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Archive for the ‘Arthritis’ Category

‘Lifestyle is important in treating arthritis’ | Ahmedabad News – Times … – Times of India

Wednesday, February 8th, 2017

AHMEDABAD: City-based rheumatologist Dr Vishnu Sharma, at a press meet on Tuesday, spoke about an alarming increase in incidence of arthritis in people, especially younger people, and how a lack of awareness is causing health problems and deformities."There are as many as a hundred types of arthritis, of which more than 90% are curable if diagnosed on time. Some 80% to 90% of patients respond positively to treatment. We want to improve these results and hence want to raise awareness about rheumatology," Dr Sharma said. Dr Sharma then shed more light on 'inflammatory arthritis', the type more prevalent among young and middle-aged people. According to Dr Sharma, inflammatory arthritis has two causes, the first is a genetic tendency and the second is environmental factors like simple viral infections or physical and mental stress. About the influence of lifestyle on arthritis, Dr Sharma said: "Experts have found significant correlation between smoking and arthritis.Arthritis, conventionally a problem for old people and women, is increasing in male patients and the severity is greater in men who are frequent smokers." Dr Sharma said that as part of healthy lifestyle, the patient should have minimal stress levels, a high protein diet and should engage in exercise and yoga.

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What to Know About the Link Between Vitamin D and Psoriatic Arthritis – Health.com

Wednesday, February 8th, 2017

If you have psoriatic arthritis, you may have heard that people withthe conditionwhich causes painful, swollen, stiff jointsoften havelow levels ofvitamin D.In a 2015 study published in Arthritis Research & Therapy, researchers found that 40.9% of participants with psoriatic arthritis had a vitamin D deficiency, compared to 26.7% of control participants.Other autoimmune diseases have also been linked to low levels of the sunshine vitamin (so-called because the body produces vitamin D when it's exposed to sunlightyou can also get some vitamin Dfrom food, but sunshine is the main source). In the same study as above, 40.5% of rheumatoid arthritis patients were found to havea deficiency, as did 57.8% of psoriasis patients in earlier research from the British Journal of Dermatology.

Experts believe inflammation may have something to do with this.Autoimmune diseases like psoriatic arthritis and psoriasisinvolve an inflammation process,explainsWaseem Mir, MD, a rheumatologist at Lenox Hill Hospital in New York City."We think that inflammation causes a decrease in vitamin D," he told Health."[Its] not because [people] dont have enough vitamin D in their body, but theyre not processing it correctly."

It makes sense. The body needs vitamin D to absorb calcium. Both calcium and vitamin D work to promotehealthy bones, and vitamin D also seems to be involved in proper functioning of the immune system. And the bones and immune systemare both compromised in people who have psoriatic arthritis.

RELATED: 31 Ways to Manage Your Psoriatic Arthritis

Dr. Mir points out that there's been some research to suggest that vitamin D treatment may help ease joint pain in certain people with psoriatic arthritis. One such treatment is vitamin D supplements.If you have psoriatic arthritis, speak to your doctor about your vitamin D levels to find out if supplements are right for you.

Another treatment is phototherapy (careful exposure to ultraviolet rays), but there isn't enough research to recommend this for psoriatic arthritis patients.And although you can feel free to add morevitamin D-rich foods to your plate (think: fatty fish like salmon and tuna, certain kinds of mushrooms, and fortified milk) it's unlikely that you'd be able to reverse a true deficiency through diet alone.

In his own practice, Dr. Mir usually prescribes liquid vitamin D to patients, which he says helps get a better response.

"That is the most effective," he says. "A lot of it is absorbed through the mouth."

However, it is possible to get too much vitamin D, which can result in a build-up of calcium in the bloodand possibly lead to nausea, vomiting, and kidney problems.Speak to your doctor before adding any new supplements to your diet.

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Kaden Hadfield, 5, died from arthritis after doctors failed to diagnose … – Metro

Tuesday, February 7th, 2017

Kaden Hadfield was just five years old when he died from arthritis (Picture: MEN)

A five-year-old boy who suffered arthritis so bad he could barely walk at times died after doctors failed to diagnose him, his family has said.

Kaden Hadfield attended hospital more than 20 times over a two-year course, but nobody diagnosedhis arthritis and sent him home with Calpol and Ibuprofen.

Despite the pain and struggling to walk at times, Kaden continued to go to school.

It was only when he was finally referred to Alder Hey two years after his symptoms began that he was diagnosed and prescribed steroids.

But by that time the disease had ravaged his body and although treatment seemed to work at first, he sadly died.

Mum Caitlin Tattersall, 25, from Bolton, and dad Lee Hadfield, 29, of Oldham, are now awaiting an inquest this month, when they hope to discover the truth surrounding his death.

Meanwhile, the Trust which runs Blackpool Hospital where he was originally treated has confirmed launching a case review into his treatment.

Caitlin, who lived in Blackpool at the time after she and Lee separated, said: It was heartbreaking, the last time I saw Kaden he was in intensive care, they had his chest open, I could see his heart and lungs.

They tried to save him for 13 hours. But I dont understand. I feel like if Kaden had just had the medication he needed earlier he would be here today.

He had been so unwell for so long he never even complained from the pain, but he needed help. I was taking him to school he was sitting through it and not complaining.

It took two years to get Kaden an appointment at Alder Hey, they diagnosed him straight away but it was too late.

The familys ordeal began two years ago, when Kaden woke up one day with pain in one of his ankles, which a GP diagnosed as a sprain.

But the pain grew worse, and 18 months ago later when it moved to his other ankle, Caitlin took him to Blackpool Victoria Hospitals A&E.

Blood tests showed him to have a vitamin D deficiency and anaemia.

In hospital for a week, he was discharged with a bottle of Calpol and Ibuprofen as well as vitamin D and iron tablets.

The pain spread to Kadens knees then all his joints.

Referred to Rheumatology at Blackpool, Caitlin claims they gave him more Calpol despite an ultrasound showing tissue damage.

Caitlin added: It was worse in the morning, he couldnt walk, he couldnt even scratch his own nose his hands were so swollen and stiff.

We got referred to a physio the therapist said I was doing too much for Kaden and thats why he wasnt able to do things himself. I felt like I was banging my head against a brick wall.

At Blackpool Hospital, blood tests showed again showed that he was anaemic, despite the iron tablets.

Finally, after months of delays, Kaden got an appointment at Alder Hey Hospital, where doctors were so shocked they suspected leukaemia.

They diagnosed systemic onset juvenile arthritis and started a course of steroids which immediately began to ease his pain.

But the arthritis was already attacking Kadens joints and organs and he was placed on a high dependency unit.

After six weeks in hospital, he finally turned a corner and his family celebrated with the nurses as he took his first steps in months.

But the next day, Kaden complained of a stabbing pain in his stomach and he was taken to intensive care where his heart stopped.

Caitlin added: They had all these wires on him, they had to open his chest, I could see his heart and his lungs. They were trying to stop him bleeding but it was just pouring from him.

I knew he was going and there was nothing they could do. I was just screaming at them to try.

Kaden died the following day and doctorstold the family it was caused by sepsis as a result of his arthritis.

Caitlin, who is training to be a social worker, added: I want to know exactly what happened.

I want everyone to know. How can a healthy boy go from having a sore ankle two years ago to being gone?

Im training to be a social worker, I know what the standards should be.

Why did it take so long to get a diagnosis?

Describing Kaden as loving, kind and caring, she added: If he was in pain he would just entertain himself, play on his computer. When his friends came round Sometimes he was too weak to play with them. I had to take him to school in a pram in the end, he didnt like it, he said everyone would think he was a baby.

He was in agony every day and he never moaned. Everyone who ever met him loved him.

A spokesman for Blackpool Teaching Hospitals NHS Foundation Trust said: Our thoughts are with Kadens family at this sad time. Upon hearing of his death the trust initiated a case review which is ongoing and is standard procedure in all childrens deaths.

A spokeswoman for Alder Hey Childrens NHS Foundation Trust said: Our thoughts remain with the family at this extremely difficult time.

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Muscle Speed Affects Arthritis Prevention as Much as Strength, Study Finds – West Virginia Public Broadcasting

Tuesday, February 7th, 2017

Studies have found that strengthening the quadriceps or thigh muscles may help prevent knee osteoarthritis. But a new study has found that how fast the quadricep muscle is able to generate force for example pushing the leg out may impact knee osteoarthritis too.

More than a third of West Virginian adults report experiencing arthritis, according to the Centers for Disease Control and Prevention.

The studys authors followed 3,996 participants for 12 months, 3,820 for 24 months and 3,623 for 36 months. They measured quadricep speed and force by using a special chair with a cable that recorded muscle strength when pushing the leg out. They also tested how well participants walked for 20 and 400 meters and how well the participant was able to stand from after being seated in a chair. Finally, participants completed self-assessments of how well they were able to do daily activities like bathing, getting in a car and getting dressed.

The studys authors found that people with slower muscle responses are more likely to suffer from worse physical function in the future.

We know that maintaining quadriceps strength is important for protection against painful knee OA, said Neil Segal, one of the studys authors. Now, we know the ability to move the muscle quickly is important for keeping people able to walk, stand from a chair and do other functional activities.

Appalachia Health Newsis a project of West Virginia Public Broadcasting, with support from theBenedumFoundation, Charleston Area Medical Center andWVUMedicine.

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GB Sciences Files Patent Application for the Treatment of Chronic Arthritis, Crohn’s Disease, Inflammatory Bowel … – Investing News Network (press…

Tuesday, February 7th, 2017

GB Sciences, Inc. (OTCQB:GBLX) announced filing the second in a series of patent applications for life science inventions by its wholly-owned subsidiary, Growblox Life Sciences, LLC.

Inflammatory disorders represent a serious health and economic burden in the US with over $200 billion spent annually. GB Sciences novel cannabis-based therapies could significantly help both patients and society. According to the CDC, arthritis affects 22.7% (52.5 million) of adults in the US (2010-2012), and the prevalence is projected to increase to an estimated 26% (78 million of the projected total adult population) by 2040. The total costs associated with arthritis were $128 billion in 2003, and they have been increasing over time. Additionally, 8.6% (7 million) children and 7.4% (17.8 million) adults had asthma (2014), which costs the US $56 billion per year. Inflammatory Bowel Disease (IBD), which includes Crohns disease and ulcerative colitis) affected between 1 and 1.3 million people in the US (2007). Per the CDC, IBD is an expensive, chronic disease, which cost the US $11.8 billion in 2008, despite the lower prevalence rates.

The current provisional patent application covers cannabinoid-containing complex mixtures (CCCM) capable of preventing and treating a spectrum of inflammatory disorders. The application focuses on the use of CCCM to disrupt the signaling pathways in certain immune cells that lead to the initiation and maintenance of inflammatory responses. Both common and uncommon inflammatory disorders, ranging from chronic arthritis to acute responses to insect stings, are likely to be effectively targeted by this therapeutic approach.

Although inflammatory reactions are a necessary part of human immunity in some situations (e.g., fighting pathogens), humans (and animals) suffer from multiple inflammatory disorders involving hyper-inflammatory responses. Our novel CCCM strategically target multiple arms of these hyper-inflammatory responses in parallel for maximal effect, rather than inhibiting a single arm like other commonly available anti-inflammatory therapies, explains Dr. Andrea Small-Howard, Chief Science Officer of GB Sciences. For example, anti-histamines are partly effective, but leave untouched those inflammatory pathways that lead to release of other pro-inflammatory mediators, such as bioactive lipids and cytokines. GB Sciences approach is to simultaneously target as many inflammatory outputs as possible with our CCCM, leading to more comprehensive relief from tissue inflammation.

John Poss, CEO, GB Sciences states: GB Sciences is committed to developing cannabis-based therapies for inflammatory disorders that affect large numbers of patients (arthritis, dermatitis, allergic asthma, eczema, IBD, Crohns disease, etc.). Our CCCM products will be developed to the same efficacy and safety standards as other commercially available anti-inflammatory therapies; however, cannabis-based medicines often have more favorable side effect profiles than traditional pharmaceuticals.

About GB Sciences, Inc.

GB Sciences, Inc. (GBLX) is a diverse cannabis company, focused on standardized cultivation and production methods; as well as biopharmaceutical research and development. The Companys goal is creating safe, standardized, pharmaceutical-grade, cannabinoid therapies that target a variety of medical conditions. To learn more about GB Sciences, Inc., go to: http://growblox.com

Forward-Looking Statements

This press release may contain statements relating to future results or events, which are forward-looking statements. Words such as expects, intends, plans, may, could, should, anticipates, likely, believes and words of similar import may identify forward-looking statements. These statements are not historical facts, but instead represent only the Companys belief regarding future events, many of which, by their nature, are inherently uncertain and outside of the Companys control. It is possible that the Companys actual results and financial condition may differ, possibly materially, from the anticipated results and financial condition indicated in these forward-looking statements. Further, information concerning the Company and its business, including factors that potentially could materially affect the Companys business and financial and other results, are contained in the Companys filings with the Securities and Exchange Commission, available at http://www.sec.gov. All forward-looking statements included in this press release are made only as of the date of this press release, and we do not undertake any obligation to publicly update or correct any forward-looking statements to reflect events or circumstances that subsequently occur or of which we hereafter become aware.

Note: Although the Companys research and development activities are not illegal, the production and sale of cannabis products violate federal laws as they presently exist.

Contact Information

Corporate: GB Sciences, Inc., 3550 West Teco Ave., Las Vegas, NV 89118 866-721-0297, or Liz Bianco Publicity Director, liz@gbsciences.com, http://growblox.com Investors: John Poss, j.poss@gbsciences.com

creating safe, standardized, pharmaceutical-grade, cannabinoid therapies that target a variety of medical conditions. To learn more about GB Sciences, Inc., go to: http://growblox.com

SOURCE Growblox Sciences, Inc.

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Health Short: Arthritis pain supplements fare poorly in new study – Sarasota Herald-Tribune

Tuesday, February 7th, 2017

Arthritis pain supplements fare poorly in new study

Many people take glucosamine and chondroitin supplements for arthritis pain, but a controlled trial has found no evidence that the combination works. In fact, in this study, the placebo worked better.

Spanish researchers randomized 164 men and women with knee osteoarthritis to take a single daily dose of 1,500 milligrams of glucosamine and 1,200 of chondroitin, or an identical looking placebo. The study is in Arthritis & Rheumatology.

The researchers used a scale that shows 10 faces with increasingly pained expressions and asks patients which picture matches their degree of pain. People who took the medicines had a 19 percent reduction in pain scores after six months on the regimen. But those who took the placebo had a 33 percent reduction.

On scales measuring how well the knee worked, there was no difference between the treatment and control groups.

A lot of money is spent on these drugs, and people have thought they were useful to decrease pain and increase function, said the senior author, Dr. Gabriel Herrero-Beaumont, a professor of medicine at the Autonomous University of Madrid. But its difficult to demonstrate that they work. We have not found any kind of pharmacological effect of these drugs.

Nicholas Bakalar, The New York Times

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Local effects of adipose tissue in psoriasis and psoriatic arthritis – Dove Medical Press

Tuesday, February 7th, 2017

Back to Browse Journals Psoriasis: Targets and Therapy Volume 7

Ilja L Kruglikov,1 Uwe Wollina2

1Scientific Department, Wellcomet GmbH, Karlsruhe, 2Department of Dermatology and Allergology, Hospital Dresden-Friedrichstadt Academic Teaching Hospital of the Technical University of Dresden, Dresden, Germany

Abstract: The structure and physiological state of the local white adipose tissue (WAT) located underneath the lesional psoriatic skin and inside of the joints affected by psoriatic arthritis play an important role in the pathophysiology of these diseases. WAT pads associated with inflammatory sites in psoriasis and psoriatic arthritis are, correspondingly, dermal WAT and articular adipose tissue; these pads demonstrate inflammatory phenotypes in both diseases. Such local WAT inflammation could be the primary effect in the pathophysiology of psoriasis leading to the modification of the local expression of adipokines, a change in the structure of the basement membrane and the release of keratinocytes with consequent epidermal hyperproliferation during psoriasis. Similar articular adipose tissue inflammation can lead to the induction of structural modifications and synovial inflammation in the joints of patients with psoriatic arthritis.

Keywords: psoriasis, psoriatic arthritis, pathophysiology, adipose tissue, dermal adipocytes, articular adipose tissue

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Rheumatoid arthritis and feet: The connection and feet arthritis pain relief tips – Bel Marra Health

Monday, February 6th, 2017

Home Anti-Aging Arthritis Rheumatoid arthritis and feet: The connection and feet arthritis pain relief tips

Rheumatoid arthritis is a chronic disease involving the immune system, in which joints undergo inflammation. causing pain and stiffness.People with rheumatoid arthritis generally find difficulty performing simple movements that involve the joints, such as walking, standing up, and sitting down.

This condition has also affected individual performance at work or school, prompting the medical field to identify an effective treatment. Having this inflammatory condition affecting the joints may also be responsible for certain emergency visits to the hospital, especially when a person suffers from a decreased ability to operate a motor vehicle or machine. In other cases, visits to the emergency room may be due to extreme pain experienced by a patient with rheumatoid arthritis.

Common treatment plans for rheumatoid arthritis include anti-inflammatory drugs, such as aspirin, ibuprofen, and naproxen. It is also possible to prescribe disease-modifying antirheumatic drugs for the treatment of rheumatoid arthritis, although this type of treatment may also increase the risk of developing severe side effects, which may also require emergency medical attention. More recent improvements in treatment include the use of biologics, which are proteins that influence the immune system to slow down the progression of rheumatoid arthritis.

In extreme cases of rheumatoid arthritiswhere drug treatment appears to be ineffectivesurgery may also be recommended. It is important to understand that this disorder involves the immune system and the joints, and may also decrease the ability of a person to move. Many emergency calls involving the elderly are caused by rheumatoid arthritis increasing slips and falls.

Based on the severity of rheumatoid arthritis and its association with emergency medical treatments caused by accidents, health groups and researchers have looked into specific signs and symptoms that could be detected at an early stage. Using this information, people who are at a higher risk of developing rheumatoid arthritis may be educated on how to maintain their healthy bodies at an earlier age and possibly prevent the development of this immune system-related inflammatory disease. This information may also decrease the incidence of emergency visits to the hospital and ultimately lower the need for aggressive treatment of the disease.

According to a recent medical report, the features of the feet may serve as a reliable indicator for signs of rheumatoid arthritis at its early stages and the condition of an individuals immune system. For example, the ankle is composed of several joints and generally responsible for the stability of the body while standing upright. Any signs of stiffness, swelling, and pain in the ankle may indicate that this foot area may need emergency treatment in order to prevent further deterioration.

The report presented the findings of 100 individuals with rheumatoid arthritis who were interviewed during their earlier stages of the disease. The results of the study showed that the earliest symptoms of foot problems involved the ankle, followed by the forefoot. Years after, these individuals also experienced pain and stiffness in the hindfoot and midfoot. The study participants also admitted that they used insoles as primary treatment of the pain they encounter in their feet. The report also showed that aside from early foot problems, these patients also presented higher body weight, so it is possible that the rheumatoid arthritis development was faster due to this specific feature.

This recent medical report provides direct proof that certain foot features could serve as indicators of rheumatoid arthritis.

Below are some tips that may help you manage foot pain caused by arthritis. Be sure to check with your doctor before making any changes to your pain relief regimen.

Visit your doctor: The first step in seeking pain relief should always be to see your doctor to obtain a proper diagnosis. Your family doctor can refer you to a podiatrist or rheumatologist, who will check your feet annually to look for signs of arthritis and evaluate if any medications or exercise regimens are working.

Pick the right shoes: Ensure that your shoes have arch support, are wide enough for your feet, and are comfortable enough to minimize any pain you may feel. Toning athletic shoes with rocker bottoms are a good choice for a supportive, comfortable shoe.

Stretch: Stretching your Achilles tendons, along with the tendons in the balls of your feet and toes, can help improve joint mobility and relieve pain.

Get a foot massage: A foot massage that focuses on the balls of your feet and your toes can help relax the muscles in your feet and provide pain relief.

Topical ointments: Ointments that contain capsaicin can help reduce inflammation when applied topically to problem areas. Try using one of these creams or ointments on your feet for arthritis pain relief.

Related: Rheumatoid arthritis (RA): Causes, symptoms, and treatment

Related Reading:

Rheumatoid arthritis patients are at a higher risk for heart failure: Study

Rheumatoid arthritis and skin problems: Causes and treatment

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New Synthetic Cartilage Being Used To Treat Common Foot Arthritis – CBS Local

Monday, February 6th, 2017

February 3, 2017 6:18 PM

PITTSBURGH (KDKA) Logan Snyder has grown up playing softball, but then her big toes started to bother her.

Once I got to about 12 or 13, says Logan, I started to experience some pain and it just sort of escalated from there.

Her problem: hallux rigidus, or arthritis of the big toes the most common form of arthritis in the foot. The joint degenerates and becomes stiff.

Steps, walking, even just standing became agony.

Aching, almost like a stabbing. Any time the toe would bend, it would hurt. So that was pretty much all the time, Logan said.

Usual measures include shoe inserts, rocker sole shoes, anti-inflammatories, and steroid injections.

Logan had a number of operations to cut away some of the toe bones to relieve pressure, but it didnt help, and she got sick from the pain medicines after surgery.

She sought another opinion from West Penn Hospital foot orthopedist Dr. Victor Prisk, who brought up a new synthetic cartilage.

Its a hydrogel, kind of brings in water. Almost like a contact lens can breathe and bring in water, says Dr. Prisk. Its almost squishy, but firm. It has very similar wear characteristics to our own human cartilage.

It was just approved by the FDA a few months ago. So, Logan was a little hesitant.

Not only is it brand new, but its brand new to him, as well. It was his first one if I remember correctly. So that made me a little nervous, and the fact that it was approved the morning of my surgery, which I didnt know until afterwards, Logan said.

The procedure involves drilling the end of the toe bone and inserting the implant with a special instrument.

The other main surgical option is to fuse the bones together. You gain pain relief, but lose motion.

Using a plug of synthetic cartilage has some advantages.

When they come back in for the two-week post-op visit, they have more motion than they had after any other procedure. And they have more pain relief than with the other procedure, which has been amazing even to me, because I did not expect that, says Dr. Prisk. Its a very fast recovery compared to other procedures. Most people are kind of getting into a shoe within three weeks.

Aside from passive stretching prevent stiffness, there is no required physical therapy.

I had to do it a couple times a day. Just pull it back and like hold it there for as long as I could, which was really rough. But, it was necessary, though, says Logan.

In studies, there is a 4 percent failure rate. The implant was removed because the foot pain persisted, not because there were any problems with the implant. Its not for patients with gout, rheumatoid arthritis certain deformities, or for patients under 18.

It is covered by insurance, but out of pocket, the implant itself runs about $3,500.

I have a lot of movement out of it compared to the previous surgeries, Logan said. Im not quite up to running yet, but walking is still good, going up stairs is good. So, now that I can do that without pain, its just a huge change. Its really nice.

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Local woman honored for arthritis advocacy – Brainerd Dispatch

Monday, February 6th, 2017

For more than 8 years, Sundquist has been learning to manage and overcome juvenile rheumatoid arthritisa diagnosis she received when she was 7 years old, according to a news release. Now, as a young adult, she is becoming an outspoken advocate for the Arthritis Foundation.

As the Arthritis Foundation's signature, national fundraising event, the Walk to Cure Arthritis brings together communities to fight arthritis and is a great way to experience the power of giving back to your community. The local Walk to Cure Arthritis is May 20 at the Paul Bunyan Trailhead in Baxter. For more information, visit http://www.walktocurearthritis.org/northernlakes or call Brekka Nessler at 651-229-5368.

In the United States, more than 50 million adults and 300,000 children live with arthritis and it affects one in five Americans. The Walk to Cure Arthritis will help those living with arthritis by supporting programs, research and advocacy initiatives as well as fund crucial research aimed at finding a cure for the disease.

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Fred Lee’s Social Network: Full house for arthritis poker; sipping wine to aid Cambodia children; Year of the … – The Province

Monday, February 6th, 2017

Dianne Watts, the MP for South Surrey White Rock, and Liberal MLA hopeful Karen Wang, right, helped usher in the Year of the Rooster at the Bell Centre for Performing Arts. Fred Lee / Postmedia News

John and Nina Cassils once again fronted their eighth annual Taste the World Gala benefiting Cambodias Angkor Childrens Hospital.

After vacationing and falling in love with Myanmar and its people, the couple has rallied others to visit, and created Taste the World to support Cambodias Ankor Childrens Hospital a non-profit pediatrics teaching hospital and the countrys need for better health education and care.

As usual, a raucous crowd filled the Four Seasons Hotel ballroom in Vancouver for the wine and cheese grazer and fundraising event, held in partnership with the Import Vitners and Spirits Association.

Brenda McAllister and Karen Carmichael steered this years tipple fest the first major wine shindig of 2017. Oenophiles sipped and swirled to their hearts content, while bidding on an array of silent and live auction items in support of the worthy cause.

Event emcees Sophie Lui and Brad Jefferson saw for themselves the need to support the effort. Their travel stories to Southeast Asia along with others in the room buoyed the well-heeled crowd to empty their designer purses and wallets of $180,000 and change.

The impressive tally pushed the Cassils humanitarian efforts beyond the $1 million mark. The evenings proceeds will treat some 35,000 children this year who otherwise would not be able to afford health care, says McAllister.

Nina and John Cassils Taste the World event in Vancouver has generated more than $1 million for Cambodias Angkor Childrens Hospital, thanks to the generosity of friends and British Columbians.

Brenda McAllister and Karen Carmichael held the prestigious positions as event co-chairs of the annual Taste the World tipple fest. Their efforts resulted in $180,000 being raised which will help treat some 35,000 patients at the non-profit pediatrics hospital.

Goldcorps David Garofalo escorted his girlfriend Christie King to the wine and cheese grazer at the Four Seasons Hotel in Vancouver. The eighth annual event netted organizers $180,000 for Angkor Childrens Hospital.

Bill Sanford and Danielle Roberts of Appellation Wine offered oenophiles a taste of their Rocca delle Macie wines from Italy and Lake Sonoma wines from California.

After visiting the Angkor Childrens Hospital in Cambodia, Richard and Heidi Coglon were moved to help the children and families there that otherwise could not afford to access basic health care.

The White Rock Chinese Association ushered in the Year of the Rooster at the Bell Performing Arts Centre.

A gala celebration featuring 80 international and local musicians, singers and dancers, the Spring China at White Rock festival sponsored by local developer Landmark Premier Properties benefited the Peace Arch Hospital Foundation and its $15 million ER Campaign.

Several hundred guests, including a gaggle of glad-handing politicos, took in the multicultural arts extravaganza. The yearly party which began in South Surreys Life Church marked its sophomore year at the Bell Centre; a recognition of the growing Chinese community in White Rock and South Surrey.

Yours truly orchestrated the live auction in advance of the two-hour gala performance led by WRCA president Joanne Ding, Landmark PropertiesRaymond Chen and event emcee Lisa Wu.

Auction proceeds contributed to the $18,000 haul. That number quickly rose when Landmark matched every dollar. Not to be outdone, Dave and Rani Mann of Isle of Mann Construction further matched donations.

Before the final curtain fell on the cultural exchange, $72,000 was presented to hospital foundation chair Siobhan Philips and executive director Stephanie Beck.

Stella Chen and Bingqing Lin were among a host of local and international musicians, singers and dancers that performed at the Spring China at White Rock New Year Festival.

Building community, Raymond Chens Landmark Properties sponsored, and Jennifer Dings White Rock Chinese Association produced, the multicultural extravaganza Spring China at White Rock.

Beneficiary of the Chinese New Year party, Peace Arch Hospital Foundation board chair Siobhan Philips and executive director Stephanie Beck collected a $72,000 cheque for its ER Fundraising Campaign.

More than 650,000 British Columbians young and old live with arthritis. And three out of five people are under the age of 65.

The idea that there are more than 100 types of arthritis, and that many can be devastating, debilitating and even fatal, is shocking.

Putting a spotlight on an underestimated, often invisible disease, the B.C. and Yukon chapter of the Arthritis Society presented its inaugural All-in for Arthritis Poker Gala.

Fronted by party chair Dave Turner, tournament chair Sameer Ismailand executive directorChristine Basque, a capacity crowd filled the Stanley Park Pavilion for the charity poker tournament and a chance to play a hand to send kids with arthritis to summer camp.

Celebrating its 35th year, the Arthritis Camp provides a unique opportunity for children to meet others who understand what its like to grow up with the disorder.

Keynote speakerAdrienne Dalla-Longa knows first hand the magic of the camp. Diagnosed with juvenile arthritis, she had to wear ankle, knee and wrist braces in school, and was prevented from participating in many activities.

Bullied by peers who did not understand why she was unable to play, the camp introduced her to others with shared challenges and highlighted she was not alone in her journey. Dalla-Longas compelling story helped table $85,000 for the society.

Rheumatologist Dr. Jean Gillies was all-in for Samantha Rogers poker charity tournament. The inaugural event raised $85,000 for the Arthritis Societys B.C. and Yukon chapter.

Arthritis ambassador Adrienne Dalla-Longa joined Arthritis Society executive director Christine Basque and gala emcee Dawn Chubai for all the fun and games at the Stanley Park Pavilion.

Tournament chair Sameer Ismail congratulated Clark Wilsons Ryan Tam, the inaugural winner of the Arthritis Societys All-In for Kids Poker Championship. Monies will go toward sending children with arthritis to summer camp.

Drew McArthur, past chair of the national board of The Arthritis Society, and his wife Heather, helped mark the 35th anniversary of the arthritis kids camp, a summer program that gives children with arthritis the chance to meet others who live with similar challenges and to make lasting memories.

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Discovery of new T-cell subtype opens window on rheumatoid … – Science Daily

Monday, February 6th, 2017

A research team led by scientists from Brigham and Women's Hospital (BWH) has carefully scrutinized the immune cells from patients with rheumatoid arthritis, revealing a striking new subset of T-cells that collaborate with other immune cells to drive inflammation in peripheral tissues. The work, which was propelled by technologies that enable the detailed analysis of even a handful of cells, opens a critical window on the biology of the disease and suggests a strategy for the development of more precise, powerful treatments. The study appears in the February 1st advance online edition of the journal Nature.

"While the newest therapies for rheumatoid arthritis have helped transform our ability to treat the disease, they are fairly blunt instruments -- blocking components of the immune system in a non-specific, global way," said first author Deepak Rao, who co-directs the Human Immunology Center at BWH. "Our results help illuminate a path toward treatments that are much more precise and focused only on the most relevant immune cells."

Rheumatoid arthritis is an autoimmune condition in which the immune system attacks the joints, causing inflammation, pain, and eventually destruction of the tissues that make up this essential body part. The disorder affects roughly 1 percent of the world's population, and disproportionately afflicts women. Although there is significant evidence implicating T-cells -- particularly their interactions with B-cells, which produce antibodies -- it has been unclear which T-cell subtypes help orchestrate the damaging immune responses that underlie rheumatoid arthritis.

Rao, together with senior author Michael Brenner, set out to explore these questions by studying patient samples in remarkable detail not achieved in earlier studies. This "disease deconstruction" approach relies on sophisticated technologies, such as mass cytometry, which allowed the researchers to rapidly sift through blood, joint tissue, and the fluid surrounding joints to isolate specific cells, defined by the assortment of molecules on their surfaces. Rao and his colleagues also harnessed RNA sequencing methods that can characterize even very small numbers of cells, revealing which genes are turned on or off.

By using these and other high-tech tools, the researchers homed in on a unique population of T-cells that are highly prevalent in the joints of rheumatoid arthritis patients. These cells, a kind of CD4+ or "helper" T-cell, represent roughly one-quarter of the helper T-cells found in patients' joints. Yet abundance is not their only noteworthy attribute.

"These cells don't adhere to the conventional view of helper T-cells, and that is really interesting," said Rao.

By taking a deep look at these unique helper T-cells, Rao and his colleagues discovered that they display some unusual biological features. These T-cells are programmed to infiltrate parts of the body that are inflamed, and there they stimulate B-cells to produce antibodies. Antibodies are specialized proteins that usually recognize foreign substances and help rally the immune system to eliminate them. In autoimmune diseases, so-called autoantibodies instead recognize normal components of the human body and contribute to tissue damage. The Nature study represents the first detailed description of a type of T-cell with these features.

To extend their initial findings, the researchers seek to understand the signals that coax these cells to develop, and whether they play roles in other autoimmune diseases, such as lupus, multiple sclerosis, and type 1 diabetes. The BWH team also plans to explore whether targeting these unique T-cells hold promise as a treatment for rheumatoid arthritis.

"This work is a remarkable illustration of the power of our disease deconstruction approach," said Brenner, who also directs BWH's Human Immunology Center together with Rao. "We hope it will prove equally illuminating as we apply it to other immune-mediated diseases."

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Materials provided by Brigham and Women's Hospital. Note: Content may be edited for style and length.

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Drug combination effective against chikungunya arthritis in mice … – Science Daily

Monday, February 6th, 2017

Combining a drug for rheumatoid arthritis with one that targets the chikungunya virus can eliminate the signs of chikungunya arthritis in mice in the disease's earliest stage, according to researchers at Washington University School of Medicine in St. Louis.

The findings could lead to a drug therapy for the painful, debilitating condition for which there currently is no treatment.

"We found that combining these two drugs could abolish the signs of arthritis in mice during the acute phase," said Deborah Lenschow, MD, PhD, an associate professor of medicine and the study's co-senior author, referring to the phase in the first weeks after infection.

The study is published Feb. 1 in Science Translational Medicine.

Until about a decade ago, chikungunya virus, which is transmitted by mosquitoes, mainly was restricted to East Africa and South Asia. But in recent years the virus has spread around the world. The first case originating in the Western Hemisphere was reported in late 2013, and by the end of 2015, the virus had infected an estimated 1.8 million people in the Americas.

Chikungunya infection causes fever and severe joint pain, as well as rash, muscle pain and fatigue. The majority of patients continue to experience joint pain six months after infection, and for some, the arthritis continues for years.

"We were seeing people at our rheumatology clinic whose signs and symptoms really mimicked rheumatoid arthritis but who had been infected with chikungunya," Lenschow said. "This raised the question in our minds, 'Would therapeutics we use to treat rheumatoid arthritis be of any benefit to patients with chikungunya arthritis?'"

To find out, Lenschow, co-senior author Michael Diamond, MD, PhD, and colleagues tested a panel of six rheumatoid arthritis drugs -- all approved by the Food and Drug Administration for use in patients -- on mice infected with chikungunya virus.

All six drugs work by suppressing the activity of the immune system. Although different in many ways, rheumatoid arthritis and chikungunya arthritis both involve out-of-control immune activity in the joints.

The researchers injected seven groups of mice with the virus and three days later administered one of the six arthritis drugs or a placebo to each group of mice. A week after infection -- when the mice's arthritis signs were at their peak -- the researchers measured the amount of swelling around the joints as well as the numbers of immune cells and molecules in the affected areas.

Two of the drugs -- abatacept and tofacitinib -- significantly reduced the swelling and the levels of immune cells and molecules. Importantly, the levels of live virus did not increase in the animals given the immunosuppressive arthritis drugs.

"There was a significant concern that administering any immunosuppressive drug would allow the virus to escape from immune control, leading to worse outcomes in the long term," said Diamond, the Herbert S. Gasser Professor of Medicine. "We've seen that with other viruses, but in this case, none of the drugs seemed to exacerbate viral replication. This raises the possibility that these drugs can be safely investigated in humans."

The treatment was only partially successful at resolving the arthritis, however, which led the researchers to test whether adding a human antibody against chikungunya virus could improve the effectiveness.

As before, the researchers infected mice with the virus and three days later dosed them with the arthritis drug abatacept, the antiviral drug or both. Each drug individually reduced joint swelling a week after infection. But when abatacept and the antiviral drug were used together, the joint swelling and the infectious virus in the animals' joints were eliminated.

"We saw real improvement in the acute phase, but unfortunately, the drug interventions we tried failed to correct the chronic phase," Diamond said.

In humans, the chronic phase of chikungunya arthritis starts three weeks after initial infection and lasts as long as the patient continues to experience joint pain, which can be three or four years. During the chronic phase, infectious virus is no longer detectable in the joints, but viral genetic material persists and may be sufficient to trigger an ongoing immune response, causing the tissue damage that patients perceive as arthritis.

The researchers found a similar pattern in the mice treated with the drug combination: By four weeks after infection, live virus was no longer present in the animals' joints, but viral genetic material remained, suggesting that the drugs had not eliminated the chronic phase of the disease.

It is possible that a treatment that reduces arthritis symptoms in the first weeks after infection could lower the chance that the disease becomes chronic, but no data has yet been published for or against the possibility. Still, any effective treatment, even if short-lived, would be a boon for chikungunya patients, who currently have no proven treatment options. Lenschow has discussed beginning a human study with colleagues in Brazil, but plans are not yet finalized.

"In those first weeks, people are really very sick with a high fever and a lot of pain, so if further studies show that this combination treatment is effective in humans, that will have real benefits for patients," Diamond said. "As for the chronic phase, we're going to continue looking for other treatment strategies."

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Taking on Arthritis: 3 Unique Ideas for Pain Relief – Care2.com

Monday, February 6th, 2017

Few people escape the daily aches and pains that come with aging. But persistent joint pain and stiffness can be a sign of something more: arthritis.

Arthritis affects more than 50 million adults and 300,000 children, according tothe Arthritis Foundation, making it the most common cause of disabilityin America. Maybe you know a parent or grandparent who suffers from arthritis; ormaybe you deal with it yourself.

There are two types of arthritis: rheumatoid arthritis, which is an inflammatory disease, and osteoarthritis, a type that is caused by the wearing away of joint cartillage. Either way, the most common symptom is pain and stiffness around the joints knees, hips, hands, etc.

Most people who suffer from arthritis turn to solutions like pain medications and stretching exercises to find relief. However, there are a number of other natural ways to soothe arthritis pain!

Here are a few oddball ideas you may not have heard of before.

3 Unique Ideas for Arthritis Pain Relief

Drink White Willow Tea

Before there was aspirin, white willow tea was the pain killer of choice. In fact, this remedy stretches all the way back to Hippocrates, a Greek physician who was operating back in 5th century BC!

White willow contains an active ingredient called salicin, a chemical that is converted in the body into salicylic acid. Sound familiar? Its essentially a less irritating form of acetyl salicylic acid, theactive ingredient in aspirin.

How to Make White Willow Tea:

Massage Sore Joints with Olive Oil

Extra virgin olive oil (sometimes abbreviated to EVOO)has anti-inflammatory properties that can actually inhibit inflammation just like aspirin or Advil.

To soothe your joints, gently massage a bit of cold-pressed, extra virgin olive oil into your sore joints, twice daily or more. You can also take a spoonful or two internally to reap its benefits as a reducer of swelling.

Related: 4 Myths About Olive Oil Debunked

Enjoy Turmeric-Based Foods

Turmeric(an earthy yellow spice you may recognize from Indian and East Asian dishes) is well-known for its anti-inflammatory properties. Its active ingredient is a naturally-occurring chemical called curcumin, which is a powerful antioxidant that lowers the levels of the enzymes responsible for causing inflammation.

There are several ways to enjoy turmeric, so stock up on those recipes; however, the simplest way to enjoy its benefits is through delicious golden milk or a lovely turmeric and ginger tea.

How to Make Turmeric & Ginger Tea:

Arthritis is a challenging, painful disease that can be hard to manage, but you dont have to suffer without aid. Test these three natural remedies throughout your day and trust what works. You may just find the relief youve been looking for.

How do you manage arthritis in your body? Do you have any tips that may help someone else find relief?

Disclaimer: The views expressed above are solely those of the author and may not reflect those of Care2, Inc., its employees or advertisers.

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Rheumatoid Arthritis: An Introduction

Sunday, February 5th, 2017

Rheumatoid arthritis (RA) is starting to cement itself as a debilitating disease that affects people of all ages.1 In fact, its now the third most common type of arthritis, in terms of incidence, behind osteoarthritis and gout.2

According to the Arthritis Foundation, as many as 1.5 million people in the United States are affected by rheumatoid arthritis, with 41 out of 100,000 people being diagnosed with the disease annually.

Women are three times more likely to have rheumatoid arthritis, commonly occurring between the ages of 30 and 60. Men are also prone to experiencing the disease, but at a later age in their lives.3

Rheumatoid arthritis accounts for 22 percent of deaths from arthritis and other rheumatic conditions in the U.S., as noted in a report entitled Science has ARTHRITIS on the Run , written by Dr. Walter G. Barr and published by the Arthritis Foundation.4

Globally, rheumatoid arthritis is said to affect 1 about percent of the population. While this seems like a small number, its not an amount that should be taken lightly, since in other countries, RA is already gaining ground.

In a report published in 2009, The Australian Institute of Health and Welfare Agency stated that around 400,000 Australians were diagnosed with rheumatoid arthritis.5 That number rose slightly to 445,000 following self-reported estimates in 2011 to 2012.6

Meanwhile, information by Arthritis Research U.K. published in 2014 showed that around 400,000 adults in the U.K. already have rheumatoid arthritis, with 20,000 new patients being diagnosed every year.7

In 2016, Glenn Frey, co-founder and front man of the band The Eagles passed away at age 67 due to complications from rheumatoid arthritis, acute ulcerative colitis, and pneumonia. But what ultimately played a part in his untimely demise was the rheumatoid arthritis medication he was using.

The thing about rheumatoid arthritis is that one can heal from it if the disease is treated immediately, but in Freys case, the medication that was supposed to help him heal didnt work, but instead set him up for devastating effects.

This is why if you use or know someone who uses rheumatoid arthritis medications, it pays to be vigilant as common treatment protocols used for RA patients nowadays can pose health risks and lead to serious consequences.

Not all of the drugs in the market used to treat different diseases are as efficient and effective as they claim to be.

The good news is that an autoimmune disease like rheumatoid arthritis, and the pain that arises from it, can be treated naturally. Read this guide and get all the information you need to know about rheumatoid arthritis.

What Is Rheumatoid Arthritis?

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Rheumatoid Arthritis – National Library of Medicine – PubMed …

Monday, December 19th, 2016

Evidence reviews Antimalarials for treating rheumatoid arthritis

Antimalarials have been used for the treatment of rheumatoid arthritis (RA) for several decades. This review found four trials, with 300 patients receiving hydrochloroquine and 292 receiving placebo. A benefit was observed in the patients taking hydroxychloroquine compared to placebo. There was no difference between the two groups in terms of those who had to withdraw from trials due to side effects.

The purpose was to examine the effectiveness of patient education interventions on health status (pain, functional disability, psychological wellbeing and disease activity) in patients with rheumatoid arthritis (RA). Patient education had a small beneficial effect at first followup for disability, joint counts, patient global assessment, psychological status, and depression. At final followup (314 months) no evidence of significant benefits was found.

In rheumatoid arthritis (RA), the joints are swollen, stiff and painful. Nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen are often recommended to ease the pain and swelling in the joints. Paracetamol (also known as acetaminophen) is another type of medication to relieve pain in RA.

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Antimalarials have been used for the treatment of rheumatoid arthritis (RA) for several decades. This review found four trials, with 300 patients receiving hydrochloroquine and 292 receiving placebo. A benefit was observed in the patients taking hydroxychloroquine compared to placebo. There was no difference between the two groups in terms of those who had to withdraw from trials due to side effects.

The purpose was to examine the effectiveness of patient education interventions on health status (pain, functional disability, psychological wellbeing and disease activity) in patients with rheumatoid arthritis (RA). Patient education had a small beneficial effect at first followup for disability, joint counts, patient global assessment, psychological status, and depression. At final followup (314 months) no evidence of significant benefits was found.

In rheumatoid arthritis (RA), the joints are swollen, stiff and painful. Nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen are often recommended to ease the pain and swelling in the joints. Paracetamol (also known as acetaminophen) is another type of medication to relieve pain in RA.

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Psoriatic arthritis – Wikipedia

Wednesday, December 14th, 2016

Psoriatic arthritis (also arthritis psoriatica, arthropathic psoriasis or psoriatic arthropathy) is a type of inflammatory arthritis[1][2] that will develop in between 6 and 42% of people who have the chronic skin condition psoriasis.[3] Psoriatic arthritis is classified as a seronegative spondyloarthropathy and therefore occurs more commonly in patients with tissue type HLA-B27.

Pain, swelling, or stiffness in one or more joints is commonly present in psoriatic arthritis.[4] Psoriatic arthritis is inflammatory, and affected joints are generally red or warm to the touch.[4] Asymmetrical oligoarthritis, defined as inflammation affecting one to four joints during the first six months of disease, is present in 70% of cases. However, in 15% of cases the arthritis is symmetrical. The joints of the hand that are involved in psoriasis are the proximal interphalangeal (PIP), the distal interphalangeal (DIP), the metacarpophalangeal (MCP), and the wrist. Involvement of the distal interphalangeal joints (DIP) is a characteristic feature and is present in 15% of cases.

In addition to affecting the joints of the hands and wrists, psoriatic arthritis may affect the fingers, nails, and skin. Sausage-like swelling in the fingers or toes, known as dactylitis, may occur.[4] Psoriasis can also cause changes to the nails, such as pitting or separation from the nail bed,[4]onycholysis, hyperkeratosis under the nails, and horizontal ridging.[5] Psoriasis classically presents with scaly skin lesions, which are most commonly seen over extensor surfaces such as the scalp, natal cleft and umbilicus.

In psoriatic arthritis, pain can occur in the area of the sacrum (the lower back, above the tailbone),[4] as a result of sacroiliitis or spondylitis, which is present in 40% of cases. Pain can occur in and around the feet and ankles, especially enthesitis in the Achilles tendon (inflammation of the Achilles tendon where it inserts into the bone) or plantar fasciitis in the sole of the foot.[4]

Along with the above noted pain and inflammation, there is extreme exhaustion that does not go away with adequate rest. The exhaustion may last for days or weeks without abatement. Psoriatic arthritis may remain mild, or may progress to more destructive joint disease. Periods of active disease, or flares, will typically alternate with periods of remission. In severe forms, psoriatic arthritis may progress to arthritis mutilans[6] which on X-ray gives a "pencil-in-cup" appearance.

Because prolonged inflammation can lead to joint damage, early diagnosis and treatment to slow or prevent joint damage is recommended.[7]

The exact causes are not yet known, but a number of genetic associations have been identified in a genome-wide association study of psoriasis and psoriatic arthritis including HLA-B27.[8][9]

There is no definitive test to diagnose psoriatic arthritis. Symptoms of psoriatic arthritis may closely resemble other diseases, including rheumatoid arthritis. A rheumatologist (a doctor specializing in diseases affecting the joints) may use physical examinations, health history, blood tests and x-rays to accurately diagnose psoriatic arthritis.

Factors that contribute to a diagnosis of psoriatic arthritis include:

Other symptoms that are more typical of psoriatic arthritis than other forms of arthritis include inflammation in the Achilles tendon (at the back of the heel) or the Plantar fascia (bottom of the feet), and dactylitis (sausage-like swelling of the fingers or toes).[10]

Magnetic resonance image of the index finger in psoriatic arthritis (mutilans form). Shown is a T2 weighted fat suppressed sagittal image. Focal increased signal (probable erosion) is seen at the base of the middle phalanx (long thin arrow). There is synovitis at the proximal interphalangeal joint (long thick arrow) plus increased signal in the overlying soft tissues indicating oedema (short thick arrow). There is also diffuse bone oedema (short thin arrows) involving the head of the proximal phalanx and extending distally down the shaft.

Magnetic resonance images of the fingers in psoriatic arthritis. Shown are T1 weighted axial (a) pre-contrast and (b) post-contrast images exhibiting dactylitis due to flexor tenosynovitis at the second finger with enhancement and thickening of the tendon sheath (large arrow). Synovitis is seen in the fourth proximal interphalangeal joint (small arrow).

(a) T1-weighted and (b) short tau inversion recovery (STIR) magnetic resonance images of lumbar and lower thoracic spine in psoriatic arthritis. Signs of active inflammation are seen at several levels (arrows). In particular, anterior spondylitis is seen at level L1/L2 and an inflammatory Andersson lesion at the upper vertebral endplate of L3.

Magnetic resonance images of sacroiliac joints. Shown are T1-weighted semi-coronal magnetic resonance images through the sacroiliac joints (a) before and (b) after intravenous contrast injection. Enhancement is seen at the right sacroiliac joint (arrow, left side of image), indicating active sacroiliitis.

There are five main types of psoriatic arthritis:

The underlying process in psoriatic arthritis is inflammation; therefore, treatments are directed at reducing and controlling inflammation. Milder cases of psoriatic arthritis may be treated with NSAIDs alone; however, there is a trend toward earlier use of disease-modifying antirheumatic drugs or biological response modifiers to prevent irreversible joint destruction.

Typically the medications first prescribed for psoriatic arthritis are NSAIDs such as ibuprofen and naproxen, followed by more potent NSAIDs like diclofenac, indomethacin, and etodolac. NSAIDs can irritate the stomach and intestine, and long-term use can lead to gastrointestinal bleeding.[11][12] Coxibs (COX-2 inhibitors) e.g. Celecoxib or Etoricoxib, are associated with a statistically significant 50 to 66% relative risk reduction in gastrointestinal ulcers and bleeding complications compared to traditional NSAIDs, but carry an increased rate of cardiovascular events such as myocardial infarction (MI) or heart attack, and stroke.[13][14] Both COX-2 inhibitors and other non-selective NSAIDS have potential adverse effects that include damage to the kidneys.

These are used in persistent symptomatic cases without exacerbation. Rather than just reducing pain and inflammation, this class of drugs helps limit the amount of joint damage that occurs in psoriatic arthritis. Most DMARDs act slowly and may take weeks or even months to take full effect. Drugs such as methotrexate or leflunomide are commonly prescribed; other DMARDS used to treat psoriatic arthritis include cyclosporin, azathioprine, and sulfasalazine. These immunosuppressant drugs can also reduce psoriasis skin symptoms but can lead to liver and kidney problems and an increased risk of serious infection.

The most recent class of treatment is called biological response modifiers or biologics has been developed using recombinant DNA technology. Biologic medications are derived from living cells cultured in a laboratory. Unlike traditional DMARDS that affect the entire immune system, biologics target specific parts of the immune system. They are given by injection or intravenous (IV) infusion.

Biologics prescribed for psoriatic arthritis are TNF- inhibitors, including infliximab, etanercept, golimumab, certolizumab pegol and adalimumab, as well as the IL-12/IL-23 inhibitor ustekinumab.

Biologics may increase the risk of minor and serious infections.[citation needed] More rarely, they may be associated with nervous system disorders, blood disorders or certain types of cancer.[citation needed]

A first-in-class treatment option for the management of psoriatic arthritis, apremilast is a small molecule phosphodiesterase-4 inhibitor approved for use by the FDA in 2014. By inhibiting PDE4, an enzyme which breaks down cyclic adenosine monophosphate, cAMP levels rise, resulting in the down-regulation of various pro-inflammatory factors inlcuding TNF- and the up-regulation of anti-inflammatory factor interleukin 10.

It is given in tablet form and taken by mouth. Side effects include headache, back pain, nausea, diarrhea, fatigue, nasopharyngitis and upper respiratory tract infections, as well as depression and weight loss.

Patented in 2014 and manufactured by Celgene, there is no current generic equivalent available on the market.

A review found tentative evidence of benefit of low level laser therapy and concluded that it could be considered for relief of pain and stiffness associated RA.[15]

Retinoid etretinate is effective for both arthritis and skin lesions. Photochemotherapy with methoxy psoralen and long wave ultraviolet light (PUVA) are used for severe skin lesions. Doctors may use joint injections with corticosteroids in cases where one joint is severely affected. In psoriatic arthritis patients with severe joint damage orthopedic surgery may be implemented to correct joint destruction, usually with use of a joint replacement. Surgery is effective for pain alleviation, correcting joint disfigurement, and reinforcing joint usefulness and strength.

Seventy percent of people who develop psoriatic arthritis first show signs of psoriasis on the skin, 15 percent develop skin psoriasis and arthritis at the same time, and 15 percent develop skin psoriasis following the onset of psoriatic arthritis.[16]

Psoriatic arthritis can develop in people who have any level severity of psoriatic skin disease, ranging from mild to very severe.[17]

Psoriatic arthritis tends to appear about 10 years after the first signs of psoriasis. For the majority of people this is between the ages of 30 and 55, but the disease can also affect children. The onset of psoriatic arthritis symptoms before symptoms of skin psoriasis is more common in children than adults.[18]

More than 80% of patients with psoriatic arthritis will have psoriatic nail lesions characterized by nail pitting, separation of the nail from the underlying nail bed, ridging and cracking, or more extremely, loss of the nail itself (onycholysis).[18]

Men and women are equally affected by this condition. Like psoriasis, psoriatic arthritis is more common among Caucasians than Africans or Asians.[19]

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Induced pluripotent stem cell – Wikipedia

Tuesday, December 13th, 2016

Induced pluripotent stem cells (also known as iPS cells or iPSCs) are a type of pluripotent stem cell that can be generated directly from adult cells. The iPSC technology was pioneered by Shinya Yamanakas lab in Kyoto, Japan, who showed in 2006 that the introduction of four specific genes encoding transcription factors could convert adult cells into pluripotent stem cells.[1] He was awarded the 2012 Nobel Prize along with Sir John Gurdon "for the discovery that mature cells can be reprogrammed to become pluripotent." [2]

Pluripotent stem cells hold great promise in the field of regenerative medicine. Because they can propagate indefinitely, as well as give rise to every other cell type in the body (such as neurons, heart, pancreatic, and liver cells), they represent a single source of cells that could be used to replace those lost to damage or disease.

The most well-known type of pluripotent stem cell is the embryonic stem cell. However, since the generation of embryonic stem cells involves destruction (or at least manipulation) [3] of the pre-implantation stage embryo, there has been much controversy surrounding their use. Further, because embryonic stem cells can only be derived from embryos, it has so far not been feasible to create patient-matched embryonic stem cell lines.

Since iPSCs can be derived directly from adult tissues, they not only bypass the need for embryos, but can be made in a patient-matched manner, which means that each individual could have their own pluripotent stem cell line. These unlimited supplies of autologous cells could be used to generate transplants without the risk of immune rejection. While the iPSC technology has not yet advanced to a stage where therapeutic transplants have been deemed safe, iPSCs are readily being used in personalized drug discovery efforts and understanding the patient-specific basis of disease.[4]

iPSCs are typically derived by introducing products of specific set of pluripotency-associated genes, or reprogramming factors, into a given cell type. The original set of reprogramming factors (also dubbed Yamanaka factors) are the transcription factors Oct4 (Pou5f1), Sox2, cMyc, and Klf4. While this combination is most conventional in producing iPSCs, each of the factors can be functionally replaced by related transcription factors, miRNAs, small molecules, or even non-related genes such as lineage specifiers.

iPSC derivation is typically a slow and inefficient process, taking 12 weeks for mouse cells and 34 weeks for human cells, with efficiencies around 0.01%0.1%. However, considerable advances have been made in improving the efficiency and the time it takes to obtain iPSCs. Upon introduction of reprogramming factors, cells begin to form colonies that resemble pluripotent stem cells, which can be isolated based on their morphology, conditions that select for their growth, or through expression of surface markers or reporter genes.

Induced pluripotent stem cells were first generated by Shinya Yamanaka's team at Kyoto University, Japan, in 2006.[1] They hypothesized that genes important to embryonic stem cell (ESC) function might be able to induce an embryonic state in adult cells. They chose twenty-four genes previously identified as important in ESCs and used retroviruses to deliver these genes to mouse fibroblasts. The fibroblasts were engineered so that any cells reactivating the ESC-specific gene, Fbx15, could be isolated using antibiotic selection.

Upon delivery of all twenty-four factors, ESC-like colonies emerged that reactivated the Fbx15 reporter and could propagate indefinitely. To identify the genes necessary for reprogramming, the researchers removed one factor at a time from the pool of twenty-four. By this process, they identified four factors, Oct4, Sox2, cMyc, and Klf4, which were each necessary and together sufficient to generate ESC-like colonies under selection for reactivation of Fbx15.

Similar to ESCs, these iPSCs had unlimited self-renewal and were pluripotent, contributing to lineages from all three germ layers in the context of embryoid bodies, teratomas, and fetal chimeras. However, the molecular makeup of these cells, including gene expression and epigenetic marks, was somewhere between that of a fibroblast and an ESC, and the cells failed to produce viable chimeras when injected into developing embryos.

In June 2007, three separate research groups, including that of Yamanaka's, a Harvard/University of California, Los Angeles collaboration, and a group at MIT, published studies that substantially improved on the reprogramming approach, giving rise to iPSCs that were indistinguishable from ESCs. Unlike the first generation of iPSCs, these second generation iPSCs produced viable chimeric mice and contributed to the mouse germline, thereby achieving the 'gold standard' for pluripotent stem cells.

These second-generation iPSCs were derived from mouse fibroblasts by retroviral-mediated expression of the same four transcription factors (Oct4, Sox2, cMyc, Klf4). However, instead of using Fbx15 to select for pluripotent cells, the researchers used Nanog, a gene that is functionally important in ESCs. By using this different strategy, the researchers created iPSCs that were functionally identical to ESCs.[5][6][7][8]

Reprogramming of human cells to iPSCs was reported in November 2007 by two independent research groups: Shinya Yamanaka of Kyoto University, Japan, who pioneered the original iPSC method, and James Thomson of University of Wisconsin-Madison who was the first to derive human embryonic stem cells. With the same principle used in mouse reprogramming, Yamanaka's group successfully transformed human fibroblasts into iPSCs with the same four pivotal genes, OCT4, SOX2, KLF4, and C-MYC, using a retroviral system,[9] while Thomson and colleagues used a different set of factors, OCT4, SOX2, NANOG, and LIN28, using a lentiviral system.[10]

Obtaining fibroblasts to produce iPSCs involves a skin biopsy, and there has been a push towards identifying cell types that are more easily accessible.[11][12] In 2008, iPSCs were derived from human keratinocytes, which could be obtained from a single hair pluck.[13][14] In 2010, iPSCs were derived from peripheral blood cells,[15][16] and in 2012, iPSCs were made from renal epithelial cells in the urine.[17]

Other considerations for starting cell type include mutational load (for example, skin cells may harbor more mutations due to UV exposure),[11][12] time it takes to expand the population of starting cells,[11] and the ability to differentiate into a given cell type.[18]

[citation needed]

The generation of iPS cells is crucially dependent on the transcription factors used for the induction.

Oct-3/4 and certain products of the Sox gene family (Sox1, Sox2, Sox3, and Sox15) have been identified as crucial transcriptional regulators involved in the induction process whose absence makes induction impossible. Additional genes, however, including certain members of the Klf family (Klf1, Klf2, Klf4, and Klf5), the Myc family (c-myc, L-myc, and N-myc), Nanog, and LIN28, have been identified to increase the induction efficiency.

Although the methods pioneered by Yamanaka and others have demonstrated that adult cells can be reprogrammed to iPS cells, there are still challenges associated with this technology:

The table at right summarizes the key strategies and techniques used to develop iPS cells over the past half-decade. Rows of similar colors represents studies that used similar strategies for reprogramming.

One of the main strategies for avoiding problems (1) and (2) has been to use small compounds that can mimic the effects of transcription factors. These molecule compounds can compensate for a reprogramming factor that does not effectively target the genome or fails at reprogramming for another reason; thus they raise reprogramming efficiency. They also avoid the problem of genomic integration, which in some cases contributes to tumor genesis. Key studies using such strategy were conducted in 2008. Melton et al. studied the effects of histone deacetylase (HDAC) inhibitor valproic acid. They found that it increased reprogramming efficiency 100-fold (compared to Yamanakas traditional transcription factor method).[32] The researchers proposed that this compound was mimicking the signaling that is usually caused by the transcription factor c-Myc. A similar type of compensation mechanism was proposed to mimic the effects of Sox2. In 2008, Ding et al. used the inhibition of histone methyl transferase (HMT) with BIX-01294 in combination with the activation of calcium channels in the plasma membrane in order to increase reprogramming efficiency.[33] Deng et al. of Beijing University reported on July 2013 that induced pluripotent stem cells can be created without any genetic modification. They used a cocktail of seven small-molecule compounds including DZNep to induce the mouse somatic cells into stem cells which they called CiPS cells with the efficiency at 0.2% comparable to those using standard iPSC production techniques. The CiPS cells were introduced into developing mouse embryos and were found to contribute to all major cells types, proving its pluripotency.[34][35]

Ding et al. demonstrated an alternative to transcription factor reprogramming through the use of drug-like chemicals. By studying the MET (mesenchymal-epithelial transition) process in which fibroblasts are pushed to a stem-cell like state, Dings group identified two chemicals ALK5 inhibitor SB431412 and MEK (mitogen-activated protein kinase) inhibitor PD0325901 which was found to increase the efficiency of the classical genetic method by 100 fold. Adding a third compound known to be involved in the cell survival pathway, Thiazovivin further increases the efficiency by 200 fold. Using the combination of these three compounds also decreased the reprogramming process of the human fibroblasts from four weeks to two weeks. [36][37]

In April 2009, it was demonstrated that generation of iPS cells is possible without any genetic alteration of the adult cell: a repeated treatment of the cells with certain proteins channeled into the cells via poly-arginine anchors was sufficient to induce pluripotency.[38] The acronym given for those iPSCs is piPSCs (protein-induced pluripotent stem cells).

Another key strategy for avoiding problems such as tumor genesis and low throughput has been to use alternate forms of vectors: adenovirus, plasmids, and naked DNA and/or protein compounds.

In 2008, Hochedlinger et al. used an adenovirus to transport the requisite four transcription factors into the DNA of skin and liver cells of mice, resulting in cells identical to ESCs. The adenovirus is unique from other vectors like viruses and retroviruses because it does not incorporate any of its own genes into the targeted host and avoids the potential for insertional mutagenesis.[39] In 2009, Freed et al. demonstrated successful reprogramming of human fibroblasts to iPS cells.[40] Another advantage of using adenoviruses is that they only need to present for a brief amount of time in order for effective reprogramming to take place.

Also in 2008, Yamanaka et al. found that they could transfer the four necessary genes with a plasmid.[41] The Yamanaka group successfully reprogrammed mouse cells by transfection with two plasmid constructs carrying the reprogramming factors; the first plasmid expressed c-Myc, while the second expressed the other three factors (Oct4, Klf4, and Sox2). Although the plasmid methods avoid viruses, they still require cancer-promoting genes to accomplish reprogramming. The other main issue with these methods is that they tend to be much less efficient compared to retroviral methods. Furthermore, transfected plasmids have been shown to integrate into the host genome and therefore they still pose the risk of insertional mutagenesis. Because non-retroviral approaches have demonstrated such low efficiency levels, researchers have attempted to effectively rescue the technique with what is known as the PiggyBac Transposon System. Several studies have demonstrated that this system can effectively deliver the key reprogramming factors without leaving footprint mutations in the host cell genome. The PiggyBac Transposon System involves the re-excision of exogenous genes, which eliminates the issue of insertional mutagenesis. [42]

In January 2014, two articles were published claiming that a type of pluripotent stem cell can be generated by subjecting the cells to certain types of stress (bacterial toxin, a low pH of 5.7, or physical squeezing); the resulting cells were called STAP cells, for stimulus-triggered acquisition of pluripotency.[43]

In light of difficulties that other labs had replicating the results of the surprising study, in March 2014, one of the co-authors has called for the articles to be retracted.[44] On 4 June 2014, the lead author, Obokata agreed to retract both the papers [45] after she was found to have committed research misconduct as concluded in an investigation by RIKEN on 1 April 2014.[46]

MicroRNAs are short RNA molecules that bind to complementary sequences on messenger RNA and block expression of a gene. Measuring variations in microRNA expression in iPS cells can be used to predict their differentiation potential.[47] Addition of microRNAs can also be used to enhance iPS potential. Several mechanisms have been proposed.[47] ES cell-specific microRNA molecules (such as miR-291, miR-294 and miR-295) enhance the efficiency of induced pluripotency by acting downstream of c-Myc.[48]microRNAs can also block expression of repressors of Yamanakas four transcription factors, and there may be additional mechanisms induce reprogramming even in the absence of added exogenous transcription factors.[47]

Induced pluripotent stem cells are similar to natural pluripotent stem cells, such as embryonic stem (ES) cells, in many aspects, such as the expression of certain stem cell genes and proteins, chromatin methylation patterns, doubling time, embryoid body formation, teratoma formation, viable chimera formation, and potency and differentiability, but the full extent of their relation to natural pluripotent stem cells is still being assessed.[49]

Gene expression and genome-wide H3K4me3 and H3K27me3 were found to be extremely similar between ES and iPS cells.[50][citation needed] The generated iPSCs were remarkably similar to naturally isolated pluripotent stem cells (such as mouse and human embryonic stem cells, mESCs and hESCs, respectively) in the following respects, thus confirming the identity, authenticity, and pluripotency of iPSCs to naturally isolated pluripotent stem cells:

Recent achievements and future tasks for safe iPSC-based cell therapy are collected in the review of Okano et al.[62]

The task of producing iPS cells continues to be challenging due to the six problems mentioned above. A key tradeoff to overcome is that between efficiency and genomic integration. Most methods that do not rely on the integration of transgenes are inefficient, while those that do rely on the integration of transgenes face the problems of incomplete reprogramming and tumor genesis, although a vast number of techniques and methods have been attempted. Another large set of strategies is to perform a proteomic characterization of iPS cells.[63] Further studies and new strategies should generate optimal solutions to the five main challenges. One approach might attempt to combine the positive attributes of these strategies into an ultimately effective technique for reprogramming cells to iPS cells.

Another approach is the use of iPS cells derived from patients to identify therapeutic drugs able to rescue a phenotype. For instance, iPS cell lines derived from patients affected by ectodermal dysplasia syndrome (EEC), in which the p63 gene is mutated, display abnormal epithelial commitment that could be partially rescued by a small compound[64]

An attractive feature of human iPS cells is the ability to derive them from adult patients to study the cellular basis of human disease. Since iPS cells are self-renewing and pluripotent, they represent a theoretically unlimited source of patient-derived cells which can be turned into any type of cell in the body. This is particularly important because many other types of human cells derived from patients tend to stop growing after a few passages in laboratory culture. iPS cells have been generated for a wide variety of human genetic diseases, including common disorders such as Down syndrome and polycystic kidney disease.[65][66] In many instances, the patient-derived iPS cells exhibit cellular defects not observed in iPS cells from healthy patients, providing insight into the pathophysiology of the disease.[67] An international collaborated project, StemBANCC, was formed in 2012 to build a collection of iPS cell lines for drug screening for a variety of disease. Managed by the University of Oxford, the effort pooled funds and resources from 10 pharmaceutical companies and 23 universities. The goal is to generate a library of 1,500 iPS cell lines which will be used in early drug testing by providing a simulated human disease environment.[68] Furthermore, combining hiPSC technology and genetically-encoded voltage and calcium indicators provided a large-scale and high-throughput platform for cardiovascular drug safety screening.[69]

A proof-of-concept of using induced pluripotent stem cells (iPSCs) to generate human organ for transplantation was reported by researchers from Japan. Human liver buds (iPSC-LBs) were grown from a mixture of three different kinds of stem cells: hepatocytes (for liver function) coaxed from iPSCs; endothelial stem cells (to form lining of blood vessels) from umbilical cord blood; and mesenchymal stem cells (to form connective tissue). This new approach allows different cell types to self-organize into a complex organ, mimicking the process in fetal development. After growing in vitro for a few days, the liver buds were transplanted into mice where the liver quickly connected with the host blood vessels and continued to grow. Most importantly, it performed regular liver functions including metabolizing drugs and producing liver-specific proteins. Further studies will monitor the longevity of the transplanted organ in the host body (ability to integrate or avoid rejection) and whether it will transform into tumors.[70][71] Using this method, cells from one mouse could be used to test 1,000 drug compounds to treat liver disease, and reduce animal use by up to 50,000.[72]

Embryonic cord-blood cells were induced into pluripotent stem cells using plasmid DNA. Using cell surface endothelial/pericytic markers CD31 and CD146, researchers identified 'vascular progenitor', the high-quality, multipotent vascular stem cells. After the iPS cells were injected directly into the vitreous of the damaged retina of mice, the stem cells engrafted into the retina, grew and repaired the vascular vessels.[73][74]

Labelled iPSCs-derived NSCs injected into laboratory animals with brain lesions were shown to migrate to the lesions and some motor function improvement was observed.[75]

Although a pint of donated blood contains about two trillion red blood cells and over 107 million blood donations are collected globally, there is still a critical need for blood for transfusion. In 2014, type O red blood cells were synthesized at the Scottish National Blood Transfusion Service from iPSC. The cells were induced to become a mesoderm and then blood cells and then red blood cells. The final step was to make them eject their nuclei and mature properly. Type O can be transfused into all patients. Human clinical trials were not expected to begin before 2016.[76]

The first human clinical trial using autologous iPSCs was approved by the Japan Ministry Health and was to be conducted in 2014 in Kobe. However the trial was suspended after Japan's new regenerative medicine laws came into effect last November.[77] iPSCs derived from skin cells from six patients suffering from wet age-related macular degeneration were to be reprogrammed to differentiate into retinal pigment epithelial (RPE) cells. The cell sheet would be transplanted into the affected retina where the degenerated RPE tissue was excised. Safety and vision restoration monitoring would last one to three years.[78][79] The benefits of using autologous iPSCs are that there is theoretically no risk of rejection and it eliminates the need to use embryonic stem cells.[79]

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Rheumatoid Arthritis. Symptoms of Arthritis and … – Patient

Tuesday, November 22nd, 2016

What is rheumatoid arthritis (RA)?

Arthritis means inflammation of joints. RA is a common form of arthritis. (There are various other causes of arthritis and RA is just one cause.) About 1 in 100 people develop RA at some stage in their lives. It can happen to anyone. It is not an hereditary disease. It can develop at any age, but most commonly starts between the ages of 40 and 60. It is about three times more common in women than in men.

A joint is where two bones meet. Joints allow movement and flexibility of various parts of the body. The movement of the bones is caused by muscles which pull on tendons that are attached to bone. Cartilage covers the end of bones. Between the cartilage of two bones that form a joint there is a small amount of thick fluid called synovial fluid. This lubricates the joint, which allows smooth movement between the bones.

The synovium is the tissue that surrounds a joint. Synovial fluid is made by cells of the synovium. The outer part of the synovium is called the capsule. This is tough, gives the joint stability, and stops the bones from moving out of joint. Surrounding ligaments and muscles also help to give support and stability to joints.

RA is thought to be an autoimmune disease. The immune system normally makes antibodies (small proteins) to attack bacteria, viruses, and other germs. In people with autoimmune diseases, the immune system makes antibodies against tissues of the body. It is not clear why this happens. Some people have a tendency to develop autoimmune diseases. In such people, something might trigger the immune system to attack the body's own tissues. The trigger is not known.

In people with RA, antibodies are formed against the tissue that surrounds each joint (the synovium). This causes inflammation in and around affected joints. Over time, the inflammation can damage the joint, the cartilage, and parts of the bone near to the joint.

The most commonly affected joints are the small joints of the fingers, thumbs, wrists, feet, and ankles. However, any joint may be affected. The knees are quite commonly affected. Less commonly, the hips, shoulders, elbows, and neck are involved. It is often symmetrical. So, for example, if a joint is affected in a right arm, the same joint in the left arm is also often affected. In some people, just a few joints are affected. In others, many joints are involved.

The common main symptoms are pain and stiffness of affected joints. The stiffness is usually worse first thing in the morning, or after you have been resting. The inflammation causes swelling around the affected joints.

These are known as extra-articular symptoms of RA (meaning outside of the joints). A variety of symptoms may occur. The cause of some of these is not fully understood:

In most cases the symptoms develop gradually - over several weeks or so. Typically, you may first develop some stiffness in the hands, wrists, or soles of the feet in the morning, which eases by mid-day. This may come and go for a while, but then becomes a regular occurence. You may then notice some pain and swelling in the same joints. More joints such as the knees may then become affected.

In a small number of cases, less common patterns are seen. For example:

The severity of RA can vary greatly from person to person. It is usually a chronic relapsing condition. Chronic means that it is persistent. Relapsing means that at times the disease flares up (relapses), and at other times it settles down. There is usually no apparent reason why the inflammation may flare up for a while, and then settle down.

If untreated, most people with RA have this pattern of flare-ups followed by better spells. In some people, months or even years may go by between flare-ups. Some damage may be done to affected joints during each flare-up. The amount of disability which develops usually depends on how much damage is done over time to the affected joints. In a minority of cases the disease is constantly progressive, and severe joint damage and disability can develop quite quickly.

Inflammation can damage the cartilage which may become eroded or worn. The bone underneath may become thinned. The joint capsule and nearby ligaments and tissues around the joint may also become damaged. Joint damage develops gradually, but the speed at which damage develops varies from person to person. Over time, joint damage can lead to deformities. It may become difficult to use the affected joints. For example, the fingers and wrists are commonly affected, so a good grip and other tasks using the hands may become difficult.

Most people with RA develop some damage to affected joints. The amount of damage can range from mild to severe. At the outset of the disease it is difficult to predict for an individual how badly the disease will progress. However, modern treatments can often limit or even stop the progression of the disease and limit the joint damage (see below).

Hi! Terrified of taking Enbrel...how is anyone else coping with it?

When you first develop joint pains, it may at first be difficult for a doctor to say that you definitely have RA. This is because there are many other causes of joint pains. There is no single test which diagnoses early RA with 100% certainty. However, RA can usually be confidently diagnosed by a doctor based on the following combination of factors:

You may also be advised to have a range of other blood tests to rule out other causes of joint pains.

The risk of developing certain other conditions is higher than average in people with rheumatoid arthritis (RA). These include:

It is not clear why people with RA have a higher-than-average chance of developing these conditions. One possible reason is that, on average, people with RA tend to have more risk factors for developing some of these conditions. For example:

Other complications which may develop include:

If your doctor suspects that you have rheumatoid arthritis (RA), you will usually be referred to a joint specialist (a rheumatologist). This is to confirm the diagnosis and to advise on treatment. It is very important to start treatment as early as possible after symptoms begin. This is because any joint damage done by the disease is permanent. Therefore, it is vital to start treatment as early as possible to minimise or even prevent any permanent joint damage.

There is no cure for RA. However, treatments can make a big difference to reduce symptoms and improve the outlook. The main aims of treatment are:

There are a number of medicines called disease-modifying antirheumatic drugs (DMARDs). These are medicines that ease symptoms but also reduce the damaging effect of the disease on the joints. They work by blocking the way inflammation develops in the joints. They do this by blocking certain chemicals involved in the inflammation process. DMARDs includemethotrexate, sulfasalazine, sodium aurothiomalate, penicillamine, leflunomide, hydroxychloroquine, azathioprine, ciclosporin and mycophenolate mofetil. It is these medicines that have improved the outlook (prognosis) in recent years for many people with RA.

It is usual to start a DMARD as soon as possible after RA has been diagnosed. It is also common practice to use a combination of two or more DMARDs. This is commonly methotrexate plus at least one other DMARD. In general, the earlier you start DMARDs, the more effective they are likely to be.

DMARDs have no immediate effect on pains or inflammation. It can take several weeks, and sometimes several months, before you notice any effect. Therefore, it is important to keep taking DMARDs as prescribed, even if they do not seem to be working at first. Whilst on treatment, you are likely to have a blood test called a C-reactive protein (CRP) test every now and then. This test detects inflammation in the body. As the disease activity reduces, so should the blood level of CRP. The CRP test, in conjunction with assessing your symptoms, is a good way of monitoring disease activity and the effect of treatment in controlling the disease. If DMARDs work well, it is usual to take one or more DMARDs indefinitely. However, when a satisfactory level of disease control has been achieved, your doctor may advise a cautious reduction in doses, but not to a dose less than that required to continue to maintain disease control.

Each DMARD has different possible side-effects. If one does not suit, a different one may be fine. Some people try several DMARDs before one or more can be found to suit. Some side-effects can be serious. These are rare and include damage to the liver and blood-producing cells. Therefore, it is usual to have regular tests - usually blood tests - whilst you take DMARDs. The tests look for some possible side-effects before they become serious.

Biological medicines have been introduced more recently and also have a disease-modifying effect against RA. They are sometimes called cytokine modulators or monoclonal antibodies. Biological therapies include adalimumab, certolizumab pegol, etanercept, golimumab, infliximab, anakinra, abatacept, rituximab and tocilizumab.

They are called biological medicines because they mimic substances produced by the human body such as antibodies. Also, they are made by living organisms such as cloned human white blood cells. This is unlike most medicines that are made by chemical processes.

Biological medicines work in RA by blocking chemicals that are involved in inflammation. For example, some of these biological medicines block a chemical called TNF-alpha which plays an important role in causing inflammation in joints in RA.

One problem with biological medicines is that they need to be given by injection. They are also expensive. Recent guidelines state that two trials of six months of traditional DMARD monotherapy or combination therapy (at least one including methotrexate) should fail to control symptoms or prevent disease progression before one of these newer biological medicines may be recommended. Biological medicines may also be used in combination with methotrexate (a DMARD).

There seems to be an association between gum disease and the activity of RA. (Gum disease is very common.) One recent research trial looked at 40 people with RA who also had gum disease. The trial compared 20 people who had treatment for their gum disease with 20 people who did not. It found that the disease activity of RA seemed to decrease when gum disease was treated. The treatment for the gum disease was scaling/root planing and oral hygiene instructions. That is, basically, good dental care and oral hygiene such as tooth brushing and flossing.

Gum disease causes an ongoing inflammation in the gums. The theory is that this inflammation may in some way add to the immune mechanisms involved in the inflammation of RA. Further research is needed to confirm this association. But, in the meantime, it seems sensible to make sure your oral hygiene is good, as it may have a beneficial effect. See separate leaflet called Dental Plaque and Gum Disease for details.

DMARDs and biological medicines mentioned earlier control the activity of the disease and will ease symptoms when they take effect. However, whilst waiting for them to take effect, or if they do not work so well, you may need treatment to treat symptoms.

During a flare-up of inflammation, if you rest the affected joint(s) it helps to ease pain. Special wrist splints, footwear, gentle massage, or applying heat may also help. Medication is also helpful. Medicines which may be advised by your doctor to ease pain and stiffness include the following:

These are sometimes just called anti-inflammatories and are good at easing pain and stiffness, and also help to reduce inflammation. There are many types and brands. Each is slightly different to the others, and side-effects may vary between brands. To decide on the right brand to use, a doctor has to balance how powerful the effect is against possible side-effects and other factors. Usually one can be found to suit. However, it is not unusual to try two or more brands before finding one that suits you best.

The leaflet which comes with the tablets gives a full list of possible side-effects. The most common side-effect is stomach pain (dyspepsia). An uncommon but serious side-effect is bleeding from the stomach. Therefore, your doctor will usually prescribe another medicine to protect the stomach from these possible problems. Stop taking the tablets and see a doctor urgently if you:

After starting a DMARD (discussed earlier), many people take an anti-inflammatory tablet for several weeks until the DMARD starts to work. Once a DMARD is found to help, the dose of the anti-inflammatory tablet can be reduced or even stopped.

Paracetamol often helps. This does not have any anti-inflammatory action, but is useful for pain relief in addition to, or instead of, an anti-inflammatory tablet. Codeine is another stonger painkiller that is sometimes used.

Note: NSAIDs and painkillers ease the symptoms of RA. However, they do not alter the progression of the disease or prevent joint damage. You do not need to take them if symptoms settle with the use of disease-modifying medicines.

Steroids are good at reducing inflammation. It is common practice to advise a short course of steroids to damp down a flare-up of symptoms which has not been helped much by an NSAID. Also, when RA is first diagnosed, a short course of steroids is commonly used to control symptoms whilst waiting for DMARDs to take effect. Sometimes a steroid is used for a longer period of time in combination with a DMARD. An injection of steroid directly into a joint is sometimes used to treat a bad flare-up in one particular joint.

The main side-effects from steroids occur when they are used for more than a few weeks. The higher the dose, the more likely that side-effects become a problem. Serious side-effects that may occur if you take steroids for more than a few weeks, or if you have injections frequently, include:

As mentioned earlier, sometimes people with RA develop inflammation in other parts of the body such as the lungs, heart, blood vessels, or eyes. Also, anaemia may develop. Various treatments may be needed to treat these problems if they occur.

As mentioned earlier, if you have RA you have an increased risk of developing cardiovascular diseases (for example, angina, heart attack, and stroke), osteoporosis, and infections. Therefore, you should consider doing what you can to reduce the risk of these conditions by other means.

For example, if possible:

See separate leaflets called Preventing Cardiovascular Diseasesand Osteoporosis for more details.

To prevent certain infections, you should have:

Some people try complementary therapies such as special diets, bracelets, acupuncture, etc. There is little research evidence to say how effective such treatments are for RA. In particular, beware of paying a lot of money to people who make extravagant claims of success. For advice on the value of any treatment it is best to consult a doctor, or contact one of the groups below.

The prognosis regarding joint damage is perhaps better than many people imagine:

However, these figures are probably becoming out-of-date, as treatment has improved in recent years. Symptoms can often be well controlled with medication. Also, the outlook for a person who is diagnosed with RA these days is likely to be much better than it was a few years ago. This is because of the newer and better medicines - in particular the newer disease-modifying medicines. Follow-up studies of people being treated with the newer medicines should give a clearer idea of prognosis over the next few years.

Another factor to bear in mind is the increased risk of developing associated diseases such as cardiovascular disease (see above). Because of this, the average life expectancy of people with RA is a little reduced compared with the general population. This is why it is important to tackle any factors that you can modify such as smoking, diet, weight, etc.

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Rheumatoid Arthritis. Symptoms of Arthritis and ... - Patient

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