RÉSUMÉ
BACKGROUND: the success of strategies with earlier anti-TNF drugs for the treatment of inflammatory bowel disease (IBD) have been shadowed by the development of anti-drug antibodies that reduce their effectiveness. The HLA-DQA1*05 allele has been shown to increase the risk of immunogenicity to anti-TNF drugs by approximately two-fold. The negative impact of this allele has not been fully investigated for newer biotherapies. OBJECTIVE: whether the presence of the HLA-DQA1*05 allele is associated with a reduction of response to ustekinumab and vedolizumab was investigated. MATERIAL AND METHODS: the impact of HLA-DQA1*05 on disease activity in 93 patients with IBD, treated with ustekinumab (n = 39) or vedolizumab (n = 54) was investigated in a retrospective cohort study. Treatment response and remission was assessed at 6 and 12 months for ustekinumab, and up to 18 and 24 months for vedolizumab, using Harvey-Bradshaw index (Crohn's disease) and Mayo score (ulcerative colitis). RESULTS: the HLA-DQA1*05 allele was found in 35.9 % and 38.9 % of patients treated with ustekinumab and vedolizumab, respectively. Clinical response was not affected by the presence of the HLA-DQA1*05 allele for both treatment groups. CONCLUSIONS: in contrast to anti-TNF drugs, HLA-DQA1*05 presence does not correlate with the decreased response to ustekinumab or vedolizumab.
Sujet(s)
Maladies inflammatoires intestinales , Ustékinumab , Humains , Ustékinumab/usage thérapeutique , Études rétrospectives , Inhibiteurs du facteur de nécrose tumorale , Maladies inflammatoires intestinales/traitement médicamenteux , Maladies inflammatoires intestinales/génétique , GénotypeRÉSUMÉ
The incidence of extramammary Paget's disease (EMPD) is very low. It is very important to distinguish between primary Paget's disease and secondary to another process. An 85-year-old man consulted for the presence of an erythematous plaque located in the anal and gluteal area, confirming Paget cells in the biopsy.
Sujet(s)
Tumeurs du sein , Maladie de Paget extramammaire , Tumeurs cutanées , Mâle , Humains , Sujet âgé de 80 ans ou plus , Maladie de Paget extramammaire/diagnostic , Maladie de Paget extramammaire/anatomopathologie , Tumeurs cutanées/anatomopathologie , Canal anal/anatomopathologie , Tumeurs du sein/anatomopathologie , BiopsieRÉSUMÉ
Primary gastric melanoma is an exceptional tumour with less than 20 cases described in the literature, as its origin is not entirely clear as the presence of melanocytes in the stomach has not been demonstrated. Symptomatology is non-specific, which prevents its early detection, and it is diagnosed in late stages. We present the case of a patient who was admitted to our hospital for vomiting in coffee grounds with analytical and haemodynamic repercussions. Urgent gastroscopy revealed a gastric lesion suspicious for malignancy, which was histologically confirmed as gastric melanoma. The therapeutic approach to these tumours is complex and they have a very poor prognosis.
Sujet(s)
Tumeurs gastro-intestinales , Mélanome , Tumeurs de l'estomac , Humains , Mélanome/imagerie diagnostique , Mélanome/chirurgie , Tumeurs de l'estomac/anatomopathologie , Gastroscopie , PronosticRÉSUMÉ
Background: the success of strategies with earlier anti-TNF drugs for the treatment of inflammatory bowel disease (IBD) have been shadowed by the development of anti-drug antibodies that reduce their effectiveness. The HLA-DQA1*05 allele has been shown to increase the risk of immunogenicity to anti-TNF drugs by approximately two-fold. The negative impact of this allele has not been fully investigated for newer biotherapies. Objective: whether the presence of the HLA-DQA1*05 allele is associated with a reduction of response to ustekinumab and vedolizumab was investigated. Material and methods: the impact of HLA-DQA1*05 on disease activity in 93 patients with IBD, treated with ustekinumab (n = 39) or vedolizumab (n = 54) was investigated in a retrospective cohort study. Treatment response and remission was assessed at 6 and 12 months for ustekinumab, and up to 18 and 24 months for vedolizumab, using Harvey-Bradshaw index (Crohns disease) and Mayo score (ulcerative colitis). Results: the HLA-DQA1*05 allele was found in 35.9 % and 38.9 % of patients treated with ustekinumab and vedolizumab, respectively. Clinical response was not affected by the presence of the HLA-DQA1*05 allele for both treatment groups. Conclusions: in contrast to anti-TNF drugs, HLA-DQA1*05 presence does not correlate with the decreased response to ustekinumab or vedolizumab (AU)
Sujet(s)
Humains , Mâle , Femelle , Adulte , Adulte d'âge moyen , Maladies inflammatoires intestinales/traitement médicamenteux , Maladies inflammatoires intestinales/génétique , Ustékinumab/usage thérapeutique , Anticorps monoclonaux humanisés/usage thérapeutique , Antigènes HLA-DQ/génétique , Allèles , Résultat thérapeutiqueSujet(s)
Humains , Femelle , Adulte d'âge moyen , Tumeurs de l'estomac/imagerie diagnostique , Tumeurs de l'estomac/anatomopathologie , Tumeurs de l'estomac/secondaire , Mélanome/imagerie diagnostique , Mélanome/anatomopathologie , Tomographie par émission de positons couplée à la tomodensitométrie , Endoscopie digestive , BiopsieRÉSUMÉ
BACKGROUND: tofacitinib is a Janus kinase inhibitor approved for the treatment of moderate-severe ulcerative colitis (UC). This study aimed to evaluate its efficacy in a real-life setting. METHODS: a retrospective and multicenter observational study was performed with UC patients treated with tofacitinib. Short and long-term treatment effectiveness, treatment survival, need for dose escalation and safety were analyzed. Clinical response and remission were defined in accordance with the partial Mayo score. RESULTS: seventy-four patients were included, 98.3 % had received prior biological treatment, 55.4 % with three or more biologicals and up to 64.9% with two or three different mechanisms of action. Clinical remission and response rates were 37.8 % and 77 % at eight weeks, and 41.8 % and 70.1 % at 16 weeks. With regard to non-responders at eight weeks, 37.5 % achieved a delayed clinical response at 16 weeks. Mean treatment duration was 19 months (95 % CI: 16-22), with a treatment survival of 56 % at 28 months, and remission and response rates at 24 months of 53.8 % and 61.5 %. Twenty-three treatments were withdrawn, most of them (18) during the induction period. There were adverse events in a quarter of the patients; only four were severe and led to treatment discontinuation. CONCLUSION: tofacitinib has a demonstrated efficacy in clinical practice to induce and maintain clinical response in treatment-refractory UC patients, with an acceptable safety profile.