Psoriasis is an independent risk for Type 2 Diabetes, according to a new study by researchers with the Perelman School of Medicine at the University of Pennsylvania, with the greatest risk seen in patients with severe psoriasis. Researchers estimate that an additional 115,500 people will develop diabetes each year due to the risk posed by psoriasis above and beyond conventional risk factors.
‘These data suggest that patients with psoriasis are at increased risk for developing diabetes even if they don’t have common risk factors such as obesity,’ said senior author Joel M. Gelfand, MD, MSCE, associate professor of Dermatology in the Perelman School of Medicine. ‘Patients with psoriasis should eat a healthy diet, get regular exercise, and see their physician for routine preventative health screenings such as checks of blood pressure, cholesterol, and blood sugar.’
Psoriasis is a common inflammatory skin disease affecting over 7.5 million Americans and causes thick, inflamed, scaly patches of skin. The disease has previously been associated with increased risk of myocardial infarction, stroke, metabolic syndrome and cardiovascular mortality.
This research builds on previous work demonstrating a diverse set of increased health risks for people with psoriasis,’ said lead author Rahat S. Azfar, MD, MSCE, adjunct assistant professor of Dermatology in the Perelman School of Medicine. ‘In addition to having an increased risk of diabetes, people with psoriasis are more likely to have metabolic syndrome, high triglycerides, and raised glucose levels, even if they are not overweight or have other common risk factors for these conditions. Both patients with psoriasis, especially those with severe psoriasis, and their treating physicians should be aware of the potential for systemic metabolic complications associated with this skin disease.
Both psoriasis and diabetes are diseases caused by chronic inflammation. A shared pathway — TH-1 cytokines — can promote insulin resistance and metabolic syndrome, and promote inflammatory cytokines known to drive psoriasis.
The study compared 108,132 people with psoriasis to 430,716 matched patients without psoriasis, and determined patients with mild psoriasis had an 11% increased risk of diabetes and patients with severe psoriasis had a 46% higher risk compared to patients without psoriasis. The study also looked at treatments used by those diagnosed with diabetes, and found that the patients with both psoriasis and diabetes were more likely to require pharmacological treatment of diabetes, compared to diabetics without psoriasis.
Researchers noted that future studies should look into the extent to which psoriasis and its treatment play a role in the development of Type 2 Diabetes and its complications. University of Pennsylvania School of Medicin

An international group of researchers, including those from Moffitt Cancer Center in Tampa, Fla., have published a paper reviewing the results of a study that analysed mutations in 18 genes of 398 patients who had acute myeloid leukemia (AML). They found that several mutated genes predicted improved outcomes when patients with certain gene mutations were given high-dose induction chemotherapy. Their findings suggest that mutational profiling could potentially be used for both risk stratification and also in helping health care providers make therapeutic decisions for some AML patients.
‘Previous studies have found that AML is a highly heterogenic disorder,’ said study co-author Hugo F. Fernandez, a senior member at Moffitt and associate chief of Moffitt’s Blood and Marrow Transplantation Division. ‘Moreover, recent studies have revealed that a number of genetic mutations in AML patients might have prognostic value. The question of the presence of these gene mutations altering outcomes based on current therapy had not been answered to date.’
Their paper cites a clinical trial carried out by the Eastern Co-operative Oncology Group (ECOG) in which dose-intensified chemotherapy improved outcomes in two age sets of AML patients. Based on these findings, the research team hypothesised that carrying out mutational analysis of all known molecular alterations occurring in more than 5 percent of patients with AML might allow for the identification of distinct, molecularly defined subgroups of patients who might benefit from dose-intensified chemotherapy.
The laboratory research team subsequently performed a mutational analysis on diagnostic samples from 398 patients enrolled in the ECOG clinical trial they cited and used patients’ frozen sample cells for extraction and profiling. The researchers validated the results of this latter group of 104 patients.
‘We found that intensification of the dose of anthracycline significantly improved outcomes and overall survival in patients with mutations in DNMT3A, NPM1 or MLL translocations,’ said Fernandez. ‘This finding suggests that mutational profiling could be used to determine which AML patients will benefit from dose-intensive induction therapy.’
‘Most importantly,’ said Fernandez, ‘this study demonstrates how integrated mutational profiling of samples from a clinical trial cohort can advance understanding of the biologic characteristics of AML.’ Moffitt Cancer Center

A Yale University-led research team has developed a way to measure the loss of insulin-producing islet cells in the human pancreas. The death of those beta cells leads to diabetes. The finding is a crucial step in developing therapies to preserve insulin production and slow or halt the progress of diabetes.
Until now there has been no effective method for imaging pancreatic islet beta-cell mass in a non-invasive manner. Based on the work of Paul Harris and colleagues at Columbia University, the Yale team focused on the genetically expressed protein known as vesicular monoamine transporter type 2 (VMAT2). This protein facilitates the storage and release of some neurotransmitters, and is expressed simultaneously with insulin in pancreatic beta cells.
The Yale team infused both healthy patients and those with type-1 diabetes with a radioactive tracer that targets VMAT2. Patients were then scanned with a PET camera to calculate the radioactivity concentration in the pancreatic cells and measure the binding of the tracer.
Adjusting for dosage and body weight, the radiotracer binding among pancreatic cells was 40 percent less in type-1 diabetes patients than in healthy patients.
Senior author Gary W. Cline, associate professor of endocrinology at Yale School of Medicine, explained, ‘This tells us that we can now measure the loss of the pancreatic islet cells that produce insulin in diabetic patients. Being able to make these measurements will help in the development of a drug that can stop or slow the death of these cells, and thus prevent the damaging effects of type 1 diabetes.’ Yale University

A new JDRF-funded study shows that many of the genes known to play a role in type 1 diabetes (T1D) are expressed in pancreatic beta cells, suggesting that the cell responsible for producing insulin may be playing a part in its own destruction to lead to T1D. Researchers in Belgium suggest this interpretation after producing an extensive catalogue of more than 15,000 genes expressed in human islets, forming the most extensive characterisation of human islets reported to date.
The researchers, led by Decio Eizirik, M.D., Ph.D., professor and director of the Laboratory of Experimental Medicine at Universite Libre de Bruxelles in Brussels, Belgium, used a technique called RNA sequencing—a method that identifies all forms of transcribed RNAs in a cell—to assemble a catalogue that showed that more than 15,000 genes are expressed in healthy human islets. Transcribed RNA (ribonucleic acid) molecules serve as the vehicles through which a cell’s genetic information is expressed. The data has been made available to other researchers to be used for future studies of beta cell function.
In the study, the researchers found many of the previously known genes associated with T1D among the genes expressed in human islets. When the researchers exposed the human islets to agents (cytokines) released by immune cells that may trigger T1D, they noted changes in the expression patterns of these genes. This finding suggested that the islets may be contributing to the recruitment of immune cells as T1D starts to develop.
While conventional wisdom was that these genes played a role in T1D by affecting the function of the immune system, their expression in human islets led the scientists to consider the possibility that the beta cells—once seen as merely victims in T1D—might actually assist in their own attack by the immune system.
‘Based on our research, our understanding now is that type 1 diabetes in its early stages, is characterised by a dialog between beta cells and the immune system, instead of the previous view of beta cells as purely passive victims of the immune attack,’ said Dr. Eizirik. ‘We can now open our eyes a bit wider to the possible ways that type 1 diabetes can develop. As we expand our focus on beta cells, we could start to unearth more answers in the mystery of this disease.’
‘What we’re seeing is that beta cells may in fact be playing a larger role in triggering type 1 diabetes than we previously thought, and exploring this concept more deeply could lead to a better understanding of the what causes the autoimmune attack,’ said Julia Greenstein, Ph.D., JDRF’s assistant vice president for cure therapies. ‘Dr. Eizirik’s work is important to JDRF because it shows us that there is a need for more research on beta cell survival and health and its role as a potentially key part of the early disease process. Furthermore, the catalog of genes from this study will continue to support progress in many more areas of diabetes research.’ EurekAlert

The uproar that began last year when the U.S. Preventive Services Task Force stated that doctors should no longer offer regular prostate-cancer tests to healthy men continued this week when the task force released their final report. Overall, they stuck to their guns, stating that a blood test commonly used to screen for prostate cancer, the PSA test, causes more harm than good — it leads men to receive unnecessary, and sometimes even dangerous, treatments.
But many people simply don’t believe that the test is ineffective. Even faced with overwhelming evidence, such as a ten-year study of around 250,000 men that showed the test didn’t save lives, many activists and medical professionals are clamouring for men to continue receiving their annual PSA test. Why the disconnect?
In an article, researchers Hal R. Arkes, of Ohio State University, and Wolfgang Gaismaier, from the Max Planck Institute for Human Development in Berlin, Germany, picked apart lay-people’s reactions to the report, and examined the reasons why people are so reluctant to give up the PSA test.
‘Many folks who had a PSA test and think that it saved their life are infuriated that the Task Force seems to be so negative about the test,’ said Arkes.
They suggest several factors that may have contributed to the public’s condemnation of the report. Many studies have shown that anecdotes have power over a person’s perceptions of medical treatments. For example, a person can be shown statistics that Treatment A works less frequently than Treatment B, but if they read anecdotes (such as comments on a website) by other patients who had success with Treatment B, they’ll be more likely to pick Treatment B. The source of the anecdotes matters too. If a friend, a close relative, or any trusted source received successful treatment, they would be more likely to recommend that treatment to others, even if there was evidence showing the treatment only works for a minority of people.
Arkes and Gaismaier also propose that the public may have recoiled against the task force’s recommendations so fiercely because they weren’t able to properly evaluate the data in the report. Confusion over the use of control groups may have led people in the general public to weigh the data differently than medical professionals did.
‘How to change this is the million-dollar question,’ said Arkes. ‘Pictorial displays are far easier to comprehend than statistics. The two figures in our article depict the situation more clearly than text and numbers can do. I think data displayed in this manner can help change people’s view of the PSA test because we compare the relative outcomes of being tested and not being tested. Without that comparison, it is tough for the public to appreciate the relative pluses and minuses of the PSA test versus not having the PSA test.’
Men will be able to continue to request the PSA test, and it will be covered by health insurance for the foreseeable future. But psychological science suggests that unless people are convinced to choose statistics over anecdotes, confusion surrounding the test’s effectiveness will linger. Association for Psychological Science