Capsule endoscopy in young patients with iron deficiency anaemia and negative bidirectional gastrointestinal endoscopy

Background: Recent data imply young patients (age ≤50 years) undergoing small-bowel (SB) capsule endoscopy (CE) for iron deficiency anaemia (IDA) show higher diagnostic yield (DY) for sinister pathology. We aimed to investigate DY of CE in a large cohort of young IDA patients, and evaluate factors predicting significant SB pathology. Materials and methods: This was a retrospective, multicentre study (2010–2015) in consecutive, young patients (≤50 years) from 18 centres/12 countries, with negative bidirectional gastrointestinal (GI) endoscopy undergoing SBCE for IDA. Exclusion criteria: previous/ongoing obscure-overt GI bleeding; age <19 or >50 years; comorbidities associated with IDA. Data retrieved: SBCE indications; prior investigations; medications; SBCE findings; final diagnosis. Clinical and laboratory data were analysed by multivariate logistic regression. Results: Data on 389 young IDA patients were retrieved. In total, 169 (43.4%) were excluded due to incomplete clinical data; data from 220 (122F/98M; mean age 40.5 ± 8.6 years) patients were analysed. Some 71 patients had at least one clinically significant SBCE finding (DY: 32.3%). They were divided into two groups: neoplastic pathology (10/220; 4.5%), and non-neoplastic but clinically significant pathology (61/220; 27.7%). The most common significant but non-neoplastic pathologies were angioectasias (22/61) and Crohn’s disease (15/61). On multivariate analysis, weight loss and lower mean corpuscular volume(MCV) were associated with significant SB pathology (OR: 3.87; 95%CI: 1.3–11.3; p = 0.01; and OR: 0.96; 95%CI: 0.92–0.99; p = 0.03; respectively). Our model also demonstrates association between use of antiplatelets and significant SB pathology, although due to the small number of patients, definitive conclusions cannot be drawn. Conclusion: In IDA patients ≤50 years with negative bidirectional GI endoscopy, overall DY of SBCE for clinically significant findings was 32.3%. Some 5% of our cohort was diagnosed with SB neoplasia; lower MCV or weight loss were associated with higher DY for SB pathology. © 2017, © Author(s) 2017

Régulation de l'IGF-I par la nutrition: mécanismes et implications

L’IGF-I (Insulin-like Growth Factor I) est un facteur de croissance indispensable à la croissance staturopondérale. L’IGF-I présent dans la circulation est essentiellement d’origine hépatique. Sa production est stimulée par l’hormone de croissance et régulée par la nutrition. En effet, la réduction de l’apport alimentaire diminue les taux circulants d’IGF-I. Les mécanismes responsables de la régulation de la production d’IGF-I par l’apport alimentaire, notamment en protéines, ont été largement caractérisés. Le contrôle de la production d’IGF-I par l’apport nutritionnel a permis d’imaginer un mécanisme par lequel la nutrition est capable de réguler les grandes fonctions physiologiques et peut contribuer au développement de certaines pathologies. Ainsi, le retard de croissance causé par la malnutrition protéinocalorique est en partie secondaire à une réduction des taux circulants d’IGF-I. Outre le retard de croissance, la réduction de l’apport nutritionnel induit également un allongement de la durée de vie dans de nombreuses espèces. De façon surprenante, l’inhibition de l’activité d’IGF-I obtenue par des manipulations génétiques s’accompagne elle aussi d’un allongement de la durée de vie. Il est dès lors possible que la réduction des taux d’IGF-I induite par la diminution de l’apport alimentaire contribue à l’allongement de la durée de vie observé. Contrairement à la malnutrition, un apport alimentaire excessif est susceptible d’augmenter, bien que modestement, les taux circulants d’IGF-I. Sur cette base, il a été suggéré que les taux d’IGF-I élevés observés dans l’obésité pourraient contribuer au risque accru de cancer observé dans cette population. En conclusion, les variations d’IGF-I circulante induites par des changements de l’apport nutritionnel pourraient affecter la croissance staturopondérale, la longévité et le risque de cancer

FOXO transcription factors : from cell fate decisions to regulation of human female reproduction

All key reproductive events in the human ovary and uterus, including follicle activation, ovulation, implantation, decidualization, luteolysis and menstruation, are dependent upon profound tissue remodelling, characterised by cyclical waves of cell proliferation, differentiation, apoptosis, tissue breakdown and regeneration. FOXO transcription factors, an evolutionarily conserved subfamily of the forkhead transcription factors, have emerged as master regulators ofcell fate decision capable ofintegrating avariety ofstress, growth factor and cytokine signaling pathways with the transcription machinery. The ability of FOXOs to regulate seemingly opposing cellular responses, ranging from cell cycle arrest and oxidative stress responses to differentiation and apoptosis, renders these transcription factors indispensable for cyclic tissue remodelling in female reproduction. Conversely, perturbations in the expression or activity of FOXO transcription factors are increasingly linked to common reproductive disorders, such as pregnancy loss, endometriosis, endometrial cancer and primary ovarian insufficiency