Dermatological complications involve one of five patients treated with anti-TNF therapy after a 14-year follow-up. Association of cutaneous infections with higher anti-TNF dosing suggests a dose-dependent effect. Discontinuation of anti-TNF therapy due to dermatological complications is required in one out of five patients with psoriasiform lesions, but specific dermatological treatment allows to continue anti-TNF therapy in half of them.

Abbreviations: Col7, collagen type VII; DEB, dystrophic epidermolysis bullosa; RDEB-I, inversa recessive dystrophic epidermolysis bullosa

Nicorandil, a nicotinamide ester, was first reported to be involved in the induction of oral ulcers in 1997. Since then, many reports of single or multiple nicorandil-induced ulcerations (NIUs) have been reported. We hypothesised that in the case of high-dosage nicorandil or after an increased dosage of nicorandil, nicotinic acid and nicotinamide (two main metabolites of nicorandil) cannot appropriately merge into the endogenous pool of nicotinamide adenine dinucleotide/phosphate, which leads to abnormal distribution of these metabolites in the body. In recent or maintained trauma, nicotinamide increases blood flow at the edge of the raw area, inducing epithelial proliferation, while nicotinic acid ulcerates this epithelial formation, ultimately flooding the entire scar. We demonstrate, by comparison to a control patient non-exposed to nicorandil, an abnormal amount of nicotinic acid (×38) and nicotinamide (×11) in the ulcerated area in a patient with NIUs. All practitioners, especially geriatricians, dermatologists and surgeons, must be aware of these serious and insidious side effects of nicorandil. It is critical to rapidly reassess the risk-benefit ratio of this drug for any patient, and not only for those with diverticular diseases.

SUMMARY BackgroundPsoriasiform lesions associated with anti-tumour necrosis factor (TNF) therapy are frequent in patients with inflammatory bowel disease (IBD). While methotrexate is the most frequently used systemic treatment for psoriasis, its efficacy for psoriasiform lesions related to anti-TNF therapy remains unknown.

In this paper, we present a two-dimensional pore-scale numerical model to investigate the main mechanisms governing biofilm growth in porous media. The fluid flow and solute transport equations are coupled with a biofilm evolution model. Fluid flow is simulated with an immersed boundary-lattice Boltzmann model while solute transport is described with a volume-of-fluid-type approach. A cellular automaton algorithm combined with immersed boundary methods was developed to describe the spreading and distribution of biomass. Bacterial attachment and detachment mechanisms are also taken into account.The capability of this model to describe correctly the couplings involved between fluid circulation, nutrient transport and bacterial growth is tested under different hydrostatic and hydrodynamic conditions (i) on a flat medium and (ii) for a complex porous medium. For the second case, different regimes of biofilm growth are identified and are found to be related to the dimensionless parameters of the model, Damköhler and Péclet numbers and dimensionless shear stress. Finally, the impact of biofilm growth on the macroscopic properties of the porous medium is investigated and we discuss the unicity of the relationships between hydraulic conductivity and biofilm volume fraction.

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