Published on the Aug. 25, 2016, Diagnostic Imaging website
By Whitney L. Jackson
Throughout the radiology community, there’s one thing every provider has in common. At one point in time, you all completed a residency as part of your training.
Some radiologists never left academia. Instead of opting for private practice or choosing a career in teleradiology, they’ve chosen to remain in the “Ivory Tower.” They’re providing care to your patients like every other provider, but being a radiologist in an academic setting carries its own habits, benefits, and challenges.
And, according to Vijay Rao, MD, chair of the Board of Directors for the Radiological Society of North American and radiology chair at Jefferson Medical School at Thomas Jefferson University, as well as Tejas Mehta, MD, MPH, chief of breast imaging at Harvard Medical School, it’s a job selection that they are frequently thankful for.
“I love what I do, and if I had to do it all over again, I wouldn’t change a thing,” Mehta said. “You need to be passionate about what you do, and academic radiology provides a great work-life balance at the same time.”
Still, there is much to consider if you’re contemplating an academic radiology career – or much to learn if you’ve never experienced radiology practice from this perspective.
Benefits of Academic Radiology
Alongside being able to, potentially, work side-by-side with some of radiology’s thought leaders, being an academic radiology has some upshots.
1. Subspecialty Reads: The same way your residency gives you the opportunity to concentrate on a subspecialty, opting for an academic career allows you to focus your efforts in one specific area, said Rao, who has spent her career as in head and neck imaging.
“Only academic radiology allows you the luxury of practicing only in your field rather than having to do reads of all types,” she said. “This is very meaningful in contributing to providing the highest levels of care.”
2. Staying Young: Yes, you’ll age in your career, but choosing to remain in an educational institution ensures you’ll be surrounded by the next generation of radiologists at all times. Not only are they likely to be forward-thinking as individuals, but it’s also a requirement that they keep up with the most up-to-date data and technology in providing radiological care. If you’re constantly training aspiring radiologists, your skill set won’t have time to get rusty or dated.
To read the remainder of the article at its original location: http://www.diagnosticimaging.com/practice-management/imaging-ivory-tower-academic-radiology
Published on the Aug. 18, 2016, Rheumatology Network website
By Whitney L. J. Howell
For nearly seven decades, glucocorticoid treatment has been a common therapy for rheumatoid arthritis patients. It’s popular for other rheumatic conditions, as well, because it’s cost effective and offers strong anti-inflammatory and immunosuppressive effects. But, awareness of the negative effects is growing.
Glucocorticoids can have detrimental impacts: osteoporosis, hyperglycemia, diabetes, cardiovascular disease and infections. Weight gain, including a red, round face, abdominal obesity with thin limbs, fat pad growth around the neck and back are also common. This weight increase, called the Cushingoid appearance, has been identified for decades and shows how glucocorticoids can impact fat metabolism. But, to date, there’s been little knowledge about how glucocorticoids can change fat mass and redistribution.
Consequently, understanding has also been minimal about the overall combination effect of rheumatoid arthritis and glucocorticoid treatments on body composition. While healthy body compositions have lower proportional body fat and higher proportional fat free mass, obesity increases the risk of high blood pressure, high cholesterol, diabetes, and cardiovascular disease.
To investigate these effects, Nicole P.C. Konijn from the Department of Rheumatology in the Amsterdam Rheumatology and Immunology Center and VU University Medical Center and colleagues conducted a study, published in Rheumatology, on the short-term effects of two high dose, step down prednisolone regimens on body composition in early rheumatoid arthritis patients. In turn, two international glucocorticoid experts from the Department of Rheumatology and Clinical Immunology at Germany’s Carité University Medicine — Frank Buttgereit and Gerd R. Burmester — analyzed the research and published a commentary in Nature Reviews.
Rheumatoid arthritis and the associated chronic inflammation affects between 0.5 percent and 1.0 percent of adults. The joint pain and stiffness associated with the condition is often attributed to a night-time rise of proteins, called cytokines, and hormones in the blood. In particular, these patients see a rise in pro-inflammatory cytokines, such as interleukin-6 and tumor necrosis factor. The same phenomenon is not seen in patients without rheumatoid arthritis.
It’s less widely known, though, that these changes also contribute to the abnormal body composition found in rheumatoid arthritis patients. Understanding this interaction is important, Buttgereit and Burmester wrote, because glucocorticoid treatment is known to facilitate fat accumulation and redistribution between the body’s trunk and limbs.
“Disease exacerbations, decreased physical activity and disuse of muscles can further reduce lean mass, leading to decreased functional capacity and serious consequences for morbidity and mortality,” Buttgereit and Burmester wrote.
Rheumatoid arthritis patients often experience rheumatoid cachexia — the replacement of lean body mass with fat mass. This condition can raise the risk for comorbidities, including diabetes and cardiovascular disease.
According to Buttgereit and Burmester, the data from Konijn’s study is particularly important because it fills in the knowledge gap, affirming there are no major changes in relative body composition that occur with some forms of glucocorticoid treatments. The researchers obtained their results by recording total body mass and using dual energy X-ray absorptiometry, a straight-forward, fast, non-invasive technique for gathering body composition measurements. They measured total fat mass, total lean mass, and trunk:peripheral fat ratio at baseline and after 26 weeks of glucocorticoid treatment.
Overall, Buttgereit and Burmester said, Konijn’s study has two major results. First, in early on-set rheumatoid arthritis patients who had never received glucocorticoid or disease modifying anti-rheumatic drug therapies, total body mass increased by 1.6 kg after 26 weeks of treatment.
The body mass index of glucocorticoid treated patients rose from 25.6 kg to 26.2 kg. That increase makes the presence of overweight and obesity at 26 weeks higher than at baseline. In fact, the 20 patients who were treated with higher cumulative glucocorticoid dose presented a 2.1 kg weight gain – more than the 1.1 kg seen in the 18 patients who received lower cumulative glucocorticoid doses. The 20 patients received a total of 2,275 mg via a combination-therapy regimen called COBRA, and their average daily dose was 12.5 mg. The 18 patients received, 1,750 mg via the same COBRA regimen, and their daily average dose was 9.6 mg.
Based on the second major result, glucocorticoid-treated patients maintained their trunk: peripheral fat ratio and proportional distribution of total body mass and fat mass. In essence, researchers observed no fat redistribution from the body’s limbs to the trunk within the study’s timeframe. The study also didn’t point to a dose-dependent effect of COBRA versus COBRA-light body composition treatment.
These observations were surprising, however, Buttgereit and Burmester said, because it’s known that glucocorticoid treatments alter energy metabolism, induce muscle wasting and fat accumulation, and redistribute fat from body’s limbs to its trunk.
But, Buttgereit and Burmester said, Konijn’s study isn’t without its limitations. Not only was the study short at 26 weeks, but it also included a small number of patients with no control group. In addition, the difference in cumulative glucocorticoid doses between the two groups — only 525 mg after 26 weeks — could be too small to cause a dose-dependent effect.
Researchers also didn’t record any data from the time period prior to rheumatoid arthritis onset, so they can’t determine if the observed total body mass and body mass index changes truly represent a real increase or whether they can be credited to the recovery of body mass previously lost to disease and, then, regained through successful glucocorticoid treatment.
Ultimately, Buttgereit and Burmester wrote, further research should investigate the long-term effects of glucocorticoid treatment in rheumatoid arthritis and other rheumatic diseases. It should also look at how disease processes influence body composition, as well as address whether cytokine-targeting biologic drugs influence body composition.
To read the article at its original location: http://www.rheumatologynetwork.com/rheumatoid-arthritis/how-glucocorticoids-can-change-fat-mass-and-redistribution
Published Aug. 19, 2016, Rheumatology Network website
By Whitney L. Jackson
Genetic variations identified in patients with rheumatological diseases could facilitate designing clinical interventions and developing therapeutic treatments, according to a recent existing literature review.
Known as Mendelian randomization, this technique uses genetic variants, called alleles, to test whether specific risk factors are associated with or cause certain disease outcomes. This strategy could help researchers better understand existing, unmeasured confounding factors that can correlate to both dependent and independent variables, particularly environmental exposures, impacting observational studies.
The basic Mendelian randomization principle is if an environmental exposure, such a urate levels, is linked to an outcome, such as cardiovascular disease, a genetic variation will be present. Identifying these genetic variants could be helpful with rheumatological diseases.
To better understand Mendelian randomization and how it touches rheumatological conditions, researchers, led by Philp C. Robinson from the University of Queensland School of Medicine in Australia, published a systematic literature review in Nature, analyzing existing results and how they can be applied to rheumatology.
“Mendelian randomization can shed new light on cause-effect relationships in rheumatology, helping to make the case for investment in confirmatory intervention trials and to generate new hypotheses regarding pathological mechanisms and aetiology,” investigators wrote. “The technique also enables experiments to be performed that would otherwise be unethical, logistically difficult or prohibitively expensive.”
Not only can Mendelian randomization studies potentially direct clinical practice, but it can also help prioritize causal pathway interventions and help avoid unnecessary clinical trials. It can be incorporated into randomized clinical trials that test therapies for common disease risk factors, potentially explaining why targeted-intervention benefits often are lower than expected, researchers said.
Understanding the Mendelian Method
Overall, successful observational studies rely on accurate confounding factor measurements. Without that, research is hampered. However, Mendelian randomization can potentially side-step the limitation by examining single-nucleotide polymorphisms. Single-nucleotide polymorphism generally explains less than 1 percent of any observed variance, so Mendelian randomization studies typically require 10,000+ individual data sets.
Any selected genetic variants shouldn’t be associated with confounders, and they shouldn’t have pleiotropic effects. For Mendelian randomization results to be valid, investigators must satisfy three criteria:
1. Genetic variants used should be associated with – and explain between 0.5 percent to 1.0 percent of – exposure variance to give the study adequate power.
2. Genetic variants shouldn’t be associated with any factors that confound the exposure-outcome relationship.
3. Genetic variants should only influence outcome through exposure and shouldn’t have pleiotropic effects.
Mendelian Randomization & Rheumatology
To date, Mendelian randomization has been applied mainly to the cause-effect relationship between urate levels and cardiometabolic traits, including coronary heart disease, high blood pressure, diabetes, obesity, body mass index, and kidney function. These studies, which also test for reverse causality, have found genetic variants associated with both hyperuricemia and gout have causal relationships with urate levels. Other studies suggest a causal role for vitamin D levels in determining responses to rheumatoid arthritis therapies and disease outcomes, as well as a causal role for high body mass index and osteoarthritis risk.
An existing literature review also revealed causal relationship results based on Mendelian randomization.
N-glycosylation of IgG in Rheumatoid Arthritis: Researchers tested 16 variants associated with IgG-N glycosylation with 14,361 rheumatoid arthritis patients and 43,923 healthy individuals. They didn’t find a causal association of any genetic variants with rheumatoid arthritis, but a lack of data meant the genetic variants weren’t directly associated with the trait. Consequently, via Mendelian randomization, IgG-N glycosylation doesn’t cause rheumatoid arthritis, but it is a disease biomarker.
IL-1 signalling in Rheumatoid Arthritis: Investigators used Mendelian randomization to unearth cardiovascular risks of long-term inhibition of IL-1 signalling. The study used two genetic variants affecting the gene that encodes IL-1 receptor antagonist (IL-1RA) and included 453,411 participants. Results indicated alleles associated with elevated IL-1RA expression were also linked to protection from rheumatoid arthritis and a cardiovascular disease increase.
Phosphate and Bone Mineral Density: According to Mendelian randomization, high phosphate intake affects calcium metabolism. The study, involving fewer than 200 patients, tested the genetic variant FGF23 associated with phosphate levels to identify any causal relationship with bone mineral density in children. The result was null.
Serum urate levels: Although genetic variation in five genes involved with uric acid excretion account for 3 percent to 4 percent of variance in serum urate levels, Mendelian randomization studies don’t point to a causal role for serum urate levels in hyperuricemia phenotypes, including poor kidney function, ischemic heart disease, diabetes, high blood pressure, high cholesterol, high bone mineral density, and high body mass index.
However, researchers said, reverse causality studies identify a causal effect of body fat measurements on urate levels or triglyceride levels. Among 26 serum-urate modifying genetic variants, only four revealed weak associations with blood pressure.
Additionally, a study into five urate-associated variants identified a positive serum urate level-kidney function relationship.
Rheumatoid Arthritis and Cardiovascular Disease: Rheumatoid arthritis is associated with a higher cardiovascular disease risk, and LDL cholesterol-associated genetic variants could help determine which drives the other. Mendelian randomization could also inform the paradoxical relationship between low body mass index and high mortality with rheumatoid arthritis.
Gout and Other Metabolic Diseases: Any causal relationships between gout and comorbidities are unknown. According to researchers, Mendelian randomization studies could be designed to focus on the disease’s inflammatory aspects to reveal existing links.
IL-6 Pathways and Rheumatoid Arthritis: Rheumatoid arthritis is characterized by high interleukin-6 levels with interleukin-6 inhibitors treating established cases. Mendelian randomization cardiovascular studies suggest interleukin-6 receptor inhibition is associated with cardiovascular-disease prevalence. Mendelian randomization can also address whether interleukin-6 or interleukin-6 receptor pathways contribute to cardiovascular disease development in rheumatoid arthritis patients.
Urate Levels and Neurological Disease: Research shows urate levels protect against neurodegenerative condition development, including Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. Using Mendelian randomization to determine whether this relationship is causal could play into how aggressively providers approach reducing urate in gout.
Alcohol Intake and Rheumatoid Arthritis: Large, existing epidemiological studies suggest moderate alcohol intake reduces rheumatoid arthritis risk. Since alcohol dependence carries a substantial genetic component – approximately 30 percent heritability based on analyzed single-nucleotide polymorphism – Mendelian randomization could further investigate if alcohol intake influences rheumatoid arthritis susceptibility.
Urate Levels and Cancer: The potential urate level and cancer risk link has been well reported and is assumed to be the result of urate’s oxidative intracellular action. However, some studies find those resuls inconclusive. It’s possible the serum urate level effect on cancer risk could be location and malignancy-type dependent.
Overall, researchers said, the urate, gout, and cancer association is complex. Existing studies found higher cancer rates in patients with gout versus those without the condition. Others found no association.
Mendelian randomization isn’t a silver bullet for solving all observational-study problems, though. It’s difficult to verify the technique’s underlying assumptions aren’t being violated. And, using genetic risk scores based on multiple variants increases analysis power, but using individual variants provides for easier interpretations of biological function.
Additionally, genetic variants are mostly pulled from genome-wide association studies conducted on middle-aged and older adults. Consequently, any detected effects could arise from years of cumulative environmental exposures. As a result, investigators recommended returning to Mendelian randomization’s origins where any exposure effect on outcomes would be tested with linear or logistic regression only.
“This proposal also contains the suggestion,” researchers wrote, “that Mendelian randomization is particularly valuable in establishing null results in a large, well-powered sample sets with an established association between genetic variant and exposure but no association between genetic variant and outcomes, supporting the conclusion that little or no effect of exposure on outcome exists.”
To read the article at its original location: http://www.rheumatologynetwork.com/rheumatoid-arthritis/assessing-risk-factors-disease-outcomes
Published on the Aug. 15, 2016, Rheumatology Network website
By Whitney L.J. Howell
Published on the July 28, 2016, DiagnosticImaging.com website
By Whitney L.J. Howell
Recently, a New Jersey court handed down a decision that could potential change the role radiologists play when it comes to determining the medical necessity of a study ordered by a referring physician.
Although the current ruling only applies to New Jersey radiologists, industry experts are talking about how it could possibly affect your responsibilities, daily work flow, and liabilities.
Allstate Insurance brought suit against radiologists who conducted MRIs and X-rays on patients who had submitted personal injury claims. The company argued the providers had not completed their due diligence in checking into whether these studies were warranted, suing to recoup $200,000 of expenditures.
Company lawyers asserted the radiologists were the imaging center’s medical directors and, therefore, bore the responsibility of verifying medical necessity. The radiologists countered that the chiropractors and other referring physicians who send them patients satisfy the state’s requirement of being “verified” providers. But, the judge ultimately ruled the onus of ensuring proper clinical evidence exists to support medical necessity and appropriateness lies with the radiologist.
According to Greg Nicola, MD, treasurer of the Radiological Society of New Jersey, the organization is filing an appeal of the ruling. The American College of Radiology (ACR) also considers the case to be unique – one that will likely only bind New Jersey radiologists, said Tom Hoffman, JD, the ACR’s associate general counsel.
“The lesson remains to realize that the radiologists aren’t in the driver’s seat about medical necessity decisions because they don’t interact daily with the patient,” Hoffman said. “They’re hard pressed to have all the sufficient clinical background on a patient.”
To read the remainder of the article at its original location: http://www.diagnosticimaging.com/practice-management/radiology-role-determining-medical-necessity
Published on the July 13, 2016, Rheumatology Network website
By Whitney L.J. Howell
Advances in drug development and management strategies for rheumatoid arthritis over the past 15 years have improved survival rates for patients, researchers say.
The study appears in the June 23, 2016,Annuals of the Rheumatic Diseases.
To date, there have been no investigations into whether these improvements have positively impacted the lifespan of patients with rheumatoid arthritis. A few studies exist, researchers said, looking into how treatments impacted mortality up to 2004. However, there are none that look at later dates.
In a population-based cohort study, researchers reviewed how standard rheumatoid arthritis treatments impacted patients with this condition and compared the results to similar patients who did not have rheumatoid arthritis. They were also interested in whether other co-morbidities impacted survival.
Led by Yuqing Zhang, M.D., professor of medicine and epidemiology at Boston University School of Medicine, investigators determined rheumatoid arthritis patients treated after the advent of new drugs and management strategies had a longer survival rate than those treated earlier. The study, which looked at patients treated from 1999 to 2014, also revealed co-morbidities did not significantly impact life span.
Throughout the study, researchers surveyed electronic medical records from The Health Improvement Network in the United Kingdom for 10.2 million patients from 580 general practice clinics. They identified all patients, ages 18 to 89, with rheumatoid arthritis and up to five similar individuals who didn’t have the condition. They, then, divided patients into two cohorts: those treated between 1999 and 2006 (10, 126 rheumatoid arthritis patients and 50,546 non-rheumatoid arthritis patients) and those treated between 2007 and 2014 (10, 769 rheumatoid arthritis patients and 53, 749 non-rheumatoid patients).
According to study results, more patients from the early cohort died – and died younger – than patients from the later cohort. Based on the data, 936 rheumatoid arthritis patients from the early cohort, and 2,968 non-rheumatoid arthritis, died. The average ages were 77 and 78.4, respectively. In the later cohort, 605 rheumatoid arthritis patients, and 2,293 non-arthritis patients, died. The average ages were 77.9 and 78.4 respectively.
In terms of relative risk, rheumatoid arthritis patients in the early cohort had a 56 percent higher risk of all-cause mortality, and the later cohort had a 29 percent higher risk, researchers reported.
Investigators also found disease-modifying anti-rheumatic drug use was greater in the later cohort than the earlier one – 81 percent to 65 percent, respectively. And, of those using these medicines, 85 percent of late cohort and 68 percent of early cohort received methotrexate. Dosing and administration modes for these medications also improved between early to later cohorts.
“While patients with rheumatoid arthritis had higher mortality rates than individuals without rheumatoid arthritis in either the early or the late cohorts, the magnitude of difference in mortality was smaller in the late cohorts compared with that in earlier cohorts,” researchers said.
Investigators found age, sex, body mass index, alcohol consumption, and medication use didn’t impact results. However, rheumatoid arthritis patients were more likely to smoke and did have more co-morbidities.
Recent U.K. studies show a tripling (156 percent) of methotrexate use between 2001 and 2012. There was also an increase in the use of tumor necrosis factor inhibitor. Seen together, these measures are seen to reduce rheumatoid arthritis disease activity and to have led to improved longevity for patients.
Not only does this data indicate that early and effective interventions for rheumatoid arthritis help prevent permanent damage, but it also demonstrates that treat-to-target strategies have been utilized more frequently. When taken together, all the findings point to a reduction in rheumatoid arthritis disease activity and improved life longevity.
Further study is needed, however, because not enough data existed to determine actual cause of death in a large number of cases. Researchers also said future studies would be valuable to assess the extent to which improved survival among rheumatoid arthritis patients is directly attributable to the improvement of rheumatoid arthritis management and disease activity.
To read the article at its original location: http://www.rheumatologynetwork.com/rheumatoid-arthritis/ra-survival-rates-outpacing-general-population
Published on the June 27, 2016, Rheumatology Network website
By Whitney L.J. Howell
Methotrexate therapy in patients with rheumatoid arthritis can cause significant changes in clinical disease activity, researchers say.
The study appears in the June 16 issue of RMD Open.
To date, researchers said, there have been no studies into the mechanism of action of methotrexate which look at serial prospective measures of serum cytokines and simultaneous measures of pharmacokinetics and clinical variables.
In this prospective, open-label, long-term mechanism of action study, investigators looked to describe changes in immune parameters that are observed during long-term methotrexate therapy in patients with active rheumatoid arthritis. They also wanted to explore correlations with simultaneously measured methotrexate pharmacokinetic parameters.
Led by Joel M. Kremer, M.D., from the Division of Rheumatology at Albany Medical College, researchers demonstrated that methotrexate treatment is associated with serum interleukin-6 (IL-6) and interleukin-8 (IL-8) decreases. This three-year study, conducted in the 1990s, also shows these drops correlate well with long-term, sequential measures of methotrexate pharmacokinetics and with clinical outcomes.
Throughout the study, 17 patients received single, weekly 7.5 mg doses of methotrexate. The doses were adjusted for efficacy and toxicity throughout the study, and researchers gathered baseline measures for disease activity and took follow-up measurements every six months for three years. Each clinical evaluation assessed serum cytokine measurements in blood together with lymphocyte surface immunophenotypes and stimulated peripheral blood mononuclear cell cytokine production.
According to study results, cytokine concentrations revealed several significant correlations over time with disease activity measures. The two strongest were: interleukin-6 (r=0.45, p<0.0001 for swollen joints and r=0.32, p=0.002 for tender joints) and interleukin-8 (r=0.25, p=0.01 for swollen joints).
Results also found significant decreases for serum interleukin-1B, interleukin-6, and interleukin-8 from baseline measurements with interleukin-6 being the most substantial change (p<0.001). Data also revealed noteworthy increases from baseline for interleukin-2 release from peripheral blood mononuclear cells ex vivo (p<0.01). However, the change in swollen joint count correlated inversely with the changes for methotrexate (r=-0.63, p=0.007).
“These data strongly support the notion that MTX (methotrexate) mediates profound and functionally relevant effects on the immunological hierarchy in the RA lesion,” the researchers wrote.
Ultimately, investigators said, knowing methotrexate can significantly affect serum interleukin-6 will increase understanding around methotrexate’s mechanism of action. It also offers insight into further changes in transaminase levels and possible additive effects on interleukin-6 when used with biological response modifiers and Janus kinase inhibitors.
“The compelling relationship between the immune changes reported and simultaneous pharmacokinetic measures strongly suggest that the findings are related to methotrexate intervention and are not simply a surrogate for general disease improvement,” investigators said.
In addition, they said, the significant decrease in serum interleukin-6 observed with methotrexate may further explain increases in transaminase enzymes when the drug is combined with either interleukin-6 or Janus kinase inhibitors.
To read the article at its original location: http://www.rheumatologynetwork.com/rheumatoid-arthritis/methotrexate-associated-%E2%80%9Cprofound%E2%80%9D-improvements-ra?GUID=EF943FEE-BD0C-44C7-A1BC-C82F32210979&XGUID=&rememberme=1&ts=28062016
Published on the June 22, 2016, Rheumatology Network website
By Whitney L.J. Howell
Researchers say it is not necessary to take body mass index into account when assessing disease activity in axial spondyloarthritis patients.
The study appears in the June 16 issue of RMD Open.
Physicians primarily rely on two measures to assess axial spondyloarthritis (axSpA) and ankylosing spondylitis disease status: the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and the Ankylosing Spondylitis Disease Activity Score (ASDAS). While BASDAI relies on patient-reported outcomes to measure ankylosing spondylitis in patients, ASDAS combines patient-reported outcomes with C reactive protein (CRP) to assess axial spondyloarthritis status.
Because adipose tissue is frequently associated with increased production of pro-inflammatory cytokines, such as C reactive protein, investigators hypothesized whether an elevated body mass index could be an accurate disease-activity indicator. Obesity, measured by body mass index (BMI), is associated with increased levels of C reactive protein (CRP). High levels occur in response to inflammation, including that associated with ankylosing spondylitis.
Led by Roxana Rubio Vargas of the Leiden University Medical Center in The Netherlands, researchers found body mass index only influences CRP blood serum levels in women. But, the impact is not clinically relevant.
Knowing whether body mass index and excess adipose tissue contributed to CRP levels and self-reported outcomes could influence how providers guide patients on how best to control their axial spondyloarthritis.
Using patients and data from the existing SPondyloArthritis Caught Early (SPACE) cohort, launched in January 2009, researchers evaluated 428 patients over age 16 who had chronic back pain for more than three months, but less than two years. Investigators divided patients into normal weight (body mass index ≤24.9) and overweight (≥25). Collected C reactive protein levels of ≥5 mg/L were considered elevated.
Of the 428 patients, 168 (39.3%) fulfilled the Assessment in SpondyloArthritis International Society axial spondyloarthritis classification. This group had statistically lower rates of overweight and obesity— 18.4% and 11.9%, respectively — than those without the condition — 31.5% and 14.2%, respectively. Among patients with axial spondyloarthritis and those without, overweight patients had statistically significant higher C reactive protein rates (p=0.02 and 0.01, respectively). Researchers also discovered body mass index increases C reactive protein blood serum levels by 0.35 mg/L for each body mass index point – but only for women.
Overall, the researchers found, the impact of body mass index on C reactive protein in women isn’t enough to warrant using it as a measure of disease activity. It also doesn’t significantly impact any patient-reported outcomes.
“In general, it is not necessary to take BMI into account when assessing disease activity by ASDAS in axSpA patients with high BMI, but there may be a slight increase in ASDAS in female patients with very high BMI,” researchers wrote.
Further research into the influence of body mass index on CRP is needed, though. Researchers recommend conducting MRI and spectroscopy studies on a larger sample size of overweight women with axial spondyloarthritis to achieve more accurate results.
To read the story at its original location: http://www.rheumatologynetwork.com/spondyloarthritis/high-bmi-not-factor-axial-spondyloarthritis
Published on the June 9, 2016, DiagnosticImaging.com website
By Whitney L.J. Howell
In radiology, there’s no more important – no closer relationship – than the one between the radiologist and the radiologic technologist (RT). You work together day-in and day-out, but there’s no guarantee that your partnership is as healthy as it should be.
According to industry experts, effective radiologist-RT work habits should share some of the same characteristics, enabling those pairs to provide quality patient care. But, radiology has changed drastically over the past 25 years, and stumbling blocks challenge how smoothly your daily interactions will be in today’s environment.
“I remember the days of film in the 1990s when technologists would come into the reading room and hang the film,” said Paul Nagy, PhD, associate professor of radiology and radiological sciences at Johns Hopkins School of Medicine. “It was great because of the cross-section of interaction that happened when the radiologists looked at the film and gathered information from the tech for diagnostic purposes. But, there are several strains on the relationship today.”
There are strategies in place that are working to fortify the partnership, though, because this interaction is necessary to produce an actionable radiology report.
“The radiologist is very dependent upon the technologist to get the most information from patients,” said Michael Delvecchio, technical director of radiology at Brigham and Women’s Hospital. “It helps them get better reads and provide a better diagnosis.”
To read the remainder of the article at its original location: http://www.diagnosticimaging.com/practice-management/challenges-radiologist-technologist-relationship