Summary
Background
With the expanding list of medications available to treat patients with inflammatory bowel disease (IBD), it is important to recognise adverse events, including those involving the skin. Dermatological adverse events may be confused with extra‐intestinal manifestations of IBD.
Aim
To review drug‐related dermatological manifestations associated with immunosuppressive and anti‐tumour necrosis factor (anti‐TNF) therapy.
Methods
The literature was searched on PubMed for dermatological adverse events in IBD.
Results
Present thiopurine exposure was associated with a 5.9‐fold [95% confidence interval (CI), 2.1–16.4] increased risk of developing non‐melanoma skin cancer (NMSC). The peak incidence is highest in Caucasians over the age of 65 years with crude incidence rates of 4.0 and 5.7/1000 patient‐years for present and previous use. In anti‐TNF‐exposed subjects, drug‐induced lupus was reported in 1% of the cases and a psoriatic rash in up to 3% of the cases. Anti‐TNF monotherapy increases the risk of NMSC ~2‐fold to a rate of 0.5 cases per 1000 person‐years. Cutaneous lymphomas have been rarely reported in subjects on thiopurine or anti‐TNF drug monotherapy. Combination therapy seems to have an additive effect on the risk of developing NMSC and lymphoma.
Conclusions
Physicians need to be aware of the wide spectrum of dermatological complications of immunosuppressive and anti‐TNF therapy in IBD, especially psoriasis and non‐melanoma skin cancer. Vigilance and regular screening for non‐melanoma skin cancer is recommended. Case discussions between gastroenterologists and dermatologists should be undertaken to best manage dermatological adverse events.
We demonstrate increasing body weight over time from 1991 to 2008 in CD as evidenced by baseline data from randomized clinical trials. Adiposity may play a potential role in initiating and perpetuating intestinal inflammation, a hypothesis that should be explored further.
The pathogenesis of inflammatory bowel disease (IBD) is multifactorial and results from an interaction between genetic, immunologic, microbial, and environmental factors. Certain drugs could act as a trigger for the disease and have been implicated in the development of new onset IBD in a number a studies. These relationships are based on case reports and cohort studies, as proving this in the context of randomized controlled trials would be difficult. Drugs that have been linked to causing or worsening IBD include isotretinoin, antibiotics, nonsteroidal antiinflammatory drugs, oral contraceptives, mycophenolate mofetil, etanercept, ipilimumab, and rituximab. Bowel preparation for colonoscopy has also been associated with aphthoid lesions that may be confused with IBD. However, given the source of these reports we have to be cautious in the interpretation of the data before concluding that these drugs trigger IBD and what is being observed is not related to other confounding factors. Different pathogenic mechanisms have been suggested for the different drugs listed above. In order to clarify the confusion a comprehensive literature review was performed with the goal of advancing the knowledge on this subject.
Thiopurine withdrawal due to adverse events is commoner in women over the age of 40 at prescription. These findings need to be replicated in other cohorts.
LE PPtESENT T R A V A I L rut entrepns h la sm~e e pubhcahons recentes attrlbuant ou sugg6rant une achon anhbact6rmnne atll melhoxyflurane et a l'halothane Les avantages 6v~dents que pr~senteraaent des anesth6s~ques possddant une telle a c ' ' ue preventmn des ~omphcataons pulmonmres post-operatw~te, au point de, v ' l ' to~res, nous ont motes a pr~caser ces propnetes
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