Category Archives: Prednisone

Rheumatoid arthritis drugs… which ones are friendly to the heart and which ones aren’t!

Rheumatoid arthritis (RA) is a chronic, autoimmune systemic disease which affects approximately two million Americans. While the symptoms that bring the patient to the doctor are the joint swelling and pain, the area of most concern may not be the joints.  It is well established that cardiovascular risk is markedly increased in RA and in fact it is this complication that shortens lifespan by between ten to fifteen years.

A number of clinical studies have retrospectively examined the relationship between certain medications and the risk of cardiovascular events.  The report card has provided some real surprises.heart-attack_0

For example, methotrexate, the workhorse disease modifying anti-rheumatic drug (DMARD) of choice reduces cardiovascular mortality by almost 70 per cent. The mechanism is felt to be due to a reduction of atherosclerotic plaque formation as well as increased clearance of foam cells (Solomon DH, et al. Circulation 2003; 11: 1303-1307).

The other major player in the treatment of RA is the TNF inhibitor group.  These are used in more than 50 per cent of RA patients in the US. These drugs apparently reduce the risk of cardiovascular events by almost 50 per cent (Gonzalaz A, et al. Ann Rheum Dis. 2008; 67: 64-69). Why this occurs is still not clearly understood.

Steroids have been used to treat RA since the early 1950’s.  Steroids have been shown to worsen cardiovascular risk because of their effects on both blood pressure as well as blood glucose.  Steroid use in RA has been associated with increased carotid plaque formation as well as increased arterial stiffness.  So what dose is a safe dose?  The answer is still unknown.

Non-steroidal anti-inflammatory drugs (NSAIDS) raise blood pressure.  Randomized clinical trials have shown that cardiovascular risk is associated with COX-2 inhibitors but also with non-selective COX drugs also.  The upshot? All NSAIDS regardless of class, are associated with increased cardiovascular risk.

Hydroxychloroquine, a drug often used to treat mild RA, is associated with a decrease in diabetes and may also improve lipid status.  Actemra increases lipid profile but the long term effects are still unknown.  Leflunomide (Arava) increases blood pressure.  The eventual effects are still a subject of conjecture.

So what about aspirin?  This medication is used for cardiovascular prophylaxis.  In higher doses it also has anti-inflammatory effects although these are limited by the potential gastrointestinal side effects known to be caused by high dose aspirin. It is well known that other NSAIDS should not be used in patients taking aspirin for cardiovascular prophylaxis since they blunt that effect.

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What’s a safe dose of prednisone? Is there such a thing?

A spirited debate was published in the Rheumatologist, a magazine I get. The topic was the use of prednisone in rheumatoid arthritis.  Recent guidelines produced by the American College of Rheumatology regarding treatment of rheumatoid arthritis omitted the use of prednisone.

prednisone-5Dr. John Kirwan, a professor at the University of Bristol, who wrote several papers showing that prednisone had disease-modifying effects and held back the destructive processes of rheumatoid arthritis (RA) made his pitch. He advocated the use of prednisone in combination therapy for this condition.

Dr. Theodore Pincus, a professor at NYU, advocated the use of low dose prednisone (less than or equal to 5 mgs a day). He provided evidence that it was safe and effective at that dose.

Dr. Anthony S. Russell, a professor at the University of Alberta issued the counterpoint. He provided historical data showing that prednisone had long term toxicity without significant benefit (in his opinion.)

With all due respect to Dr. Russell, much of the data he cited was old data when higher doses of prednisone were used.  He also contended that primary care doctors would be tempted to use prednisone if they saw rheumatologists using it.

My opinion is this.  I use low dose prednisone a lot in my practice.  By low dose, I mean 5 mgs or less. I think it is effective as an add- on therapy.  It is also a great “bridge” if the patient is transitioning therapies. I have seen very little long term toxicity associated with this low dose approach.  And I think the benefits derived from improved activities of daily living far outweigh the negatives. I do think that doses higher than 5 mgs should be avoided if possible. I also don’t think the primary care issue is that big a deal although I admit… I have seen some indiscriminate use in my community.


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Rheumatoid Arthritis Treatments

Of all of the inflammatory forms of arthritis, rheumatoid arthritis (RA) is the most common. It affects about 2 million Americans, about 60% of whom are women.  RA affects people of all ages including infants and children.

It is an autoimmune disorder characterized by chronic inflammation in the joints which causes pain, swelling, and stiffness. What is generally not understood is that it affects not only joints but internal organs as well.

Data has indicated that early aggressive treatment of RA can limit joint damage. RA is a major contributor to morbidity and mortality.  Mortality rates among people with RA are twice that of the general population and disease severity is an independent risk factor of mortality regardless of other co-morbid conditions.  People with RA are twice as likely to develop congestive heart failure is compared to those without RA. Cardiovascular disease is a major cause of mortality in patients with RA.

RA , if not treated aggressively, can cause permanent joint damage leading to deformity and loss of joint movement.  As a result, many people with RA experience limitations in their ability to perform daily activities which impacts quality of life.

woman-with-a-walkerRA is the most common cause of disability in the United States and the third leading cause of work limitations.  Medical and indirect costs due to lost wages are estimated at $3 billion annually and fewer than 50% of working age adults with RA are still employed 10 years after onset of the disease.

The cause of RA is unknown, but multiple genetic and environmental factors (infectious agents, reproductive status, and smoking) are thought to be involved.

When it comes to treatment, the primary goals are to relieve pain, swelling, and fatigue; improve joint function; slow down or stop joint damage; and prevent disability and disease-related morbidity.rub-hands

RA is a complex disease.  There are many cells, proteins, and processes involved in the genesis of RA.   T cells mediate joint damage both directly and indirectly by driving non-T  cells to release inflammatory cytokines.  Also,  B cells play a role in RA pathology by producing autoantibodies and triggering cytokine secretion by T cells as well as by acting as antigen-presenting cells (APCs) to trigger T-cell activation. This entire machinery is driven by multiple cytokines.

In the past the traditional treatment pyramid for rheumatoid arthritis was to start with anti-inflammatory drugs, move onto mild disease-modifying drugs (DMARDS), step up to more aggressive disease-modifying drugs if they didn’t work, and finally use powerful immunosuppressive drugs as a last resort.  The treatment approach now is to stand the pyramid on its head and use more aggressive therapies in concert with methotrexate to effect remission as soon as possible.

A newer approach is to “treat to target.”  This means that a specific goal of remission is aimed for and adjustments in medications are made regularly in order to achieve

Anti-inflammatory drugs- either non-steroidal drugs or low dose corticosteroids are an adjunctive therapy but are not considered as important as remission-inducing drugs. These drugs are initiated at the start of treatment to give the patient some relief- to serve as a “bridge” until the disease-modifying anti-rheumatic drugs (DMARDS) can kick in. Full therapeutic doses of non-steroidal anti-inflammatory drugs (NSAIDS) or prednisone in doses ranging from 5-10mgs/day are helpful for symptoms. Side effects related to an increase in cardiovascular events as well as gastrointestinal issues must be balanced against benefit.

Remission-inducing agents (DMARDS) are started at the same time or shortly thereafter.  Besides methotrexate, other DMARD drugs include hydroxychloroquine (Plaquenil), azathioprine (Imuran), sulfasalazine (Azulfidine), cyclosporine (Sandimmune), and leflunomide (Arava).

By far, the most commonly used is methotrexate.

Treatment options including combination DMARD therapy and  biologic response modifier are used by rheumatologists to induce remission.

Therapeutic agents including TNF antagonists and IL-6 inhibitors were developed to block cytokine-mediated processes.  Co-stimulatory pathway T-cell drugs were developed to inhibit T-cell mediated processes.  Elucidation of the role of B cells in the inflammation cascade has provided the rationale for the institution of B-cell targeted therapies.

Biologic drugs have revolutionized the treatment of rheumatoid arthritis and have permitted rheumatologists to achieve remission in many patients with RA.

Examples of biologics include the following: TNF inhibitors consist of Enbrel, Humira, Remicade, Cimzia, and Simponi.  Anti-interleukin 6 drugs are represented by Actemra.  The primary  T-cell drug is Orencia and the B-cell drug is Rituxan.  Many other drugs are in the pipeline.

In addition to the existing biologics, new oral kinase inhibitors (JAK and SYK) are exciting new drugs.

Objective measurement of remission include reduction in joint swelling and pain scores, improvement in health assessment and activities of daily living, reduction in blood measures of inflammation, and cessation of disease activity by magnetic resonance imaging.

Newer measurement criteria that will ensure uniformity of definition of remission are also being created.


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Prednisone Side Effects

Prednisone – sometimes it’s mispelled as “prednizone”-is a generic, inexpensive, and commonly used medicine in arthritis treatment.

The diseases for which corticosteroids are most often used are rheumatoid arthritis, lupus, psoriatic arthritis, ankylosing spondylitis, Reiter’s disease, polymyalgia rheumatica and temporal arteritis, polymyositis and dermatomyositis, gout and pseudogout, sarcoidosis, and the arthritis accompanying inflammatory bowel disease.

It is catabolic (meaning it breaks down tissue) and anti-inflammatory.

When taken chronically it can suppress the ability of the adrenal glands to make its own steroid, particularly if the average daily dose of prednisone is greater than 7.5 mgs.

Other factors that constrain the ability of the adrenals to perform are if therapy continues for more than a few weeks or months, if doses are given late in the day or in divided doses throughout the day, or if long-acting corticosteroid preparations are used.

Patients who require high doses of prednisone (more than 20 mgs a day) for extended periods of time always develop side-effects.

Taking steroids on an alternate day (every other day) schedule reduces the chance of adrenal insufficiency but does not eliminate it.

Other side-effects include:

“Moon face”

Elevated blood sugar and diabetes

Elevated cholesterol and triglycerides

Fluid retention



Increased blood pressure

Electrolyte abnormalities such as low potassium serum levels

Hardening of the arteries

Hirsutism (abnormal hair distribution)

Easy bruising

Thinning of the skin

Cataracts and glaucoma

Purple striae (stretch marks)

Poor wound healing

Muscle wasting

Susceptibility to infection and masking of infection leading to sepsis and death


Avascular necrosis (dead bone)


Inflammation of the pancreas

Stomach ulcers (particularly if used with non-steroidal anti-inflammatory drugs

Obviously, patients must be counseled as to the relative risks and benefits, and the lowest possible steroid dose should be used.

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