Biological therapies for immune based chronic inflammatory diseases, especially
cytokine inhibitors such as
TNF-alpha antagonists, have been acceptably well tolerated in clinical trials with patients suffering rheumatic, dermatologic and
intestinal diseases in which they have been subsequently indicated. However, the pharmacovigilance studies and long-term follow-up have clarified several aspects on their safety in the everyday clinical use. The adverse effects associated with
TNF-alpha inhibitors can generally be classified into those related to the target (or class) and those related to the agent. Target-related adverse events include those potentially attributable to the immunosuppression inherent in blocking a key
cytokine, a phenomenon that could increase the susceptibility to
infections and
neoplasms. Specific inhibition of
TNF-alpha could also facilitate hepatotoxicity, production of
autoantibodies, development of demyelinizing diseases and it is also possibly associated to the worsening of
congestive heart failure. The side effects related to the agent itself, such as
allergic reactions and immunogenicity, are idiosyncratic phenomena of each molecule.
Infliximab is an
IgG1 class chimeric
monoclonal antibody with extensive accumulated experience in the treatment of
rheumatoid arthritis,
ankylosing spondylitis,
psoriatic arthritis, intestinal inflammatory disease and, recently, moderate-to-severe plaque
psoriasis. It is also being evaluated in other inflammatory
dermatitis and systemic diseases with skin expression, such as severe
atopic dermatitis,
pityriasis rubra pilaris,
pyoderma gangrenosum, cutaneous
sarcoidosis, Adult Still's disease, inverted
acne and refractory
graft -versus- host disease. Predisposition of
infliximab-treated individuals, as occurs with other anti-
TNF-alpha agents, to cause an increase of conventional pyogenic
infections (of the skin and soft tissues, respiratory tract, genitourinary tracts and bacteriemias) and an increase in granulomatous and
opportunistic infections due to invasive or intracellular pathogens (such as Mycobacterium tuberculosis), has been well established and quantified in the last five years. We presently know that the initiation of screening strategies of
latent infections (especially
tuberculosis) in the host candidate to receive anti-
TNF-alpha drugs, with their corresponding early treatment to avoid reactivations, and other prophylaxis, hygiene and vaccination measures have not only minimized these risks of suffering
infections but also have practically reduced and equalized the different capacity to trigger
infections belonging to each one of the
biological agents individually.