Development Of Psoriasiform Lesions Research Articles

Anti-Tumor Necrosis Factor-α-Induced Dermatological Complications in a Large Cohort of Inflammatory Bowel Disease Patients.

The broader use of anti-tumor necrosis factor (TNF) agents in inflammatory bowel disease (IBD) has been associated with a high rate of adverse reactions. Dermatological complications are among the most common adverse events. We assessed the incidence, risk factors, management, and outcome of anti-TNF-induced dermatological complications in a large cohort of IBD patients. This was an observational retrospective study at a single tertiary referral center. All consecutive adult IBD patients treated with anti-TNF agents between 2005 and 2015 were identified. Patients who developed at least one dermatological complication while on anti-TNF therapy were included. From the 732 patients treated with anti-TNF agents, 211 (29%) developed at least one dermatological complication: 52% women (mean age of 42±13years), 85% with Crohn's disease, 67% were under infliximab. Median follow-up time under anti-TNF therapy was 53 (27-77) months. Dermatological complications recorded were: infections (13.5%), psoriasiform lesions (5.3%), injection/infusion reactions (3.8%), skin cancer (0.5%), and miscellaneous (5.6%). Overall, female gender (OR=1.658, p=0.029), smoking (OR=2.021, p=0.003), and treatment with an infliximab dose of 10mg/kg (OR=2.012, p=0.007) were independent risk factors for dermatological complications in multivariable analysis. Female gender (OR=3.63, p=0.017), smoking (OR=2.846, p=0.041), and treatment with adalimumab (OR=8.894, p<0.001) were independently associated with development of psoriasiform lesions. Three (3%) patients with infectious complications and 12 (31%) patients with psoriasiform lesions discontinued anti-TNF therapy definitively. Dermatological manifestations occurred in almost one-third of our population. Infections were the most common complication, but anti-TNF-induced psoriasiform lesions were the most common cause for anti-TNF therapy definitive discontinuation.

Psoriasiform Skin Lesions Are Caused by Anti-TNF Agents Used for the Treatment of Inflammatory Bowel Disease.

Tumor necrosis factor (TNF) antagonists used for the treatment of inflammatory bowel disease (IBD) have been associated with the development of psoriasiform skin lesions. We assessed the demographic and clinical characteristics associated with and outcomes of patients with anti-TNF-induced psoriasiform lesions. Patients with Crohn's disease (CD) and ulcerative colitis (UC) receiving treatment with anti-TNF therapy (infliximab, adalimumab, or certolizumab pegol) at a tertiary referral center were identified using an IRB-approved clinical data repository. Patients that developed psoriasiform skin lesions after initiation of anti-TNF therapy were included as cases. A group of anti-TNF-treated patients without drug-related psoriasiform lesions were identified as controls. The association between demographic and clinical variables and psoriasiform lesions was assessed using Chi-square analyses and multivariable logistic regression. Five hundred twenty-one patients with IBD undergoing treatment with anti-TNF therapy were identified; of these, 18 (3.5%) had psoriasiform lesions (16 CD and 2 UC). Seventy-two patients were identified as controls. Lesions developed a mean of 58 weeks (range 4-240 weeks) after starting anti-TNF therapy. The majority of patients were female and Caucasian (63 and 78%, respectively). Thirty-nine percent of patients had upper tract disease location. Forty-five patients (50%) were current or former smokers. Location of psoriasiform lesions included palmo-plantar (53%), trunk (47%), and scalp (53%), with 88% reporting involvement of ≥2 locations. Treatment of psoriasiform lesions was instituted with topical therapy in eight patients and systemic therapy (± phototherapy) in five patients. Discontinuation of anti-TNF therapy was recommended in nine patients (50%); of those, three were retreated with a second anti-TNF agent and all had recurrence of psoriasiform lesions. When adjusted for multiple variables, upper GI tract disease was significantly associated with psoriasiform lesions. Anti-TNF-induced psoriasiform lesions developed in 3.5% of patients with IBD at a tertiary referral center. Similar to prior published studies, most patients were female, had involvement of the palmo-plantar and scalp regions, and did not have severe IBD activity. The presence of upper tract disease was associated with the development of psoriasiform lesions. Skin lesions led to discontinuation of anti-TNF therapy in 50% of patients. Based upon these results, IBD providers should educate patients about this adverse effect, refer to dermatology for treatment, and discuss alternative IBD therapeutic options early if a severe psoriasiform rash develops.

The association of psoriasiform rash with anti-tumor necrosis factor (anti-TNF) therapy in inflammatory bowel disease: A single academic center case series

Background & AimsAnti-tumor necrosis factors (anti-TNF) including infliximab, adalimumab and certolizumab pegol are used to treat Crohn's disease (CD) and ulcerative colitis (UC). Paradoxically, while also indicated for the treatment of psoriasis, anti-TNF therapy has been associated with development of psoriasiform lesions in IBD patients and can compel discontinuation of therapy. We aim to investigate IBD patient, clinical characteristics, and frequency for the development of and outcomes associated with anti-TNF induced psoriasiform rash. MethodsWe identify IBD patients on anti-TNFs with an onset of a psoriasiform rash. Patient characteristics, duration of anti-TNF, concomitant immunosuppressants, lesion distribution, and outcomes of rash are described. ResultsOf 1004 IBD patients with exposure to anti-TNF therapy, 27 patients (2.7%) developed psoriasiform lesions. Psoriasiform rash cases stratified by biologic use were 1.3% for infliximab, 4.1% for adalimumab, and 6.4% for certolizumab. Average time on treatment (206.3weeks) and time on treatment until onset of psoriasiform lesions (126.9weeks) was significantly higher in the infliximab group. The adalimumab group had the highest need for treatment discontinuation (60%). The majority (59.3%) of patients were able to maintain on anti-TNFs despite rash onset. Among patients that required discontinuation (40.7%), the majority experienced improvement with a subsequent anti-TNF (66.7%). Conclusion27 cases of anti-TNF associated psoriasiform lesions are reported. Discontinuation of anti-TNF treatment is unnecessary in the majority. Dermatologic improvement was achieved in the majority with a subsequent anti-TNF, suggesting anti-TNF induced psoriasiform rash is not necessarily a class effect.

What's New in Laboratory Research?

Psoriasis is a multigenic disease with a number of susceptibility loci on different chromosomes predisposing to the disease, which is in turn triggered by environmental factors. The pathogenesis of psoriasis is characterized by 2 main components, the dysfunctions of the immune system and the alteration of keratinocyte homeostasis. While the Th1 T cell response has long been considered the sole immune agent in the pathomechanisms of psoriasis, recently, the role of IL-23-driven Th17 has been shown to be predominant. Subsequently, only effector memory T cells expressing alpha1beta1 integrin migrate into the epidermis, and psoriasis development is inhibited by blocking this integrin. Psoriatic epidermis contains high amounts of antimicrobial peptides, which have been shown to be a key mediator of plasmocytoid dendritic cell activation in psoriasis. The keratinocyte component has recently regained the central stage, as the abrogation of JunB/activator protein 1 in mouse keratinocytes induces development of psoriasiform lesions in T cell deficient mice. Moreover, inhibition of nerve growth factor and its receptor in keratinocytes strikingly improves psoriatic lesions.

Psoriasis Following Growth Hormone Therapy in a Child

To report a case of psoriasis that developed following growth hormone treatment. An 8-year-old boy was admitted to our pediatric endocrinology department because of short stature (<3rd percentile). A dopamine stimulation test and an insulin tolerance test revealed growth hormone (GH) deficiency with a normal cortisol response. His insulin-like growth factor 1 (IGF-1) level (9 ng/mL; reference range 113-261) was under the limits for his age and sex. Six months after the initiation of treatment with recombinant human GH 0.33 mg/kg/wk, the patient presented with a 10 day history of desquamation and a burning sensation in his right knee and hip. Lesions of erythematous papules consistent with plaques of psoriasis were present. Histologic findings from skin biopsies were consistent with psoriasis. The GH dose was reduced to 0.2 mg/kg/wk and treatment for psoriasis (including hydrocortisone and clemastine) was started. Three months after those interventions, the plaques had resolved. Previous studies proposed that the extent and severity of psoriasis correlate with GH levels, although psoriatic patients, in general, have normal GH and IGF-1 levels. The Naranjo probability scale indicated that the development of psoriasis was probably associated with GH therapy. This case suggests that the development of psoriasiform lesions in a previously unaffected individual represents an adverse effect of GH treatment, occurring at higher doses, with higher IGF-1 levels.