Plaque psoriasis patients could develop resistance against adalimumab (Humira), says study

Plaque psoriasis patients taking adalimumab (Humira) could develop resistance to the drug, studies indicate.

A new study from the Netherlands researchers indicate that a large portion of patients taking the immunosuppressant adalimumab (Humira) for plaque psoriasis developed antibodies to the drug.

The study conducted in two Dutch dermatology departments in university hospitals detected antibodies to adalimumab in 13 of 29 patients (45%) during 24 weeks of treatment.

The patients had an average age of 44 years and average disease duration of 22 years. They were given an initial 80mg dose of Humira, followed by 40mg doses.

Patients responded with differing rates low, high, and no titers of antibodies to adalimumab were significant at weeks 12 and 24.

The median adalimumab trough concentrations varied significantly among patients with low, high, and no titers of antibodies to adalimumab.

The median adalimumab trough concentrations also differed significantly at week 24,among good responders, moderate responders, and nonresponders.

Twelve out of 13 patients, or 92 per cent, who developed antibodies to adalimumab (Humira) had previously also been treated with Enbrel (etanercept), while only half of those who hadn’t developed Humira antibodies had been treated with Enbrel (etanercept).

“Antibodies to adalimumab are associated with lower serum adalimumab trough concentrations and with nonresponse or loss of response to adalimumab in patients with plaque psoriasis,” the researchers wrote in the latest issue of Archives of Dermatology.

However, the researchers recommended testing for antibodies to adalimumab when patients lose response to adalimumab or do not respond at all.

They also emphasized the need for further research to identify risk factors for antibody development and factors affecting antibody development. Investigations are also needed to study how the effect of antibodies to adalimumab can be minimized.

Adalimumab, which is marketed by Abbott under the brand name Humira, is the third TNF inhibitor, after infliximab and etanercept, to be approved by USFDA. Adalimumab binds to TNF?, preventing it from activating TNF receptors.

Adalimumab is constructed from a fully human monoclonal antibody. TNF? inactivation has proven to be important in the inflammatory reactions associated with autoimmune diseases.

Humira affects immune system, and hence can lower the ability of the immune system to fight infections.

Serious infections have happened in patients taking Humira. These infections include tuberculosis (TB) and infections caused by viruses, fungi, or bacteria that have spread throughout the body. Some patients have died from these infections. HUMIRA may increase the chance of getting lymphoma or other cancers.

Adalimumab has been approved by the FDA for the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, moderate to severe chronic psoriasis and juvenile idiopathic arthritis.

Humira is a prescription medicine used to treat moderate to severe chronic (lasting a long time) plaque psoriasis.

Plaque psoriasis is red, scaly skin.

In one clinical trial for moderate to severe chronic plaque psoriasis patients, 7 out of 10 adults taking Humira saw 75% skin clearance and 6 out of 10 patients had clear or almost clear skin at 16 weeks.

US FDA approved Humira for treatment of rheumatoid arthritis in 2002. The $3 billion Humira was submitted for the fifth new indication for global regulatory approval for psoriasis in 2007.