March 2017

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Warfarin-Associated Nonuremic Calciphylaxis

Question  Is warfarin-associated calciphylaxis a distinct disease when compared with classic calciphylaxis, and, if so, what are its features?

Findings  In this review of reports of 18 patients with warfarin-associated calciphylaxis, 15 had used warfarin for an average of 32 months prior to calciphylaxis onset, and the most common treatments were substitution of heparin or low-molecular weight heparin for warfarin, intravenous sodium thiosulfate, and hyperbaric oxygen. Survival after hospital discharge was high with 15 cases (83%) reporting full recovery and 3 cases ending in death.

Meaning  Warfarin-associated calciphylaxis is distinct from classic calciphylaxis in pathogenesis, course, and outcome.


Importance  Classic calciphylaxis associated with renal failure is a life-threatening disease. Warfarin-associated calciphylaxis without renal injury has been described, but whether it is a subset of classic calciphylaxis or a different entity remains unknown. We describe 1 case of warfarin-associated calciphylaxis, present data from 2 others from our institution, and review all cases of warfarin-associated calciphylaxis available in the literature. Our review indicates that warfarin-associated calciphylaxis is clinically and pathophysiologically distinct from classic calciphylaxis.

Objective  To review warfarin-associated calciphylaxis and determine its relationship to classic calciphylaxis.

Design, Setting, and Participants  We searched MEDLINE and Ovid without language or date restrictions for case reports of calciphylaxis from the inpatient setting using the terms “calciphylaxis and warfarin,” “non-uremic calciphylaxis,” and “nonuremic calciphylaxis.” We defined nonuremic calciphylaxis as a histopathologic diagnosis of calciphylaxis without severe kidney disease (serum creatinine level >3 mg/dL; glomerular filtration rate <15 mL/min; acute kidney injury requiring dialysis; and renal transplantation).

Exposures  Each patient had been exposed to warfarin before the onset of calciphylaxis.

Main Outcomes and Measures  Patient data were abstracted from published reports. Original patient medical records were requested and reviewed when possible.

Results  We identified 18 patients with nonuremic calciphylaxis, 15 from the literature, and 3 from our institution. Patients were predominantly female (15 of 18 [83%]) with ages ranging from 19 to 86 years. Duration of warfarin therapy prior to calciphylaxis onset averaged 32 months. Lesions were usually located below the knees (in 12 of 18 [67%]). No cases reported elevated calcium-phosphate products (0 of 17 [0%]). Calcifications were most often noted in the tunica media (n = 8 [44%]) or in the vessel lumen and tunica intima (n = 7 [39%]). The most common treatments included substitution of heparin or low-molecular weight heparin for warfarin (n = 13 [72%]), intravenous sodium thiosulfate (n = 9 [50%]), and hyperbaric oxygen (n = 3 [17%]). The survival rate on hospital discharge was remarkably high, with 15 cases (83%) reporting full recovery and 3 cases ending in death.

Conclusions and Relevance  Warfarin-associated calciphylaxis is distinct from classic calciphylaxis in pathogenesis, course, and, particularly, outcome. This finding should influence clinical management of the disease and informs targeted treatment of the disease.




Deadly fungal infection that doctors have been fearing now reported in U.S.

March 10

A strain of Candida auris cultured in a petri dish at the Centers for Disease Control and Prevention. (Shawn Lockhart/CDC)

Nearly three dozen people in the United States have been diagnosed with a deadly and highly drug-resistant fungal infection since federal health officials first warned U.S. clinicians last June to be on the lookout for the emerging pathogen that has been spreading around the world.

The fungus, a strain of a kind of yeast known as Candida auris, has been reported in a dozen countries on five continents starting in 2009, when it was found in an ear infection in a patient in Japan. Since then, the fungus has been reported in Colombia, India, Israel, Kenya, Kuwait, Pakistan, South Korea, Venezuela and the United Kingdom.

Unlike garden variety yeast infections, this one causes serious bloodstream infections, spreads easily from person to person in health-care settings, and survives for months on skin and for weeks on bed rails, chairs and other hospital equipment. Some strains are resistant to all three major classes of antifungal drugs. Based on information from a limited number of patients, up to 60 percent of people with these infection have died. Many of them also had other serious underlying illnesses.

Those at greatest risk are individuals who have been in intensive care for a long time or who are on ventilators or have central line catheters inserted into a large vein.

In the United States, the largest number of infections has been reported in New York, with at least 28 cases, according to the Centers for Disease Control and Prevention. Infections have also been reported in Illinois, Maryland, Massachusetts and New Jersey. Last June, the CDC sent an urgent alert to clinicians to start looking for the infections, which are difficult to identify with standard laboratory methods.

“As soon as we put out that alert, we started to get information about cases and now we know more about how it spreads and how it’s acting,” Tom Chiller, the CDC’s top fungal expert, said in an interview Thursday. The CDC now tracks the number of infections, updating the case count every few weeks.
In addition to the 35 infected patients, an additional 18 were carrying the organism but weren’t sickened by it.

The microbe is among a group of newly emerging drug-resistant threats, health officials said.

“These pathogens are increasing, they’re new, they’re scary and they’re very difficult to combat,” said Anne Schuchat, CDC’s acting director, during a briefing in Washington this week about the growing danger from antimicrobial resistance.

Of the first seven cases that were reported to the CDC last fall, four patients had bloodstream infections and died during the weeks to months after the pathogen was identified. Officials said they couldn’t be sure whether the deaths were caused by the infection because all the individuals had other serious medical conditions. Five patients had the fungus initially isolated from blood, one from urine, and one from the ear.

The infection is still relatively rare. “It’s really hitting the sickest of the sick,” Chiller said.

So far, the fungus doesn’t seem to be evolving into new strains within the United States. Because the country doesn’t yet have any “homegrown” strains of the deadly fungus, “it gives us a better opportunity to contain it and stop it from spreading,” Chiller said.

In other countries, infections have been resistant to all three major types of antifungal drugs, but so far the U.S. cases have been treatable with existing drugs.

Because invasive bloodstream infections with Candida are common in hospitalized patients in the United States, health officials are concerned that this deadly strain could “get into that mix,” Chiller said. Unlike Candida infections in the mouth, throat or vagina (which are typically called yeast infections), invasive yeast infections can affect the blood, heart, brain, eyes, bones and other parts of the body and are more dangerous.

Among infectious disease clinicians and laboratory personnel, infections involving fungi don’t typically ring the same kind of alarm bells as antibiotic-resistant bacteria — until now.

“This is a paradigm shift, because Candida is not generally thought of as highly resistant or passed person to person,” Chiller said.

Since the CDC issued its alert in June, the agency has provided funds and additional expertise to help regional laboratories and hospitals identify the organism.


Hospital Floors May Pose a Larger Health Risk Than Previously Thought

Hospital room floors may be an overlooked source of infection, according to a study published in the March issue of the American Journal of Infection Control, Because items in the patient’s room may touch the floor, pathogens on hospital floors can rapidly move to the hands and high-touch surfaces throughout a hospital room.

“Understanding gaps in infection prevention is critically important for institutions seeking to improve the quality of care offered to patients,” said 2017 APIC president Linda Greene, RN, MPS, CIC, FAPIC. “Even though most facilities believe they are taking the proper precautions, this study points out the importance of ensuring cleanliness of the hospital environment and the need for education of both staff and patients on this issue.”

In the study by Abhishek Deshpande, MD, PhD, and colleagues, researchers cultured 318 floor sites from 159 patient rooms (two sites per room) in five Cleveland-area hospitals. The hospital rooms included both C. difficile infection (CDI) isolation rooms and non-CDI rooms. Researchers also cultured hands (gloved and bare) as well as other high-touch surfaces such as clothing, call buttons, medical devices, linens, and medical supplies.

The researchers found that floors in patient rooms were often contaminated with Methicillin-resistant Staphylococcus aureus (MRSA), VRE, and C. difficile, with C. difficile being the most frequently recovered pathogen found in both CDI isolation rooms and non-CDI rooms.

Of 100 occupied rooms surveyed, 41 percent had one or more high-touch objects in contact with the floor. These included personal items, medical devices, and supplies. MRSA, VRE, and C. difficile were recovered from 6 (18 percent), 2 (6 percent), and 1 (3 percent), respectively of bare or gloved hands that handled the items.

“Efforts to improve disinfection in the hospital environment usually focus on surfaces that are frequently touched by the hands of healthcare workers or patients,” said Deshpande, et al. “Although healthcare facility floors are often heavily contaminated, limited attention has been paid to disinfection of floors because they are not frequently touched. The results of our study suggest that floors in hospital rooms could be an underappreciated source for dissemination of pathogens and are an important area for additional research.”

Reference: “Are hospital floors an underappreciated reservoir for transmission of health care-associated pathogens?” Abhishek Deshpande; Jennifer L. Cadnum; Dennis Fertelli; Brett Sitzlar; Priyaleela Thota; Thriveen Sankar C.; Annette Jencso; Heba Alhmidi; Sreelatha Koganti; and Curtis J. Donskey appears in the American Journal of Infection Control, Volume 45, Issue 3 (March 2017).


Autoimmune Diseases Linked to Dementia

Pauline Anderson

March 03, 2017


A new study provides additional evidence linking autoimmune diseases to dementia, including Alzheimer’s disease (AD).

Researchers showed that compared with a control group admitted to the hospital for another reason, people hospitalized with an autoimmune disease were more likely to be later admitted with dementia.

“Fundamentally, this is an epidemiology study using the power of big numbers of patients to look at a hypothesis, namely that Alzheimer’s disease may have an autoimmune component, and our bottom line in epidemiological and population terms is that yes, the study supports that hypothesis,” study author Michael J. Goldacre, emeritus professor of public health, University of Oxford, United Kingdom, told Medscape Medical News.

It’s important for clinicians to recognize that their patients with multiple sclerosis, type 1 diabetes, rheumatoid arthritis, or other autoimmune disorders may have an increased risk for dementia, said Dr Goldacre.

The study was published online March 1 in the Journal of Epidemiology & Community Health.

Common Chronic Diseases

Researchers used the Hospital Episode Statistics database, which includes clinical, demographic, and administrative information on hospital admissions (including day cases) in England. They constructed retrospective cohorts of patients admitted to the hospital with a range of autoimmune diseases and followed them to see which patients were later admitted with a record of dementia.

The 25 diseases on the list for evaluation included those that are common and chronic and for which there’s an accepted autoimmune component. The list did not include type 1 diabetes because, as Dr Goldacre explained, he and his colleagues had already published a paper that linked diabetes with subsequent dementia.

The researchers also constructed a control cohort of patients hospitalized with various other medical and surgical conditions and injuries.

From April 1, 1998, to March 31, 2012, over 1.8 million people were admitted to the hospital with an autoimmune disease. The number in the different autoimmune groups ranged from 1019 for Goodpasture’s syndrome (where antibodies attack the lungs and kidneys), to 316,043 for rheumatoid arthritis (RA). About 7 million people were included in the control cohort.

The autoimmune disease cohort that eventually had the most dementia cases (48,146) was myxoedema (hypothyroidism). This condition “is quite common in elderly people, particularly women,” commented Dr Goldacre.

Overall, patients admitted to the hospital with an autoimmune disease were 20% more likely to have a subsequent admission for dementia than those without an admission for an autoimmune disease (adjusted rate ratio [RR], 1.20; 95% confidence interval [CI], 1.19 – 1.21).

Of the 25 diseases studied, 18 showed significant positive associations with dementia at P < .05 (with 14 significant at P < .001), including multiple sclerosis (RR, 1.97; 95% CI, 1.88 – 2.07), psoriasis (RR, 1.29; 95% CI, 1.25 – 1.34), and systemic lupus erythematosus (RR, 1.46; 95% CI, 1.32 – 1.61).

The authors noted that by chance alone, only one or two would be significant at P = .05.

However, although significant, effect sizes were small.

“As risks go, it’s a relatively small elevation,” said Dr Goldacre. “Risks start to seem important at the individual patient level when they are about two-fold or over, when the risk is something like doubled.”

Researchers found no notable differences in the RRs for dementia after excluding cases of dementia recorded within a year of the autoimmune disease admission. This suggests that the dementia diagnosis was not the result of being admitted soon after an autoimmune disease admission.

Different Dementias

Investigators subdivided patients admitted with a record of dementia into those having AD and those having vascular dementia.

Of the 81,502 people with an autoimmune disease and dementia, 20,032 had a record of AD and 22,536 a record of vascular dementia. The risk for vascular dementia after an admission with an autoimmune disease was higher (RR, 1.28; 95% CI, 1.26 – 1.31) than the risk for AD (RR, 1.06; 95% CI, 1.04 – 1.08).

“We think that’s probably because these autoimmune diseases are themselves conditions that predispose to atherosclerotic vascular disease,” said Dr Goldacre.

Some autoimmune diseases were associated with an elevated risk for future vascular dementia but not AD. This was the case for RA, where the RR for vascular dementia was 1.16 (95% CI, 1.12 – 1.20) but for AD, it was 0.89 (95% CI, 0.86 – 0.93).

“We might have been tempted to just dismiss the seemingly protective effect — the inverse relationship between RA and AD — were it not for the fact that others have reported on that before, so it’s not an entirely sort of eccentric finding,” said Dr. Goldacre.

The finding helps support the hypothesis that nonsteroidal anti-inflammatory drugs (NSAIDs) protect against AD. “People with rheumatoid arthritis generally take NSAIDs to manage their condition, so if rheumatoid arthritis is at least partially a proxy for NSAID use, the real association may be between NSAID use and a reduced risk of AD,” write the authors.

Since dementia subgroups were not well coded on hospital records, the authors cautioned that the separate analyses of AD and vascular dementia should be viewed with caution.

In analyzing the data separately for men and women, the researchers found that the adjusted RRs for dementia were broadly similar when they looked at individual diseases, but for all of them together, the RR was higher in men than women.

Dr Goldacre pointed out that autoimmune diseases are generally more common in women than men. “It’s often the case that the sex with the lower disease frequency has outcomes that are worse than the sex with the higher disease frequency.”

For example, he said, although women don’t develop myocardial infarction as often as men, they tend to have a slightly higher death rate from it, he said. “I am highly speculative, but that pattern might fit here.”

The researchers also analyzed the data according to time interval between the autoimmune disease and dementia admissions. Most associations remained significant for 5 or more years, although they were generally stronger with shorter time intervals.

Emerging Field

Medscape Medical News invited James A. Hendrix, PhD, director, Global Science Initiatives, Alzheimer’s Association, to comment on the study.

“We certainly are seeing more and more research on the link between AD and the immune system and neuroinflammation,” said Dr Hendrix. “This kind of paper helps show that there is something going on and we need to do more research to really understand it.”

An “emerging” field of research for the Alzheimer’s Association is developing anti-inflammatory agents targeted to the brain, he said.

“A possible strategy would be to develop a drug that has excellent brain penetration and has brain-specific targets, so it targets the microglia or other cells in the brain that are associated with the immune system and neuroinflammation.”

Another strategy might be to “repurpose” anti-inflammatory drugs and see whether they can affect neuroinflammation with limited side effects.

“We will leave no stone unturned with this,” said Dr Hendrix.

Indeed, last summer, the Alzheimer’s Association announced a $7 million investment in clinical trials targeting brain inflammation (see Medscape Medical News’ coverage of the Part the Cloud Challenge on Neuroinflammation).

Dr Hendrix said the association between RA and vascular dementia uncovered by the study was news to him. “That says that we really don’t have a good understanding of the role of the immune system and inflammation when it comes to vascular dementia. For me, that was the one of the things that stood out in the paper generally.”

He outlined a number of “caveats” to the research. For one thing, the authors looked only at hospital records. “These were people who went into hospital complaining of an autoimmune disease or disorder, so it was probably pretty severe to force them to go to a hospital for care,” said Dr Hendrix.

Also, only about half of those who developed dementia were classified as having AD or vascular dementia. “It’s really challenging under the best of circumstances to do a differential diagnosis of dementia,” said Dr Hendrix.

The Unit of Health-Care Epidemiology was funded by the English National Institute for Health Research to build the linked data set. The authors have disclosed no relevant financial relationships.

J Epidemiol Community Health. Published online March 1, 2017. Abstract


Eczema Relief: Probiotic Lotion Shows Early Promise

Scanning electron microscopic image of Staphylococcus aureus bacteria (orange).
Credit: CDC/Jeff Hageman, MHS

Over the years, people suffering from eczema have slathered their skin with lotions containing everything from avocado oil to zinc oxide. So, what about a lotion that features bacteria as the active ingredient? That might seem like the last thing a person with a skin problem would want to do, but it’s actually a very real possibility, based on new findings that build upon the growing realization that many microbes living in and on the human body—our microbiome—are essential for good health. The idea behind such a bacterial lotion is that good bugs can displace bad bugs.

Eczema is a noncontagious inflammatory skin condition characterized by a dry, itchy rash. It most commonly affects the cheeks, arms, and legs. Previous studies have suggested that the balance of microbes present on people with eczema is different than on those with healthy skin [1]. One major difference is a proliferation of a bad type of bacteria, called Staphylococcus aureus.

Recently, an NIH-funded research team found that healthy human skin harbors beneficial strains of Staphylococcus bacteria with the power to keep Staph aureus in check. To see if there might be a way to restore this natural balance artificially, the researchers created a lotion containing the protective bacteria and tested it on the arms of volunteers who had eczema [2]. Just 24 hours after one dose of the lotion was applied, the researchers found the volunteers’ skin had greatly reduced levels of Staph aureus. While further study is needed to learn whether the treatment can improve skin health, the findings suggest that similar lotions might offer a new approach for treating eczema and other skin conditions. Think of it as a probiotic for the skin!

In their study published in Science Translational Medicine, Richard Gallo, of the University of California, San Diego and his colleagues, set out to connect the dots between eczema, Staph aureus, and changes to the skin microbiome. Step one involved swabbing the forearms of 30 people with healthy skin and almost 50 people with outbreaks of the most common form of eczema, atopic dermatitis. From each swab, the researchers isolated hundreds of bacterial colonies and tested their ability to inhibit the growth of Staph aureus in lab dishes.

Gallo’s team found that bacterial strains collected from the skin of healthy people showed antimicrobial activity that inhibited the growth of Staph aureus. The researchers traced that inhibition to previously unknown antimicrobial peptides produced by certain strains of Staphylococcus hominis and Staphylococcus epidermidis, which are benign bacteria that are quite abundant on the skin. The researchers then discovered that the antimicrobial strains not only kill Staph aureus quite effectively, they do so without causing harm to other beneficial bacteria commonly found on healthy skin. In contrast to the healthy people, people with eczema had much lower levels of the two strains of protective bacteria.

Based on encouraging results in a mouse model, Gallo and his colleague initiated a Phase I clinical trial involving five volunteers with atopic dermatitis that tested positive for Staph aureus. To beef up the amount of protective Staph bacteria on the volunteers’ skin, the researchers took a small sample of each patients’ skin micriobiome, grew up more of the good Staph strains in the lab, and used them to create a personalized probiotic lotion. The volunteers then each received a single dose of probiotic lotion on one arm and regular lotion on the other. Twenty-four hours later, it was clear—the probiotic lotion reduced levels of the bad bug, Staph aureus, on the participants’ skin.

The researchers report that a larger human clinical trial is now underway, designed to test whether continued use of probiotic lotion can provide lasting protection against Staph aureus and improve eczema symptoms. Hopefully, the promise of these new findings can provide some encouragement to the more than 31 million Americans, many of them children, who now suffer from eczema


Association Between Dietary Factors and Mortality From Heart Disease, Stroke, and Type 2 Diabetes in the United States

March 7, 2017
JAMA. 2017;317(9):912-924. doi:10.1001/jama.2017.0947
Key Points

Question  What is the estimated mortality due to heart disease, stroke, or type 2 diabetes (cardiometabolic deaths) associated with suboptimal intakes of 10 dietary factors in the United States?

Findings  In 2012, suboptimal intake of dietary factors was associated with an estimated 318 656 cardiometabolic deaths, representing 45.4% of cardiometabolic deaths. The highest proportions of cardiometabolic deaths were estimated to be related to excess sodium intake, insufficient intake of nuts/seeds, high intake of processed meats, and low intake of seafood omega-3 fats.

Meaning  Suboptimal intake of specific foods and nutrients was associated with a substantial proportion of deaths due to heart disease, stroke, or type 2 diabetes.


Importance  In the United States, national associations of individual dietary factors with specific cardiometabolic diseases are not well established.

Objective  To estimate associations of intake of 10 specific dietary factors with mortality due to heart disease, stroke, and type 2 diabetes (cardiometabolic mortality) among US adults.

Design, Setting, and Participants  A comparative risk assessment model incorporated data and corresponding uncertainty on population demographics and dietary habits from National Health and Nutrition Examination Surveys (1999-2002: n = 8104; 2009-2012: n = 8516); estimated associations of diet and disease from meta-analyses of prospective studies and clinical trials with validity analyses to assess potential bias; and estimated disease-specific national mortality from the National Center for Health Statistics.

Exposures  Consumption of 10 foods/nutrients associated with cardiometabolic diseases: fruits, vegetables, nuts/seeds, whole grains, unprocessed red meats, processed meats, sugar-sweetened beverages (SSBs), polyunsaturated fats, seafood omega-3 fats, and sodium.

Main Outcomes and Measures  Estimated absolute and percentage mortality due to heart disease, stroke, and type 2 diabetes in 2012. Disease-specific and demographic-specific (age, sex, race, and education) mortality and trends between 2002 and 2012 were also evaluated.

Results  In 2012, 702 308 cardiometabolic deaths occurred in US adults, including 506 100 from heart disease (371 266 coronary heart disease, 35 019 hypertensive heart disease, and 99 815 other cardiovascular disease), 128 294 from stroke (16 125 ischemic, 32 591 hemorrhagic, and 79 578 other), and 67 914 from type 2 diabetes. Of these, an estimated 318 656 (95% uncertainty interval [UI], 306 064-329 755; 45.4%) cardiometabolic deaths per year were associated with suboptimal intakes—48.6% (95% UI, 46.2%-50.9%) of cardiometabolic deaths in men and 41.8% (95% UI, 39.3%-44.2%) in women; 64.2% (95% UI, 60.6%-67.9%) at younger ages (25-34 years) and 35.7% (95% UI, 33.1%-38.1%) at older ages (≥75 years); 53.1% (95% UI, 51.6%-54.8%) among blacks, 50.0% (95% UI, 48.2%-51.8%) among Hispanics, and 42.8% (95% UI, 40.9%-44.5%) among whites; and 46.8% (95% UI, 44.9%-48.7%) among lower-, 45.7% (95% UI, 44.2%-47.4%) among medium-, and 39.1% (95% UI, 37.2%-41.2%) among higher-educated individuals. The largest numbers of estimated diet-related cardiometabolic deaths were related to high sodium (66 508 deaths in 2012; 9.5% of all cardiometabolic deaths), low nuts/seeds (59 374; 8.5%), high processed meats (57 766; 8.2%), low seafood omega-3 fats (54 626; 7.8%), low vegetables (53 410; 7.6%), low fruits (52 547; 7.5%), and high SSBs (51 694; 7.4%). Between 2002 and 2012, population-adjusted US cardiometabolic deaths per year decreased by 26.5%. The greatest decline was associated with insufficient polyunsaturated fats (−20.8% relative change [95% UI, −18.5% to −22.8%]), nuts/seeds (−18.0% [95% UI, −14.6% to −21.0%]), and excess SSBs (−14.5% [95% UI, −12.0% to −16.9%]). The greatest increase was associated with unprocessed red meats (+14.4% [95% UI, 9.1%-19.5%]).

Conclusions and Relevance  Dietary factors were estimated to be associated with a substantial proportion of deaths from heart disease, stroke, and type 2 diabetes. These results should help identify priorities, guide public health planning, and inform strategies to alter dietary habits and improve health.

Scientists Have Developed a Patch That Could Stop Severe Peanut Allergies

It just passed a phase II clinical trial.

6 MAR 2017

A treatment for one of the most common food allergies out there just got even more data that it’s working. Roughly 1.5 million children in the US are allergic to peanuts, an allergy that can often be so severe that even the smallest amount of contact can set off an extreme reaction.

To counter that, DBV Technologies is working on a patch that works to lessen that severity.

In new phase two data presented at the American Academy of Allergy, Asthma and Immunology conference on Sunday, the company showed that 83 percent of children ages 6 to 11 who took part in the trial could eat 1,000 milligrams of peanuts without having an allergic reaction after wearing a patch for three years.

That’s 10-times the amount of peanut that the participants could handle when they first joined the trial. Though the phase two data looked at people between the ages of 6 and 55, the best responses came from children on the trial.

Allergies are your immune system’s response to a substance that may not be harmful to others. They’re the sixth leading cause of chronic disease in the US.

According to the CDC, an estimated 4-6 percent of children in the US have food allergies, with peanuts being one of the worst offenders.

In December 2015, DBV kicked off a phase 3 trial that looks at how the patch works in kids aged 4-11, which along with this data will set the company up for the FDA approval process.

How the patch works Video

The immune-system-targeting drug is delivered through the skin through a process called epicutaneous immunotherapy.

Inside each patch is a sprayed-on sample of peanut protein. Once you put it on, the protein makes its way into your immune system through your skin.

Since it’s delivered this way, the allergen never makes it to the blood stream, which would cause the allergic reaction you’re trying to avoid.

Based on the data from DBV’s phase two trial, those who used the patch for three years at the 250 microgram dose (the highest dose) had the best responses to the treatment.

The patch treatment is a departure from the way allergies are typically treated.

Typically, the only way to lessen an allergic reaction is through ‘desensitisation’, a process in which you gradually introduce small amounts of the allergen into your body. In the case of peanut allergies, that means eating the peanut outright.

The problem with this method is that it can be risky, since it can cause an allergic reaction that spreads throughout the body through the blood stream.

Other, more common methods, for treating allergies have been focused around treating the symptoms of the allergic reaction; i.e. using antihistamines like Benadryl or shots of epinephrine in extreme cases.

Beyond peanut allergies, DBV is developing patches to treat other food allergies such as milk and eggs – among the most common food allergies – and other non-food allergies that are connected to asthma.

The company’s also exploring treatments for Crohn’s disease, celiac disease, and type 1 diabetes that use the same immunotherapy technology.

This article was originally published by Business Insider.

Scientists Reverse Sickle Cell Disease for the First Time Using Gene Therapy


4 MAR 2017

A new gene therapy technique has been used to successfully reverse sickle cell disease for the first time, scientists report.

While this is just one case study involving a single French teenager, the early signs are encouraging, and the therapy could eventually lead to an effective treatment for the millions of people with this crippling disease worldwide.

Sickle-cell disease occurs when one of the proteins making up a type of haemoglobin we use to carry oxygen through our body takes a slightly different form.

This small change is enough to make the red blood cells they occupy lose elasticity, deforming them into a curved ‘sickle’ shape and risking clumps of cells piling up as they struggle to slip through blood vessels.

But by using a virus to insert genes for the correct form of this protein into the bone marrow of a French teenager, researchers have been able to restore the elasticity to the patient’s blood cells.

After 15 months of therapy, the patient is off medication, and while it’s far too early to say he’s been functionally cured, it’s a case of ‘so far so good’ for this pioneering kind of treatment.

“So far the patient has no sign of the disease, no pain, no hospitalisation,” one of the team, Philippe Leboulch from the University of Paris in France, told the BBC. “He no longer requires a transfusion so we are quite pleased with that.”

“But of course we need to perform the same therapy in many patients to feel confident that it is robust enough to propose it as a mainstream therapy.”

Sickle cell disease causes a condition called ischemia – an interruption of the flow of oxygen to parts of the body that causes pain, organ damage, and in some cases, eventually death.

The only existing long-term treatment is a bone marrow transplant, a high-risk and difficult operation that not everyone is eligible for.

But because sickle cell disease involves a mutation of just a small part of the body’s genetic code – producing an abnormal beta-globin protein known as haemoglobin S – it’s a prime candidate for genetic therapy treatments that could reverse the mutation.

Although there are still concerns over how modern gene therapy techniquescould be abused, scientists now have the know-how to ‘correct’ certain genetic mutations.

In this case scientists removed bone marrow stem cells from the teen’s body and added a specially made virus, designed to recode the cells to produce normal haemoglobin again. The cells were then transfused back into the patient.

Doctors are reporting that half the patient’s red blood cells are now regular and healthy, and he hasn’t needed any blood transfusions since three months after his first treatment.

We’ve come a long way – this type of treatment was first tested on mice back in 2001 – but there’s still a great way to go before we can say we have an effective, long-term treatment for sickle cell disease.

A number of other gene therapy techniques are currently being tested, and not all of them are as promising as this one, but scientists are continuing to tweak their approach to find a therapy that can work for the majority of patients, while still being affordable.

“I’ve worked in gene therapy for a long time and we make small steps and know there’s years more work,” Deborah Gill, from the gene medicine research group at the University of Oxford, who wasn’t involved in this study, told the BBC.

“But here you have someone who has received gene therapy and has complete clinical remission – that’s a huge step forward.”

The research has been published in the New England Journal of Medicine.


Even More Evidence Has Linked Parkinson’s Disease to Our Gut Bacteria

Parkinson’s isn’t just in our brains

4 MAR 2017
Researchers have found yet another reason to think the symptoms of Parkinson’s disease could be a consequence of the type of bacteria living in our gut.

Such discoveries could help us use changes in our gut bacteria to not only diagnose the debilitating disorder earlier, but potentially create better targeted treatments.

Once referred to as ‘the shaking palsy‘, Parkinson’s disease is mostly characterised by tremors and a loss of fine motor control, later progressing into dementia, difficulty walking, and sometimes chronic depression.

In most studies on the condition the brain has been the focus, with the blame for the disease primarily falling on the death of cells in a part of the brain called the substantia nigra – a lump of tissue responsible for movement and reward.

In recent years, however, scientists studying the root cause of Parkinson’s disease have shifted their attention from the nervous system onto the denizens of our gut, identifying significant differences in the types of bacteria living in the guts of those with the condition and those who don’t.

Now a team of scientists at the University of Alabama at Birmingham in the US have contributed yet another piece of evidence tying Parkinson’s disease with our personal community of microorganisms – or microbiota.

“We know that a well-balanced gut microbiota is critical for maintaining general health, and alterations in the composition of gut microbiota have been linked to a range of disorders,” said researcher Haydeh Payami.

The researchers analysed samples of gut microbes from 197 patients with Parkinson’s disease from Seattle, New York, and Atlanta – representing three distinct regions around the US – and compared their species and functions with samples taken from 130 individuals without the condition.

Not only did the results show marked differences in the numbers and types of bacteria between the two groups, they also noticed a difference in the metabolism of various medications.

In other words, either the various drugs taken by those with Parkinson’s disease were also having a unique impact on the bacteria, or their microbiota was affecting how their bodies responded to pharmaceutical treatments.

Microorganisms in our digestive system have been found to play an important role in breaking down so-called xenobiotics – chemicals which aren’t usually expected to be present inside an organism.

This includes not only the medications used to treat conditions such as Parkinson’s disease, but chemicals in their environment such as pesticides and herbicides.

Given farmers seem to be more prone to Parkinson’s disease than the general population, thanks possibly to the chemicals they use, it’s possible that the bacteria in their guts could be their body’s first casualties.

“It could be that, in some people, a drug alters the microbiome so that it causes additional health problems in the form of side effects,” Payami said.

“Another consideration is that the natural variability in the microbiome could be a reason some people benefit from a given drug and others are unresponsive. The growing field of pharmacogenomics – tailoring drugs based on an individual’s genetic makeup – may need to take the microbiome into consideration.”

One of the early symptoms of Parkinson’s disease is constipation, so correlations such as these shouldn’t come as much of a surprise.

As with many things in science, however, it’s hard to tell if a difference in microbiota is a cause of Parkinson’s disease or an effect.

Last year researchers at the Californian Institute of Technology found mice who had been engineered to be susceptible to Parkinson’s disease developed less severe symptoms if they were raised in sterile conditions.

Injecting microflora from the guts of human Parkinson’s patients led to a rapid deterioration, suggesting the type of microbes could be at least partially responsible for the severity of the symptoms.

However it’s clear the relationship is a two-way street, making for a complex interaction which demands further study.

We’re only beginning to learn how important our body’s tiny citizens are, but as we find more links like these, we open up new horizons to treating or even preventing diseases such as Parkinson’s.

This research was published in Movement Disorders.


Carri’s Corner – The Quality Payment Program/MIPS/APMs – How do you begin?

Taking care of and making patients healthier is the main concern of clinicians. As a special gift, Medicare has devoted itself to help you focus on quality care! The MACRA final rule has introduced, as you all know by now, the Quality Payment Program (QPP) where clinicians either choose the MIPS (Merit-Based Incentive Payment System) or the APMs (Advanced Alternative Payment Models) track. It was published this past October and the new programs begin in 2017, with payment adjustments beginning in 2019.  Most providers will be part of the MIPS program which combines elements of three programs whose performance period ended in 2016: PQRS, VM, and the Medicare EHR incentive program. I am sure many of you have already begun the work, however for some who really do not understand what the new programs are about, I thought I would do my best to explain what I know.


MIPS is comprised of four performance categories which include Quality (formerly PQRS), Cost (formerly Value-Based Modifier),Improvement Activities (this is new) and Advancing Care Information (formerly Meaningful Use). Performance will be measured for clinicians under these categories and a final score will be issued. For the first year, clinicians will be able to pick their pace and participate as minimally or as fully as they are able to. Data will then be received by CMS, who will then issue feedback to clinicians to let them know how they performed under the MIPS program. Higher scores will be associated with higher reimbursement in 2019.


Let’s look at how you can begin participating in MIPS. First, you must determine if you are eligible. Next you need to decide if you will be submitting as an individual or a group and lastly you must decide your method of submission and verify its capabilities.


As you prepare to partake, I would like to offer a few suggestions. Begin with considering your practice’s readiness and evaluate your ability to begin reporting data for the 2017 transition year. Then, review the Pick Your Pace options as to whether you would like to participate as a test, partial or full-year. Start selecting your measures and/or improvement activities. CMS has given clinicians increased flexibility to choose the improvement activities and measures, within the performance categories, that are most meaningful to their practice. You may choose one or more performance categories, the more you choose the more your reimbursement will be. Go to and click on explore measures. There you will find a list of specialties, unfortunately Podiatry is not yet listed, but you can find quality measures that apply to your specialty. Verify the information you need to report and review the specifications for any measures you will be reporting. As you care for and treat your patients during 2017, you will be tracking your data. Finally, you will take that captured data and submit it to CMS by March 31, 2018.


Hopefully every physician in our group, who is eligible, is prepared. The better prepared and the more you participate in MIPS, the more you will get paid.


For any technical support, or any other questions on these programs go to


Next month in Carri’s Corner- Part 2 explanation of MIPS including more specific information on elements of reporting, length of participation, performance categories and scoring.


Please contact me for guidance with EHR programs that can help with MIPS and reporting.


I would also like to remind everyone that we are available for any billing help that you need. We can take on your whole account or customize our service to what you need. How is you AR doing? Please do not hesitate to contact us for help. We are Sammy experts and also work on other systems.