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Two biological response modifiers that are approved for treatment for psoriasis and psoriatic arthritis are the fusion protein, etanercept, and the monoclonal antibody, adalimumab. These are their "generic names"—etanercept is manufactured and marketed under the trade name Enbrel by the pharmaceutical company Wyeth. Adalimumab is produced by Abbott Labs and marketed as Humira, an abbreviation of "human monoclonal antibody in rheumatoid arthritis" derived from the treatment for which adalimumab was first developed.
Both of these biological response modifiers work by inhibiting the pro-inflammatory role of the cytokine, tumor necrosis factor-alpha, or TNF-a, within the body's immune system. Both drugs are the product of recombinant DNA technology, and are engineered to consist of the constant F portion of human IgG antibodies and a TNF-a binding component. Both are priced at roughly the same cost for patients: $1200 to $1700 per month. And both companies offer the drugs through patient assistance programs for those who have difficulty with the cost of treatment, although the terms and length of time each program is available to patients may vary.
Recombinant DNA technologies are the methods that have been developed to splice two or more individual gene segments together with the intent to design a protein that possesses particular qualities or activities. In a very simplified version of normal gene expression, a gene, made up of a double helix of DNA, is "transcribed" by certain cell components to form a single strand of RNA. The RNA strand can then be "processed" through other cell "machinery" to create specific proteins that the cell then uses to send signals, or messages, to yet other cell components, or that carry out specific functions critical to cell metabolism, such as peptides, cellular membrane portals, or activation factors. Many things can happen along this pathway to modify the protein and its specific functions or activities. Recombinant DNA technology takes advantage of these processes to customize and synthesize a final protein product for use as a drug, as is the case with these biologics. (And again, this description is a highly simplified explanation of a very complex set of reactions that take place continually in a living organism.)
In the case of Enbrel, the gene segment for the human p75 TNF receptor is coupled with the gene segment that produces the Fc portion of human IgG (immunoglobulin G, the body's most common antibody). When this recombinant DNA structure is expressed by a Chinese hamster ovary (mammalian) cell expression system, the "fusion protein" that emerges has the ability to bind to TNF-a when injected into a patient, rendering TNF-a biologically inactive. With Humira, recombinant technology is used to create fully human monoclonal antibodies with an affinity for TNF-a, which similarly when injected into a patient renders TNF-a inactive. In psoriasis and psoriatic arthritis there is an abundance of TNF-a generated at the sites of inflammation by the autoimmune reaction at the heart of the disease. Rendering excess TNF-a inactive reduces inflammation by limiting the generation of additional pro-inflammatory factors to what the immune system considers a challenge.
A cytokine is a signaling protein that facilitates cellular communication, often in response to injury, infection, or an autoimmune reaction. TNF-a is a key cytokine that plays many amazing roles in the body, from regulating inflammation to assisting in the normal and necessary apoptosis, or programmed cell death. Apoptosis is the process responsible for fingers and toes differentiating into hands and feet in the developing fetus, or for breaking down unneeded cell components that the body recycles and reuses. A chief role, though, for TNF-a is as a signal protein regulating inflammation in the body, and as such, it is found in high concentrations in skin involved in psoriatic lesions.
TNF-a is secreted by many different cells in the body, but primarily from the white blood cells called macrophages. When TNF-a is released in response to a challenge to the immune system, it binds with either of two receptors, TNF-R1 or TNF-R2, which in turn act to initiate additional reactions. TNF-R1 is by far the more active TNF-a binding site, where binding leads to a set of complex reactions that increase inflammation in the area where the immune system senses a challenge is taking place. In psoriasis, an unknown trigger challenges the body's immune system which responds by producing excessive TNF-a, along with a number of other pro-inflammatory factors, such as T-cells, interferons, and interleukins which have been shown to play roles in the rapid skin turnover that is behind plaque formation.
By designing drugs that place the TNF-R1 receptor onto human IgG antibodies, TNF-a can be selectively removed from the sequence of events that cause inflammation. For some, these drugs reduce inflammation and provide relief from their psoriasis symptoms, while for others the effect seems to be less effective, or not effective at all.
Because these drugs act directly upon a key component of our body's natural immunity mechanism, they both carry significant risks with their use. The strikingly cautionary tone of the labeling required by the FDA on all marketing materials in print and online clearly indicates this risk. TNF-a is a critical component of our body's natural defense system. Deliberately interfering with this system, in particular, can and has resulted in severe unintended consequences. Serious bacterial and fungal infections, tuberculosis, cancer, blood and nervous system problems, and even deaths have occurred in patients using these treatments. They have offered many psoriasis patients significant benefits with few to no apparent side effects, while others have found the treatments to be only marginally effective, or not effective at all. Some patients have used one treatment over a period of time, before switching to another in the effort to find relief. Some have experienced upon stopping a treatment "rebound" effects, with their psoriatic flares returning to the same or worse status than before treatment was started. Psoriasis is a highly individualized disease and patient experience has shown that what works for one person may not work at all, or only marginally for another. Any psoriasis sufferer must weigh the risks and benefits of these treatments very carefully before beginning their use.
Strictly approved for those with moderate to severe psoriasis, these and the other biological response modifiers that are on the market have shown some promise in relieving the symptoms and discomfort experienced in psoriasis and psoriatic arthritis. But to date, all come with serious risks of severe infection, disease, and even death. Great care should be taken when considering their use. A good starting point for undertaking such considerations is arguably one that includes making deliberate diet and lifestyle changes that promote systemic good health: Eliminate any dietary, environmental, and emotional factors that trigger or exacerbate psoriasis flares. Ensure any nutritional gaps are covered by taking a high-grade multivitamin–mineral complex daily. Avoid unhealthy lifestyle choices that compromise one's general good health. If one can make deliberate improvements to one's general state of health, this launching point is optimum for finding lasting, effective relief through any number of psoriasis treatments available.
In 2005 DermaHarmony began to "rethink" psoriasis — its nature, causes and treatment — starting a revolution natural in skin health that continues to this day. Our programs and products promote healthy skin with nutritional supplements, cleansing and detoxification, pH balancing, mild topical treatments and dietary guidance.