Implant-Related Lymphoma Cases Rise

https://goo.gl/GzqBUe

More than 400 cases reported to FDA

The number of cases of a rare type of lymphoma linked to breast implants has surpassed 400, according to updated information from the FDA.

As of Sept. 30, 2017, the FDA had received 414 medical device reports (MDRs) of breast implant-associated anaplastic large-cell lymphoma (BIA-ALCL), a 15% increase since agency's previous report on the issue in March 2017. The MDRs included nine patients who died.

Not all reports included complete information, but from the information available, the FDA determined that:

  • 242 involved implants with textured surfaces and 30 with smooth surfaces
  • 234 implants were filled with silicone gel and 179 with saline
  • In about half the cases, the BIA-ALCL diagnosis occurred 7-8 years after implantation

As part of the update, the FDA reviewed reported cases of BIA-ALCL in the medical literature and found that the estimated lifetime risk of developing BIA-ALCL for a women with textured breast implants rages from 1 in 3,817 to 1 in 30,000. However, the FDA emphasized that it is not changing its recommendations on use of breast implants.

Non-antibiotic drugs promote antibiotic resistance

This is scary and complex.....

https://goo.gl/evArgC

THE widespread use of antibiotics encourages the pathogens they are directed against to become inured to their effects. That is well known. But antibiotics cause damage to non-target species as well, so these, too, tend to evolve immunity. Since most antibiotics are administered by mouth, the many bacteria that live peacefully in the human gut are particularly susceptible to such evolutionary pressures.

The medical consequences of this are ill-understood, in part because most gut bacteria are anaerobes (meaning they flourish only in the absence of oxygen) and so are difficult to culture. But Lisa Maier of the European Molecular Biology Laboratory, in Heidelberg, and her colleagues have, nevertheless, grown 40 of the most common strains of them in anaerobic conditions. They have then gone on to expose those cultures to hundreds of drugs for a range of ailments, at the sorts of concentrations that might be encountered in the human intestine. Their study, published this week in Nature, has revealed an unexpected avenue by which gut bacteria can become resistant to antibiotics: exposure to drugs that were designed to act on human cells rather than microbial ones.

Of the drugs in the study, 156 were antibacterials (144 antibiotics and 12 antiseptics). But a further 835, such as painkillers and blood-pressure pills, were not intended to harm bacteria. Yet almost a quarter (203) did. These accidental bactericides included proton-pump inhibitors such as omeprazole (used to treat acid reflux), calcium-channel blockers (to lower blood pressure), antihistamines, painkillers and antipsychotics. (In the case of antipsychotics, these chemically diverse drugs seemed to affect many of the same strains of gut bacteria. That suggests their effects on the brain could, in part, be a result of their influence on gut flora).

The researchers noticed too that the strains of bacteria most resistant to the effects of drugs not aimed at them were also those most resistant to antibiotics. This observation implied that these bacteria were using similar means to defend themselves against both sorts of medicine.

Did a Sugar Called Trehalose Contribute to the Clostridium difficile Epidemic?

https://goo.gl/m5QhhR

Scientists have recently discovered that a form of sugar called trehalose could be partly to blame for the rapid emergence around the turn of the millennium of certain epidemic-associated strains of the gut bacterium Clostridium difficile. The research, published in Nature and led by Baylor College of Medicine microbiologist Robert Britton, PhD, suggests that these strains have a unique ability to grow on low amounts of the sugar, which entered the North American and European food systems around the same time as C difficileoutbreaks in these regions.

The strains belong to 2 C difficile ribotypes, RT027 and RT078. Infections from C difficile had always caused diarrhea and colitis, sometimes leading to surgery and even death. But starting around 2000, as the previously rare ribotype RT027 spread, the infections became more common, more severe, more resistant to treatment, more likely to relapse, and more deadly.

Between 2001 and 2010, the US rate of C difficile hospitalizations per 1000 adult discharges roughly doubledfrom 5.6 to 11.5. In 2011, C difficile caused almost half a million infections and approximately 15 000 deaths. That year, RT027 was associated with around a third of health care–associated C difficile infections.

Antibiotic resistance alone doesn’t fully explain the trends. Although RT027 strains are resistant to fluoroquinolone antibiotics, so are other nonepidemic ribotypes. So what was giving this particular brand of C difficile its edge?

In 2014, Britton demonstrated that epidemic RT027 strains outcompete other nonepidemic C difficile strains in human fecal bioreactors and mouse models. But the mechanism behind their advantage was still unknown.

In their recent Nature study, funded by the National Institutes of Health, Britton and collaborators looked at how an epidemic strain of RT027 responds to around 200 food sources—sugars and sugar alcohols, amino acids, and proteins—found in the large intestine, where C difficile causes disease. One food source in particular—trehalose—stood out as increasing growth 5-fold compared with a non-RT027 strain.

The researchers then supplemented 21 strains from 9 C difficile ribotypes commonly found in the clinical setting with either glucose or trehalose alone. Most of the strains grew on low amounts of glucose, but only epidemic strains of RT027 and another outbreak-associated ribotype, RT078, grew on low amounts of trehalose.

“That was a smoking gun for us,” Britton said.

The Underrepresentation of You in Medical Research

https://goo.gl/MRb6FK

You probably think taking a baby aspirin daily will reduce your risk of getting a blood clot. You’ve likely heard that a thousand times. It’s one of those pieces of medical common knowledge. But here’s the thing: it doesn’t work in about a third of people, and doctors don’t know why. It’s a phenomenon called aspirin resistance, and people who have it don’t get the anti-blood-clot benefits from the drug. But for people who do respond to aspirin, it works pretty well.

At the individual level, aspirin resistance is really important, obviously. But big randomized controlled trials suppress these important individual factors, leading to generic conclusions that don’t apply to a large swath of patients. Let’s simplify things a bit in attempt to discern how this works, then we’ll consider some other individual factors that don’t get captured by broad research conclusions.

What we’ve started to realize over the last few decades is just how unique each person really is. And we don’t have good systems in place for taking into account these individual factors in health research. Not long ago, scientists assumed that once we’d figured out the human genetic sequence, miraculous medical feats would become commonplace and amazing drugs that cured everybody would be rapidly developed. Well, we found the human genome sequence in 2001, and we still haven’t developed those miracle cures.

Part of the problem, scientists now realize, has to do with what we call epigenetics. Epigenetic processes regulate the real-world effects of our genes by modulating the rate at which genes are changed into proteins. Even identical twins, whose gene sequence is shared, often turn out quite different because of epigenetics. How we respond to a given medication has a lot to do with epigenetics too.

Many factors influence epigenetics — what you eat, your environment, what medications you take, etc. But there’s one factor that makes this issue more complicated: a person’s microbiome also influences his or her epigenetics. Your microbiome consists of all the non-human organisms in and on your body. You’re composed of at least as many non-human cells as you are human cells.

And here’s where it get’s bewilderingly complex: the cumulative genome of the microbiome, called the metagenome, is way, way bigger than the human genome, and it’s influenced by its own epigenetic processes.

What this all means is this: there are no two individuals on the planet whose genetics, epigenetics, microbiome, metagenome, and meta-epigenetics all match exactly. And all of these things influence how we respond to medications.

ACP Recommends Less-Intensive HbA1c Target for T2D

https://goo.gl/jU1nf2

No proof of benefit for targets below 7%, new guidelines say.

New type 2 diabetes guidelines from the American College of Physicians (ACP) recommend less-intensive blood sugar control for most patients, with a glycated hemoglobin (HbA1c) target between 7% and 8%.

"Studies have not consistently shown that intensive glycemic control to HbA1c levels below 7% reduces clinical microvascular events, such as loss or impairment of vision, end-stage renal disease, or painful neuropathy, or reduces macrovascular events and death," said first author Amir Qaseem, MD, PhD, ACP vice president for clinical policy, and colleagues.

To develop the new recommendations, the authors evaluated six sets of current guidelines from other organizations and reviewed five important clinical trials on which those guidelines are based. The updated guidance, published online in Annals of Internal Medicine, offers four key statements:

  • Statement 1: Clinicians should personalize goals for glycemic control in patients with type 2 diabetes on the basis of a discussion of the benefits and harms of pharmacotherapy, patients' preferences, patients' general health and life expectancy, treatment burden, and costs of care
  • Statement 2: Clinicians should aim to achieve an HbA1c level between 7% and 8% in most patients with type 2 diabetes
  • Statement 3: Clinicians should consider de-intensifying pharmacologic therapy in patients with type 2 diabetes who achieve HbA1c levels less than 6.5%
  • Statement 4: Clinicians should treat patients with type 2 diabetes to minimize symptoms related to hyperglycemia and avoid targeting an HbA1c level in patients with a life expectancy less than 10 years due to advanced age (80 years or older), residence in a nursing home, or chronic conditions (such as dementia, cancer, end-stage kidney disease, or severe chronic obstructive pulmonary disease or congestive heart failure) because the harms outweigh the benefits in this population


U of R researchers developing automated pain detection system for dementia patients

https://goo.gl/X5dQ1E

'This sounds like science fiction to a lot of people, but it's a lot more feasible than people think.'

It sounds like science fiction, but University of Regina researchers are developing cameras to flag when non-verbal adults with dementia are in pain and a notification system to alert staff of their anguish.

For many years, Thomas Hadjistavropoulos, co-leader of the research project, has studied the problem of people with severe dementia, such as Alzheimer’s disease, who can’t communicate they are in pain.

“You can have somebody with a tooth abscess, which is tremendously painful, and the pain can go undetected for days, sometimes longer,” he said. 

People with severe dementia who have untreated pain can turn aggressive. The aggression is attributed to a psychiatric problem and psychotropic medications are prescribed, which don’t treat the pain, but increase the risk of death by falls or stroke.

“For frail people with dementia, psychotropic medications should be used with a great deal of caution,” Hadjistavropoulos said.

He and his graduate students have developed methods for detecting, evaluating and measuring pain in adults with dementia through pain behaviours — specific facial responses that are relatively uncommon in situations other than pain. 

A lowered eyebrow or wince are things staff would notice if they had time to watch residents closely, but often resources are limited.

“That got us thinking, what if we were able to detect and monitor these behaviours in an automated way and reduce the need for a nurse or another clinician to go around and look for pain behaviours on a regular basis — what if a system could do that?” Hadjistavropoulos said.

They’ve come up with a system of strategically placed cameras that send information to a computer which analyzes it based on an algorithm.

When the system detects patients who are in pain, nursing staff will be sent an email, and a light at the nursing station would flash indicating an email was sent.

Sick and Struggling: High-Need Adults with Financial Difficulties Have Worse Access to the Quality Care They Need

https://goo.gl/t1pDJp

High-need adults — those with multiple physical or cognitive limitations — are almost twice as likely to struggle financially as adults who are not high-need. Such financial difficulties can lead people to avoid getting the care they need, when they need it. Furthermore, research shows adults experiencing financial hardship are at increased risk for chronic disease and early death.

To explore how financial difficulties affect the health care of high-need adults,1 we analyzed data from the Commonwealth Fund Survey of High-Need Patients conducted from June to September 2016. We defined financial difficulties as worrying about having enough money to pay for housing or monthly bills, or making less than $15,000 a year.

Our analysis finds an interaction between financial hardship, complex medical needs, and access to high-quality care. In light of this, and the large body of research which shows that financial difficulties can have adverse implications on patients’ health, providers and health systems should consider the benefits of systematically screening patients to understand their financial needs, and then linking them to services to help meet those needs.

PHYSICALLY FIT WOMEN NEARLY 90 PERCENT LESS LIKELY TO DEVELOP DEMENTIA

https://goo.gl/Tv1Qub

Women with high physical fitness at middle age were nearly 90 percent less likely to develop dementia decades later, compared to women who were moderately fit, according to a study published the March 14, 2018, online issue of Neurology®, the medical journal of the American Academy of Neurology. The study measured the women’s cardiovascular fitness based on an exercise test. 

 When the highly fit women did develop dementia, they developed the disease an average of 11 years later than women who were moderately fit, or at age 90 instead of age 79. “These findings are exciting because it’s possible that improving people’s cardiovascular fitness in middle age could delay or even prevent them from developing dementia,” said study author Helena Hörder, PhD, of the University of Gothenburg in Gothenburg, Sweden.

“However, this study does not show cause and effect between cardiovascular fitness and dementia, it only shows an association. More research is needed to see if improved fitness could have a positive effect on the risk of dementia and also to look at when during a lifetime a high fitness level is most important.”


America Has A Massive Hepatitis A Problem, And No One Is Talking About It

https://goo.gl/UsgY2f

San Diego’s huge outbreak of hepatitis A ― a preventable but deadly virus that is spread through contact with human feces ― captured national media attention in September. The city began washing streets it believed were contributing to the problem with bleach and initiated a local vaccination campaign among the communities most affected. Soon, it was out of the national conversation.

But similar outbreaks have continued throughout the country, still largely among the homeless and illicit drug-using populations who are most vulnerable to the disease, with few national headlines in sight. Meanwhile, the Morbidity and Mortality Weekly Report out of the Centers for Disease Control and Prevention ― which the agency itself calls the “voice of the CDC” ― has not provided accurate year-end numbers for hepatitis A, making the disease appear less widespread than it truly is.

A HuffPost analysis of CDC and California Department of Health data has found that from 2016 to 2017, hepatitis A cases shot up 48.7 percent nationwide ― an unprecedented spread of the sometimes deadly virus. That contrasts with what the CDC has reported in the MMWR: a mere 5.4 percent increase.  

The CDC declined to publicly comment on the 48.7 percent figure.

But public health experts across the country point to a combination of forces that are driving the nationwide outbreak ― the vulnerable homeless population, whose numbers rose last year for the first time since 2010; rising illegal drug users, who often don’t seek or are unable to access medical care; and a lack of alternative sanitary services for those who don’t have housing.

“We’re continuing to have an affordable housing crunch, which means you have more homeless people. And oftentimes communities close the public bathrooms because of the opioid epidemic and people overdosing,” said Laura Hanen, interim executive director and chief of public affairs of the National Association of County and City Health Officials. “Some of that is likely contributing to what we’re seeing.”

What results are outbreaks like San Diego’s, which numbered over 580 cases from late 2016 through this March, including 20 deaths. Responding to the disaster has cost San Diego County’s health department more than $9.5 million. Michigan has seen its own outbreak spread across the state, culminating in 777 illnesses and 25 deaths since it began in a southeastern pocket of the state in August 2016. Louisville, Kentucky, which is the latest city to face an outbreak, has 128 sick and one dead since declaring that outbreak in November 2017, health officials told HuffPost.

“My guess is that we’re closer to the beginning than the end” of fighting the outbreak in Kentucky, said Dave Langdon, a public information officer for the Louisville Metro Department of Health and Wellness.

Chronic Care Management Reduces Costs, Provides Better Support

https://goo.gl/ds83n4

A new study shows that a government program for managing chronic care cuts costs while also improving care for the chronically ill.

A federal program for chronic care management (CCM) slows the increase in Medicare costs, helps keep people out of the hospital, and connects them with community-based resources, according to a recent report from the Center for Medicare and Medicaid Innovation (CMMI).

The program results could be replicated by private health plans.

The Centers for Medicare and Medicaid Services (CMS) established CMMI in 2015 to help provide support for patients with multiple chronic conditions in-between their provider visits and episodes of care, creating a new Medicare benefit. The program helps beneficiaries with two or more chronic conditions by providing new “in-between visit” payments to participating providers.

That revenue encourages healthcare providers to focus more on goal-directed, person-centered care planning, and to provide "aging-in-place" resources such as proactive care management, the report explains.

Over 684,000 beneficiaries received CCM services during the first two years of the new payment policy, the report says. They were generally concentrated in the South and had poorer health status than the general Medicare fee-for-service (FFS) population.