Survey estimates extent of nontreatment and undertreatment of psoriasis and psoriatic arthritis in U.S. patients

Main Category: Eczema / Psoriasis
Article Date: 15 Aug 2013 - 2:00 PDT Current ratings for:
Survey estimates extent of nontreatment and undertreatment of psoriasis and psoriatic arthritis in U.S. patients

Nontreatment and undertreatment of patients with psoriasis and psoriatic arthritis appears to still be a significant problem in the United States, according to a study by April W. Armstrong, M.D., M.P.H., of University of California-Davis, Sacramento, and colleagues.

A total of 5,604 patients with psoriasis or psoriatic arthritis completed surveys collected by the National Psoriasis Foundation from January 2003 through December 2011.

From 2003 through 2011, patients who were untreated ranged from 36.6 percent to 49.2 percent of patients with mild psoriasis, 23.6 percent to 35.5 percent of patients with moderate psoriasis, and 9.4 percent to 29.7 percent of patients with severe psoriasis. Among those receiving treatment, 29.5 percent of patients with moderate psoriasis and 21.5 percent of patients with severe psoriasis were treated with topical agents alone. Although adverse effects and a lack of effectiveness were primary reasons for discontinuing biological agents, the inability to obtain adequate insurance coverage was among the top reasons for discontinuation. Overall, 52.3 percent of patients with psoriasis and 45.5 percent of patients with psoriatic arthritis were dissatisfied with their treatment, according to study results.

"While various treatment modalities are available for psoriasis and psoriatic arthritis, widespread treatment dissatisfaction exists. Efforts in advocacy and education are necessary to ensure that effective treatments are accessible to this patient population," the authors conclude.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our eczema / psoriasis section for the latest news on this subject.

JAMA Dermatol. Published August 14, 2013. doi:10.1001/jamadermatol.2013.5264.

JAMA

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Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

Main Category: Arthritis / Rheumatology
Also Included In: Immune System / Vaccines;  Pediatrics / Children's Health;  Seniors / Aging
Article Date: 31 Jul 2013 - 1:00 PDT Current ratings for:
Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

The joints of children with the most common form of chronic inflammatory arthritis contain immune cells that resemble those of 90-year-olds, according to a new study led by researchers at Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. The findings, published in the August issue of Arthritis and Rheumatism, suggest that innovative treatment approaches could aim to prevent premature aging of immune cells.

Juvenile idiopathic arthritis, or JIA, is the most prevalent rheumatic condition in the world and affects one of every 1,000 children in the U.S., said senior researcher Abbe de Vallejo, Ph.D., associate professor of pediatrics and immunology, Pitt School of Medicine. It usually starts with a swollen ankle, knee or wrist that parents often assume is due to a minor injury sustained while playing.

"Untreated JIA has devastating consequences," Dr. de Vallejo said. "It can slow growth and, in extreme cases, the child can be physically disfigured. It's a degenerative disease that eats up the joints."

Doctors have long thought of JIA as an autoimmune disease, meaning the body attacks itself. But previous studies by Dr. de Vallejo of young adults with rheumatoid arthritis indicated that a certain population of cells present in the joint synovial fluid and blood displayed telltale signs of abnormal cell division and premature aging. His current team at Children's wanted to see if that was true in pediatric arthritis.

They examined immune cells called T-cells in the synovial fluid and blood from 98 children ages 1 to 17 and known to have JIA, as well as 46 blood samples from children who didn't have the disease. T-cells are the army of immune cells that eradicate infection, tumors and other dangerous agents to which people may be exposed.

The research team found about one-third of the T-cells of children with JIA had shortened telomeres and had reduced, or in some cases lost, the capacity to proliferate. Telomeres are the ends of chromosomes that don't code for proteins and, because they are not fully copied by enzyme mechanisms, are trimmed slightly during each DNA replication cycle. It is thought that aging occurs when the telomeres become too short for DNA replication and cell division to proceed normally.

"The T-cells of the children with JIA had very short telomeres, about the length we see in a 90-year-old or a young adult with rheumatoid arthritis. Those same T-cells express unusually high levels of several classic protein markers of cell aging and exhaustion," Dr. de Vallejo said. "These kids haven't lived long enough to have cells that look that old. This is the first indication that premature aging in occurring in this childhood condition."

In addition, the T-cells had become dysregulated, and their immune activity could be stimulated through atypical cell surface receptors. Much more must be learned about the unusual cells and about genetic mechanisms that might contribute to the development of JIA, Dr. de Vallejo said, but these findings could point the way to new therapies.

"JIA is typically treated with broad-spectrum drugs such as steroids and biologics that essentially paralyze the entire immune system, but only a third of the cells are affected and their abnormality seems to be premature aging, rather than autoimmune activity," he noted. "This study suggests cell-targeted treatments could be developed to prevent this premature immune aging."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our arthritis / rheumatology section for the latest news on this subject.

Co-authors of the paper include other researchers from Children’s Hospital of Pittsburgh of UPMC; Pitt School of Medicine; and the Mayo Clinic. The project was funded by the Nancy E. Taylor Foundation for Chronic Diseases, the Arthritis Foundation, and National Institutes of Health grant AR052282.

Children’s Hospital of Pittsburgh of UPMC & University of Pittsburgh Schools of the Health Sciences

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University of Pittsburgh Medical Center. (2013, July 31). "Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says." Medical News Today. Retrieved from
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Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

Main Category: Arthritis / Rheumatology
Also Included In: Immune System / Vaccines;  Pediatrics / Children's Health;  Seniors / Aging
Article Date: 31 Jul 2013 - 1:00 PDT Current ratings for:
Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

The joints of children with the most common form of chronic inflammatory arthritis contain immune cells that resemble those of 90-year-olds, according to a new study led by researchers at Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. The findings, published in the August issue of Arthritis and Rheumatism, suggest that innovative treatment approaches could aim to prevent premature aging of immune cells.

Juvenile idiopathic arthritis, or JIA, is the most prevalent rheumatic condition in the world and affects one of every 1,000 children in the U.S., said senior researcher Abbe de Vallejo, Ph.D., associate professor of pediatrics and immunology, Pitt School of Medicine. It usually starts with a swollen ankle, knee or wrist that parents often assume is due to a minor injury sustained while playing.

"Untreated JIA has devastating consequences," Dr. de Vallejo said. "It can slow growth and, in extreme cases, the child can be physically disfigured. It's a degenerative disease that eats up the joints."

Doctors have long thought of JIA as an autoimmune disease, meaning the body attacks itself. But previous studies by Dr. de Vallejo of young adults with rheumatoid arthritis indicated that a certain population of cells present in the joint synovial fluid and blood displayed telltale signs of abnormal cell division and premature aging. His current team at Children's wanted to see if that was true in pediatric arthritis.

They examined immune cells called T-cells in the synovial fluid and blood from 98 children ages 1 to 17 and known to have JIA, as well as 46 blood samples from children who didn't have the disease. T-cells are the army of immune cells that eradicate infection, tumors and other dangerous agents to which people may be exposed.

The research team found about one-third of the T-cells of children with JIA had shortened telomeres and had reduced, or in some cases lost, the capacity to proliferate. Telomeres are the ends of chromosomes that don't code for proteins and, because they are not fully copied by enzyme mechanisms, are trimmed slightly during each DNA replication cycle. It is thought that aging occurs when the telomeres become too short for DNA replication and cell division to proceed normally.

"The T-cells of the children with JIA had very short telomeres, about the length we see in a 90-year-old or a young adult with rheumatoid arthritis. Those same T-cells express unusually high levels of several classic protein markers of cell aging and exhaustion," Dr. de Vallejo said. "These kids haven't lived long enough to have cells that look that old. This is the first indication that premature aging in occurring in this childhood condition."

In addition, the T-cells had become dysregulated, and their immune activity could be stimulated through atypical cell surface receptors. Much more must be learned about the unusual cells and about genetic mechanisms that might contribute to the development of JIA, Dr. de Vallejo said, but these findings could point the way to new therapies.

"JIA is typically treated with broad-spectrum drugs such as steroids and biologics that essentially paralyze the entire immune system, but only a third of the cells are affected and their abnormality seems to be premature aging, rather than autoimmune activity," he noted. "This study suggests cell-targeted treatments could be developed to prevent this premature immune aging."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our arthritis / rheumatology section for the latest news on this subject.

Co-authors of the paper include other researchers from Children’s Hospital of Pittsburgh of UPMC; Pitt School of Medicine; and the Mayo Clinic. The project was funded by the Nancy E. Taylor Foundation for Chronic Diseases, the Arthritis Foundation, and National Institutes of Health grant AR052282.

Children’s Hospital of Pittsburgh of UPMC & University of Pittsburgh Schools of the Health Sciences

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University of Pittsburgh Medical Center. "Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says." Medical News Today. MediLexicon, Intl., 31 Jul. 2013. Web.
31 Jul. 2013. APA
University of Pittsburgh Medical Center. (2013, July 31). "Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/264123.php.

Please note: If no author information is provided, the source is cited instead.

'Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says'

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Technique to create better anti-cancer agents, arthritis drugs, and more

Main Category: Lymphoma / Leukemia / Myeloma
Also Included In: Medical Devices / Diagnostics;  Arthritis / Rheumatology
Article Date: 30 Jul 2013 - 0:00 PDT Current ratings for:
Technique to create better anti-cancer agents, arthritis drugs, and more

Many drugs such as agents for cancer or autoimmune diseases have nasty side effects because while they kill disease-causing cells, they also affect healthy cells. Now a new study has demonstrated a technique for developing more targeted drugs, by using molecular "robots" to hone in on more specific populations of cells.

"This is a proof of concept study using human cells," said Sergei Rudchenko, Ph.D., director of flow cytometry at Hospital for Special Surgery (HSS) in New York City and a senior author of the study. "The next step is to conduct tests in a mouse model of leukemia." The study, a collaboration between researchers from HSS and Columbia University, is in Advance Online Publication on the website of Nature Nanotechnology.

All cells have many receptors on their cell surface. When antibodies or drugs bind to a receptor, a cell is triggered to perform a certain function or behave in a certain manner. Drugs can target disease-causing cells by binding to a receptor, but in some cases, disease-causing cells do not have unique receptors and therefore drugs also bind to healthy cells and cause "off-target" side effects.

Rituximab (Rituxan, Genentech), for example, is used to treat rheumatoid arthritis, non-Hodgkin's lymphoma and chronic lymphocytic leukemia by docking on CD20 receptors of aberrant cells that are causing the diseases. However, certain immune cells also have CD20 receptors and thus the drug can interfere with a person's ability to mount a fight against infection.

In the new study, scientists have designed molecular robots that can identify multiple receptors on cell surfaces, thereby effectively labeling more specific subpopulations of cells. The molecular robots, called molecular automata, are composed of a mixture of antibodies and short strands of DNA. These short DNA strands, otherwise called oligonucleotides, can be manufactured by researchers in a laboratory with any user-specified sequence.

The researchers conducted their experiments using white blood cells. All white blood cells have CD45 receptors, but only subsets have other receptors such as CD20, CD3, and CD8. In one experiment, HSS researchers created three different molecular robots. Each one had an antibody component of either CD45, CD3 or CD8 and a DNA component. The DNA components of the robots were created to have a high affinity to the DNA components of another robot. DNA can be thought of as a double stranded helix that contains two strands of coded letters, and certain strands have a higher affinity to particular strands than others.

The researchers mixed human blood from healthy donors with their molecular robots. When a molecular robot carrying a CD45 antibody latched on to a CD45 receptor of a cell and a molecular robot carrying a CD3 antibody latched on to a different welcoming receptor of the same cell, the close proximity of the DNA strands from the two robots triggered a cascade reaction, where certain strands were ripped apart and more complementary strands joined together. The result was a unique, single strand of DNA that was displayed only on a cell that had these two receptors.

The addition of a molecular robot carrying a CD8 antibody docking on a cell that expressed CD45, CD3 and CD8 caused this strand to grow. The researchers also showed that the strand could be programmed to fluoresce when exposed to a solution. The robots can essentially label a subpopulation of cells allowing for more targeted therapy. The researchers say the use of increasing numbers of molecular robots will allow researchers to zero in on more and more specific subsets of cell populations. In computer programming language, the molecular robots are performing what is known as an "if yes, then proceed to X function."

"The automata trigger the growth of more strongly complementary oligonucleotides. The reactions occur fast. In about 15 minutes, we can label cells," said Maria Rudchenko, M.S., the first author of the paper and a research associate at Hospital for Special Surgery. In terms of clinical applications, researchers could either label cells that they want to target or cells they want to avoid.

"This is a proof of concept study that it works in human whole blood," said Dr. Rudchenko. "The next step is to test it in animals."

If molecular robots work in studies with mice and eventually human clinical trials, the researches say there are a wide range of possible clinical applications. For example, cancer patients could benefit from more targeted chemotherapeutics. Drugs for autoimmune diseases could be more specifically tailored to impact disease-causing autoimmune cells and not the immune cells that people need to fight infection.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our lymphoma / leukemia / myeloma section for the latest news on this subject.

The study was funded, in part, by the National Institutes of Health, National Science Foundation, and the Lymphoma and Leukemia Foundation.

Other researchers involved with the study are Alesia Dechkovskaia from Hospital for Special Surgery, and Steven Taylor, Ph.D., Payal Pallavi, B.A., Safana Khan, Vincent Butler, M.D., and Milan Stojanovic, Ph.D., from Columbia University. Dr. Stojanovich is also a senior author.

Hospital for Special Surgery

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