New Update: Vitamin D has No Effect on Knee Osteoarthritis

Vitamin D supplementation for individuals with knee osteoarthritis and low 25-hydroxyvitamin D levels did not reduce knee pain or slow cartilage loss, according to a study appearing in the March 8 issue of JAMA.
 
Symptomatic knee osteoarthritis occurs among 10 percent of men and 13 percent of women age 60 years or older. Currently, there are no disease-modifying therapies for osteoarthritis. Vitamin D can reduce bone turnover and cartilage degradation, thus potentially preventing the development and progression of knee osteoarthritis. Observational studies suggest vitamin D supplementation is associated with benefits for knee osteoarthritis, but current evidence from clinical trials is contradictory.
 
Changhai Ding, MD, PhD, of the University of Tasmania, Hobart, Tasmania, Australia, and colleagues randomly assigned 413 patients with symptomatic knee osteoarthritis and low 25-hydroxyvitamin D to receive monthly treatment with oral vitamin D3 (50,000 IU; n = 209) or an identical placebo (n = 204) for 2 years. The study was conducted in Tasmania and Melbourne, Australia.
 
Of 413 enrolled participants (average age, 63 years; 50 percent women), 340 (82 percent) completed the study. The researchers found that vitamin D supplementation, compared with placebo, did not result in significant differences in change in MRI-measured tibial cartilage volume or a measure of knee pain over 2 years. There were also no significant differences in change of tibiofemoral cartilage defects or change in tibiofemoral bone marrow lesions. Vitamin D levels did increase more in the vitamin D group than in the placebo group over 2 years.
 
“These data suggest a lack of evidence to support vitamin D supplementation for slowing disease progression or structural change in knee osteoarthritis,” the authors write. 

Patients Believe Lab Tests More Than Doctors

A colleague recently made this declaration among a group of rheumatologists. There was a long group pause that made me consider this observation. This is an important issue, because it is sad if true and we may be leaving our patients with the wrong impression. It’s also important as new laws have liberalized the patients’ rights to his/her lab tests and records.

Thus, why do patients believe their labs more so than their doctors? And what do physicians do with this open sharing of lab values? To understand this we should look at both the patient and physician perspective on this issue.

The Patient Perspective

• Trust a doctor or trust a lab number? Doctors are human, occasionally fallible or poorly groomed. Not surprisingly, it takes a while for patients to learn to trust a physician. Urgency and severity don’t engender trust either. My new patient with the melon-sized, swollen, hot knee may trust the prescription given but will trust less when I’m wielding a large needle and 20 cc syringe. Physicians’ lingo also undermines trust. I think patients are perplexed when we deliver the shortest possible message using the longest possible polysyllabic terminology. Medical speak is the third leading cause of patient bewilderment and malpractice suits. Patients are keenly aware that if a doctor cannot speak plainly, there must be something wrong with the doctor, rather than the patient.
• Laboratory tests on the other hand, are numbers - and numbers don’t lie (the latter is likely to be attributed to an accountant or administrator, not Osler). Numbers are countable, incremental and delivered by and/or on computer printouts. Hence, those values that appear in red and are “out of range” are meaningful to the owner or those red values. Even though I try to convince my patients that the red, seemingly elevated BUN/Creatinine ratio is not important, my patients are not easily convinced. I use the analogy that driving at 37 MPH (in a 35 MPH zone) may be considered speeding; no one gets a policeman’s ticket for such a number. Or that the number has to be interpreted in context. So if I’m driving 37 MPH in a school zone full of flashing buses and crossing guards, a penal code prize will be duly served.
• Everyone values free stuff. You don’t always get your money's worth in healthcare and when you don’t, it costs more. These are the built in pitfalls of healthcare and physicians that every patient must cope with. Cognitive dissonance may explain why humans value that which is free, but still I’m amazed when patients are compelled to react (without calling me) to a TV news report or a pharmacy six-page printout or a lab report. These info bits, presumably from authoritative sources, are valued and believable as they are free, personalized and clear in their message. This contrasts with physician messages that are expensive, occasionally uninterpretable and delivered at the end of a rushed medical visit.
• Doctors specialize in messaging that isn’t so clear.  We commonly use statements like, “you’re much better or “this is a setback”. Patients wonder whether “better” is relative to my last visit or other patients on the better to worse scale. This contrasts with lab tests are quantitative and digital. Patients believe that a lab test is a numeric systematic representation their biology and a pivotal arbiter of wellness. This they can understand – or at least look up on Google. My labs say I’m either normal like everyone else or a red number, falling out of range. “Doc my lab must mean I’m at least as abnormal as the test says I am”.
• Doctors are to blame. Patients think labs are important because doctors tell them so. “Let’s wait and see what the labs show” (meaning I can’t make a diagnosis without them). “Your labs are just fine” (implying the patient must be also). “Mr. Sample there’s a problem with your labs” (uh-oh, sell the farm Mr. Sample!). Then Dr. Jekyll becomes Dr. Hyde when the patient wishes to discuss lab abnormalities only to observe the doctor dismiss the labs as either hanging chads in a meaningless election or a result that should never have been reported (because it takes too long to explain why the result in physiologically unimportant even though it may be psychologically damaging). I’m not surprised when my patients struggle and say it’s sometimes hard to tell who I should believe, the lab test or the doctor.

The Physician Perspective

Laboratory testing is usually an integral part of comprehensive healthcare delivery. Testing can be used to assess a patients metabolic status, organ function, immunologic abnormalities, disease risk, drug safety or toxicity, and occasionally a diagnosis.

Labs are important. But a lab is meaningless without a symptom narrative, list of diagnoses or drugs, or a detailed patient examination. Clinicians need labs to answer specific questions and use them as adjunctive “info bits” to enhance their understanding of the disease, management of the patient and safety of therapies given.

Patients want and should have their lab results. But it is the physician’s responsibility to educate their patients about labs, why they are being done, what is being examined and looked for. Here are a few principles of lab testing that clinicians need clearly communicate to their patients and payers of labs:

• A lab test does not equal a diagnosis. Hence, while we would like to see a positive rheumatoid factor in someone with suspected of rheumatoid arthritis, this test is not required to establish the diagnosis.
• More labs means more chances for an abnormal finding. The more lab tests that are ordered, the more likely one or more will fall out of normal range. Normal values of a particular lab reflect the bell curve limits established in a large number of “normal” people. Values that fall “out of range” beg the question, “when is abnormal really abnormal?” Explaining the difference between a random spurious finding and a pathologic result can be difficult, but requires trust and communication between patient and physician.
• Monitoring and serial labs. Labs are important when monitoring disease status (e.g., sed rate or creatinine) or drug toxicity. This is why repeated or serial labs may be necessary.
• Once is enough!  Many autoimmune laboratory tests need only be done once or confirmed by a second by different lab. Hence there is no value in repeating and following the following tests: ANA, RF, CCP, ENA or ANCA as these have not been shown to change as the disease does. There are other tests often used as a “disease activity” measure – these can be quite valuable in certain clinical situations.
• Result communication.  Physicians and patients need to have an agreed upon plan addressing how the patient will learn about his/her lab results.
• Patient folders.  Patients need to keep copies of their labs in a folder, bring these to all medical visits and share the results with all caregivers.

Patients should understand their labs and believe that they are being used to effectively diagnose and treat their medical predicament. They should be given copies and encouraged to maintain a file of their wellness and labs to share with other doctors. Patients who are overly fixated on a specific lab result are that way because we made them that way! It’s the physicians’ responsibility to educate the patient on which labs are needed or important and when concern over a lab results is appropriate.

Diabolical Negativism

I’m often perplexed when I say one thing, but my patient hears something totally different. Where did my advice get derailed? Or was my advice too weak or too wild to take seriously? Is it the patients’ perspective, or education, or am I not clear in my messaging?

“Here’s your new medicine, hydroxychloroquine. It’s quite effective (at controlling joint and skin symptoms) and is one of the safest medicines we prescribe.”  That was my lead sentence; but instead the patient heard and clung to the last sentence: “Oh, and it rarely affects the eyes. So you’ll need to have an annual eye exam to assure the drug’s safety.”  The subtext became a headline and the patient heard “potential blindness”.  Importance is justified when you find she makes her living as a sharp-shooter and her grandmother had macular degeneration.

Negative thinking is the constitutive skepticism that comes with new diagnoses, new drugs, car salesmen and prospective suitors. It is an anchor for self-preservation, especially in such naïve situations. However, in the case of medical care it can be diabolical, destructive and damaging to outcomes. Such thinking is not devilish or ill-intended; instead it is misinformed, pessimistic and restraining. Left unchecked, it stagnates care, averts interventions and drives nonadherence – much to the detriment of the worried patient.

Research on patient compliance and drug adherence has shown that nearly all patients have some degree of noncompliance, with medication compliance ranging from 50-70% in most.  We see this in patients who confess to taking their etanercept once every two weeks or sleep apnea patients who admit to using CPAP, but only once a week when their spouse nags them to do it.

There are two approaches to negative thinking physicians need to consider proactively. First, is the need to teach the consequences of not treating a problem or disorder and second, teaching the patient how to correct the negative narrative they tell and convince themselves of.

The Consequences
Teaching the consequences is easy, but it takes time and pastoral patience. Patients can easily comprehend the consequences of not treating HIV, a cancer or mental illness. But applying the same clarity to their own clinical situation requires coaching and simple logic. 

Recognize that many patients will not take a drug or even fill the prescription.  Consumer Reports states that half of patients assume grave risks by skipping doses, taking expired medications or not filling a prescription. Several sources indicate that 23-33% of all prescriptions go unfilled, especially in the elderly, low-income groups, chronic conditions and expensive drugs. Nonadherence is willful inaction owing to risk aversion, bolstered by inexperience in making value-based choices.  

Patients struggle with the balance of potential benefits and risks of a particular therapy. Many believe there is more harm in taking meds than in avoiding meds. When confronted with new, confusing or ambiguous situations, decision avoidance may appear to be the easiest and safest option. Worse is the belief that all adverse events are likely for those with the misfortune of having an autoimmune (or like) chronic condition.  An RA patient may immediately reject the appropriate option of rituximab because of the very rare risk of progressive multifocal leukoencephalopathy (PML).  When informed that the risk of getting PML from rituximab is 1 in 30,000; such patients quip “oh don’t worry, I’m unlucky enough to get it!”  They truly don’t accept that their individual risk is the same as the next RA patient, 1 in 30,000. 

Unfortunately, such magical thinking (rooted in what is not known) and non-treatment is predictably rewarded with poor outcomes and more difficulty and distress for all. This is where an experienced clinician can teach the likely consequence of not treating (active lupus nephritis, inflammatory symptoms of PMR or swollen joints with RA). Patients can be counseled that:

1. they are often avoiding that which they are misinformed or know little about;
2. they are stuck and without a plan to fix their problem;
3. that time and natural cures/interventions were prevalent at the turn of the century when the average life span was 48 years; and
4. it is wrong to view or equally consider information that is free (internet, sales people, television) versus that which is the best money can buy (consultation with a specialist). 

Risk communication takes time and careful wording.  But I like to end my rationale for a prescriptive plan with proclaiming this medicine was made for them and their situation, it cost $1-2 billion dollars to develop and has been given to thousands or millions of patients for the same reason AND that my research and 30 years of experience are on your side for the best possible outcome.  Reinforce that the patient needs to read, do research and have a voice.  But at some point, they will have to trust someone (of their choosing) to guide them as they forge ahead through scary waters. Who will guide them?  A website, vitamin maker, and brother-in-law surgeon, or the rheumatologist they’ve chosen to see?   

The Negative Narrator
We all have a narrator in our head and at times, it just won’t quit. “You’re not good enough”. “That would be a bad choice.”  “Let someone else go first”. The narrative inside your head is often negative and constraining and while it may be self-protective, it can also be a detriment to health and happiness. 

The television series “Ray Donovan” is about a nefarious Irish family who moves from Boston to Los Angeles and becomes involved in a fast paced, shady sub-culture. The lead character, Ray Donovan (played by Liev Schreiber), is a “fixer” or “mechanic” of bad predicaments that happen to good and bad people.  When asked what his job is, he proclaims, “I change the story” (meaning he delivers the desired outcome he is paid for). 

Changing the story, especially the story patients tell themselves, can be done with clarity, guidance, risk communication and recognition of the negative narrator within. Instea of thinking, "dang! I've got to take this drug for the rest of my life?" the inner voice should be taught to think, "thank goodness there is a long-term treatment so that I can have long-term normalcy!" 

Michael Hyatt is an author, publisher, mentor and podcaster who speaks on many areas of self-improvement. One of his podcasts (listen here(link is external)) covers how to  “change your story” and in essence, deal with the negative narrative in a more productive and planful way.

Tenets to Changing the Story include:

1. Recognize that there is a narrator/voice within;
2. Jot down what that voice tells you – “don’t take that medication, you’ll be the one in 30,000 to get that deadly brain infection”;
3. Evaluate the “story” – is it holding you back or empowering you forward; is it leading to action or stagnation;
4. Write a different story – with a better or more informed outcome. What you should tell yourself or what your doctor would tell you.

Patients need to recognize the voice isn’t always positive or productive.  The narrator often leaves you stuck where you are with what you don’t know.  The patient needs to know what are the consequences? What is at stake?  What choices leave you the victim or the one in control? Also, remind them it’s unwise to make judgments (or listen to the narrator) when they are stressed, tired, in pain or after hearing bad news.  A good night's sleep and repeat conversation is likely to be more productive.

Lastly, and most importantly, physicians need to prescribe more than the drug. They need to deliver hope and be clear about their expectations and how this patient’s story will play out. Patients desperately want to hear “the rest of the story”, when and what will happen when the right choices are made. Tell them what it is about their situation makes them ideal or suboptimal candidates for your prescribed plan.

Give them the positive voice they need to move forward!

6,000 steps a day keeps knee osteoarthritis limitations away

New study shows that walking reduces risk of functional limitation associated with knee osteoarthritis (OA). In fact, the study funded in part by grants from the National Institutes of Health (NIH) and published in the American College of Rheumatology (ACR) journal, Arthritis Care & Research, suggests that walking 6,000 or more steps per day may protect those with or at risk of knee of OA from developing mobility issues, such as difficulty getting up from a chair and climbing stairs.
http://jaipurrheumatologist.com/6000-steps-day-keeps-knee-osteoarthritis-limitations-away/

RA Impacts Much More than Bones and Joints

When people hear the general term arthritis, they typically think of an older person with joint pain as in osteoarthritis – common wear and tear on the joints. But this term can miss the mark when describing the systemic impact of autoimmune rheumatoid disease on the entire body. One of the first symptoms that doctors often examine for establishing a diagnosis of RA is bone erosion – typically in the fingers. But as an autoimmune disease, RA can impact much more than the bones as it can damage a variety of soft tissues including the eyes (iritis), lungs (fibrosis), heart, blood vessels (vasculitis), nerves (carpal tunnel), and skin (nodules, ulcers), and connective tissue (cartilage, tendons, ligaments)

. Often-times, the soft tissue damage occurs long before bone erosion is visible or even before an official RA diagnosis comes.

Besides bone erosion, RA can impact other parts of the joint including the surrounding connective soft tissues comprised of tendons, ligaments, and cartilage. Chronic tenosynovitis, inflammation of the sheath of a tendon, is common in rheumatoid arthritis and can result in the permanent damage and tearing of the involved tendons. Such tendon problems caused by RA are well known by the scientific community and are linked to joint deformities.^{1, 2} Tendon problems have even been posited as being one of the most powerful predictors of early RA.³ Sophisticated imaging techniques developed in the last few decades, such as MRIs and ultrasound, can reveal connective tissue damage in joints caused from RA that are not seen in x-rays.⁴ Bursitis, inflammation of the fluid-filled sacs that protect joints⁵, often accompanies tenosynovitis. RA is also implicated as a cause of cartilage damage in knees.⁴

In my particular RA case, damage to soft and connective tissue before bone damage to joints occurs is a typical presentation. Two symptoms now linked to RA which I personally experienced before an official diagnosis were iritis – inflammation in the eyes, and torn Achilles tendons and bursitis in myankles resulting in three surgeries. An MRI taken at the onset of my RA diagnosis revealed cartilage damage in one knee. And just last week, an MRI revealed a 50% tear of a tendon in my elbow. Theelbow joint, while actively inflamed, did not yet show bone erosions.

Although not publicly well known, scientists and doctors have recognized for some time that rheumatoid arthritis is also linked to an increased risk for cardiovascular disease (CVD) including heart attack, stroke and diabetes. Systemic inflammation inherent in rheumatoid arthritis may play a role in the increased CVD risk.⁷ Some researchers have even called for the development of specific CVD predictors for RA patients as a special population with unique characteristics.⁸ Systemic inflammation involved with RA can impact the complex metabolic processes of the body including use of food for energy, sugar processing, insulin production, production of fats and lipids, body weight, and physical activity. Whenever one of these interconnected systems gets out of normal parameters, a cascade of problems may occur which can impact cardiovascular health. This is called metabolic syndrome and involves a set of interconnected risk factors which are related to cardiovascular disease and diabetes.⁹In a study published in 2013, it was found that 18-49% of RA patients also had metabolic syndrome which was significantly higher than general populations.¹⁰ These researchers also found that RA patients with higher inflammatory blood markers and those who used corticosteroids were more likely to show signs of metabolic syndrome leading to increased cardiovascular risk which can have serious and fatal consequences.

As an autoimmune disease, RA can cause the body to attack itself in many different ways – not just in bones and joints. RA patients and doctors need to be aware of the numerous extra-articular (outside the joint) manifestations of the disease, carefully monitor them, and treat as needed. The stereotype of RA as “just arthritis” needs to be challenged and it needs to be seen as a hideous disease that can attack many different tissues and systems in the body.

Osteoarthritis

What Is Osteoarthritis (OA)?

Osteoarthritis is a condition that affects the joints. It is as a result of the wearing off of the cartilage that serves as cushion where two bones meet. Cartilage is slippery and firm and works by allowing the joints to move without friction. When it gets worn out, the surface roughens and gradually it deteriorates completely leaving the bones to rub against each other. Although it can affect any joint in the body, the most affected joints remain those of the knees, hips, hands and the lower back. Of all forms of arthritis, OA remains the highest ranked in patient numbers with over 27 million people in the U.S.

Signs and Symptoms of Osteoarthritis

Progression of the disease can be very gradual sometimes taking years to develop. Symptoms may begin with a single joint and progress to others.

1. Pain
This is the first symptom you will experience with OA. It may be painful to move your joint or the pain may come after flexing it.

2. Stiffness
When you stay inactive for some time, your joints become stiff. This may be common in the morning after waking up. It ceases after the joint becomes active again.

3. Loss of Flexibility
He joint becomes rigid and painful to move it around

4. Reduced Range Of Motion
The ability to turn your joint to a full range motion is lost.

5. Tenderness
When little or much pressure is applied to the joint, it feels tender

6. Swelling
You may notice hard or soft swelling on the joint. The hard is caused by bone spurs while the soft is as a result of the thickening of synovial fluid.

7. Specific Joints Are Affected
Pain will be common in specific joints in the body. These are the knees, hands, spine and the hips.

8. Grating Sensation
A small movement of the joint causes a grating sensation.

9. Noisy Joints
Joints become creaky on movement especially when you stand from a sitting position.

10. Changes in Joint Appearance
Inflammation, growth of bone spurs and swelling may deform the joint and change its appearance altogether.

11. Bone Spurs
In advanced OA, the bones around the joint develop outgrowths known as spurs which appear as painful hard lumps.

What Causes Osteoarthritis?

Osteoarthritis is as a result of the deterioration of cartilage that serves as a cushion at the end of bones. That deterioration (wearing off) can be as a result of several factors

A. Joint Injury
A joint that suffered a serious injury or underwent a form of operation is likely to suffer OA later in life. People who engage in strenuous jobs and extremely physically demanding chores are at risk of OA.

B. Getting Older
As one’s age advances, joints and bones wear out slowly. The body’s ability to heal itself weakens too and one becomes susceptible to getting OA. It is common to people above the age of 40.

C. Obesity
Knee osteoarthritis is common in overweight people. If you have excess weight, it means that the body exerts more pressure to the knees than they can bear. This poses a risk to the knees.

D. Genetics
Genes play a small yet an important part on OA. Some forms of the condition run through a blood line. Nodal OA which is known to affect middle aged women particularly in the hands is inherited.

E. Inactivity
If you stay inactive for long periods of time, it means the muscles and tendons around your joints become weak. Strong muscles and tendons keep the stability of joints and when this is altered you are at the risk of OA. Light exercises like walking, cycling or swimming will keep your muscles strong.

F. Joints That Are Not Properly Formed
Sometimes one is born with malformed joints. You may also develop this in childhood. Such can lead to getting OA earlier in life of increase the severity of the condition in people.

G. Stresses on the Joints
Some activities like sports can impose a lot of stress on joints. Games like basketball involve jumping and landing which may stress the joints, reduce cartilage and risk OA.

Types of Osteoarthritis

1. Primary Osteoarthritis
This is the type of Osteoarthritis which is as a result of natural wear and tear of the cartilage. Medics associate it with aging and it does not have a specific trigger.

2. Secondary Osteoarthritis
This type of OA is initiated by a secondary factor. These factors may include injuries, obesity, genetic make-up or diseases.

Risk Factors

The risk factors involved with osteoarthritis include old age, gender, obesity, injuries on joints, occupations that stress joints, genetic make-up, malformed bones and infections or diseases.

Complications

Some of the complications of osteoarthritis include an increased risk of contracting gout and chondrocalcionosis. Gout sets in when uric acid forms crystals which are deposited around joints. The changes that occur to a joint when you get OA can lead to the formation of these crystals. On the other hand, having chondrocalcionosis means calcium pyrophosphate crystals have formed around your joints. It may be a joint with OA or without. The severity of OA worsens when you get these crystals around the same joint.

Who Gets Osteoarthritis?

Anybody can get OA whether young or old. However, primary OA is basically associated with age and is common with the aged. Secondary OA however affects both the young and the old.

How Does Osteoarthritis Affect People?

Osteoarthritis affects people in every aspect of life; emotionally, socially and economically. People with OA perceive their health status as ill. The limitations that come with OA impose anxiety, pain and emotional distress to patients. Treating or finding means to deal with the condition can also be expensive and burdensome to one’s finances.

How Do You Know If You Have Osteoarthritis?

When you experience symptoms that relate to OA, it is not advisable to be conclusive. Seek a medical practitioner who will test and deduce whether it is OA. Early testing will keep you away from many complications.

What Research Is Being Done On Osteoarthritis?

Research on OA is at an advanced state with medics digging to know how to counter this disease which has affected people for ages. At a congregation of researchers at American College of Rheumatology, several research reports revealed the possible causes of OA, the concept of patho-mechanics and how this is going to affect the treatment of OA.

New research being conducted in Harvard seems to be shedding light on this condition. Dr. Antonios Aliprantis says “we’re beginning to realize that there are important changes happening in the bone underneath the cartilage and in the joint lining itself”. There is a new development to incorporate strontium effectively, a drug which has been used in Europe to treat osteoporosis.

How Is Osteoarthritis Diagnosed?

There is no single method that is defined to diagnose osteoarthritis. Your doctor will ask you a series of questions and your health history. He may then perform some blood tests on you which will rule out other diseases that pose similar symptoms.

Arthroscopy may also be used where by the doctor inserts a viewing tube into the affected joint. From this tube the condition of the joint can be seen and at times repaired through the same. Repair of the joint through arthroscopy heals faster than the usual open operation

X-rays and MRI imaging are also used. They help the doctor in evaluating the extent of the condition and also rule out other similar conditions. Repeats of imaging also give the rate of progression of the disease.

How Is Osteoarthritis Treated?

Treatment of Osteoarthritis will depend on the extent of the disease and also the joint involved. Your physician will advise on possible treatment procedures that best suit you.

1. Surgery
This may be the last resolve after the rest have failed. Your physician will advise you on the kind of surgery. It may involve total replacement of the affected joint, bone realignment or lubrication injections on the joint.

2. Therapy
There are therapeutically effective measures that can help you in managing OA. Your doctor will advise on the need for a therapist. He may also recommend braces or shoe inserts which will minimize the pain when you move. They also take up the pressure exerted on the joint.

3. Supplements
You may consider taking nutritional supplements to curb pain.

4. Physical Measures
Giving physical support to joints like bracing them will relieve the pain and improve flexibility. You can also combine these with a regular exercise program to obtain maximum benefits.

5. Using Heat or Ice on the Painful Joint
Some people will respond to heat while others cold. Find what is appropriate for your pain.

6. Exercising
Exercising strengthens the muscles and joints. It also allows you to lose extra weight and thereby reducing the pressure you place on your joints.

7. Lifestyle Changes
Your lifestyle will define how far the severity of OA will go. Eat a healthy diet, maintain your weight and avoid foods that trigger flare-ups.

8. Losing Weight, If You’re Overweight
Extra body weight strains your joints. Getting involved in a program that allows you to shed it does your joints a lot of good.

9. Medications 
Osteoarthritis remains without a cure but there are drugs that help to relieve pain. They may include non-steroidal anti-inflammatory drugs and other pain killers. Flexoplex is a drug that has been proved to counter OA by lubricating the joint, repairing it and curbing the pain with all these benefits packed in a single tablet.

10. Alternative Treatments
Complementary or alternative therapy may include aromatherapy, taking supplements like glucosamine and chondroitin or application of gels and creams. It is essential that you involve your physician when you choose to take alternative therapy.

Prevention

Although all of us develop OA at some point in life as we age, it is possible for you to control the onset or progression of the disease. Indulge in regular exercises and check your weight. These will ensure the strength in your muscles and joints and that you do not strain your joints excessively.

Conclusion

With OA, you can live a meaningful and productive life if you learn how to manage the pain in early stages. Leading a healthy lifestyle in vital in a person with OA.

Raynaud's phenomenon: a whiter shade to winter's pale

Raynaud's phenomenon is a circulatory disorder, characterised by episodic attacks where arteries in the fingers and toes spasm, restricting blood flow and causing pain and marked colour changes of the skin.

During the winter months, complaints of pain associated with cold fingers and toes increase. 

In New Zealand, it is estimated that 19% of females and 5% of males experience symptoms 

consistent with Raynaud’s phenomenon.¹ This is a circulatory disorder, characterised by 

episodic attacks where arteries in the fingers and toes spasm, restricting blood flow and

 causing pain and marked colour changes of the skin.² In some people it may also affect 

other peripheral areas, such as the tip of the nose and ears.

In New Zealand, Raynaud’s phenomenon is reported to affect Māori and people with 

manual occupations more severely.¹ Initial vasoconstriction causes a white appearance 

to the skin as blood flow decreases, which is often followed by a cyanotic blue phase, as 

the trapped blood deoxygenates.² Attacks may last from minutes to hours and usually end 

with rapid perfusion of blood back into the digits, which then appear red. Episodes of

 Raynaud’s frequently cause pain and a “pins and needles” sensation due to sensory nerve 

ischaemia.² The cause of Raynaud’s is unknown, however, it is likely to involve increased 

activation of sympathetic nerves due to cold, or emotional stimulus.² In secondary
Raynaud’s, abnormalities of vascular structure and function from the underlying
condition contribute to the phenomenon.

Diagnosis is based on clinical symptoms and signs

A diagnosis of Raynaud’s phenomenon is based on a history of repeated and sudden

 episodes with the characteristics as described above. Patients may report attacks being 

triggered by cold weather, or other cold environments such as refrigerated areas in 

supermarkets or from cold air conditioning.³ There may be a family history present. 

An occupational history should be taken – people who use vibrating hand tools or 

have ongoing exposure to cold, e.g. meat packers, are at an increased risk of
 Raynaud’s.³

Raynaud’s can be primary or secondary

It is important to distinguish between primary and secondary Raynaud’s so that a
potentially serious, underlying condition, is not overlooked. Primary Raynaud’s has 
no underlying etiology and clinical examination may be normal, therefore it is a diagnosis
of exclusion.

Secondary Raynaud’s can occur due to a number of connective tissue diseases such as 

systemic sclerosis (scleroderma), systemic lupus erythematosus and rheumatoid arthritis, 

but can also occur with a range of other conditions, including carpal tunnel syndrome and 

hypothyroidism. Raynaud’s may also be secondary to medicines or trauma, particularly 

vibration injury.³ Patients with secondary Raynaud’s may have skin changes such as 

ulcerated or necrotic patches around the affected area.⁴

The presence of any of the following factors suggest a diagnosis of secondary Raynaud’s:³

• Age of onset > 30 years
• Intense, painful, asymmetric attacks or attacks associated with ischaemic skin lesions
• Symptoms suggestive of an underlying disorder, especially a connective tissue disease
•  – such as systemic sclerosis, where in up to 90% of cases Raynaud’s is one of the 
• presenting symptoms.⁵

Laboratory testing is unhelpful in people with primary Raynaud’s, but if a diagnosis of 

secondary Raynaud’s is suspected, testing may help confirm the presence of an
underlying condition. Initially, testing may include complete blood count, CRP and 
antinuclear antibody (ANA), however, other tests may be indicated depending on the 
clinical findings and suspected underlying condition. In some cases, treating the 
underlying condition will also ameliorate Raynaud’s phenomenon.⁶

Conservative treatment is often the best

Behaviour modification is the first strategy for alleviating symptoms of Raynaud’s 

phenomenon. A “common sense” strategy of avoiding abrupt changes in temperatures, 

therefore preventing peripheral vasoconstriction, can be effective. Considerations include 

clothing, home heating and workplace conditions.

Practical tips for avoiding or minimising episodes of Raynaud’s include:⁷

• Keep the whole body warm and wear warm socks, gloves and a hat when going out 
• in cold weather
• Avoid carrying objects in the hand, e.g. a handbag, which can restrict blood to the 
• fingers when gripped
• Maintain regular movement, e.g. squeezing a stress ball or walking round the room
• Avoid smoking as this causes vasoconstriction
• The consumption of “warming” foods such as porridge or chilli has been reported by
•  some people to ameliorate symptoms⁶
• When an attack occurs, place hands in warm water or under the armpits, or rotate
•  arms in a windmill pattern

People who experience Raynaud’s should avoid medicines which reduce blood flow to the 

peripheries, such as:⁴

• Serotonin receptor agonists, e.g triptans used to treat migraines
• Ergots (Claviceps fungi derivatives), e.g. ergotamine used to treat migraines
• Clonidine (which decreases cardiac output)

Historically there have been reports that non-selective beta-blockers, e.g. propanolol, 

carvedilol, nadolol, exacerbate Raynaud’s. Recent studies have shown that beta blockers 

with beta-1 selectivity, e.g. metoprolol, are less likely to cause vasoconstriction in patients 

with Raynaud’s. However, beta blockers should be used cautiously, in people who 

experience severe Raynaud’s symptoms.⁸

Medication is the second option

In severe cases of Raynaud’s, the use of medicines that cause vasodilation of the digits may be 

considered. Calcium channel antagonists such as nifedipine, amlodipine and felodipine are
frequently  effective in the treatment of Raynaud’s and are all fully funded in New Zealand.
However, calcium channel blockers are less effective for treating patients with secondary Raynaud’s,
 notably Raynaud’s secondary to systemic sclerosis (sclerodoma).⁹

Adverse effects of treatment are experienced by up to three-quarters of patients with Raynaud’s
and may include headache, flushing, dizziness and peripheral oedema. However, these effects can
be controlled with careful dosing and if mild, are often considered by the patient to be preferable to
the symptoms of Raynaud’s itself.⁹

Table 1: Calcium channel blockers for Raynaud’s phenomenon9

Medicine Dose Nifedipine (sustained-release) 30 – 120 mg/day Amlodipine 5 – 10 mg/day Felodipine (extended release) 2.5 – 10 mg/day

It is recommended that patients are started on the lowest dose of the chosen medicine (Table 1). 

The dose can then be increased incrementally as required and tolerated. If a patient reports that one 

calcium channel blocker is ineffective then another can be trialled.⁹ Primary Raynaud’s may 

spontaneously remit, therefore treatment can be stopped from time to time in order to confirm

 persistence.⁴ Some people report that intermittent use of the medicine prior to exposure to cold 

weather is sufficient.

Patients with secondary Raynaud’s, who find calcium channel blockers ineffective, may benefit 

from the concomitant administration of an additional vasodilator such as transdermal nitroglycerin.⁹

Many other medicines, such as other vasodilators, endothelin antagonists, phosphodiesterase-5 

inhibitors, prostaglandin derivatives, statins, botulinum toxin and N-acetyl-cysteine have been

 trialled in patients unresponsive to calcium channel blockers, however, there is limited evidence 

as to their effectiveness.

Rarely, in severe cases, surgical destruction of sympathetic nerves (sympathectomy) may be 

required to alleviate symptoms.

For video- Raynauds-real time

For further information: Centre for Arthritis & Autoimmune Rheumatic Disorders