Category Archives: JAK drugs

Treat To Target for Rheumatoid Arthritis

Dr. Steve Paget summarized the “treat to target” approach for rheumatoid arthritis (RA) elegantly in a recent article.  He laid out ten principles that make sense.

rheumatoid-arthritisThey are:

1. The primary target for RA treatment should be clinical remission.

2. Clinical remission is defined as the absence of signs and symptoms of significant inflammation.

3. While remission is the target, low disease activity is an acceptable alternative.

4. Until the treatment target is reached, drug therapy should be adjusted every three months.

5. Measures of disease activity need to be obtained and documented every month for patients with high disease activity and every three months for patients with low disease activity.

6. Validated measures of disease activity should guide treatment decisions.

7. Structural changes and functional impairment shoulkd be considered when making clinical decisions.

8. The treatment target should be maintained indefinitely.

9. The choice of the disease measuring and the level of target should take patient factors, co-morbidities, and drug-related risk into consideration.

10. The patient needs to be informed about the treatment target and how it will be achieved.

For more information on arthritis treatments and other arthritis problems,  go to:

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New rheumatoid arthritis drug… the inside scoop!

The first oral biologic drug has finally hit the runway.

Here’s the “skinny” on it from the American College of Rheumatology…

Xeljanz (tofacitinib) is a first-in-class oral JAK inhibitor which has shown clinical effectoveness in patients with moderate to severe rheumatoid arthritis. xeljanz

Tofacitinib is approved for patients with an inadequate response to both biologic and non-biologic disease-modifying anti-rheumatic drugs (DMARDS) .

It should not be used in combination with other biologic agents. Current labeling for tofacitinib does not include an indication for inhibition of structural damage.

Data on safety suggests that infections, including severe “traditional” infections, as well as opportunistic infections and Herpes zoster, have occurred. Long-term safety studies and post-marketing safety data is being collected. Monitoring for blood abnormalities, liver enzyme abnormalities, lipid abnormalities and kidney damage is appropriate prior to initiation of therapy and throughout treatment.

For more information on arthritis treatments and other arthritis problems,  go to:

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Rheumatoid Arthritis: The scientific explanation of the new oral biologic therapies

rheumatoid-handRheumatoid arthritis is a chronic, systemic, autoimmune disease that is driven by inflammatory protein messengers, called cytokines.  Cytokines are produced by cells in the immune system including macrophages, dendritic cells, T cells and B cells. Abnormal regulation of cytokine production leads to the inflammation and tissue destruction that is characteristic of rheumatoid arthritis.

While much attention has been focused on what happens outside immune system cells, more recently, there has been interest in what happens inside these cells that might explain the abnormal regulation of cytokines.

Multiple pathways inside immune cells include pathways with such interesting alphabet soup names like the MAPK pathway, the JAK pathway, the Syk pathway, the NFK pathway, and the PI-3K pathway.

By way of background, if you’ve forgotten your biology, cells consist of an envelope called the cell wall, an inside soup called the cytoplasm, and a core called a nucleus.cell

Cytokines released by immune system cells bind to receptors located on the cell wall.  This binding then sends signals into the cytoplasm of the cell. In the example of the JAK pathway, the receptor on the cell wall, when activated by cytokine binding, sends a signal into the cytoplasm which activates the JAK pathway.

Activated JAKs do something weird then.  They phosphorylate (not an obscene word… just the action of adding a tag) other protein receptors found in the cytoplasm.  These protein receptors act as docking stations for another type of protein called STATs.  Once the STATs dock, they also become activated.  Yes… activation is contagious. These activated STATs then enter the nucleus of the cell and activate genes that lead to the production of more inflammatory cytokines. Pretty complicated, huh?

Why is this important?

It’s because these inflammatory cytokines activate, recruit, and attract more immune cells.  This leads to more inflammation and tissue damage… more or less an endless loop of destruction.

Understanding these mechanisms is what is now driving the pursuit of newer rheumatoid arthritis drugs, called small molecule drugs.  These are oral drugs that have a biologic action.

Clinical trial data has shown these drugs to be effective.  However, like other biologic therapies, they do have potential side effects including elevation of blood pressure, elevation of blood lipids, alterations in blood counts, decrease in kidney function and a few other issues.

Nonetheless, they will prove to be a helpful addition to our arsenal of rheumatoid arthritis treatments.

For more information on rheumatoid arthritis treatments and other arthritis problems go to:

Arthritis Treatment

And don’t forget to sign up for  free weekly arthritis tips and a free copy of our special report “The Consumer’s Guide to Arthritis”

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