they also found higher levels in people who were smokers.

The researchers then checked their new findings against two existing study groups, which together contain data on a further 249 people – some non-smokers, some current smokers and some former smokers. Again, they found levels of ACE-2 were higher in current smokers but lower in non-smokers and in those who were former smokers.

Dr Leung said: “We found that patients with COPD and people who are still smoking have higher levels of ACE-2 in their airways, which might put them at an increased risk of developing severe COVID-19 infections. Patients with COPD should be counselled to strictly abide by social distancing and proper hand hygiene to prevent infection.

“We also found that former smokers had similar levels of ACE-2 to people who had never smoked. This suggests that there has never been a better time to quit smoking to protect yourself from COVID-19.”

HRCT findings in various ILDs

By Dr Deepu
Here is an easy pictorial representation of the various ILD.

Anti-malondialdehyde-acetaldehyde adducts antibodies in lung tissues may play important role in pathogenesis of RA-associated interstitial lung disease, study indicates

By Dr Deepu

Anti-malondialdehyde-acetaldehyde adducts (MAA) antibodies and MAA expression in lung tissues of patients with rheumatoid arthritis-associated interstitial lung disease (RA-ILD) likely play an important role in RA-ILD pathogenesis, and anti-MAA antibodies may function well as serum biomarkers in the identification of this disease manifestation.

Patients with RA face premature mortality and RA-ILD is a major determinant of worse long-term outcomes, with a median survival as short as 3 years after diagnosis. In the present study, researchers compared serum anti-MAA antibodies and MAA expression in lung tissues of patients from 13 sites fulfilling the 1987 American College of Rheumatology criteria by selecting participants from the Veterans Affairs Rheumatoid Arthritis Registry.

Multivariable logistic regression models were used to assess the association between anti-MAA antibodies (immunoglobulins A, M, and G [IgA, IgM, IgG]) and RA-ILD status by combining RA alone with RA+chronic obstructive pulmonary disease (COPD) for a comparator group, as unadjusted comparisons found no significant differences in concentrations of anti-MAA antibodies between these groups. Lung tissues from RA-ILD patients, and other patients with ILD, emphysema, and controls were stained for MAA, macrophages (CD68), citrulline, B cells (CD19/CD27), T cells (CD3), and extracellular matrix proteins (fibronectin, vimentin, type-II collagen). Lung tissue expression and MAA co-localization were quantified and compared.

Among the total 1823 participants with RA, 90 had RA-ILD. Higher serum concentrations of IgM and IgA anti-MAA antibodies were seen in RA-ILD vs RA+COPD or RA alone (P =.005). After adjustment for covariates, the highest quartiles of IgM (odds ratio [OR] 2.23; 95% CI, 1.19-4.15) and IgA (OR 2.09; 95% CI, 1.11-3.90) anti-MAA antibody were significantly associated with RA-ILD. MAA expression in lung tissue was greater in RA-ILD than all other groups (P  <.001). The RA-ILD group also showed the greatest degree of MAA co-localized with CD19+ B cells (r =0.78), citrulline (r =0.79), and extracellular matrix proteins (type-II collagen [r =0.72] and vimentin [r =0.77]).

The study authors concluded the study by noting "These findings suggest that MAA immune responses could play an important role in the pathogenesis of RA-ILD and anti-MAA antibodies may be promising serum biomarkers in the identification of this extra-articular disease manifestation"

The finding were published in arthritis and rheumatology

Many children with asthma do not use inhalers properly, study indicates

By Dr Deepu

Research indicates “many children with asthma don’t use their inhalers properly and don’t get a full dose of medicine.” Investigators looked at “inhaler use among 113 children between the ages of 2 and 16 who were hospitalized for asthma.” The researchers found that “at least one crucial step in inhaler technique was missed by 42% of the children,” and approximately “18% did not use a spacer device with their inhaler.” The findings were published in the Journal of Hospital Medicine.

Tuberculosis could be eliminated by 2045, researchers suggest

By Dr Deepu

A new study by researchers  suggests that “increased investment in evidence-based interventions to diagnose, treat, and prevent tuberculosis (TB), especially in high-burden countries, could help end TB” by the year 2045. These interventions should not only “be scaled up, but greater investment and research is needed to develop new methods of diagnosis, treatment, and prevention around the world, [researchers] reported.” Additionally, they suggest that “responsibility for investing in TB programs should be shared between domestic allocation in these countries, as well as external funding through increased developmental assistance.”

The authors mentioned that”to reach these goals, global investment in TB research and development will need to increase to at least $2 billion per year during the next 4 years”.

With the goals of treating 40 million people and preventing 30 million new cases from 2018-2022, the United Nations held its first-ever "high-level meeting" about TB,in September 2018

A TB-free world is possible by 2045 if "increased political will and financial resources" are targeted towards areas where they are needed most, as stated in the report

 In India, the country with the highest burden of TB,  "unavoidable tuberculosis deaths" will cost the country at least $32 billion each year over the next 30 years, even with "optimal implementation of existing tools." The authors also have mentioned that the savings from averting a TB death can be three times the costs in certain countries.

Tuberculosis was declared a global emergency by WHO in 1993. Then, about a third of the world’s population was infected with the bacteria that cause tuberculosis, and the disease was responsible for an estimated 3 million deaths each year. Today, around a quarter of the world’s population has a tuberculosis infection, which causes about 1·6 million annual deaths, making it the leading infectious killer of our time. Although progress has been made in reducing the global burden of tuberculosis in the past 25 years, it has occurred at a frustratingly slow rate. Declines in tuberculosis mortality are not keeping pace with reductions in deaths from other infectious diseases of global importance such as HIV and malaria, and the world is not on track to meet targets set out in the Sustainable Development Goals and the WHO End TB Strategy.

The findings were published in The Lancet.

Statins in Asthma COPD overlap may bring down the risk of CAD and stroke risk

By Dr Deepu

Recently published study in atherosclerosis journal has found that the risk for CAD was lower in all statin-treated patients with ACOS. Whereas the risk for ischemic stroke was lower only in long-term statin users with ACOS. There was no link  between risk for hemorrhagic stroke and  statin use.

A retrospective cohort study was conducted using data from the Longitudinal Health Insurance Database, which included 1 million enrollees in the Taiwan National Health Insurance program from January 1, 2000, through December 31, 2011.

Patients ≥20 years of age with ACOS who were treated with statins (n=916) and those who did not receive statin therapy (n=6338) were enrolled in the study. Investigators examined the cumulative incidence of CAD and stroke (both ischemic and hemorrhagic) with the use of time-dependent Cox proportional regression. Following adjustments for age, sex, inhaled corticosteroid use, oral steroid use, and comorbidities, adjusted hazard ratios (aHRs) and 95% CIs for CAD or stroke in statin users (long-term statin use: >600 days; short-term statin use: ≤600 days) were compared with these values in statin nonusers.

In statin users, the aHRs for CAD and stroke were 0.50 (95% CI, 0.41-0.62) and 0.83 (95% CI, 0.63-1.09), respectively. Furthermore, aHRs for ischemic and hemorrhagic stroke were 0.30 (95% CI, 0.09-0.99) and 0.90 (95% CI, 0.68-1.20), respectively. In addition, in long-term statin users, aHRs for CAD and stroke were 0.23 (95% CI, 0.13-0.41) and 0.42 (95% CI, 0.19-0.89), respectively. In short-term statin users, aHRs for CAD and stroke were 0.58 (95% CI, 0.47-0.71) and 0.93 (95% CI, 0.70-1.23), respectively.

A major limitation of the current study is that lipid levels were not taken into account. Moreover, although a new-user study design was employed, with propensity score matching and a time-dependent model for analysis, results were not as accurate as those derived from randomized controlled trials.

The investigators concluded that regardless of the duration of statin use, the risk for CAD was lower in all statin-treated patients with ACOS. In contrast, the risk for ischemic stroke was lower only in long-term statin users with ACOS, and no link was observed between risk for hemorrhagic stroke and use of statin therapy.

The study was published in atherosclerosis journal

Exposure to silica dust may trigger pulmonary fibrosis in human and mouse cells, study indicates

By Dr Deepu

Researchers found in “both human cells and mice” that “exposure to silica dust may trigger pulmonary fibrosis (PF) because silica particles block a self-cleansing process used by cells, termed autophagy, which drives cell death in the lungs.”

The researchers have summarized their study by saying” we have shown that autophagy participates in SiNPs-induced PF. We have also identified that the autophagic flux blockage results from lysosomal acidification inhibition, which then triggers apoptosis in AECs and subsequent PF. These findings provide a new mechanism by which SiNPs trigger PF by targeting AECs. Furthermore, these results may lead to new strategies to prevent SiNPs-induced PF by enhancing autophagic degradation”.

The findings were published in Cell Death & Disease.

One-year treatment with cyclophosphamide tied to short-term improvements in patients with symptomatic systemic sclerosis-related interstitial lung disease, study indicates

By Dr Deepu

Researchers found that “in patients with symptomatic systemic sclerosis (SSc)-related interstitial lung disease (ILD), 1-year treatment with the immunosuppressant cyclophosphamide (CYC) is associated with short-term improvements in forced vital capacity (FVC)%-predicted and the modified Rodnan skin score (mRSS), but not in the diffusing capacity of the lungs for carbon monoxide (DLCO)%-predicted.”

Participants enrolled in the CYC arms of SLS I (n = 79) and II (n = 69) were included in the study. SLS I and II randomized participants to oral CYC for 1 year and followed patients for an additional year off therapy (in SLS II, patients received placebo in Year 2). Outcomes included the forced vital capacity (FVC%)-predicted and DLCO%-predicted (measured every 3 months) and quantitative radiographic extent of interstitial lung disease (measured at 1 and 2 yearsrs for SLS I and SLS II, respectively). Joint models were created to evaluate the treatment effect on the course of the FVC/DLCO over 2 years while controlling for baseline disease severity.

Researchers found that SLS I and II CYC participants had similar baseline characteristics. After adjusting for baseline disease severity, there was no difference in the course of the FVC%-predicted (p = 0.535) nor the DLCO%-predicted (p = 0.172) between the SLS I and II CYC arms. In both groups, treatment with CYC led to a significant improvement in the FVC%-predicted from 3 to 12 months, but no significant improvement beyond this point. Treatment with CYC had no effect on the DLCO for either group.

Finally they could conclude that Treatment with 1 year of oral CYC led to similar improvements in lung function in both SLS I and II, although the effects were not sustained following cessation of CYC. These results suggest that increasing the duration of ILD therapy may improve outcomes for patients with systemic sclerosis–ILD.

The findings were published in the Journal of Rheumatology.

People who receive flu vaccine while hospitalized no more likely to require extra care than inpatients who are not vaccinated, suggests a large study

By Dr Deepu

 In a recent study, the researchers evaluated the risk of outcomes of interest between those who received influenza vaccination during their hospitalization vs those who were never vaccinated that season or were vaccinated at other times using propensity score analyses with inverse probability of treatment weighting. Outcomes of interest included rates of outpatient and emergency department visits, readmissions, fever, and clinical laboratory evaluations for infection (urine, blood, and wound culture; complete blood cell count) in the 7 days following discharge. Data on 290,149 US hospitalizations involving 255,737 patients over three consecutive flu seasons has suggested that patients who receive the flu vaccine while hospitalized are no more likely to develop fever or require extra doctor or hospital visits after they go home than inpatients who don’t get vaccinated. The author's have concluded that findings provide reassurance about the safety of influenza vaccination during hospitalization. Every contact with a health care professional, including during a hospitalization, is an opportunity to vaccinate. The findings were published in Mayo Clinic Proceedings.

Research looks into COPD risk among never-smokers

By Dr Deepu

Data from the years 2012-2015 was pulled from the National Health Interview Survey (NHIS), a cross-sectional household survey conducted annually by the National Center for Health Statistics (NCHS). All subjects were aged 40 years or older and self-reported a COPD diagnosis.
Urbanization was evaluated using the 2013 NCHS Urban-Rural Classification that divides counties into 6 categories: large metro, central (urban); large metro, fringe( suburban); medium metro; small metro, micropolitan (rural), and non-core (rural).
The American Community Survey was used to collect information about environmental exposures at the census level that may increase COPD risk, including poverty, jobs associated with developing lung disease, and household heating sources. Census tracts were divided into poor and non-poor, based on whether 20% of households were living below poverty line.
Never-smokers were defined as those that smoked less than 100 cigarettes in their lifetime; smoking exposure was appraised by the number of smoking years per participant.
Of the 90,334 subjects, 14.9% lived in rural counties, and 15.7% lived in poor census tracts. Almost half were current or former smokers (43.9%), while 23.2% were never-smokers. Among the current or former smokers, 13.5% had COPD and 4.3% of never-smokers had COPD.
Rural regions had the highest prevalence of COPD (12.7%). Within those areas, the rural poor had the highest occurrence of COPD (15.7%), compared to 12% in rural non-poor communities. Non-poor urban communities had the lowest prevalence of COPD (6.1%).
Living in a rural census tract predicted COPD even after adjusting for residence, age, sex, race, smoking status, household wealth, education, community poverty, health insurance, and solid fuel use. The association was the same among never-smokers (OR 1.34, p<.001) and current or former smokers (OR 1.19, p .031).
Poverty increased the chances of COPD by 8%, while wealth (including college education) and home ownership lowered those chances.

For never-smokers, there was a strong link between using coal as a fuel source and developing COPD, increasing the odds by 9%.
The study demonstrates the high burden of COPD in poor, rural communities and gives insight into the role that environmental exposures—including heating with coal—play in COPD development.
However, some of this is changing. The COPD Foundation and the National Institutes of Health (NIH) COPD National Action Plan are beginning to focus efforts on improving care and building a research infrastructure for patients with COPD in rural areas. McCormack’s research group at JHU has partnered with Eastern Tennessee State University to launch a study focused on understanding the impact of household air pollution on individuals living with COPD in Appalachia.
The study, “Rural Residence and Poverty are Independent Risk Factors for COPD in the United States”, was published on November 2, 2018, in the American Thoracic Society’s American Journal of Respiratory and Critical Care.

Absence of Alveolar Neutrophilia Predictive of Negative Bacterial Pneumonia

By Dr Deepu

Results of a study published in the American Journal of Respiratory and Critical Care Medicine has revealed that  Patients undergoing evaluation for ventilator-associated pneumonia who had an alveolar neutrophil percentage <50% had a negative predictive value >90% for bacterial pneumonia.
Bronchoalveolar lavage specimens from patients undergoing evaluation for ventilator-associated pneumonia at an urban academic medical center were analyzed retrospectively for associations between alveolar neutrophilia and bacterial pneumonia diagnosis. All lavage samples were processed for flow-cytometry sorting within 12 hours of collection. Pneumonia was defined as ≥104 colony-forming units/mL of a bacterial species on quantitative culture in the setting of a clinical suspicion of infection and an abnormal chest radiograph.
Of the 1156 bronchoalveolar lavage specimens screened for inclusion, 851 were included in the final analysis. Of these 851 specimens, 344 (40.4%) met the definition for bacterial pneumonia. The most common pathogens isolated were Pseudomonas aeruginosa, methicillin-resistant Staphylococcus aureus, and Klebsiella pneumoniae. The area under the curve for bronchoalveolar lavage neutrophilia was 0.751 (95% CI, 0.719-0.784). When bronchoalveolar lavage neutrophils were <50%, the negative predictive value for pneumonia was 91.5%.
 the researchers concluded The absence of alveolar neutrophilia is useful in ruling out bacterial pneumonia in mechanically ventilated patients with suspected infection. A combination of cellular and molecular analysis of the host and pathogen in [bronchoalveolar lavage] fluid shows promise for improving the diagnosis and management of pneumonia.

Original article reference
Walter J, Ren Z, Yacoub T, et al. Multidimensional assessment of the host response in mechanically ventilated patients with suspected pneumonia [published online November 6, 2018]. Am J Respir Crit Care Med. doi:10.1164/rccm.201804-0650OC