RA causes many changes in how your body looks and functions. Whether it’s due to joint swelling, fatigue, or another symptom of the condition, your experience of living in your body is different from how used to be, in ways that can be distressing.

Experiencing pain, developing a limp, and moving more slowly than you used to are also common RA-related physical changes, said Dr. Fields. “The general psychological effect that patients talk about … is that it is making them ‘a different person,’” he explained. 

It is important for people with RA patients to optimize their disease-modifying medications so they have good control of disease activity and less unpredictable disease flares. This will improve swelling, pain, and possibly any visible abnormalities. Adjunctive (complementary) treatments can also help such as "physical therapy, local injections, topical pain relievers, nonsteroidal anti-inflammatory agents," Dr. Fields continued.

Read the full article at everydayhealth.com. 

Call it the canary in the coal mine — or maybe a screaming eagle, to more aptly describe the pain. Identifying gout usually requires taking a patient’s medical history, conducting a physical exam and testing, Dr. Fields noted. A joint fluid analysis can detect the presence of monosodium urate crystals under a microscope.

Flares are typically treated with anti-inflammatory drugs and, in some cases, a cortisone injection in the affected joint. Medicine to lower uric acid levels, most commonly allopurinol, can prevent future flares, Dr. Fields noted, if a person is able to continue taking it. Medication side effects range from drowsiness and dizziness to joint pain, stiffness and swelling. 

Read the full article at aarp.org. 

Apps and wearables aren’t substitutes for seeing your doctor regularly, explained Dr. Fields. But by helping you track your needs and making it easier to notice symptom changes, they offer insight into when you should be coming in, and what to share during your visit. “That can improve care and make visits more effective,” Dr. Fields said. 

“Our orthopedic surgeons have been using electronic step-counters to follow their patients after joint surgery, and this can be helpful to see how psoriatic arthritis patients are getting around,” Dr. Fields noted.

Read the full article at healthcentral.com. 

If you often find yourself sidelined by a sudden, throbbing pain in your joints, especially in your big toe, you may be suffering from a gout attack. Flare ups of this common type of arthritis can also cause the affected joint to feel swollen, tender and warm to the touch. 

“Gout is caused by an excess of uric acid in the body, which deposits in joints and causes intermittent episodes of inflammatory arthritis,” explained Dr. Fields. 

Uric acid is a waste product that the body creates when it breaks down chemicals called purines. These compounds are found in alcohol, high-sugar foods, red meat, turkey, certain seafood and high fructose corn syrup (as well as in some other foods). Everyone has uric acid in their body, but it’s when levels get too high that gout can be triggered. “If you have elevated uric acid, over time the blood carrying the uric acid ‘drops off’ some of the uric acid into the joints,” explained. Fields. “Gradually, the joints build up more and more uric acid. Ultimately, a person reaches a ‘critical level’ of uric acid in the joint, and then gets an ‘overflow’ of uric acid crystals into the joint fluid. Those crystals set off the inflammatory response we call a gout flare.”

While the joints are the most common place for uric acid to build up in gout patients, they aren’t the only spots. “Uric acid can deposit elsewhere in the body as part of the gout process, such as by having collections of uric acid form into kidney stones,” revealed Dr. Fields. “You can also get collections of uric acid felt below the skin, called tophi.” These are large bumps you can see and feel, though they usually aren’t painful. Common spots to develop tophi include the elbows, hands, feet, and the outer edge of the ear.

Read the full article at womansworld.com

If naproxen is your go-to pain reliever for things like everyday muscle aches, headaches, arthritis pain, or period cramps, you might wonder how much of this medication you can safely take. You might also be curious about what could happen if you pop too many naproxen pills in your quest for pain relief.

In general, you don’t want to take more than 500 milligrams of naproxen twice a day (a daily total of 1,000 mg), said Dr. Fields.

It’s worth checking your medicine chest and talking to your doctor before you take naproxen, because this drug can interact with many other medications. One of the most important interactions is with other NSAIDs, like ibuprofen, says Dr. Fields. “Combining them increases the risk of excessive dosing and side effects,” he said.

Naproxen also doesn’t mix well with blood thinners . That’s because naproxen impairs the ability of tiny blood cells called platelets to clot, resulting in a blood thinning effect. Taking naproxen plus another blood thinner increases this effect and could cause excessive bleeding, explained Dr. Fields.

Also, if you’re taking medication to lower your blood pressure, naproxen may be a no-no: “Because naproxen can raise blood pressure, it can oppose the effects of medications you take to control high blood pressure,” Dr. Fields said. Check with your doctor before using naproxen if you’re on a blood pressure-lowering drug like an ACE inhibitor, angiotensin receptor blocker (ARB), or calcium channel blocker.

Read the full article at healthcentral.com. 

 For roughly 50 years, lupus has been recognized as a disease that involves the immune system. In the 1960s, investigators made important discoveries about the autoantibodies that are hallmarks of the disease, how they function, and what they react to. Further studies of the immune system in general added understanding of changes in certain immune cells that contribute to lupus. For example, research on the function of immune cells such as T cells and B cells allowed for understanding how autoantibodies are produced and contribute to lupus.

 Over the last several decades, researchers have discovered that cytokines, a type of protein, are key components in the body’s response to infection. They provide chemical signals to immune system cells that help them eliminate other cells infected with bacteria or viruses, but in rheumatic diseases, cytokines can play a role in inflammation. For example, in rheumatoid arthritis, cytokines were found to activate cells in the lining of joints, resulting in joint swelling and damage to healthy tissues like cartilage.

 In the early 2000s, researchers including myself discovered that cytokines called interferons are significant players in lupus. Normally, interferons orchestrate a response to virus infection. But in people with lupus, interferon levels are elevated and cause inflammation in many parts of the body. In a healthy situation, a virus infection will stimulate rapid production of interferons, then go back to normal in several days; however, in most lupus patients, interferon levels remain elevated for months and years. Researchers have also identified many lupus-associated genetic changes that affect molecular pathways involved in the development of lupus, including the interferon pathway. Any one of these common genetic variants has a modest effect on risk of disease, but when multiple variants occur in an individual, risk of disease is significantly increased.

 Based on what has been learned about the mechanisms involved in lupus over the last 20 years, researchers have made great efforts to develop new drugs to more effectively treat the disease. Roughly ten years ago, the FDA approved belimumab, which blocks the activity of a molecule called BAFF (B-cell activating factor) that drives B cells to become active and contributes to their ability to make damaging autoantibodies. A year and a half ago, the FDA approved anifrolumab, an antibody that blocks the cell surface receptor for the type I interferons that are particularly elevated in lupus patients.

 Lupus research is conducted by investigators around the world, with many opportunities for progress being pursued. Sunlight, for example, can trigger flares of lupus, but we don’t really understand why. One possibility is that the ultraviolet rays of sunlight could damage DNA. Studies have supported an association between herpes virus, particularly Epstein-Barr virus, and lupus, and researchers have been working out the mechanisms. My laboratory has investigated the possibility that virus-like sequences in DNA, called genomic retroelements, can sometimes result in production of interferon in patients with lupus. There are currently many ongoing studies aimed at understanding why the interferon pathway is activated in lupus patients or why the body produces autoantibodies.

 Clinical drug development studies have exploded in recent years, with candidate drugs focused on many immune components involved in the disease. Rituximab, for example, which is approved for other uses, is sometimes used for lupus patients. Rituximab depletes B lymphocytes, which are the cells that make autoantibodies. Future drugs will aim to achieve optimal B cell depletion or reduce the function of interferon-producing cells. Other drugs that inhibit cellular signaling pathways involved in lupus are being developed, some of which may be administered as a pill rather than as an injection. I believe that multiple components of the immune response represent rational therapeutic targets for treatment of patients with lupus, and in the end, it may be necessary to target several parts of the immune system to achieve long-lasting responses or even cure. One approach of great current interest is administration of CD19-CAR T cells, a novel therapy that involves modification of a patient’s T cells followed by injection of those cells back into the body. A study of a small number of patients with lupus nephritis, a form of disease that involves the kidneys, has shown impressive responses that last as long as a year. Longer studies are necessary to fully assess the efficacy of the CAR T cell approach. Furthermore, some research is focused on why some patients develop disease of the vasculature, kidneys, heart, spleen, skin, and brain while others do not, drawing attention to alterations in cells outside of the immune system that impact the vulnerability of those organs for developing chronic damage.  

 Lupus is very variable in how an individual person will react to having the disease, even given the same degree of immune system activation. Though people do better with lupus now than they did 50 years ago, they can be quite damaged by the disease, and experience severe organ involvement, such as kidney failure or cardiovascular disease. Even those patients who do not experience organ damage can report life-altering symptoms such as fatigue and what they describe as “brain fog”.

 Because so much of the immune system is involved in lupus, studying lupus patients has taught us a lot about the immune system that can be applicable to many other diseases that rheumatologists treat, as well as about how the immune system responds in the setting of infection or cancer. An example of that is COVID-19; there was a lot of study of the immune system in people who got sick with COVID. This created an opportunity to relate that data on how the immune system was behaving to what we have been studying in lupus.

 My research efforts are focused on better understanding the underlying biology that results in the development of lupus and its complications. This includes the contributions of genetic risk factors, understanding what activates the immune system and results in the autoimmunity characteristic of lupus, and how patients can be characterized based on their unique immune response and disease symptoms. The overall objective is to gain enough new information that we can propose targets for more effective therapies, ultimately improving the lives of patients. More specifically, our current research is defining differences between those patients who maintain high levels of interferon chronically and those patients who only increase their interferon levels at times of disease flare. Other current projects include defining the immune mechanisms that are associated with different specificities of autoantibodies, understanding the molecular pathways that trigger flares of lupus nephritis, and understanding genetic risks for chronic inflammation in lupus.

 Despite all we’ve learned, we still have a lot of work to do to understand what drives lupus, what activates the immune system, and what causes organ vulnerabilities. If we understand the mechanisms of the disease, the whys and what’s of the immune system becoming altered in its behavior, then we will have relevant ideas of what would be good approaches for development of novel therapies. There are many points of attack for this disease that are being considered and tested in clinical trials, so there is a lot of optimism that some of these will pan out as effective and relatively safe.

 — Mary Crow, MD, physician-in-chief emerita and senior scientist at the HSS Research Institute

Rheumatoid arthritis (RA) is rising: In 2019, 18 million people worldwide were living with RA, according to the World Health Organization.

The good news is that, thanks to early diagnosis and new treatment options, people with RA – even younger adults in the midst of career development, family-building, and active lives – can experience remission.

“There is a lot of hope these days for someone with RA, and we can give young patients a lot of reassurance,” said Dr. Fields.

Rheumatologists say that catching RA early is key; telltale signs are pain and swelling of the smaller joints in both hands, wrists, or feet. “The reason to get treatment started early is that our medications can not only reduce or stop symptoms such as fatigue, stiffness, and joint swelling and pain, but they can reduce or stop damage to bone,” explained Dr. Fields.

Read the full article at WebMD.com. 

The connection between osteoarthritis and allergic diseases could be the low-grade inflammation, said Theodore R. Fields, MD, FACP, rheumatologist at HSS, who was not involved in the study, but commented on the findings.

"If treatment of atopic disease helps prevent or lessen osteoarthritis, there are a lot of options and will be more," said Dr. Fields.

"For patients with eczema or asthma, this data can make them aware that they might be more likely to get osteoarthritis," he continued.

If you have an allergic disease and develop aches and pains in your joints, see your doctor, advised Dr. Fields.

"We have many strategies to improve the symptoms of osteoarthritis but don't yet have a disease-modifying treatment," said Dr. Fields. 

"There can be some hope in this study for patients with eczema or asthma that their treatment for atopic disease might prevent or diminish their potential to develop osteoarthritis," he added.

Read the full article at healthday.com. 

The body makes uric acid when it breaks down purines found in the body, meat and some beverages. Hyperuricemia, an elevated level of uric acid in the blood, can lead to the formation of uric acid crystals in a joint, causing inflammation. People with gout also often have high levels of uric acid in their synovial fluid. However, hyperuricemia does not always cause gout.

Theodore R. Fields, MD, FACP,  rheumatologist at HSS who was not involved in the study, said the results illustrate more can be learned about the pathogenesis of gout.

“It makes sense that factors like lubricin deficiency might play a role in some patients, because we still have major gaps in our knowledge of why some patients get gout and others don’t, even when both have the same serum uric acid levels,” he said.

Read the full article at ustoday.news. 

Dr. Fields discussed stand out studies, including the MIRROR trial, a study pinpointing the role of lubricin deficiency in the pathogenesis of gout, and a Korean study that compared febuxostat and allopurinol treatment and the impact they had on adverse cardiovascular reactions. He went on to discuss regulatory news updates and issues that he hopes will be addressed in 2023, including continued education of the physician community about the patient benefit from an aggressive and targeted approach. 

Read the full article at rheumatologynetwork.com. 

A rheumatologist may suggest seeing an OT to help make everyday tasks easier and cut down on the pain, stress, and fatigue that comes with having an inflammatory or degenerative condition.

When it comes to pain relief, Dr. Fields said that OTs may engage in pain-reducing treatments such as wax baths and heated corn husks for painful hands.

Read the full article at CreakyJoints.org.

Some experts think PPIs are overprescribed and should be reserved for the most serious conditions like erosive esophageal disease and bleeding ulcers.

According to HSS rheumatologist Theodore R. Fields, MD, FACP, acid-blocking drugs called H2 receptor blockers are a safer choice for people with arthritis who use NSAIDs.

He said, “Since data came out increasing the list of potential side effects of PPIs, such as low magnesium, increased kidney risk, and increased fracture risk … many [doctors] will substitute [H2-blockers] for PPIs.”

Read the full article at Arthritis.com.

Considered a type of arthritis, gout is very common, however “the thumb is quite an unusual place for gout to make its first appearance,” said Dr. Fields. Gout can occur in any joint in the body, but the most common spot for a first flare of gout is at the bunion joint of the big toe, followed by the mid-foot, then the ankle and the knee. “There’s some thought that gout in the lower extremity, and especially the big toe, may happen earlier than in other joints because of pressure from walking,” he explained. “In the first toe, it has been postulated that it being the coolest part of the body, you get more gout since we know that gout crystals are more likely to come out of solution in cooler temperatures.”

“For a flare of gout in the thumb, the treatment is similar to that of other sites of gout flares,” counseled Dr. Fields. Gout pain is generally treated in two ways: Medications to relieve gout attacks in the short-term; and preventive medications taken regularly to lower uric acid and stop gout attacks from occurring. Since gout in the thumb typically occurs later in the course of disease and is not the first sign of gout, it can be easily avoided if people seek medical attention for recurrent gout and adhere to their treatment, said Dr. Fields. If this is the case, people “will likely never get gout in the thumb, since their gout problem likely started in the foot or ankle and once on [medication like allopurinol] for a period of time gout almost always is ‘cured’ as long as the medication is continued.”

Read the full article at CreakyJoints.org.

People may be good candidates for an intravenous medication called pegloticase, which can dramatically lower uric acid levels over a short time. However, pegloticase is only effective about 40 percent of the time because many people form antibodies to it. This causes the medication to stop working for them or causes them to have reactions to it, explained Dr. Fields. At ACR this year, “a number of studies addressed a new strategy to prevent people from forming antibodies to pegloticase by using a medication with the pegloticase that suppresses antibody formation,” he continued. “These studies were small, but all suggested that the medications added to pegloticase all had a low risk of side effects during the treatment period, generally three to six months. All of them increased the effectiveness of the pegloticase.”

Read the full article at Creakyjoints.org.

To listen to episodes featuring Dr. Fields, visit Creakyjoints.org/thegoutshow/.

According to new data, seeing a rheumatologist shortly after the onset of RA symptoms leads to better outcomes. HSS rheumatologist, Theodore R. Fields, MD, FAACP, who was not involved with this research, provided commentary on the findings, noting, “They [researchers] found that patients who saw a rheumatologist within six weeks were more likely to ultimately be in remission without strong RA medication than those seen in seven to 12 weeks or more than 12 weeks.” Dr. Fields added, “This argues for earlier referral of patients with RA to a rheumatologist.”

Findings of a separate study also indicate RA patients who are in remission should not taper the dose of their biologics. “This study raises questions about whether to taper a TNF inhibitor in view of the high flare rate. However, since patients did well with restart of the TNF inhibitor, tapering and withdrawal is still an option for some patients,” explained Dr. Fields.

Read the full article at Creakyjoints.org.

Researchers used ultrasounds to determine how common entheses abnormalities are among gout patients who were in the midst of a gout flare. Out of 31 participants, 22 had an abnormality in at least one enthesis — most often in the area where the quadriceps tendon connects to the patella in the knee.

HSS rheumatologist Theodore R. Fields, MD, FACP, who wasn’t involved in the study, commented on the findings, noting, “People with gout who get pain and swelling in the Achilles’ tendon, for example, may think it’s a tendon strain or other tendon injury, but there is a good chance it is a gout flare and will respond to gout treatment.”

Read the full article at Creakyjoints.org.

Dr. Fields explained the risk factors that affect both gout and COVID-19 such as obesity and cardiovascular disease, and suggested to work on improving any comorbidities that can make COVID-19 more risky. “Obesity is more common in gout patients [as overweight people produce more uric acid, which is what accumulates in the joints and triggers inflammation] than in the general population. There is evidence that obesity is also a risk factor for having more complications of COVID-19,” said Dr. Fields. Heart disease is more common in people with gout, and it is also linked with increased complications of COVID-19, he added, noting, “Elevated uric acid [in gout] may also raise blood pressure.”

Dr. Fields advised to not stop taking gout medications and also recommended exercise, prioritizing sleep, manage stress, and to also quit smoking and limit alcohol intake.

Read the full article at Creakyjoints.org.

CreakyJoints spoke to Theodore R. Fields, MD, FACP, rheumatologist at HSS, who explained, “Alcohol makes the uric acid be pulled back into the body, with less [expelled] in the urine. This leads to elevated blood levels of uric acid.” Dr. Fields added, “If you’ve been diagnosed with gout and are managing it with medication for the long term, occasional intake of high-purine foods, like red meat and shellfish, and a small amount of alcohol is generally okay. High quantities of any of these have a good chance of setting off gout flares, especially in the untreated patient or the patient early-on in the use of a medication such as allopurinol.”

Read the article at Creakyjoints.org.

CreakyJoints spoke to Theodore R. Fields, MD, FACP, rheumatologist at HSS, who explained the lack of symptoms during the first stage. “In this first stage of gout, the person has no joint pain, no red or swollen joints, just an elevated uric acid blood test,” said Dr. Fields. “This is the time that the uric acid, or urate, crystals are collecting in the joints and can cause inflammation later on,” he added.

In the second stage, otherwise known as acute gout, an unexpected attack might occur. “This is when the person has pain, redness, and swelling of a joint, most commonly in the big toe, the foot, the ankle or the knee, but gout can start in other joints as well,” cited Dr. Fields. “This is when the urate crystals are released into the joint fluid and cause an inflammatory reaction, bringing in many white blood cells and releasing inflammatory chemicals that cause the pain, redness, and swelling.”

Additionally, 75 percent of people will experience a second flare within a year, however some can go years before another attack. Dr. Fields cited this third, or in-between stage is where a person has had a gout flare but is presently not having any joint pain or swelling. “Almost all gout patients will go through this phase, since it is the nature of gout to have flares and then quiet down for a period of time before the next flare.”

The fourth stage is called “tophaceous gout” as uric acid deposits can form nodules called “tophi” develop at the big toe or at the elbow. “This stage is where a person can have some joint pain from gout just about all the time,” said Dr. Fields. “It usually takes many years of uncontrolled gout for someone to get into this stage,” he added.

“Anything that makes urate levels go suddenly up or down can set off gout,” said Dr. Fields. Factors include eating a diet high in purines (i.e., red meat and shell fish), alcohol, obesity, emotional or physical trauma. However, weight loss, diet and exercise, medications to limit the amount of uric acid the body produces, and treatments to calm gout flares, can aid with progression.

Dr. Fields concluded, “Treatments for gout are extremely good, and the vast majority of gout patients can expect to be ‘cured. ‘Cured’ is in quotes since it means that gout flares can completely disappear, but the person would need to stay on their medicine.”

Read the article at Creakyjoints.org.

CreakyJoints spoke to Theodore R. Fields, MD, FACP, rheumatologist at HSS, who explained why the enthesis is susceptible this issue, the types of arthritis that can cause enthesitis, treatment and home remedies.

Dr. Fields explained, “The enthesis has a lot of blood flow and [thus] is subject to both infection and inflammation.” He mentioned there are two common entheses where enthesitis often occurs. “Two of the most common entheses are the area where the Achilles’ tendon inserts on the back of the heel, which causes Achilles’ tendonitis, and where the sheet of connective tissue, or fascia, inserts on the bottom of the heel, which causes plantar fasciitis.” Additionally, about half of people with psoriatic arthritis and ankylosing spondylitis have enthesitis, said Dr. Fields. “In both psoriatic arthritis and ankylosing spondylitis, the back and under portions of the heel are common sites of enthesitis,” he cited.

Dr. Fields underscored the importance of taking the affected area(s) into account when deciding on a treatment regimen. “In patients where enthesitis is the major issue, and more severe than the arthritis, we may skip the non-biologic agents and go directly to biologic therapies, since they tend to be more effective for enthesitis.” Additionally, local injection of corticosteroids can be used in enthesitis at times, however this needs to be used carefully to avoid weakening of the surrounding tendons and ligaments, advised Dr. Fields.

Dr. Fields concluded a physical therapist can provide you with gentle stretches to do at home to relieve the pain. Furthermore, he suggested maintaining a healthy weight to take the pressure off of involved areas, and wearing special shoes.

Read the full article at CreakyJoints.org.

CreakyJoints spoke to Theodore R. Fields, MD, FACP, rheumatologist at HSS, and Juliette Kleinman, LCSW, ACSW, senior social work manager, rheumatology at HSS, to discuss what this process entails for arthritis patients. Dr. Fields noted, “Some of the Department of Motor Vehicles’ list of disabilities that qualify for the placard and which especially relate to people with arthritis are: inability to walk 200 feet without stopping and severe limitation in the ability to walk due to an arthritic, neurological, or orthopedic condition.” Dr. Fields continued on saying people should be comfortable addressing this issue with their doctor, even if that conversation means you learn you don’t yet meet the requirements. Klienman added, “Bringing up this request early on in the appointment is important, so that you have enough time to be evaluated by your doctor.”

Dr. Fields further explained, “There are a number of conditions where a patient’s source of disability is not visible to an observer. The key issue is how these issues are affecting the patient rather than how they look to others.” Klienman concluded, “The pain and fatigue from arthritis is internal and may not be visible to others, however, you are the one who experiences it day to day. It’s understandable that we may be concerned about what others think, but remember, the handicap placard is there to help you take care of yourself and get you to where you need to be to maintain your independence.”

Read the full article at CreakyJoints.org.

Arthritis Today spoke to Theodore R. Fields, MD, FACP, rheumatologist at HSS, who said many people with sleep apnea go undiagnosed, and advised those who suspect they have apnea to speak with their doctor because as there are treatments. Treatments include using a continuous positive airway pressure (CPAP) mask or mandibular advancement device (through people with arthritis of the jaw should avoid the latter.)

Studies have demonstrated poor sleep contributes to higher levels of next-day arthritis pain – but it also may help reduce the risk of heart disease. Dr. Fields added, “It is especially important for people with inflammatory arthritis to be screened for sleep apnea, since they are already at risk for cardiac disease.”

This article appeared in the May-June 2019 print issue.