Recent studies in USA, Europe, and across the world have revealed a continuous increase of mean birth weight in the last 2 decades. Strong evidence exists from several studies indicating that individuals born with a low birth weight are more likely to present cardiometabolic complications in later life. So far, the long-term consequences of high birth weight have not been clearly defined. This review examines the role of high birth weight on the development of cardiometabolic consequences (obesity, body composition, type 2 diabetes mellitus, and cardiovascular disease) in childhood and adulthood. The majority of the studies show that high BW is associated with an increased risk for obesity. To a certain extent high birth weight affects diseases of the heart and circulatory, but does not constitutes a risk for the development of type 2 diabetes mellitus in the general population. Maternal glycemia and the subsequent fetus hyperinsulinemia appear to be the key component for increased fetal growth. With the increase in incidence of diabetes mellitus and obesity over the years, the number of high birth weight infants is likely to increase. The elucidation of the relationship between high birth weight and the cardiometabolic disorders will be particularly important.

Background Anemia is a common extraintestinal manifestation of Inflammatory Bowel Disease (IBD) affecting negatively the patients’ quality of life. The aim of this study was to determine the frequency and real-life management of anemia in IBD patients in Greece. Methods This study was conducted in 17 Greek IBD referral centers. Demographic, clinical, laboratory, IBD and anemia treatment data were collected and analyzed retrospectively. Results A total of 1394 IBD patients [560 ulcerative colitis (UC), 834 Crohn’s disease (CD)] were enrolled. Anemia at any time was reported in 687 (49.3%) patients of whom 413 (29.6%) had episodic and 274 (19.7%) had recurrent/persistent anemia. Anemia was diagnosed before IBD in 45 (6.5%), along with IBD in 269 (39.2%) and after IBD in 373 (54.3%) patients. In the multivariate analysis the presence of extraintestinal manifestations (p = 0.0008), IBD duration (p = 0.026), IBD related surgeries and hospitalizations (p = 0.026 and p = 0.004 accordingly) were risk factors of recurrent/persistent anemia. Serum ferritin was measured in 839 (60.2%) IBD patients. Among anemic patients, 535 (77.9%) received treatment. Iron supplementation was administered in 485 (90.6%) patients, oral in 142 (29.3%) and intravenous in 393 (81%). Conclusions The frequency of anemia in IBD patients, followed at Greek referral centers, is approximately 50%. Development of recurrent/persistent anemia may be observed in 20% of cases and is independently associated with the presence of extraintestinal manifestations, IBD duration, IBD related surgeries and hospitalizations. Anemia treatment is administered in up to $$4/5$$ 4 / 5 of anemia IBD patients with the majority of them receiving iron intravenously.

The aim of this study was to investigate the cytotoxic effect cisplatin in combination with epigallocatechin-3-gallate (EGCG) on leiomyosarcoma cells (LMS cells) in order to identify a less toxic but equally effective alternative. Assays for cell proliferation, colony formation efficiency, induction of apoptosis and cell cycle arrest were performed using the IC of cisplatin (8.6 μΜ) as a reference value and a concentration of EGCG (30 μΜ) that caused a non-significant reduction in cell proliferation. Pre-treatment of cells with EGCG for 24 h before the addition of cisplatin increased cytotoxicity up to 8.5% (p < 0.05) and the number of apoptotic cells by 40%. Epigallocatechin-3-gallate failed to alter S-phase cell cycle arrest induced by cisplatin and to modulate cisplatin effects on mitochondrial function. These results indicate that pre-treatment with EGCG could be used as an adjunctive therapy to maximise effectiveness of chemotherapy.

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract characterized in many patients by extraintestinal manifestations. One of the most common comorbidities seen in IBD patients is a significant reduction in their bone mass. The pathogenesis of IBD is mainly attributed to the disrupted immune responses in the gastrointestinal mucosa and putative disruptions in the gut microbiomes. The excessive inflammation of the gastrointestinal tract activates different systems, such as the RANKL/RANK/OPG and the Wnt pathways linked with bone alterations in IBD patients, thereby suggesting a multifactorial etiology. The mechanism responsible for the reduced bone mineral density in IBD patients is thought to be multifactorial, and, so far, the principal pathophysiological pathway has not been well established. However, in recent years, many investigations have increased our understanding of the effect of gut inflammation on the systemic immune response and bone metabolism. Here, we review the main signaling pathways associated with altered bone metabolism in IBD.