Hereditary hemorrhagic telangiectasia (HHT) also known as Rendu Osler syndrome is a vascular hereditary autosomal dominant disease, leading to a dysfunction in the development of arteriovenous capillaries, usually resulting in epistaxis, gastrointestinal (GI) bleeding, and iron deficiency anemia. It is believed that by interfering and stopping angiogenesis, anti-vascular endothelial growth factor molecules could be an option for HHT patients. Indeed, an intranasal treatment regime of diluted Avastin (bevacizumab; recombinant humanized antivascular epithelial growth factor immunoglobin G1) has proven clinically efficacious in patients with HHT1. However, there are no data available regarding bevacizumab's effect in patients with HHT and GI bleeding. We report here the case of an 85-year-old woman, suffering from life-threatening GI bleeding due to HHT with an impressive clinical response using anti-vascular endothelial growth factor infusion.

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SRSB allows a gain in macronutrient absorption, which is associated with a lower HPN dependence. To our view, SRSB should be integrated in intestinal rehabilitative adult programs.

Summary Background Phase III trials have demonstrated the efficacy of risankizumab in moderate‐to‐severe Crohn's disease (CD), but no real‐world data are currently available. We aimed to assess the short‐term effectiveness and safety of risankizumab in patients with CD. Methods From May 2021 to May 2022, all patients with refractory luminal CD treated with risankizumab in 22 French GETAID centres were retrospectively included. The primary endpoint was steroid‐free clinical remission at week 12 (Harvey‐Bradshaw [HB] score <5). Secondary endpoints included clinical response (≥3‐point decrease of HB score and/or (HB) score <5), biochemical remission (CRP ≤ 5 mg/L), need for CD‐related surgery and adverse events. Results Among the 100 patients included, all have been previously exposed to anti‐TNF agents, 94 to vedolizumab, 98 to ustekinumab (all exposed to at least three biologics) and 61 had a previous intestinal resection. All but three (97%) received a 600 mg risankizumab intravenous induction at weeks 0–4–8. At week 12, steroid‐free clinical remission was observed in 45.8% of patients, clinical remission in 58% and clinical response in 78.5%. In subgroup analysis restricted to patients with objective signs of inflammation at baseline (n = 79), steroid‐free clinical remission at week 12 was observed in 39.2% of patients. Biochemical remission was observed in 50% of patients. Six patients discontinued risankizumab before the week 12 visit due to lack of efficacy. CD‐related hospitalisation was needed in six patients, and three underwent intestinal resection. In multivariable analysis, only a history of ustekinumab loss of response (vs primary failure) (odds ratio (OR), 2.80; 95% CI: 1.07–7.82; p = 0.041) was significantly associated with clinical remission at week 12. Twenty adverse events (AE) occurred in 20 patients including 7 serious AE corresponding to 6 CD exacerbation and one severe hypertension. Conclusion In a cohort of highly refractory patients with luminal CD and multiple prior drug failures including ustekinumab, risankizumab induction provided a clinical response in about 3 out of 4 patients and steroid‐free clinical remission in about half of patients.

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