Adalimumab (Humira) is a human monoclonal antibody that binds to tumour necrosis factor alpha (TNF). TNF is a protein called a cytokine, produced mainly by white cells (leukocytes). In RA, TNF is produced by cells inside the joint and plays an important role in stimulating joint inflammation. When adalimumab binds to TNF, it neutralises the function of TNF and reduces joint inflammation and damage. Adalimumab is one of the licensed TNF-blocker or anti-TNF drugs (the others are infliximab and etanercept).
A monoclonal antibody is a protein and, therefore, cannot be taken by mouth as it would be digested. Adalimumab is given by an injection just under the skin, usually once every two weeks, using a special pre-filled syringe.
In the 1380 patients receiving adalimumab in the detailed clinical trials described above common side-effects included, injection site reaction, headaches and rashes. Many of these effects were transient and only 0.2% of patients had to stop treatment because of the most common side-effect of injection site reaction. These localised skin reactions usually disappear after a few injections.
Possibly the most serious side-effects to be considered with TNF-blocking treatment is that of infections. TNF plays an important helpful role in the body to fight infections. Studies of adalimumab have shown, as with other TNF-blocking drugs, a slight increase in serious infections such as pneumonia, pyelonephritis or joint infections. In particular, TNF-blocking drugs are associated with re-activation of previously undetected infections with tuberculosis (TB, previously known as consumption). Therefore, before taking adalimumab, or any TNF blocker, you will be asked about any previous infections, or contact with people with TB, including other family members and a chest x-ray will be performed. Sometimes a skin test will also be performed to assess if any dormant (latent) TB may be present. If there are signs of previous TB which has not been thoroughly treated, you will be asked to take anti-TB treatment before starting adalimumab (or any other TNF-blocking treatment).
TNF-blockers have all been reported to exacerbate multiple sclerosis and you will be asked if you have ever experienced symptoms such as transient loss of vision that could indicate a previous attack of multiple sclerosis.
There seems to be no increased risk of most cancers. However, although it is unclear if cancer has been previously treated and cured, how long the interval between cancer treatment and starting anti-TNF treatment should be. A cancer of lymph glands called lymphoma is known to be increased in patients with persistent active RA (as well as psoriasis and Crohn’s disease). The clinical trials of adalimumab have recorded 10 cases of lymphoma. This is higher than would be expected in the normal population, but is in keeping with the rate observed in patients with active RA, and this (ie no increased risk of lymphoma) is supported by data from larger groups of patients in the BSR biologics register (BSRBR).
Blocking TNF with drugs in RA is associated with a slight increase in the levels of auto-antibodies in the blood. These auto-antibodies are usually found in a condition called lupus. One patient out of 2334 RA patients treated with adalimumab developed new onset lupus. The patient improved following discontinuation of therapy.
Blocking TNF may worsen moderate to severe congestive heart failure. Therefore, adalimumab (and other anti-TNF therapies) is also not recommended for RA patients with moderate to severe heart failure.
http://www.nras.org.uk/about_rheumatoid_arthritis/newly_diagnosed/which_drugs_are_used/adalimumab_humira.aspx