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Innate defenses to intestinal cell death in necrotizing enterocolitis – spotlight on macrophage efferocytosis and its efficacy in rescuing inflamed intestinal mucosa

100%
Kanuri S. H., Bagang N., Ulucay A. S., Pandey P., Singh G.
European Journal of Clinical and Experimental Medicine
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2023
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issue 2
365-396
EN
Introduction and aim. Necrotizing enterocolitis (NEC) is a grave gastrointestinal disease of preterm infants which is widely prevalent in the neonatal intensive care units. Current treatment options are very limited with high mortality and morbidity. With no disease specific interventions, understanding nascent cellular events that occur immediately after microbial insult can offer insights for devising novel treatment options for curtailing the disease progression in NEC. In this regard, intestinal cell death in NEC is a primordial cell-signaling event and is regarded as a harbinger of future pathological derangements such as increased intestinal permeability, intestinal dys-homeostasis, and systemic inflammation. Material and methods. We performed PubMed search of relevant articles that describes the host response to intestinal cell death in NEC by cellular battalion including dendritic cells, lymphocytes, neutrophils and macrophages which are important in containing intestinal inflammation. Analysis of the literature. We particularly focused this review on enumerating macrophage efferocytosis, and pertinent novel treatment modalities based on this physiological process that has inherent capability for down regulating inflammation and promoting tissue repair in NEC. We highlighted its mechanistic aspect including mediators, receptors and signaling mechanisms and its physiological significance. Conclusion. Macrophage efferocytosis is an overlooked and undervalued physiological defense mechanism to clear the dying intestinal epithelial cells for facilitating tissue healing and restoring the intestinal homeostasis. Any impairment of this critical defense mechanism can result in rapid clinical progression and systemic complications. Understanding its importance in the pathogenesis of NEC is important for designing novel therapeutic interventions to attenuate disease progression.
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Acute mercuric chloride poisoning at a potentially lethal dose ended with survival: symptoms, concentration in cerebrospinal fluid, treatment

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Krakowiak A., Janasik B., Sadowski Ł., Szwabe K., Machała W.
International Journal of Occupational Medicine and Environmental Health
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2023
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vol. 36
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issue 5
685-692
EN
This study aims to present a case of acute mercuric chloride poisoning at a potentially lethal dose treated with the antidote – 2,3-dimercapto- 1-propanesulfonic acid (DMPS) and continuous renal replacement therapy (CRRT) combined with CytoSorb. A 21-year-old woman was admitted to a hospital with abdominal pain, vomiting, and suspected gastrointestinal bleeding after taking 5000 mg of mercuric chloride for suicidal purposes. Due to the patient deteriorating general condition and multiple organ damage, on the third day she was transported to the Clinic of Anaesthesiology and Intensive Care (CAaIC), Łódź, Poland. Laboratory tests confirmed features of acute kidney injury and high mercury levels in the blood (1051 μg/l) and urine (22 960 μg/l) – DMPS therapy and CRRT combined with CytoSorb were instituted. Due to nervous system complaints (headache, dizziness), a lumbosacral puncture was performed – the mercury concentration in the cerebrospinal fluid (CSF) was 5.45 μg/l. During a colonoscopy, significant diagnostic abnormalities revealed features of colonic mucosal necrosis. The treatment resulted in a decrease in subjective complaints, decreased mercury levels in biological material, and improved parenchymal organ function. On the 15th day of therapy, the patient was transferred to the primary care center for further treatment. The case confirms the possibility of improvement of patient condition following ingestion of a potentially lethal dose (5 g) as a result of the initiation of appropriate therapy even on the third day. The presence of mercury in CSF confirms that inorganic mercury compounds (mercuric chloride) can pass through the blood-brain barrier after oral ingestion.
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