Depression worsens COPD symptom

Date:
May 3, 2016
Source:

Manchester Metropolitan University

Summary:
Debilitating symptoms from chronic obstructive pulmonary disease (COPD)
can worsen in patients who also experience depression, research
suggests. Patients who had pre-existing depression or developed
depression after COPD diagnosis were more likely to experience
heightened COPD symptoms, such as increased breathlessness, reduced
exercise tolerance and hopelessness.

Debilitating symptoms from chronic obstructive pulmonary

disease (COPD) can worsen in patients who also experience
depression, research suggests.

A new study, published in journal CHEST , demonstrates a link between an

exacerbation of COPD in patients and depression.

Patients who had pre-existing depression or developed depression after COPD

diagnosis were more likely to experience heightened COPD symptoms, such as
increased breathlessness, reduced exercise tolerance and hopelessness.

Patients with the obstructive lung condition and depression also performed
worse than COPD patients without depression in exercise tests, showing a
pronounced loss in performance in their daily activities.

The results have implications for healthcare practitioners who could potentially
screen for mental health problems periodically in those patients with a history of
difficulty coping at home, poor adherence to therapy or experience of a recent
bereavement, in a bid to reduce COPD-related hospital readmission.

Lead researcher Dr Abebaw Mengistu Yohannes, Reader at Manchester

Metropolitan University, an expert in COPD and mental health, said: "We have
found a previously unknown link between the brain and COPD. Mental health can
have repercussions elsewhere in body, in this case, exacerbating the negative
effects of COPD and poor prognosis in health outcomes.
 "Essentially, we can treat the brain to treat the lungs and this is something
health practitioners should be aware of when working with COPD patients.

"It creates a strong argument for vigorous screening of mental health problems
in patients who are admitted in the short term for exacerbations of COPD.
Managing mental health problems associated with COPD should be an important
part of the management plan for the short term as well as the discharge planning
with longer-term follow-up."

The research looked at 1,589 patients over a three-year period. It found that
more than half did not experience any depressive symptoms. Almost a quarter of
COPD patients were classified as permanently depressed while 14 per cent
developed a 'case' for depression during the three-year follow-up.

COPD patients were asked to complete a six-minute walking test and quality of
life scale. Those with depression performed worse in exercise tolerance and
impaired quality of life than COPD patients without depression. Researchers
concluded that depression in COPD is chronic and inadequately treated.

Journal Reference:

1. Abebaw Mengistu Yohannes et al. Long-term Course of Depression

Trajectories in Patients With COPD: A 3-Year Follow-up Analysis of the Evaluation
of COPD Longitudinally to Identify Predictive Surrogate Endpoints Cohort. Chest,
May 2016 DOI:10.1016/j.chest.2015
New way to predict COPD progression; new
treatment may be on the horizon

Date:

May 15, 2016

Source:

American Thoracic Society

Summary:

New research has found that a process initiated in white blood cells
known as neutrophils may lead to worse outcomes for some patients with
chronic obstructive pulmonary disease (COPD). The discovery may help
identify patients at higher risk for COPD progression, who might also show
little benefit from standard treatments.

New research has found that a process initiated in white blood

cells known as neutrophils may lead to worse outcomes for
some patients with chronic obstructive pulmonary disease
(COPD). The discovery may help identify patients at higher risk
for COPD progression, who might also show little benefit from
standard treatments. The study was presented at the ATS 2016
International Conference.

"We have known for many years that neutrophils should be able to fight infection,
but we haven't fully understood why they don't work in COPD," said lead author
James D. Chalmers, MD, PhD, from the University of Dundee, Scotland. "Our study
found that a recently identified form of neutrophil behavior called neutrophil
extracellular trap (NET) formation is present in the lungs of COPD patients, and
may weaken their ability to eat and kill bacteria."
Dr. Chalmers noted his team found that when NET formation weakens
neutrophils' bacteria-fighting capability, patients experience more frequent chest
infections and worse lung function and quality of life.

"This marker may help us identify patients at higher risk of disease progression,"
he said. "And it identifies a subset of patients who may need treatments other
than corticosteroids. Our data show that inhaled steroids may even exacerbate
NETs, so we need to identify new COPD treatments and discover whether
inhibiting NET formation will result in improved clinical outcomes for patients
with COPD."

Dr. Chalmers and colleagues recruited 141 patients with stable COPD for the
study. Sputum and blood were collected at the beginning of the study, during
acute COPD exacerbations, and at the end of exacerbations. NETs were
measured using a validated enzyme-linked immunosorbent assay targeting
specific DNA associated NET/protein complexes.

The amount of NET complexes in the lungs of patients in the study was directly
related to the severity of their COPD and the risk of exacerbations. NETs
increased significantly during exacerbations that did not respond to
corticosteroid treatment.

Neutrophilic airway inflammation has been known for some time to be a

characteristic feature of COPD. NETs were discovered as an essential part of
innate immune response to infection approximately 10 years ago, and scientists
are only beginning to understand how NETs impact disease outcomes.

"Some recent studies described the presence of NETs in the COPD lung, so we
wanted to know whether there was any relationship between NETs and
outcomes in COPD patients," said Dr. Chalmers.

"We are now keen to find out if we can identify why NET formation occurs in
these patients and whether it can be prevented or treated. While our new
research is at an early stage, we hope that detecting NETs may be a biomarker
that can identify patients at risk of deterioration, and that we can work toward
testing whether inhibiting NET formation would be a beneficial treatment in
COPD."
Being fit may slow lung function decline as we
age

Date:

May 16, 2016

Source:

American Thoracic Society (ATS)

Summary:

Being fit may reduce the decline in lung function that occurs as we grow
older, according to new research.

Being fit may reduce the decline in lung function that occurs
as we grow older, according to research presented at the ATS
2016 International Conference.

"While everyone's lung function declines with age, the actual trajectory of this
decline varies among individuals, " said Lillian Benck, MD, a medical resident at
Northwestern University Feinberg School of Medicine, Chicago, Illinois, and study
lead investigator. "What is less known is, beyond smoking, what factors affect
this rate of decline."

Dr. Benck added that even though the majority of people will not develop lung
disease in their lifetime, "declining lung function is known to increase overall
morbidity and mortality even in the absence of overt pulmonary disease."

Dr. Benck and her colleagues analyzed data from the National Heart, Lung, and
Blood Institute's CARDIA (Coronary Risk Development in Young Adults Study),
which began in 1985-86 with 5,115 healthy black and white men and women,
aged 18-30. The study has measured participant's cardiopulmonary fitness
periodically over 20 years using a graded treadmill test. At the beginning of the
study and at each follow-up assessment, pulmonary function (PF) was also
assessed by measuring forced expiratory volume in one second (FEV1) and
forced vital capacity (FVC).

After adjusting for age, smoking, body mass index and change in BMI, the
association between fitness and lung function remained statistically significant.

Researchers found that participants: in the top quartile of baseline fitness

experienced the least annual decline in PF.

with the greatest decline in fitness experienced the greatest decline in

FEV1and PF over 20 years.

with sustained or improved fitness experienced the least decline in PF over 20

years.

Dr. Benck said that the last finding is noteworthy because it indicates that
fitness matters, not just at a single point in time but over many years. "Fitness
early in life and at middle age appears to attenuate this natural decline," she
said, noting that the benefit of fitness was even seen among smokers.

Because it is an observational study, researchers cannot claim cause and effect.

However, they noted several important strengths, including a large study
population and long-term follow-up and objective measurements of fitness and
lung health.

Dr. Benck said that CARDIA will continue to follow participants and may
eventually provide insights into whether fitness not only preserves lung function,
but also reduces the risk of developing lung disease.

Story Source:

The above post is reprinted from materials provided by American Thoracic

Society (ATS). Note: Materials may be edited for content and length.
Exposure to cigarette smoke and flu virus may
prevent lung medications working properly

Date:

April 10, 2016

Source:

Biochemical Society

Summary:

A new study backs up observations in chronic obstructive pulmonary

disease patients showing reduced effectiveness of symptom-reliever
 medication in flare-ups linked to cigarette smoking and infection with
viruses such as influenza.

New study backs up observations in Chronic Obstructive

Pulmonary Disease (COPD) patients showing reduced
effectiveness of symptom-reliever medication (2-adrenoceptor
agonists) in flare-ups linked to cigarette smoking and infection
with viruses such as influenza.

Research suggests a need for new drugs to treat COPD patients in these
categories and a model that could be used to test new medications.

According to the study, which is published in the Portland Press journal Clinical
Science, the effectiveness of the commonly used COPD symptom-reliever
medication salbutamol is reduced on exposure to cigarette smoke and influenza
A infection in an animal model of the respiratory disease.

"There is a clear need for new therapies that can overcome the limitations of
current drugs used to treat COPD and associated flare-ups. When combined with
knowledge gained through clinical research, animal models utilizing cigarette
smoke exposure are a valuable tool in the quest to identify new therapies for this
life-changing condition," commented senior study author Dr Ross Vlahos,
Associate Professor at RMIT University in Melbourne, Australia.

COPD is the collective name for lung diseases including emphysema, chronic
bronchitis and chronic obstructive airways disease. Smoking is currently the
main cause of COPD and the chances of developing COPD increases the longer
an individual has been smoking. Patients suffering from COPD have difficulties
breathing, mainly due to the airflow becoming obstructed, persistent production
of phlegm and frequent chest infections. Over time, the inflammation leads to
permanent changes in the lung and walls of the airways thicken with more
mucus being produced. This inflammation is caused by inflammatory proteins, for
example tumour necrosis factor-alpha and interleukin-1 beta, which are involved
in systemic inflammation or chronic activation of the immune system.

Cigarette smoke is a major contributor to COPD as it alters immunity and can

increase a patient's susceptibility to infection, which can worsen symptoms and
cause flare-ups.

One of the most common reliever drugs used to treat flare-ups of the common
lung disease known as COPD is salbutamol, a 2-adrenoceptor agonist. This drug,
which is also used to treat asthma, works by dilating a patients airways making
 it easier for them to breathe. The effectiveness of drugs such as salbutamol in
cigarette smoke-induced lung diseases such as COPD is limited. To date, the
mechanisms involved in loss of responsiveness to therapy remain poorly
understood.

The study assessed sections of lung exposed to cigarette smoke and a version of
the influenza A virus. Overall, the researchers found that the lung tissue exposed
to cigarette smoke and viral infection was less responsive to salbutamol than
tissue that was not.

Commenting on the research, lead author Dr Chantal Donovan, from Monash

University in Victoria, Australia, said: "By understanding the mechanisms
responsible for reduced sensitivity to current bronchodilators, we can then
design alternative, more efficacious agents to help treat people with COPD,
especially during a viral exacerbation."

The researchers hope that their technique will help identify new targets that can
be exploited therapeutically to help patients with COPD who do not respond to
current therapy.

A commentary article accompanying this paper will shortly be published

inClinical Science to accompany this research.

Discussing the significance of the study, Professor Sebastian Johnston from

Imperial College London, UK, one of the authors of the upcoming commentary,
said: "The findings of this study suggest that cigarette smoke and respiratory
virus infections may impair the ability of salbutamol to effectively bronchodilate
the airways. These findings emphasise yet again that smoking is bad for you, and
especially so if you have asthma or COPD."

He added: "It would be interesting to determine whether the other commonly

used reliever bronchodilator ipratropium bromide, which acts via a different
mechanism, is similarly impaired by cigarette smoke and/or viral infection."

Story Source:

The above post is reprinted from materials provided by Biochemical

Society. Note: Materials may be edited for content and length.

Journal Reference:

1. C. Donovan, H. J. Seow, J. E. Bourke, R. Vlahos. Influenza A virus infection

and cigarette smoke impair bronchodilator responsiveness to -adrenoceptor
agonists in mouse lung. Clinical Science, 2016; 130 (10): 829
DOI: 10.1042/CS20160093

Lung ultrasound may be a safe substitute for

chest x-ray when diagnosing pneumonia in
children

Date:

April 12, 2016

Source:

Mount Sinai Health System

Summary:

Pneumonia is the leading cause of death in children worldwide, according

to the World Health Organization (WHO). Lung ultrasound has been shown
to be highly effective and safe for diagnosing pneumonia in children,
scientists report in a new article.

Lung ultrasound has been shown to be highly effective and

safe for diagnosing pneumonia in children and a potential
substitute for chest X-ray, according to a study conducted at
the Icahn School of Medicine at Mount Sinai. Results are
currently published in the medical journal Chest.

Pneumonia is the leading cause of death in children worldwide, according to the

World Health Organization (WHO). Symptoms include fever, cough, and rapid
breathing. Chest X-ray is considered the test of choice for diagnosing pneumonia
in children, but the WHO estimates three-quarters of the world's population does
not have access to radiography.

Investigators conducted a randomized controlled trial in the pediatric Emergency

Department at The Mount Sinai Hospital comparing lung ultrasound to chest X-
ray in 191 children from birth to 21 years of age. The patients were randomly
assigned into an investigational arm (received a lung ultrasound and if the
physician needed additional verification, a chest X-ray) and a control arm
(received a chest X-ray followed by a lung ultrasound). Researchers found a 38.8
percent reduction in chest X-rays in the investigational arm compared to no
 reduction in the control arm, with no missed pneumonia cases and no increase in
any other adverse events.

The research team was led by James Tsung, MD, MPH, Associate Professor in the
Department of Emergency Medicine and Department of Pediatrics at the Icahn
School of Medicine at Mount Sinai, and former clinical fellow Brittany Pardue
Jones, MD, who's currently Assistant Professor in the Department of Pediatrics
at Vanderbilt University School of Medicine.

"Ultrasound is portable, cost-saving and safer for children than an X-ray because
it does not expose them to radiation," says Dr. Tsung. "Our study could have a
profound impact in the developing world where access to radiography is limited."

Furthermore, the reduction in chest X-rays in the investigational arm resulted in

an overall cost savings of $9,200, and length of stay in the Emergency
Department was decreased by 26 minutes.

"In the era of precision medicine, lung ultrasound may also be an ideal imaging
option in children who are at higher risk for radiation-induced cancers or have
received multiple radiographic or CT imaging studies," says Dr. Tsung.

As more and more handheld ultrasound machines come to market, these results
suggest that lung ultrasound has the potential to become the preferred choice
for the diagnosis of pneumonia in children. Further research is needed to
investigate the impact of lung ultrasound on antibiotic use and stewardship.

Story Source:

The above post is reprinted from materials provided by Mount Sinai Health
System. Note: Materials may be edited for content and length.

Journal Reference:

1. Brittany Pardue Jones, Ee Tein Tay, Inna Elikashvili, Jennifer E. Sanders,

Audrey Z. Paul, Bret P. Nelson, Louis A. Spina, James W. Tsung.Feasibility and
Safety of Substituting Lung Ultrasound for Chest X-ray When Diagnosing
Pneumonia in Children: A Randomized Controlled Trial. Chest, 2016;
DOI: 10.1016/j.chest.2016.02.643
Small cell lung cancer: Newly discovered clues
to cause of chemoresistance

Date:

April 4, 2016

Source:

Medical University of Vienna

Summary:

Small cell lung cancer is not usually detected until it is at an advanced

stage, when metastases have already formed. Chemotherapy is very
effective initially but, within a year, cancer recurs and this time does not
respond to a course of chemotherapy. The research group has now
managed to identify the reason for this chemoresistance.

Small cell lung cancer is not usually detected until it is at an

advanced stage, when metastases have already formed.
Chemotherapy is very effective initially but, within a year,
cancer recurs and this time does not respond to a course of
chemotherapy. The research group headed by Gerhard
Hamilton, University Department of Surgery at MedUni Vienna,
has now managed to identify the reason for this
chemoresistance. The groups results have recently been
published in the journals "Cell Adhesion and Migration" and
"Trends in Cancer".

Lung cancer is one of the most commonly occurring types of cancer in Austria.
The majority of the 4,000 people who die from it every year are long-term heavy
smokers. Approximately 85% of lung cancers are of the histological type known
as Non-Small Cell Lung Cancer (NSCLC), which responds very well to targeted
treatment and immunotherapy.

The remaining 15% of patients have Small Cell Lung Cancer (SCLC), which
consists of neuroendocrine cells and metastasizes very quickly. It is treated with
cytotoxic chemotherapy and radiotherapy. Initially patients respond very well to
platinum-based therapy in combination with the drug etoposide but, within a
year, resistant tumors recur. Further treatment is with topocetan or
anthracyclines but the response rate is poor and, at this stage, patients are only
expected to survive for a few more months.

A peculiarity of this type of cancer is that a lot of cancer cells migrate into the
blood where they circulate and form metastases elsewhere in the body. A year
ago, the research group led by Gerhard Hamilton, in collaboration with Robert
Zeillinger (Molecular Oncology Group, University Department of Gynaecology and
Obstetrics) and Maximilian Hochmair (Otto-Wagner Hospital), managed to
establish permanently cultivating tissue cultures of these circulating tumor
cells. It was found that individual circulating tumor cells were sensitive to
chemotherapy drugs but that, in every case, they spontaneously formed large
aggregations, or cancer clusters, with oxygen-deprived cores. These cancer
clusters are resistant to chemotherapy, firstly because the drugs cannot
penetrate sufficiently and secondly because many of the cells are dormant due
to the lack of oxygen. This lack of oxygen means that radiotherapy is also
ineffective, because there are no oxygen radicals available and these are
necessary to destroy the cancer cells.

The researchers were able to provide ground-breaking proof that resistance to

chemotherapy and radiotherapy is due to the circulating tumor cells forming
clusters. As far as treatment is concerned, this means that the first cycle of
chemotherapy only destroys the main tumor mass and the circulating cancer
cells, which have formed clusters, subsequently lead to recurrence. Completely
new therapeutic approaches must therefore be developed to prevent the
formation of these cancer clusters or to break them up. Small cell lung cancer
follows the model of an aggressively metastasizing cancer so that these
findings could equally well apply to other malignant diseases.

Five research clusters at MedUni Vienna

 In total, five research clusters have been established at MedUni Vienna. In these
clusters, MedUni Vienna is increasingly focusing on fundamental and clinical
research. The research clusters include medical imaging, cancer
research/oncology, cardiovascular medicine, medical neurosciences and
immunology. Research into lung cancer at MedUni Vienna falls within the remit of
the cancer research/oncology cluster.

Story Source:

The above post is reprinted from materials provided by Medical University of

Vienna. Note: Materials may be edited for content and length.

Journal Reference:

1. Gerhard Hamilton, Maximilian Hochmair, Barbara Rath, Lukas Klameth,

Robert Zeillinger. Small cell lung cancer: circulating tumor cells of extended
stage patients express a mesenchymal-epithelial transition phenotype.. Cell
Adhesion & Migration, 2016; 00 DOI:10.1080/19336918.2016.1155019

Device that detects congestion in the lung

improves heart failure outcomes
Compared with standard of care, hospitalizations and deaths
significantly reduced

Date:

April 4, 2016

Source:

American College of Cardiology

Summary:
 In patients with heart failure, use of an investigational device that
monitors the accumulation of fluid in the lungs appeared to cut heart
failure-related hospitalizations by more than half, meeting the study's
primary endpoint, and reduced deaths from any cause by 39 percent per
year compared with standard assessment and treatment, researchers
reported.

In patients with heart failure, use of an investigational device

that monitors the accumulation of fluid in the lungs appeared
to cut heart failure-related hospitalizations by more than half,
meeting the study's primary endpoint, and reduced deaths
from any cause by 39 percent per year compared with
standard assessment and treatment, researchers reported at
the American College of Cardiology's 65th Annual Scientific
Session.

The Edema Guard Monitor alerts patients to an increase in fluid in the lungs, also
called pulmonary congestion or edema, before they have symptoms, said Michael
K. Shochat, M.D., of Hillel Yaffe Heart Institute in Hadera, Israel, and lead author
of the study. Shochat is also president of RS Medical Monitoring, the Israel-based
company that manufactures the Edema Guard Monitor.

"By the time a patient shows clinical signs of pulmonary congestion, the
condition is already at an advanced stage," Shochat said. "Many patients need
emergency hospitalization and have a high probability of sustaining irreversible
damage to the heart and lungs. In this study, patients who used the Edema
Guard Monitor started taking medication well before pulmonary congestion
reached an advanced stage."

The Edema Guard Monitor--a stand-alone device--measures lung impedance, or

resistance to electrical current, Shochat said. Healthy, air-filled lungs are highly
resistant to electrical current, whereas lungs swollen by fluid are less resistant.
In pulmonary congestion, the lungs gradually become more and more swollen by
fluid. Existing techniques for monitoring worsening pulmonary congestion, such
as periodic chest X-rays or computed tomography (CT) scans of the lungs, are
costly or not highly effective. Preliminary studies had suggested that lung
impedance-guided treatment could reduce hospitalizations for heart failure.

"This study shows for the first time that a noninvasive lung impedance monitor
can be used to detect pulmonary congestion in its earliest stages and that
adequate medical treatment at that early stage can significantly reduce both
hospitalizations and mortality," Shochat said.

The IMPEDANCE-HF trial was conducted at two medical centers in Israel and
included 256 patients with chronic heart failure whose hearts were pumping
blood at less than half of the normal rate. Patients were 67 years of age on
average, and 80 percent were male. Before patients were randomized, they
received three months of treatment through outpatient clinics to achieve
maximal doses of guideline-directed medications to manage congestive heart
failure. All patients attended monthly outpatient visits during which a technician
measured their lung congestion using the Edema Guard Monitor and their
physician performed a standard clinical assessment.

Patients were randomly assigned to one of two groups. In the treatment group,
medication was prescribed or adjusted at each visit based on the results of
clinical assessment and lung congestion measurement with the Edema Guard
Monitor. In the control group, medication was prescribed or adjusted based on
clinical signs of lung congestion. The primary endpoint was hospitalizations due
to heart failure. Secondary endpoints were hospitalizations and deaths from any
cause. The average follow-up time was 48 months in the treatment group and 39
months in the control group.

In the treatment group compared with the control group, hospitalizations due to
heart failure decreased by 58 percent during the first year of treatment, and the
frequency of heart failure-related hospitalization decreased by 56 percent per
year during the entire follow-up period, meeting the study's primary endpoint. For
the entire follow-up period, deaths from heart failure were reduced by 62 percent
per year and deaths from any cause decreased by 39 percent per year in the
treatment group compared with the control group.

The hope is that patients will eventually be able to use the device at home to
measure their lung impedance once or twice a day, Shochat said.

A limitation of the study is that it excluded patients with less severe heart
failure, or those whose hearts were pumping blood at more than half of the
normal rate, and that the results cannot be extended to that group of patients,
Shochat said. Results from an ongoing randomized trial of the Edema Guard
Monitor in patients with less severe heart failure are expected in 2019.

Story Source:

The above post is reprinted from materials provided by American College of

Cardiology. Note: Materials may be edited for content and length.
 Short Prayer for Children

Dear Lord and Father of all,

Thank you for today.

Thank you for ways in which you provide for us all. For Your protection and love we
thank you.
Help us to focus our hearts and minds now on what we are about to learn.
Inspire us by Your Holy Spirit as we listen and write.
Guide us by your eternal light as we discover more about the world around us.

We ask all this in the name of Jesus.

Amen.

Thank you for today.

Thank you for ways in which you provide for us all.

For Your protection and love we thank you.

Help us to focus our hearts and minds right now on

what we are about to learn.
Inspire us by Your Holy Spirit as we listen and write.
Guide us by your eternal light as we discover more
about the world around us.

We ask all this in the name of Jesus,

Amen.
Thank you.
You promise us that when two or more come together
in Your name
You are with us.
Thank you Lord that you have been with us
throughout this lesson,
And that you are with us right now.

Inspire us as we leave this place

To love and serve You always.

In the name of Jesus,

Amen