[Infectious risk]

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.