Background: Whether the human Achilles tendon undergoes hypertrophic changes as measured by an increase in cross-sectional area, in response to endurance training exercise remains in question. We investigated the hypothesis that transition from civilian life through 6 months of elite infantry training would induce adaptive Achilles tendon hypertrophy. Methods: Seventy-two new elite infantry recruits had the cross-sectional area of their Achilles tendons measured at a point 2.5 cm proximal to the Achilles insertion by ultrasound before beginning elite infantry training. Measurements were repeated by the same ultrasonographer for those recruits who were still in the training program at 6 months. Prior to beginning the study the intraobserver reliability of the ultrasonographer’s Achilles tendon measurements was calculated (intraclass correlation coefficient = .96). Fifty-five recruits completed 6 months of training. Results: The mean cross-sectional area of their right Achilles tendon increased from 47.0 ± 11.2 to 50.2 ± 9.6 mm² ( P = .037) and the left Achilles tendon from 47.2 ± 8.9 to 51.1 ± 8.3 mm² ( P = .013). The change in cross-sectional area did not correlate with subject height, weight, prior sport history, or jumping and running abilities. Conclusions: An abrupt stimulus of 6 months of elite infantry training was adequate to induce hypertrophic changes in the Achilles tendon. This is the first human prospective study showing an increase in the Achilles tendon cross-sectional area in response to rigorous endurance type training. The finding supports the hypothesis that the Achilles tendon in response to sufficiently high and sustained loading can remodel its morphological properties and thereby strengthen itself. Level of Evidence: Level II, etiology study.

There are no data on the transfer of vedolizumab in breast milk of nursing mothers. We aimed to assess the presence of vedolizumab in breast milk of nursing inflammatory bowel disease [IBD] patients. This was a prospective observational study of vedolizumab-treated breastfeeding patients with IBD. Serum and breast milk samples were obtained at pre-defined tim -points. The in-house developed enzyme-linked immunosorbent assay [ELISA] for measuring vedolizumab in blood was adapted and validated for measurement of the drug in breast milk. The level of vedolizumab was also measured in breast milk of a control group of nursing healthy mothers. Vedolizumab was undetectable in breast milk in IBD patients before the first infusion of vedolizumab [n = 3] and in all of the healthy controls [n = 5]. Vedolizumab was measurable in all lactating women who received vedolizumab [n = 5]. However, on serial measurements in breast milk after an infusion, drug levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels. Vedolizumab can be detected in the breast milk of nursing mothers. Although more data are imperative, the concentrations of vedolizumab in breast milk are minute and are therefore unlikely to result in systemic or gastro-intestinal immune-suppression of the infant.

Inflammatory bowel diseases (IBDs) are commonly diagnosed during the reproductive years. IBD first manifested during pregnancy (pregnancy-onset IBD [POIBD]) is still an undescribed entity. The aim of the study was to evaluate the characteristics and maternal and neonatal outcomes of patients with POIBD. Data of all pregnant women with IBD within a single multidisciplinary referral clinic, IBD-MOM, between 2011–2016, were analyzed. Maternal and neonatal characteristics and outcomes were compared between the POIBD group and those diagnosed before pregnancy (non-POIBD). We identified 237 women, 31 (15%) from the POIBD group and 206 (85%) from the non-POIBD group. Eight (3.5%) patients experienced early spontaneous pregnancy loss, all in the non-POIBD group. The POIBD diagnosis occurred in 16 (52%) patients during the first trimester, 10 (32%) in second trimester, and 5 (16%) during third trimester. Diagnosis of ulcerative colitis (UC) was significantly more common in the POIBD group compared with the non-POIBD group (22/31, 71% vs 50/206, 24%, respectively, P < 0.001). More UC than Crohn’s disease patients had active disease during pregnancy (69% vs 50%, P = 0.03, respectively). POIBD patients experienced vaginal delivery in 100% of births, compared with 164 (79.6%) in the non-POIBD group (P = 0.017). The mean gestational age at birth and the neonatal weight were similar among the study groups; 38.6 weeks and 3040 g for POIBD patients, compared with 38.7 weeks and 3055 g in the non-POIBD group. POIBD is a unique clinical entity, and the diagnosis is mostly UC. However, the maternal and neonatal outcomes are similar.

Background and Aims: Sodium-glucose cotransporter-2 (SGLT2) inhibitors have shown promise in metabolic dysfunction-associated steatotic liver disease (MASLD). This large real-world study aimed to evaluate the effects of SGLT2 inhibitors on MASLD patients’ clinical outcomes and liver-related complications over extended follow-up. Patients and Method: Data were sourced from TriNetX, a global health research platform with de-identified electronic medical records spanning 135 million patients across 112 healthcare organizations worldwide. We included MASLD adults diagnosed according to ICD9/10 criteria. Following propensity score matching based on 34 variables (demographics, comorbidities, laboratory tests and medication history), SGLT2 inhibitor-treated (n = 19,922) patients were compared with non-SGLT2 inhibitor (n = 19,922) cases. Exclusion criteria included baseline improved alanine aminotransferase (ALT) and alkaline phosphatase (ALP) levels > 4 upper normal limit (UNL), baseline advanced liver disease, liver transplant and cancer, past anticoagulation and non-MASLD etiologies. Assessed outcomes included survival, biochemical, hematologic, AFP, metabolic and cardiovascular parameters, progression to advanced liver disease (ALD), synthetic function, and metabolic markers over 1, 5, and 10 years. Results: Following matching, both cohorts were well-balanced across baseline characteristics. After one year, the SGLT2 inhibitor group demonstrated significantly reduced BMI (33.2 ± 6.2 vs. 34.1 ± 6.5 kg/m², p < 0.001), improved ALT (40.3 ± 31.5 vs. 48.3 ± 41.2 U/L, p < 0.001), and better glycemic control (HbA1c 7.35 ± 1.51% vs. 7.93 ± 1.72%, p < 0.001). The SGLT2 inhibitor group showed higher 10-year survival rates (95.00% vs. 88.69%, p < 0.001), fewer cardiovascular events (10.19% vs. 11.80%, p < 0.001), and markedly reduced progression to advanced liver disease (6.90% vs. 14.15%, p < 0.001). These benefits were consistent across clinical, laboratory, and medication-defined ALD categories. Notably, rates of hepatic decompensation events were significantly lower with SGLT2 inhibitor therapy. Conclusions: In this large real-world cohort, SGLT2 inhibitor use in MASLD patients was associated with significantly improved long-term survival, cardiovascular, and liver-related outcomes over 10 years of follow-up. These benefits likely result from combined metabolic improvements, anti-inflammatory effects, and direct hepatoprotective mechanisms. SGLT2 inhibitors represent a promising therapeutic strategy for improving outcomes in MASLD.