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Objective: To determine the incidence, risk factors, and short-term maternal outcomes of women with pathologically confirmed retained products of conception (RPOC) following vaginal delivery. Methods: Prospective cohort study of women with suspicion of RPOC following vaginal delivery, from March 2018 to April 2019. Women were followed for eight weeks postpartum. Women with complete retained placenta were excluded. Women with pathologically confirmed RPOC were compared to those without. Univariate analysis was conducted (ORs; [95% CI]) and was followed by multivariate analysis (aOR; [95% CI]). Results: During the study period, there were 16,583 vaginal deliveries. A total of 96 women (0.58%) with a suspicion of RPOC were enrolled, of these, 53 women (55%) had pathologically confirmed RPOC. The most significant risk factors for pathologically confirmed RPOC were placental abruption (aOR 5.0 [2.29–11.13]) and Oxytocin augmentation of labor (aOR 1.7 [1.07–2.63]). Pathologically confirmed RPOC were associated with higher rates of prolonged hospitalization (OR 9.2 [2.83–30.05]), postpartum hemorrhage (PPH) (OR 6.6 [3.60–11.98]), hemoglobin drop > 3 g/dl (OR 11.4 [5.49–23.49]), and blood transfusion (OR 8.6 [2.07–38.18]). Women who had exploration of uterine cavity without pathological confirmation of RPOC, still had higher rates of perineal laceration (OR 17.6 [4.93–63.08]), PPH (OR 6.1 [3.05–12.21]), and a hemoglobin drop > 3 g/dl (OR 6.0 [2.13–16.95]). Conclusions: Pathologically confirmed RPOC following vaginal delivery has unique characteristics and is associated with significantly higher rates of PPH and blood transfusions. These findings may assist in the development of better criteria for selecting women for manual exploration and for preventive measures to reduce PPH and complications. [ABSTRACT FROM AUTHOR]

Introduction: There is little information in the literature on the early, sub-clinical stage and laboratory test results in patients with primary mucosa-associated lymphoid tissue (MALT) lymphoma of the lung, a rare disease., Case Description: In a 75-year-old man, an open lung biopsy-confirmed diagnosis of primary pulmonary lymphoma was preceded by almost six months of anaemia of inflammatory disease and monocytosis without any pulmonary symptoms. When he developed a dry cough, increasing dyspnoea and marked weight loss, these changes deepened and became associated with reactive thrombocytosis; markedly increased ferritin and C-reactive protein (positive acute-phase reactants), as well as reduced albumin and transferrin (negative acute-phase reactants). Globulins increased, due to an increase in the alpha1, alpha2 and gamma fractions, and mild hyponatraemia developed due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) secondary to the intrathoracic disease. All these changes were completely reversible following successful treatment and complete remission., Conclusion: The previously unreported detailed laboratory features of early, sub-clinical and advanced primary pulmonary lymphoma are presented. When a potentially susceptible patient develops an unexplained anaemia of inflammatory disease, primary pulmonary lymphoma should be added to the differential diagnosis., Learning Points: B-cell pulmonary lymphoma without extra-pulmonary disease (primary pulmonary lymphoma) remains a rare entity, often arising from mucosa-associated lymphoid tissue, presenting with non-specific symptoms (cough, dyspnoea) and imaging (nodules <5 cm or areas of consolidation on CT), and diagnosed by an adequate biopsy.Our patient's course demonstrates early, pre-clinical changes: anaemia of inflammation and monocytosis, which became more severe as symptoms developed and imaging abnormalities progressed, and was associated with marked acute-phase response (for example, substantially increased ferritin levels), increased globulins and hyponatraemia due to the syndrome of inappropriate antidiuretic hormone secretion.In patients with unexplained anaemia of inflammatory disease, occult pulmonary lymphoma should be considered in the differential diagnosis., Competing Interests: Conflicts of Interests: The Authors declare that there are no competing interests., (© EFIM 2024.)

β-Cell mitochondrial dysfunction as well as proinflammatory cytokines have been suggested to contribute to reduced glucose-stimulated insulin secretion (GSIS) in type 2 diabetes. We recently demonstrated that Cohen diabetic sensitive (CDs) rats fed a high-sucrose, low-copper diet (HSD) developed hyperglycemia and reduced GSIS in association with peri-islet infiltration of fat and interleukin (IL)-1β-expressing macrophages, whereas CD resistant (CDr) rats remained normoglycemic on HSD. We examined: 1) the correlation between copper concentration in the HSD and progression, prevention, and reversion of hyperglycemia in CDs rats, 2) the relationship between activity of the copper-dependent, respiratory-chain enzyme cytochrome c oxidase (COX), infiltration of fat, IL-1β-expressing macrophages, and defective GSIS in hyperglycemic CDs rats. CDs and CDr rats were fed HSD or copper-supplemented HSD before and during hyperglycemia development. Blood glucose and insulin concentrations were measured during glucose tolerance tests. Macrophage infiltration and IL-1β expression were evaluated in pancreatic sections by electron-microscopy and immunostaining. COX activity was measured in pancreatic sections and isolated islets. In CDs rats fed HSD, GSIS and islet COX activity decreased, while blood glucose and infiltration of fat and IL-1β-expressing macrophages increased with time on HSD (P < 0.01 vs. CDr-HSD rats, all parameters, respectively). CDs rats maintained on copper-supplemented HSD did not develop hyperglycemia, and in hyperglycemic CDs rats, copper supplementation restored GSIS and COX activity, reversed hyperglycemia and infiltration of fat and IL-1β-expressing macrophages (P < 0.01 vs. hyperglycemic CDs-HSD rats, all parameters, respectively). We provide novel evidence for a critical role of low dietary copper in diminished GSIS of susceptible CDs rats involving the combined consequence of reduced islet COX activity and pancreatic low-grade inflammation.