8 Foods That May Help Relieve Asthma Symptoms
Eliminating Infectious Diseases: Triumph Of Public Health
(In the weekly Health Matters newsletter, Ramya Kannan writes about getting to good health, and staying there. You can subscribe here to get the newsletter in your inbox.)
In what could well be tagged as a 'pioneering' move, one that is in sync with the current global concern of the effects of climate change, Tamil Nadu went ahead and declared heatwaves as State-specific disasters and announced an ex-gratia for heat-related deaths. This will allow the government to provide immediate relief to those affected by extreme temperatures and the government has claimed it will use the State Disaster Response Fund to support these efforts. This comes after many regions in Tamil Nadu recorded temperatures exceeding 40°C, and the impact on public health was perceived to be considerable. Vulnerable populations, including the elderly, children, and individuals with pre-existing health conditions, have been particularly at risk.
Heat is an important environmental and occupational health hazard. Heat stress is the leading cause of weather-related deaths and can exacerbate underlying illnesses including cardiovascular disease, diabetes, mental health, asthma, and can increase the risk of accidents and transmission of some infectious diseases. Heatstroke is a medical emergency with a high-case fatality rate. The World Health Organization says the number of people exposed to extreme heat is growing exponentially due to climate change in all world regions. Heat-related mortality for people over 65 years of age increased by approximately 85% between 2000–2004 and 2017–2021.
Tamil Nadu is arguably the first State in the country to factor in healthcare support for the crisis of excessive heat brought on by climate change. As part of relief measures, the State also plans to provide medical care, including oral rehydration salts (ORS) and access to drinking water in kiosks throughout affected areas. It would be ideal for other States to follow suit, as there is sufficient evidence that challenges from climate change will only be exacerbated in the coming years.
In other encouraging news, S. Vijay Kumar reports that the Centre is eying 'presumed consent' for cornea retrieval in hospital deaths. This comes against the backdrop of a huge demand for cornea donation, with the country being able to meet only 50% of the requirement. Going by the new initiative, corneas could be retrieved from all citizens who die in hospitals without the consent of the family. This means that every person dying in a hospital would be presumed to be a cornea donor, unless otherwise specified.
There's a lot in the area where genomics intersects with Artificial Intelligence (AI) in healthcare technology today. Sridhar Sivasubbu and Vinod Scaria enlighten us with the attempts of Researchers to meld AI and genomics to find thousands of new viruses. In recent years, metagenomics has helped scientists identify a staggering number of previously unknown microbes in diverse environments. These discoveries have significantly expanded our understanding of microbial ecosystems. As sequencing technologies continue to improve — becoming more accurate, faster, and more affordable — alongside better global data-sharing practices, scientists are beginning to unlock the secrets of the microbial world at an unprecedented pace, the authors write.
Meanwhile, in a significant move, countries are expected to reach a deal at this month's U.N. COP16 nature summit on how the world uses and pays for genetic information extracted from nature, according to negotiators. Experts refer to this data as "digital sequence information," or DSI for short. The unique genetic codes and sequences in all living organisms hold the information needed for them to develop and function. For years, researchers have been tapping the genetic codes of plants, animals and microbes in search of new compounds that can be used in pharmaceuticals, cosmetics or other commercial purposes.
Species-rich countries, including tropical giants like Brazil and India, are on guard against corporations and researchers capitalizing on their biodiversity without offering compensation or royalties to the country where a species originated. In response, a complex system of laws has cropped up to govern the use of genetic material. The laws vary widely from country to country, posing headaches for companies and complicating the sharing of biological material for research. This system has also generated little money for developing nations. Do read the story for more details.
But there is a need for caution, when using generative AI. Apparently, OpenAI's Whisper transcription tool used in hospitals invents things no one ever. Researchers have claimed that it is prone to making up chunks of text or even entire sentences, according to interviews with more than a dozen software engineers, developers and academic researchers. Those experts said some of the invented text — known in the industry as hallucinations — can include racial commentary, violent rhetoric and even imagined medical treatments.
We had some mixed news with polio last week, but this week is mostly not great news. While, so far, polio vaccinations proceeded on course even in Gaza, WHO now says 'intense bombardment' halts Gaza polio vaccinations. This will derail the vaccination programme and is bound to cause a resurgence of polio in the region. The international community must intervene at this stage in order to ensure at least basic health care services reach the Palestinians.
Meanwhile, on Polio in Pakistan: another vaccination campaign begins after worrying surge.
Back in India, if you had question about the Meghalaya vaccine-derived polio case, maybe you could check out this report by R. Prasad: Why is WHO cagey about publishing Meghalaya polio case details?
Evelyn Parr and Brooke Devlin, in the The Conversation write on how in type 2 diabetes, focusing on when you eat – not what – can help control blood sugar, pitching for the benefits of time-restricted eating.
Over 77 per cent of India's children lack WHO-suggested diversity in diet, a study finds. This refers to children in India aged 6-23 months who lack the diversity in diet as suggested by the World Health Organization.
Meanwhile, Megha,Bob Allkin and Varun Subramanya bring in the importance of Medicinal foods: A missing category on the regulator's plate. Their study found that of the 7,564 medicinal species listed in 11 referenced sources, approximately a quarter (1,788) were documented as food as well as medicine. They go on to show that when medicinal foods are regulated as foods, they are subjected to lower efficacy and safety standards than if they were medicines, putting consumers at risk
As part of The Hindu Wellness Series webinar held recently in association with Kauvery Hospital, doctors discussed factors that would ensure a healthy lifestyle, and regular check-ups to prevent strokes in young adults.
As news of the reducing air quality in the national capital region came back to hit headlines, in a letter to States and UTs, the Director General of Health Services Atul Goel has said to discourage stubble and waste burning, and spread awareness among people about reducing firecrackers during festivities, reports Bindu Shajan Perappadan. Read here.
Ashna Butani follows that up with a bunch of lifestyle recommendations to combat rising air pollution levels, that doctors advocate.
If there is a cat story, then naturally that makes it the tailpiece of the week. Susan Hazel in The Conversation asks: Are cats good for our health? The conclusions are what any cat lover will tell you: Living with a cat can have a profound – and sometimes surprising – effect on our physical and mental health. Still, living with cats is not without risks, the main downside being exposure to toxoplasmosis -a parasite excreted in cat faeces which can affect other mammals, including humans. The parasite is more likely to be carried by feral cats that hunt for their food than domestic cats. Do click on the link for more details.
In our rather substantial explainers section this week,
Sathana Dushyanthen and David Kok (in The Conversation) write on What is stereotactic radiation therapy for prostate cancer? How does it compare to other treatments?
Serena Josephine M. asks Should men be allowed into operation theatres when their wives are having a baby? Doctors weigh in after YouTuber's video sparks controversy
C. Aravinda explains Acute Flaccid Paralysis and need for surveillance and Trachoma eliminated as a public health problem in India; what next?
Why did the Centre sanction a 50% hike in prices of commonly used drugs?
Zubeda Hamid in the In Focus podcast goes back to what we have explained for a couple of weeks now: What role does microRNA play in our cells and why is this vital?
Bani Jolly and Vinod Scaria explore: What does H5N1 in cattle, humans portend?
If you have a few extra moments, do also read:
Drugs regulator finds 49 samples not of standard quality, manufacturers asked to withdraw their products
Roll back approval to import used medical devices, med-tech industry urges PM
National Testing Agency remains tight-lipped on possible changes to NEET 2025 exam pattern
30,000 critical care beds, regional centres for National Institute of Virology are among plans under PM-ABHIM: Niti Aayog member V.K. Paul
$25-million Pandemic Fund aims to curb 'zoonotic' diseases
A.S. Jayanth writes Rajasthan-based firm barred from making 'insulin' homeopathic tablets
For many more health stories, head to our health page and subscribe to the health newsletter here.
Published - October 08, 2024 05:03 pm IST
How Coloring My Hair After Chemotherapy Helped Me Feel Like Myself Again
I have hundreds of photos in my camera roll that might seem like the musings of someone who never turns down a selfie. But if you look closer, the subject of these countless photos is my hair. You might think I'm a stylist's dream—constantly chopping and coloring, with cool memories to accompany each change. But, in reality, my collection reminds me of what I've lost and how much further I must go to feel like myself again.
My diagnosisIt started in 2022 with a trip to the doctor for white bumps in the back of my throat, which I assumed was strep. From January through April, I bounced from ENT specialists, trying to figure out why these swollen bumps wouldn't disappear after treating them with rounds of steroids. By May, I found out I had Diffuse Large B Cell Lymphoma (DLBCL), a type of non-Hodgkin lymphoma (NHL) that affects white blood cells.
The irony was after years of having light brown hair, I finally started the journey to go blonde, getting it to the perfect golden shade a week before I received my diagnosis. I caught my cancer early, and everyone, from my doctor to well-intentioned friends, told me it was a "good" cancer to get, meaning my outcome would likely be positive, and after treatment, I'd remain in remission. People automatically put me in the "cancer warrior" category, but dealing with a diagnosis and starting treatment was anything but easy. My body experienced blood clots and cancer-induced asthma, to name a few. Despite all this, I made it through my six rounds of chemo and had one final PET scan standing between me and remission. I went in for my scan, and two weeks later, my doctor told me that everything looked good and that they'd see me in three months.
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It was quite surreal after twelve emergency room visits, one collapsed lung, and seeing a slew of specialists. Medically speaking, I was cleared to rejoin society, but mentally and physically, I was still in shambles. My bald head and eyebrows were the most obvious signs I was still healing. I desperately counted down the days my hair would be below my shoulders or could be thrown up into a messy bun without needing a pin to secure still-growing flyaways. I regularly dreamt of sitting in my colorist's chair, in hopes that the foils would put an end to the neon "cancer patient" sign my hair (or lack thereof) communicated.
"People automatically put me in the 'cancer warrior' category, but dealing with a diagnosis and starting treatment was anything but easy."
Hair loss and cancer treatmentSee, hair loss is a common side effect of chemotherapy and, according to Beth N. McLellan, MD, and director of supportive oncodermatology at Montefiore Einstein Comprehensive Cancer Center, hair loss during treatment happens because chemo works by attacking rapidly dividing cells, like cancer cells. "Unfortunately, some normal cells that divide rapidly can also be affected, like hair follicles, which are the second fastest-dividing cells your body produces," Dr. McLellan says.
The most common side effects of chemotherapy are fatigue, nausea, mouth sores, loss of appetite, and hair loss, but each person's experience is unique. "Hair shed typically happens in the first few weeks and grows back over the months following a patient's last treatment, but some other cancer treatments can affect the texture or color of the hair, and some can cause thinning rather than complete hair loss," Dr. McLellan says.
Hair follicles go through four stages within a growth cycle: anagen (growth), catagen (intermediate phase), telogen (where the hair stops growing and rests in the follicle), and exogen (where hair falls out). "Certain chemotherapy treatments can cause the immediate release of hairs in the growth phase known as a type of hair loss called anagen effluvium," explains Anabel Kingsley, consultant trichologist and brand president at Philip Kingsley, meaning that after completing chemotherapy, your hair will grow back, but the treatment can cause it to return with a different texture and color, which can be another emotional ordeal for some people. "For many people, it's not uncommon for hair to come back curlier, unpigmented, or slightly lighter. However, everyone's scalp and hair will be more fragile at first following chemotherapy," says Kingsley.
For me, it took about four months to go from being completely bald to having a crew cut with thin eyebrows. However, I was overjoyed because I could go about my day publicly, and no one gave me a double take of pity. Granted, I was very far from my previous mid-back length but it was a start. I'm not the first person to experience cancer-related hair loss, and there are many forums online with people offering their advice to expedite hair growth and their lists of do's and don'ts. I learned during my experience that some people instantly colored their hair after treatment, and others decided to keep their hair short and dye-free.
Dyeing my hair after chemotherapyI really wanted to dye my hair because I thought if I looked how I did pre-chemo, I could cope with the trauma of having cancer quicker. Despite this desire, I knew I had to be cautious because if I truly wanted to return to a "normal" life full of regular color appointments, I couldn't rush it. That meant letting my hair grow untouched for up to eight months before taking the plunge.
Rogério Cavalcante, stylist and owner of The Second Floor Salon tells me he always advises clients to wait six to eight months before using chemical color on regrown hair since chemotherapy makes the scalp and hair more sensitive and fragile. To ensure your hair and scalp are ready for color, most professionals recommend an allergy patch test, where your colorist will apply a small amount of dye behind your ear to see if a reaction occurs within 48 hours.
This is especially important for people who have undergone chemotherapy because many permanent and semi-permanent hair dyes contain paraphenylenediamine or PPD, a chemical known to be an irritant and allergen. It's a common cause of most reactions, and anyone can have an allergic reaction to it, especially when going brunette or shades of black, as darker dyes contain higher levels of it. Cavalacante also warns against dyes containing bleach and peroxide to avoid unnecessary breakage.
"To everyone else around me, this was just another day at the salon. To me, it was a real step forward, marking that I was done with cancer and could feel like myself again."
None of this matters, though, if your scalp isn't completely healthy. Before chemo, I had experienced outbreaks of redness around my hairline, and chemo brought this back, accompanied by flakes and itchiness. "If you don't have a healthy scalp, you can't have healthy hair," says Marisa Garshick, MD, board-certified dermatologist. "Start with a gentle, sulfate-free shampoo and conditioner to keep your hair hydrated, avoid excessive use of heat-styling tools, and opt for air-drying to minimize damage," she says.
Fortunately, my scalp issues didn't return, and by all accounts, I was a prime candidate to start coloring again. I waited 622 days, to be exact, before I could finally walk into NYC the Team on Fifth Avenue to dye my hair. To everyone else around me, this was just another day at the salon. To me, it was a real step forward, marking that I was done with cancer and could feel like myself again.
To prep for this appointment, I had a haircut three weeks prior and had both the stylist who cut my hair and my colorist sign off on my hair and scalp being strong enough for my service. I was deciding between a glaze and a balayage service. "Glazes are generally non-ammonia and don't deeply penetrate the hair. It rather just coats and smooths out the cuticle, giving the hair luster and shine," Michelle Hong, colorist and founder of NYC the Team, explained to me. The glaze results typically fade in about eight to 10 washes, so I opted for the balayage with ammonia-free dye and a lower peroxide concentration to keep my hair as healthy as possible post-color. Since my hair handled the color so well, my colorist told me to maintain my current routine and consider adding a hair SPF to protect my fresh color from the sun and a shielding finishing spray to protect it from environmental elements.
I left the salon 90 minutes later, feeling lighter both literally and figuratively. To everyone else, I was just another woman with fresh color and a bouncy blowout to match. To me? It was much more significant. Nothing about my new hairstyle says 'former chemo patient.' The experience of it all lies within my memories. My hair may not be what it once was, nor am I. However, this version of me is compelled to stop worrying and letting fear call the shots—so before leaving the salon, I made sure to put my next color appointment on the calendar.
Final thoughtsWalking home with my hair bouncing and catching the light of golden hour was truly surreal. Going through treatment and all the complications left me very anxious. With lymphoma, the chance of relapse is high—so high that I'll be seeing my doctor regularly for five more years. Many survivors report feeling symptoms they had pre-diagnosed and fearing their cancer would come back.
I can confirm: There's a real sense of waiting for the other shoe to drop when my throat tingles or my arms aches for too long. However, being able to have an experience—like finally getting that hair color I waited so long for—that silences that fear is something I'll always seek out and be grateful for. It's my reminder when I look in the mirror that I'm in recovery and that everything will be okay.
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Bronchiectasis Exacerbations: Are We Doing Everything We Can?
IntroductionThe chronic and progressive inflammatory disease bronchiectasis is characterised by permanent bronchi dilation and by symptoms such as recurrent bronchial infection, sputum production, chronic cough, dyspnoea, and exacerbations.1 Bronchiectasis prevalence estimates range by geographical region, gender, and age, with indications that prevalence is rising.2-4
One of the most common causes of bronchiectasis, as shown in 16,963 patients in the European Multicentre Bronchiectasis Registry Audit and Research Collaboration (EMBARC) registry, is post-infective disease (21.2%).5 Other causes include COPD (8.1%), asthma (6.9%), tuberculosis (4.9%), and immunodeficiency (4.1%). Of note though, 38.1% of patients in the registry had a cause listed as idiopathic. Bacteria are frequently linked with bronchiectasis, with the most common types found in the EMBARC cohort being Pseudomonas aeruginosa (in 25.1% of sputum samples) and Haemophilus influenzae (23.6%), followed by Enterobacteriaceae (15.9%), Staphylococcus aureus (8.6%), Streptococcus pneumoniae (8.5%), and Moraxella catarrhalis (5.4%). Co-infection was common, with 36.1% of patients having samples positive for at least two pathogens. Occurrence of these infectious agents may differ geographically, for example, H. Influenzae infection was lower in Southern Europe, where P. Aeruginosa predominated, and was higher in Northern and Western Europe.5
In the first two parts of this symposium, two leading experts in bronchiectasis, Goeminne and Shteinberg, discussed the pathogenesis of bronchiectasis as well as the recognition and control of exacerbations. Such exacerbations can greatly impact a patient's health-related quality of life (HRQoL).
Bronchiectasis Development and ExacerbationAs shown in Figure 1, four pathogenic components intersect to drive bronchiectasis development, persistence, and exacerbations.6 The first two, chronic infections and dysfunction of airway epithelial cells and their cilia, result in hypersecretion of mucus. Inflammation, the third component, accompanies these phenomena, and together they can result in the fourth component, characteristic of bronchiectasis, permanent airway injury, and dilatation. This opens the airways up to increased epithelial cell damage, infection, and inflammation. As each individual component may not only lead to, but also be brought about by, one of the others, and they do not necessarily occur in any particular sequence, the model of bronchiectasis has moved from being seen as a 'vicious cycle' to being recognised as a 'vicious vortex.'1,7
Figure 1: The four pathogenic components of bronchiectasisAdapted from Chalmers et al., 20236Pulmonary infection and inflammation, MCC dysfunction, and structural lung damage are common features of the pathophysiology of bronchiectasis regardless of cause. The interactions between these four aspects are not best represented as a cycle; this is due to the fact that each of the individual components can independently affect allof the other aspects, and therefore it is better described as a "vicious vortex".ASL: airway surface liquid; MCC: mucociliary clearance; NET: neutrophil extracellular trap;NTM: non-tuberculous mycobacteria.
This material has not been reviewed prior to release; therefore, the European Respiratory Society may not be responsible for any errors, omissions or inaccuracies, or for any consequences arising there from, in the content. Reproduced with permission of the ERS 2024. Chalmers JD et al. Basic, translational and clinical aspects of bronchiectasis in adults. Eur Respir Rev. 2023;32(168):230015.
The Role of Neutrophils in BronchiectasisNeutrophils usually contribute to acute infection control in a number of ways, including phagocytosis of pathogens, release of granule-resident cytotoxic and microbicidal molecules, extrudation of neutrophil extracellular traps, and generation of reactive oxygen and nitric oxide species. Neutrophils can also have a large influence on the activity of other immune cells, including macrophages and T cells.8 Such actions are usually relatively time-limited; however, a key feature of bronchiectasis is persistent overabundant neutrophil infiltration into the airways that helps drive the viscous vortex through inflammation and promotion of bacterial colonisation.7
Typically, neutrophils survive for only short periods of time; however, in bronchiectasis, their lifespan can be extended in response to bacterial products, cytokines, and interferons.7 Additionally there is a decrease in neutrophil apoptosis and impaired phagocytosis, compared with healthy controls.9
The primary protease involved in tissue damage and remodelling in bronchiectasis is neutrophil elastase. During neutrophil maturation, this protease is activated by dipeptidyl peptidase 1 (DPP1) in the bone marrow, prior to packaging into granules.10 Neutrophil elastase overabundance, along with other proteases, such as cathepsin, matrix metalloproteinase, and proteinase 3 may occur over anti-proteases such as alpha-1 antitrypsin, alpha-1 macroglobulin, secretory leukocyte protease inhibitor, and elafin.11,12 This imbalance, Goeminne posited, may be a key driver of bronchiectasis. Indeed, neutrophil elastase is found in high concentrations in patients with a number of neutrophil-associated lung diseases, including bronchiectasis11 and there is a significant positive relationship between the level of this protease and bacterial load in bronchiectasis.11,13 The pathogenesis of lung damage associated with neutrophil elastase release includes activation of pro-inflammatory cytokines and pathways; impaired immune cell function; goblet cell metaplasia and increased airway mucin expression and dehydration; impaired ciliary motility; and epithelial cell apoptosis and impaired proliferation.11,14
Bronchiectasis ExacerbationsExacerbations in bronchiectasis are important clinical entities to identify, and while precise definitions may vary slightly according to different guidelines (Table 1), common to all are a number of signs and symptoms, including increased cough and sputum purulence, volume, and/or consistency; decreased lung function; exercise intolerance and/or worsening dyspnoea; increased fatigue and/or feelings of malaise; new or increased haemoptysis; and a change required in current treatment. Also present may be fever, pleurisy, chest pain, and asthenia.15-18 However, Shteinberg discussed that typically, lung infiltrates are not shown on X-ray, and fever may not be present, so these should not be relied upon to make a positive diagnosis. Importantly, Goeminne highlighted, is the role of a healthcare professional in interpreting clinical signs and symptoms as a bronchiectasis exacerbation so that appropriate supportive treatments can be initiated.
Table 1: Definition of exacerbation according to different guidelines.
In the study utilising EMBARC data, patients had a median of two exacerbations per year, with approximately 40% having at least three per year and over a quarter (26.4%) being hospitalised during an exacerbation in the year prior to the study. Bronchiectasis was generally more severe in Eastern and Central Europe than in other regions. Patients in these parts of Europe also had increased exacerbation frequency, and 57.9% had exacerbations leading to hospitalisation.5 These findings, said Shteinberg, illustrate how common bronchiectasis exacerbations are.
Exacerbation Risk FactorsThe highest risk for bronchiectasis exacerbations, as shown in a study including 2,572 patients in Europe, is the number of previous exacerbations. Here, the adjusted incidence rate ratio of a future exacerbation following one exacerbation was 1.81 (95% CI: 1.54, 2.12; p<0.0001), following two exacerbations was 3.07 (95% CI: 2.62, 3.60; p<0.0001), and following three or more exacerbations was 5.18 (95% CI: 4.51, 5.95; p<0.0001), all compared to no exacerbations. Risk of future exacerbations was also associated with type of infection (greater with H. Influenzae or P. Aeruginosa) and comorbid medical condition (most notably COPD).19
As expected, there is an intimate relationship between lung function and bronchiectasis, with one study showing a decline in the annual rate of forced expiratory volume during the first second (FEV1) of -31.6 mL/year.20 Lower lung function increases the risk of future exacerbations.19 Additionally, more rapid lung function decline is significantly associated with more hospitalisations and/or intravenous antibiotic treatment needed due to an exacerbation.20
Notable is an association between bronchiectasis exacerbations and cardiovascular events; for example, in 1,230 patients with an exacerbation history, both risk of and time to acute myocardial infarction and congestive heart failure was higher compared to 9,484 patients with no exacerbation history.21 There is also a relationship between the number of exacerbations per year and all-cause mortality, which is particularly increased in patients who have ≥3 exacerbations per year.19
Bronchiectasis exacerbations can occur due to exogenous triggers such as pathogens6 and pollution levels.22 These may change regional growth characteristics of the disease through mechanisms such as inflammation, immune dysregulation, and cell damage at the DNA and mitochondrial level.23 There may also be changes in the endogenous microbiome during exacerbations whereby they shift from a less interactive to an 'antagonistic' relationship.24 This may occur due to changes in regional growth characteristics of the disease, as well as to changes in microbial immigration and elimination, epithelial cell interactions, and inflammatory cell concentration and activation.25,26
Neutrophils and Eosinophils in Bronchiectasis ExacerbationsNeutrophil activity is a key endogenous trigger of exacerbations. Neutrophil elastase activity is associated with increased exacerbation risk as well as with disease severity, as evidenced by clinical and radiological extent of bronchiectasis, sputum volume, and lung function decline (both occurrence and rate).11,27,28 There is also a correlation between resolution of neutrophil elastase activity after antibiotic treatment for an exacerbation,13 with neutrophil bacterial phagocytosis and killing ability only increasing following antibiotic administration.9
Notably, an association is shown between neutrophil elastase activity and post-exacerbation hospital admission, shorter time to next severe exacerbation requiring hospitalisations or intravenous antibiotic use, and all-cause mortality.11 There is also evidence of a relationship between high neutrophil extracellular trap concentration (>20 mg/mL) and both occurrence of, and shorter time to, bronchiectasis exacerbations.29
While approximately 80% of patients with bronchiectasis are classified as 'neutrophilic', with blood eosinophil counts <150 cells/mL, the remaining 20% are considered 'eosinophilic', with blood eosinophil counts >300 cells/mL and/or sputum eosinophils >3. Characteristics of such patients include having severe disease, frequent exacerbations, no history of asthma or allergic bronchopulmonary aspergillosis, and possible involvement of P. Aeruginosa.30 A relationship is shown between higher eosinophil count and higher annual hospitalisation and exacerbation rates, with the highest levels when blood eosinophil counts are >300 cells/mL. A role of these inflammatory mediators is also shown as treatment with inhaled corticosteroids of patients with eosinophils >300 cells/mL leads to lower annual bronchiectasis-related hospitalisation and exacerbation rates compared to those with low (<100 cells/mL) or interim (101–300 cells/mL) blood eosinophil counts.31
Current thinking points to the existence of a number of endotypes of bronchiectasis exacerbations based on neutrophil and eosinophil expression and bacterial species. For example, one study32 showed a neutrophilic and Pseudomonas dominated endotype, an eosinophilic endotype with no specific dominance, a Haemophilus dominated endotype that had a bacterial response, and a Streptococcus dominated endotype with excess mucus production. Differences between these endotypes were shown in neutrophil elastase activity and in the expression of the pro-inflammatory cytokine IL-1b and the hormone resistin.32 These are exciting findings regarding bronchiectasis, explained Goeminne, "as we are now realising how important inflammation really is."
Exacerbations and Health-Related Quality of LifeThe European study discussed above (n=2,572) investigated the impact of exacerbations on HRQoL utilising the St. George's Respiratory Questionnaire (SGRQ), which assesses disease-specific health status for asthma and COPD. This is scored on a scale from 0−100 (where a higher score indicates worse HRQoL), with a minimal clinically important difference of around 4.0 points.33 Here, the median SGRQ total score increased according to the number of exacerbations per year, with each additional exacerbation leading to a significant 3.7-point score increase (95% CI: 2.58, 4.87; p<0.0001). Investigation of the data according to hospitalisations found that while there was a 1.4-point increase for each individual outpatient exacerbation (95% CI: 0.57, 2.07; p=0.001), there was a 9.8-point increase for patients with a history of hospitalised exacerbations (95% CI: 6.28, 13.3; p<0.0001).19 These findings echo patient testimony shown as part of the symposium regarding how exacerbations, particularly, can impact their HRQoL.
Management of Bronchiectasis ExacerbationsThe American Lung Association suggests a number of ways to help manage bronchiectasis symptoms and limit flare-ups, including quitting smoking and avoiding second-hand smoke; maintaining a healthy diet and staying hydrated; taking medications as prescribed and staying up-to-date with recommended vaccinations; as well as performing daily mucus clearance techniques.34 However, despite prevention and management strategies, around 75% of patients with bronchiectasis experience exacerbations,5 and challenges remain regarding identifying biomarker triggers and resistance genes to help target treatments, and understanding the interactions between triggers and bronchiectasis-associated inflammation (Figure 2).
Figure 2: Challenges in the clinical management of exacerbations.24,35
Defined airway clearance techniques, as taught by a respiratory physiotherapist, are part of exacerbation management recommended in British Thoracic Society (BTS) guidelines for all patients with bronchiectasis.36 While these are recommended both during and between exacerbations, Shteinberg discussed how, for patients with mild exacerbations, increased airway clearance should be the first step recommended, reviewing their progress after 2−3 days to ascertain if further treatment is needed. The BTS also recommend using postural drainage, which may be modified and targeted in patients with radiological changes, and, for patients with ongoing airway clearance difficulties, addition of manual techniques, use of positive pressure devices, and enhanced airway humidification/hydration using isotonic or hypertonic saline if secretions are viscous.36
Antibiotics and Other TreatmentsAccording to BTS36 and ERS37 guideline recommendations, the primary treatment for acute bronchiectasis exacerbations is antibiotics. Of note, however, recommendations may be based on low-quality evidence.36,37 Eradication is not a treatment goal, discussed Shteinberg, "rather, the rationale in treating with antibiotics is to reduce bacterial load in the airways, which improves symptoms".13 According to these guidelines, standard antibiotic treatment is for 14 days, although shorter periods may be considered in patients with variable disease severity or activity.36,37 The BTS guidelines recommend intravenous antibiotics in patients who are 'particularly unwell, have resistant organisms, or who fail to respond to oral therapy'.36 Antibiotic choice can be guided by the identification of bacterial genus and species,38 and it is recommended that such treatment is always used if a patient is infected with P. Aeruginosa.36,37
Shteinberg echoed good practice points from the BTS when discussing her patient consults. These include initiating empiric antibiotics while awaiting microbiology results, taking into account results from previous exacerbations. Once microbiology results are received, antibiotic choice can be adjusted if needed.36
Microbial response to an antibacterial agent is typically assessed using one of several in vitro 'antimicrobial susceptibility testing' methods. However, these do not necessarily reflect lung diseases where there may be polymicrobial infection, anaerobic airway niches, and diversity in biofilm growth and phenotype.39 As such, instead of antimicrobial susceptibility testing, Shteinberg discussed how one challenge in bronchiectasis is the need to use genotyping methods to identify antibiotic-resistance genes (Figure 2).24 Another difficulty with regard to antibiotic use is that their primary action in the airways is usually only at the level of the mucus layer, which contains far fewer bacteria than in the underlying biofilm due to inactivation by material released from bacteria therein.40
Studies point to the feasibility of shortening the 14 days recommended for antibiotic use during exacerbations. For example, in one study involving patients with severe pulmonary exacerbations treated with an intravenous antibiotic, 47 were administered 14 days' treatment and 43 were treated according to bacterial load in sputum samples (bacterial load-guided group: BLGG). Results demonstrated that, on Day 7, 84% of all participants in both groups showed colony-forming units per mL <106. This meant that in the BLGG, bacterial load was considered low enough that treatment could be stopped in 88% of patients on Day 8. In all other participants in the BLGG, treatment could be stopped on Day 11. While clinical recovery was not affected by group, time to next exacerbation was significantly sooner in the 14-day group compared to the BLGG (p=0.0034).41
Studies have also assessed dual antibiotic use, taking advantage of different delivery methods. In one double-blind, randomised study, an oral antibiotic was combined with either an inhaled antibiotic or a placebo in 53 patients with bronchiectasis and chronic P. Aeruginosa infection. At Day 21, no differences were found in bacterial load or clinical outcome, which, the authors postulated, may have been related to the finding of more treatment-related wheeze in the inhaled antibiotic group compared with the placebo group.42
Shteinberg also highlighted the challenge of needing to find ways to reduce antibiotic use (antibiotic resistance), for example, by understanding if exacerbations are caused by viral infection, pollutants, or host inflammatory responses (Figure 2).35 Other treatments for bronchiectasis include mucolytics, the use of which is associated with significant improvements in expectoration, sputum volume, auscultatory findings, and FEV1.43 As bronchiectasis is associated with inflammation,1 an anti-inflammatory agent may be prescribed during acute exacerbations. However, in a single-centre, retrospective study (n=43), the use of systemic glucocorticoids in such cases was associated with significantly increased in-hospital mortality (p=0.0474).44
ConclusionOverall, this symposium highlighted how both patients and their primary healthcare providers need to be educated in identifying bronchiectasis exacerbations and in understanding the impact of exacerbations on a patient's general health and HRQoL. Daily airway clearance techniques should be taught and escalated if needed during exacerbations, and discussion of antibiotic treatment should include details of how this should result in clinical improvement but may not lead to pathogen eradication. Challenges that remain regarding clinical management of bronchiectasis exacerbations include understanding the interaction between associated triggers35 and identifying biomarkers for such,24 as well as providing clinically evidenced treatment regimens.
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