239receiving anti-TNF therapy for IBD, Rahier et al. found that 42/60 (68%) in the
psoriasiform group and 20/23 (87%) in the eczematiform group were females [ 25 ].
Guerra et al. and George et al. reported a similar female predominance in their stud-
ies, 15/21 (71%) and 14/18 (78%), respectively [ 31 , 32 ]. Similarly, in a systematic
literature review consisting of IBD patients who developed psoriasis during anti-
TNF therapy, 21/41 (64%) of the cases were females (see Table 14.2) [ 36 ]. This
finding may be confounded by the fact that autoimmune diseases are generally more
common in females and these inflammatory skin lesions are thought to be immune-
mediated [ 31 ].
Cigarette smoking has been linked to the development of idiopathic psoriasis
[ 37 ], and a similar association is thought to exist between smoking and anti-TNF-
related psoriasiform lesions (see Table 14.2) [ 32 , 38 ]. In a case control study consist-
ing of 373 cases with new onset of plaque psoriasis, Wolk et al. found that smoking
was associated with 70% increased risk for onset of psoriasis [ 37 ]. The ingredients
in cigarettes are thought to be pro-inflammatory which can lead to immune dysregu-
lation and the development of idiopathic psoriasis [ 37 ]. However, Guerra et al. found
that smokers and nonsmokers were equally likely to develop anti-TNF-related pso-
riasiform lesions in their cohort [ 31 ]. In a retrospective case control study consisting
of 18 anti-TNF-treated patients with psoriasiform lesions and 70 anti-TNF-treated
patients without skin lesions, smokers were numerically more likely to develop pso-
riasis than nonsmokers, 7/18 [38.9%] vs. 13/70 [18.6%] (p = 0.13) [ 32 ]. Similarly,
in a large retrospective cohort study where 42 cases of psoriasis were recorded
among 402 anti-TNF-treated IBD patients, smoking was found to be an independent
predictor of psoriasis (HR 2.37, 95% CI, 1.36–4.48; p = 0.08) [ 38 ].
Psoriasiform lesions may be more common in patients with CD than ulcerative
colitis (UC) (see Table 14.2). In a case series by Guerra et al., 17/21 (81%) of
patients with anti-TNF-related psoriasis had CD [ 32 ]. Rahier et al. also noted that
majority of patients who developed psoriasiform or eczematiform lesions during
anti-TNF therapy had CD, 52/62 (84%) and 17/23 (74%), respectively [ 25 ]. A simi-
lar finding was observed in a cross-sectional study by Hellstrom et al. where nearly
80% of patients who had eczema or psoriasiform lesions (new onset = 8, exacerba-
tion of existing lesions = 6, existing lesions not worsened = 11) had CD [ 26 ]. In a
retrospective case control study comparing demographic and clinical characteristics
between 18 anti-TNF-treated patients with psoriasis and 70 anti-TNF-treated
patients without psoriasis, those with upper tract CD were more likely to have pso-
riasis during anti-TNF therapy (39% vs. 5%, p = 0.001) [ 32 ]. This association may
be confounded by the fact that patients with CD, particularly those with upper GI
tract involvement, are more likely to receive an anti-TNF than patients with UC.
Table 14.2 Risk factors for
anti-TNF-induced
psoriasiform and
eczematiform lesions
Young age
Female gender
Smoking
Crohn’s disease14 Noninfectious and Nonmalignant Complications of Anti-TNF Therapy