National Kidney Month

National Kidney Month

National Kidney Month

Kidneys are an essential role because they help remove waste and extra water from our systems. This process is necessary because it helps maintain a stable balance of body chemicals. Kidneys also help produce hormones that affect the functions of other organs. These are hard-working organs that also help:

  1. Regulate fluid levels
  2. Activate Vitamin D
  3. Filter wastes from the body
  4. Directs production of red blood cells
  5. Regulates blood pressure
  6. Keep blood minerals in balance
Mesothelioma

Nivolumab Improves Survival in Relapsed Mesothelioma

Nivolumab Improves Survival in Relapsed Mesothelioma

In the first ever placebo-controlled phase 3 trial in patients with relapsed mesothelioma, immunotherapy with nivolumab (Opdivo) significantly improved both overall survival (OS) and progression-free survival (PFS).  

The CONFIRM trial involved 330 previously treated patients with mesothelioma who were randomly assigned to nivolumab or placebo for 1 year or until progression or unacceptable toxicity.

Although recruitment to the study was stopped early because of the COVID-19 pandemic, enough data accrued to show that the immunotherapy improved overall survival by 28% over placebo, and increased PFS by 39%.

“Nivolumab was deemed a safe and effective treatment and should be considered a new treatment option for patients with relapsed mesothelioma,” said principal investigator Dean A. Fennell, MD, PhD, professor and consultant in Thoracic Medical Oncology, University of Leicester, United Kingdom.

He presented the results at the World Conference on Lung Cancer, which was held virtually because of the ongoing pandemic.

Rina Hui, MD, PhD, Crown Princess Mary Cancer Centre, Westmead Hospital, Sydney, Australia, who was not involved in the study, told journalists that these results had been a “long time coming.”

CONFIRM has added “important, encouraging data on immunotherapy in the salvage setting, particularly that patients were heavily pretreated,” Hui said, with two thirds having received two or more lines of therapy.

Fennel noted that “a significant clinical benefit was observed in the epithelioid subtype” of the disease, but not in patients with non-epithelioid disease.

However, there was “no evidence” to support tumor programmed death ligand 1 (PD-L1) expression as predictive of outcomes, he added, which does appear to be the case in some trials on lung cancer and other tumors.

Commenting on these observations, Hui said that PD-L1 as a predictive biomarker in mesothelioma has been “controversial”, and emphasized that the results from CONFIRM indicate “no evidence of PD-L1 being predictive”.

However, she questioned the other observation that clinical benefit appeared to be seen only in the epithelioid subtype.

Hui emphasized that non-epithelioid disease is known to be a “more aggressive, chemo-resistant subtype…with a steep decline in the survival curves.”

“Therefore a lot of patients would not have made it to a subsequent line clinical trial, explaining why there were only 12% in the CONFIRM study,” and so the sample size may be “too small to detect a difference in outcome.”

Consequently, Hui said she “would not deny patients with non-epithelioid histology from considering nivolumab in the salvage setting.”

She argued that there was “no clear predictive biomarker for patient selection” emerging from the CONFIRM data.

She agreed that, in patients with mesothelioma who have progressed following platinum/pemetrexed-based chemotherapy as in the first line, “monotherapy nivolumab now can be considered as a treatment option in the second…or third-line setting, after second-line chemotherapy”.

However, outstanding questions remain, including whether nivolumab “provides better outcomes than second-line single-agent chemotherapy or second-line gemcitabine with the VGFR inhibitor ramucirumab (Cyramza).”

Source: medscape.com

ScaledBlog 12.02.20 copy 3-100

How gut microbes could drive brain disorders

How gut microbes could drive brain disorders

Scientists are starting to work out how the gut microbiome can affect brain health. That might lead to better and easier treatments for brain diseases

In 2006, soon after she launched her own laboratory, neuroscientist Jane Foster discovered something she felt sure would set her field abuzz. She and her team were working with two groups of mice: one with a healthy selection of microorganisms in their guts, and one that lacked a microbiome. They noticed that the mice without gut bacteria seemed less anxious than their healthy equivalents. When placed in a maze with some open paths and some walled-in ones, they preferred the exposed paths. The bacteria in the gut seemed to be influencing their brain and behavior.

Foster, at McMaster University in Hamilton, Canada, wrote up the study and submitted it for publication. It was rejected. She rewrote it and sent it out again. Rejected. “People didn’t buy it. They thought it was an artefact,” she says. Finally, after three years and seven submissions, she got an acceptance letter1.

John Cryan, a neuroscientist at University College Cork in Ireland, joined the field about the same time as Foster did, and knows exactly how she felt. When he began talking about the connections between bacteria living in the gut and the brain, “I felt very evangelical”, he says. He recalls one Alzheimer’s disease conference at which he presented in 2014. “I’ve never given a talk in a room where there was less interest.”

Today, however, the gut–brain axis is a feature at major neuroscience meetings, and Cryan says he is no longer “this crazy guy from Ireland”. Thousands of publications over the past decade have revealed that the trillions of bacteria in the gut could have profound effects on the brain, and might be tied to a whole host of disorders. Funders such as the US National Institutes of Health are investing millions of dollars in exploring the connection.

But along with that explosion of interest has come hype. Some gut–brain researchers claim or imply causal relationships when many studies show only correlations, and shaky ones at that, says Maureen O’Malley, a philosopher at the University of Sydney in Australia who studies the field of microbiome research. “Have you found an actual cause, or have you found just another effect?”

In recent years, however, the field has made significant strides, O’Malley says. Rather than talking about the microbiome as a whole, some research teams have begun drilling down to identify specific microbes, mapping out the complex and sometimes surprising pathways that connect them to the brain. “That is what allows causal attributions to be made,” she says. Studies in mice — and preliminary work in humans — suggest that microbes can trigger or alter the course of conditions such as Parkinson’s disease, autism spectrum disorder and more (see ‘Possible pathways to the brain’). Therapies aimed at tweaking the microbiome could help to prevent or treat these diseases, an idea that some researchers and companies are already testing in human clinical trials.

Source: Nature.com

Study links healthy sleep duration to less sick time from work

Study links healthy sleep duration to less sick time from work

Study links healthy sleep duration to less sick time from work

New research suggests that sleeping 7 to 8 hours per night is associated with the lowest risk of absence from work due to sickness. The results underscore the importance of the “Sleep Well, Be Well” campaign of the National Healthy Sleep Awareness Project, a collaboration between the Centers for Disease Control and Prevention, American Academy of Sleep Medicine, Sleep Research Society and other partners.

Results show that the risk of an extended absence from work due to sickness rose sharply among those who reported sleeping less than 6 hours or more than 9 hours per night. Further analysis found that the optimal sleep duration with the lowest risk of sickness absence from work was between 7 and 8 hours per night: 7 hours, 38 minutes for women and 7 hours, 46 minutes for men. Insomnia-related symptoms, early morning awakenings, feeling more tired than others, and using sleeping pills also were consistently associated with a significant increase in workdays lost due to sickness.

“Optimal sleep duration should be promoted, as very long and very short sleep indicate health problems and subsequent sickness absence,” said principal investigator Tea Lallukka, PhD, specialized researcher at the Finnish Institute of Occupational Health. “Those sleeping five hours or less, or 10 hours or more, were absent from work every year for 4.6 to 8.9 days more, as compared to those with the optimal sleep length.”

The study results are published in the September issue of the journal Sleep.

“Insufficient sleep – due to inadequate or mistimed sleep – contributes to the risk for several of today’s public health epidemics, including cardiovascular disease, diabetes and obesity. Getting at least seven hours of nightly sleep is a key to overall health, which translates to less sick time away from work,” said American Academy of Sleep Medicine President Dr. Timothy Morgenthaler, a national spokesperson for the Healthy Sleep Project. The “Sleep Well, Be Well” campaign was launched earlier this year to increase awareness of the importance of sleep as one of the three pillars of a healthy lifestyle.

The study involved a nationally representative survey of 3,760 men and women in Finland who had been working at any time in the prior year. Participants were 30-64 years old at baseline. Sleep characteristics were determined by questionnaire, and health measures were derived from physical examination conducted by field physicians. Data for work absences due to sickness were gathered from the Social Insurance Institution of Finland, which tracks all sickness absences lasting more than 10 days. The average follow-up period was seven years.

A novel statistical method developed by study co-authors Tommi Härkänen, PhD, and Risto Kaikkonen, MSc, was used to predict adjusted average sickness absence days per working year. Additional statistical estimates found that the direct costs of sickness absence to the Finnish government and employers could decrease by up to 28 percent if sleep disturbances could be fully addressed.

“Insomnia symptoms should be detected early to help prevent sickness absence and deterioration in health, well-being and functioning,” said Lallukka. “Successful prevention of insomnia not only promotes health and work ability among employees, but it can also lead to notable savings in reduced sickness absence costs.”###

The study was supported by the National Institute for Health and Welfare, the Academy of Finland and the Finnish Work and Environment Fund.

To request a copy of the study, “Sleep and Sickness Absence: A Nationally Representative Register-Based Follow-Up Study,” and the commentary, “Working with Poor Sleep,” or to arrange an interview with the study author or an AASM spokesperson, please contact Communications Coordinator Lynn Celmer at 630-737-9700, ext. 9364, or [email protected].

The monthly, peer-reviewed, scientific journal Sleep is published online by the Associated Professional Sleep Societies LLC, a joint venture of the American Academy of Sleep Medicine and the Sleep Research Society. The AASM is a professional membership society that improves sleep health and promotes high quality patient centered care through advocacy, education, strategic research, and practice standards.

About the National Healthy Sleep Awareness Project

The Healthy Sleep Project addresses the sleep health focus area of Healthy People 2020, which provides science-based, 10-year national objectives for improving the health of all Americans. The sleep health objectives are to increase the medical evaluation of people with symptoms of obstructive sleep apnea, reduce vehicular crashes due to drowsy driving and ensure more Americans get sufficient sleep. For more information, visit http://www.sleepeducation.org/healthysleep.

Source: EurekAlert.org

Study describes the diversity of genetic changes that cause inherited kidney disease

Study describes the diversity of genetic changes that cause inherited kidney disease

Study describes the diversity of genetic changes that cause inherited kidney disease

A study has described genetic changes in patients with the most common form of hereditary kidney disease that affects an estimated 12.5 million people worldwide. The research, which focussed on Polycystic Kidney Disease (PKD) in Ireland, provides insights into PKD that will assist doctors and patients in the management of this of inherited condition.

In the research, a cohort of 169 patients with PKD in Ireland was analyzed. The genetic changes were identified in up to 83% of cases. It is the first time that the diversity of genetic causes of PKD in Ireland have been described. The results will better assist doctors in identifying patients who may require transplantation or dialysis. The findings also have important implications for people who have a family history of PKD and are planning a family or considering kidney donation.

“This study is hugely important in providing us with an insight into the genetic landscape of Polycystic Kidney Disease, the most common form of inherited kidney disease in the world,” said first author on the study Dr Katherine Benson, School of Pharmacy and Biomolecular Sciences, RCSI.

“Our findings have implications for the prognosis of patients by helping us to further identify why the disease may progress more rapidly in some cases and how we can reduce the burden of inherited kidney disease in future.”

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The study was carried out by a team of researchers and clinician scientists under the supervision of senior authors Prof. Gianpiero Cavalleri, Professor of Human Genetics at RCSI and Prof. Peter Conlon, Associate Professor of Medicine at RCSI and Consultant Nephrologist at Beaumont Hospital.

The study was supported by an Enterprise Partnership Scheme Fellowship Award from The Irish Research Council, in conjunction with Punchestown Kidney Research Fund. The research was also funded by the Beaumont Hospital Foundation and the Royal Irish Academy.

About RCSI University of Medicine and Health Sciences

Ranked number one globally for Good Health and Well-being in the Times Higher Education (THE) University Impact Rankings 2020, RCSI University of Medicine and Health Sciences is an international not-for-profit university, with its headquarters in Dublin.

RCSI is exclusively focused on education and research to drive improvements in human health worldwide. It is among the top 250 universities worldwide in the World University Rankings (2020) and its research is ranked first in Ireland for citations. RCSI has been awarded Athena Swan Bronze accreditation for positive gender practice in higher education.

Visit the RCSI MyHealth Expert Directory to find the details of our experts across a range of healthcare issues and concerns. Recognizing their responsibility to share their knowledge and discoveries to empower people with information that leads them to better health, these clinicians and researchers are willing to engage with the media in their area of expertise.

Source: EurekAlert.org

Chronic Kidney Disease

Chronic Kidney Disease Rises While Most People with the Condition Remain Unaware

Chronic Kidney Disease Rises While Most People with the Condition Remain Unaware

A growing number of Americans have chronic kidney disease, but most remain unaware of it, hampering efforts to prevent irreversible kidney failure requiring dialysis or a transplant, according to a study funded by the National Institutes of Health and published November 7 in the Journal of the American Medical Association.

An estimated 26 million people — about 13 percent of the U.S. population — now have chronic kidney disease, say researchers at Johns Hopkins University in Baltimore, Tufts-New England Medical Center in Boston and Cleveland Clinic Foundation. The disease affected an estimated 20 million people in 1994.

“Increases in diabetes, hypertension, obesity, and the aging U.S. population explain at least some of the increase,” says co-author Paul W. Eggers, Ph.D., director of kidney disease epidemiology at the National Institute of Diabetes and Digestive and Kidney Diseases, part of the NIH. “We don’t know what may be responsible for the rest.”

The study analyzed and compared National Health and Nutrition Examination Survey data on adults age 20 or older from 1988 to 1994 and 1999 to 2004. More than 15,000 and 13,000 adults, respectively, were interviewed at home and had a physical exam and blood and urine tests. The surveys were conducted by the National Center for Health Statistics, part of the Centers for Disease Control and Prevention.

Kidney function was estimated for each participant with a formula that considers the amount of creatinine in a blood sample, along with age, gender and African American race, which can affect results. Creatinine is a waste product created by normal breakdown of muscle cells during activity. When kidneys are ailing, creatinine builds up in the blood. A small sample of urine was checked for a protein called albumin. Damaged kidneys may persistently leak albumin from the blood into the urine, sometimes even when kidney function appears normal.

Awareness of chronic kidney disease is up, but most people who have the condition still don’t know it. Between 1999 and 2004, survey participants were asked if they had been told they had “weak or failing kidneys.” The authors report that only 11.6 percent of men and 5.5 percent of women with moderate (stage 3) kidney disease knew it. Awareness increased to 22.8 percent among participants with stage 3 disease and albumin in the urine. Awareness was highest among people with severe (stage 4) kidney disease, only 42 percent of whom knew they had the condition. Stage 5 is kidney failure.

“Kidney disease is often silent until late stages, but if we can find it early we can do a lot to prevent kidney failure,” explained Andrew S. Narva, M.D., F.A.C.P., a kidney specialist at the NIH. “If you have diabetes, high blood pressure or a family history of kidney problems you are at risk and should be screened for kidney damage with routine blood and urine tests.”

“To help protect the kidneys’ small blood vessels, carefully control high blood pressure, and blood sugar if you’re diabetic, and ask your doctor if you should take an angiotensin converting enzyme inhibitor or angiotensin receptor blocker,” advised Narva, also director of the NIH’s National Kidney Disease Education Program.

Kidney disease raises the risk of early death, heart attack, stroke, and high blood pressure; causes anemia, bone disease and malnutrition; and can lead to kidney failure. In 2005, at least 107,000 Americans learned they had kidney failure. That year, more than 485,000 had dialysis or a kidney transplant, costing $32 billion, according to the NIH’s U.S. Renal Data System. The data system predicts that by 2020 nearly 785,000 people will be receiving treatment for kidney failure, costing $53.6 billion.

Source: NIH.gov

IU researchers find disease-related gene changes in kidney tissue

IU researchers find disease-related gene changes in kidney tissue

IU researchers find disease-related gene changes in kidney tissue

Researchers from Indiana University have identified key genetic changes in the interstitial kidney tissue of people with diabetes, a discovery that signifies the potential for a revolutionary new genetic approach to the treatment of kidney disease. They will contribute their findings to the Kidney Precision Medicine Project’s (KPMP) “cell atlas,” a set of maps used to classify and locate different cell types and structures within the kidney.

They shared their groundbreaking findings in a study published on February 10, 2021, in Science Advances.

In the study, researchers investigated the kidney tissue of healthy people and people with diabetes using a technique called “regional transcriptomics.” This technique involves a rapid stain of kidney tissue, and then using a laser to cut out microscopic regions of interest.

They found that important genes change when a scar forms on the interstitium, said Daria Barwinska, PhD, the lead author of the study and an Assistant Scientist in the Department of Medicine at Indiana University School of Medicine.

“The interstitium is the ‘glue’ that holds the kidney together. It is one of the least characterized parts of the kidney, but scars in the interstitium caused by diseases such as diabetes can contribute to kidney disease,” said Barwinska.

Acute kidney injury (AKI) and chronic kidney disease (CKD) affect millions of people in the United States and globally. However, no effective therapies exist for AKI, and only a few are available for CKD. The KPMP, a multi-site project focused on understanding and finding new treatments to AKI and CKD, is seeking to bring treatment for these conditions “into the molecular era,” according to Michael Eadon, MD.

IU is one of KPMP’s many “tissue interrogation sites” across the country. Collectively, these sites are working together bring cutting-edge technologies to aid in the interrogation of human kidney biopsies.

“Many diseases can look the same under the microscope, but they have very different causes,” said Eadon, who is the study’s corresponding author and an Assistant Professor of Medicine in the Department of Medicine at IU School of Medicine. “We’re seeking to understanding how different genes contribute to very common kidney diseases.”

This study could usher in the era of new and better treatments for millions of people with AKI and CKD.

“A personalized medicine approach that understands how different diseases affect a patient’s genes will aid in finding potential treatments for kidney disease,” said Barwinska. “This approach can meet any single patient’s needs.”


Source: EurekAlert.org

American Heart Month

Amerian Heart Month Awareness

Amerian Heart Month Awareness

This February we are raising awareness for American Heart Month and discussing prevention steps for heart diseases. Heart disease is the leading cause of death and every 36 seconds someone in the United States dies from a heart condition. This month Febo is focusing on adopting a healthy lifestyle to prevent heart disease. Here are some facts on heart disease:
 

  • In the US someone has a heart attack every 40 seconds
  • High blood pressure, high cholesterol and smoking are key risk factors for heart disease
  • 1 in every 4 deaths in the US is related to heart disease
  • The most common type of heart disease is Coronary Artery Disease

Some tips for adopting a healthier lifestyle:

  • Exercise for at least 30 minutes a day
  • Replace snacks for a healthy fruit or veggie
  • Plan your meals at the beginning of the month
  • Use your Febo Food Diary to track calories and nutrients
  • Swap the elevator for the stairs
  • Get 8 hours of sleep
     

Let’s have a #HearttoHeart and share these tips with your friends and family!

Source: CDC, NIH

Heart Failure

Temple researchers identify a cardiac protein that causes different types of heart failure

Temple researchers identify a cardiac protein that causes different types of heart failure

Like a failing fuel pump that causes a loss of engine power in a car, a diseased heart can take a serious toll on the body’s performance. For some patients, tasks like walking up a flight of stairs or walking across a room eventually turn into exhausting endeavors. This is because, over time, regardless of the underlying cause, heart damage typically progresses, owing to a constant barrage of oxidative stress and toxic lipids that alter heart cell energetics and, ultimately, the ability of the heart to function normally.

Oxidative stress occurs when harmful oxygen-containing molecules outnumber helpful antioxidants, leading to damaging reactions with proteins, DNA, and other cell components. Now, in two new studies, researchers at the Lewis Katz School of Medicine at Temple University (LKSOM) show that in the heart, one molecule in particular, Kruppel-like factor (KLF)-5, single-handedly fuels both the generation of oxidizing molecules and the accumulation of toxic lipids known as ceramides in the heart, exacerbating heart dysfunction. The studies are the first to identify KLF5 as a common mediator of cardiac damage in animal models of different diseases that lead to abnormal heart function, including diabetes and heart attack.

“Our findings expose KLF5 as a new target for different types of cardiac disease,” said Konstantinos Drosatos, PhD, Associate Professor of Pharmacology at the Center for Translational Medicine, the Center for Metabolic Disease Research, and Alzheimer’s Center at Temple at LKSOM. “As a unifying factor driving oxidative stress and accumulation of toxic lipids in the heart, the implications of targeting KLF5 could be far-reaching, opening up treatment for a broad range of diseases involving heart dysfunction.”

In the first study, published online December 2 in the journal Circulation Research, Dr. Drosatos and colleagues investigated the involvement of KLF5 in a mouse model of diabetic cardiomyopathy. Diabetic cardiomyopathy is a major complication of diabetes and is characterized in particular by altered heart cell metabolism and oxidative damage. The new study showed that patients with diabetes have high levels of KLF5 expression in the heart.

The researchers found that mice with diabetic cardiomyopathy similarly have high KLF5 expression, and they discovered that elevated KLF5 is linked to the build up of ceramides in the heart. Ceramides, which occur naturally in the cell membrane, are known to reach toxic levels in the presence of insulin resistance and severe heart damage, such as that inflicted by heart attack.

The Temple team showed that in mice, however, these harmful effects could be halted. “Inhibiting KLF5 with a drug, as well as with genetic interventions, not only reduced oxidative stress and prevented ceramide accumulation but also restored cardiac function,” Dr. Drosatos explained.

In the second study, published online January 12 in the journal Circulation, which was driven by LKSOM MD-PhD student, Matthew Hoffman, Dr. Drosatos’s team investigated the role of KLF5 in mice with heart failure induced by cardiac ischemia, a sudden, severe blockage of blood flow to the heart. Cardiac ischemia characteristically is followed by extensive increases in toxic lipids, particularly ceramides. The researchers were able to show that KLF5 is involved in causing the production of ceramides that underlies damage to the cardiac wall. Ceramide buildup was driven by KLF5-induced overexpression of a molecule known as SPT1.

“The next step is to determine whether the severity of heart disease or the way patients respond to treatment is associated with increased KLF5,” Dr. Drosatos said. “We know from clinical observations, for example, that some patients with heart failure are less responsive than others to therapeutic interventions. We want to know whether KLF5 is a factor that defines how well the patients will respond to treatments.”

In addition, Dr. Drosatos and colleagues plan to search for proteins that regulate KLF5, which could broaden understanding of the role and pathway of activation of KLF5 in the heart and other tissues.

The studies also mark new ground in individual and collaborative research efforts at Temple University.

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Notably, lead author of the paper in Circulation Research, Ioannis D. Kyriazis, PhD, a post-doctoral researcher in the Drosatos laboratory, was recognized as a finalist for the prestigious Melvin L. Marcus Early Career Investigator Award in Cardiovascular Sciences of the American Heart Association for his studies of KLF5 in diabetic cardiomyopathy.

Other investigators who contributed to the studies included Anna Maria Lucchese, Eftychia Markopoulou, Dimitra Palioura, Walter J. Koch, Maria Cimini, Sudarsan Rajan, Erhe Gao, Raj Kishore, Center for Translational Research at LKSOM; Lea Gaignebet, Charite? – Universita?tsmedizin Berlin, Germany; Chao Wang and Thomas D. Bannister, The Scripps Research Institute, Jupiter, Florida; Melpo Christofidou-Solomidou, Pulmonary, Allergy, and Critical Care Division, University of Pennsylvania School of Medicine, Philadelphia; Shin-ichi Oka and Junichi Sadoshima, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School; Ira J. Goldberg, Division of Endocrinology, Diabetes and Metabolism, New York University School of Medicine; Vincent W. Yang and Agnieszka B. Bialkowska, School of Medicine, Stony Brook University; Georgios Kararigas, Charite? – Universita?tsmedizin Berlin, DZHK (German Centre for Cardiovascular Research) partner site Berlin, and Department of Physiology, Faculty of Medicine, University of Iceland; Rachit Badolia and Stavros G. Drakos, University of Utah, Nora Eccles Harrison Cardiovascular Research and Training Institute, Division of Cardiovascular Medicine; Nikolas Nikolaidis, Department of Biological Science, Center for Applied Biotechnology Studies, and Center for Computational and Applied Mathematics, College of Natural Sciences and Mathematics, California State University; P. Christian Schulze, Department of Internal Medicine, Division of Cardiology, Angiology, Intensive Medical Care and Pneumology, University Hospital Jena, Germany; and Craig H. Selzman, University of Utah, Division of Cardiothoracic Surgery.

The studies were funded in part by the National Heart Lung and Blood Institute of the National Institutes of Health, the National Institute of General Medical Sciences, the W.W. Smith Charitable Trust, and the American Heart Association.


Source: EurekaAlert

Psoriasis

Study links metabolic syndrome to higher cardiovascular risk in patients with psoriasis

Study links metabolic syndrome to higher cardiovascular risk in patients with psoriasis

Psoriasis, a chronic inflammatory skin disease, has long been known to increase the risk of cardiovascular disease, which includes heart attack and stroke. Now, researchers have identified a key culprit: the presence of metabolic syndrome (MetSyn), a condition that includes obesity, diabetes, high cholesterol, and hypertension, and is highly prevalent among psoriasis patients.

The findings, which could lead to new ways to help prevent cardiovascular disease among people with psoriasis, appear online today in the Journal of the American Association of Dermatology (JAAD). The study was funded by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health.

“Metabolic syndrome, so common among our psoriasis patients, drives up coronary artery disease in this population by increasing the plaque buildup that clogs the heart’s arteries,” said Nehal N. Mehta, M.D., MSCE, preventive cardiologist and head of the NHLBI’s Lab of Inflammation and Cardiometabolic Diseases. “Our study shows that, of the MetSyn components, hypertension and obesity contribute the most to coronary plaque buildup, and hence can be good targets for intervention.”

Partly because it worsens vascular and systemic inflammation, psoriasis, a common skin disease affecting 2-3% of adults, not only increases but speeds up atherosclerosis, the plaque buildup that clogs arteries and can lead to heart attack and stroke. Metabolic syndrome affects about 25% of adults and is on the rise, and its prevalence is even greater among patients with psoriasis.

To reach their conclusions, Mehta and his team conducted an observational study of the NIH Psoriasis, Atherosclerosis, and Cardiometabolic Initiative cohort, which included 260 patients with psoriasis, 80 of whom met the criteria for metabolic syndrome. All participants underwent CT scanning to take pictures of their coronary arteries using a technique called cardiac computed tomography angiography (CTA).

The study found that systemic inflammation, insulin resistance, and blood cholesterol were significantly higher in the participants who had both psoriasis and metabolic syndrome. And those with MetSyn had higher coronary artery plaque buildup, assessed by CTA, which is a high-risk factor for heart attacks.

“Even after adjusting for individual MetSyn factors, blood pressure and obesity assessed by waist circumference were the most significant links to coronary plaque buildup,” Mehta explained. 

Obesity is the most salient aspect of MetSyn, and excess visceral fat tissue, technically known as visceral adipose tissue (VAT), plays a large role in it, the researchers concluded after the amount of VAT measured by CT scans was associated to MetSyn factors such as waist circumference, blood pressure, triglycerides, high cholesterol.

VAT is a known predictor(link is external) of cardiovascular disease in the general population, as well as a predictor of increased plaque buildup in psoriasis patients. However, due to the needed imaging technology, measuring VAT is not currently feasible in a doctor’s office.

This new study, Mehta said, demonstrates a critical link between excessive VAT and metabolic syndrome in psoriasis patients. It suggests that identifying metabolic syndrome, especially waist circumference, can significantly help in estimating VAT and assessing cardiovascular disease risk in clinical settings for patients with psoriasis.

It also showed for the first time, he said, the impact of metabolic syndrome on early vascular disease in psoriasis patients, measured through the plaque buildup.

“In psoriasis patients, traditional risk factors of cardiovascular diseases, such as age, do not relate strongly to cardiovascular risk as in the general population,” Mehta said. However, he added, the findings in the study show the importance of evaluating for the presence of the metabolic syndrome as a heretofore unexplored risk factor. 

Because this was an observational study, the researchers cannot establish cause-effect links, Mehta noted. But the new research provides strong evidence that psoriasis patients with metabolic syndrome have high levels of disease-producing plaque.    

 

Source: nih.gov