RESUMEN
Posterior reversible encephalopathy syndrome (PRES), which was first described in 1996, is a neurologic condition characterized by a combination of clinical and neuroimaging findings. PRES may arise in the context of preeclampsia, eclampsia, renal failure, and sepsis, among other conditions. Neuropsychiatric symptoms of PRES include altered mental status, agitation, and in some cases psychosis. PRES occurring in the postpartum period is understudied, especially with regard to its psychiatric manifestations. We aim to add to the literature a case of PRES associated with psychosis and agitation in a postpartum woman, highlighting clinical implications and offering suggestions for practice. A female in her late 20s, with no significant psychiatric or medical history, presented to the hospital at 29 weeks and one day of gestation following a witnessed seizure. She was found to be hypertensive and hyponatremic, was diagnosed with eclampsia, and underwent an emergent cesarean section due to fetal malpresentation. The next day, the patient developed paranoia with acute agitation, and the psychiatry team diagnosed her with delirium with psychosis/agitation secondary to her underlying medical condition. She required intramuscular medications for agitation, was placed in restraints, and was transferred to the ICU for sedation. Subsequently, CT and MRI scans of her head both indicated that she had developed PRES. The patient's delirium and psychotic behavior resolved after appropriate treatment of her eclampsia. To our knowledge, this case report is the second documented case in the literature, of a patient who presented with PRES characterized by agitation and psychotic features in the postpartum period. Due to the significant overlap in symptoms between delirium and postpartum psychosis, this case highlights the crucial importance of interdisciplinary collaboration for accurate diagnosis and prompt treatment of PRES in the postpartum period. The case also speaks to the importance of differentiating postpartum psychosis associated with a primary psychiatric disorder from delirium arising in postpartum patients with or without a previous psychiatric history.
RESUMEN
Clostridioides difficile is a Gram-positive, anaerobic, spore-forming bacterium responsible for antibiotic-associated pseudomembranous colitis. Clostridioides difficile infection (CDI) symptoms can range from diarrhea to life-threatening colon damage. Toxins produced by C. difficile (TcdA and TcdB) cause intestinal epithelial injury and lead to severe gut barrier dysfunction, stem cell damage, and impaired regeneration of the gut epithelium. Current treatment options for intestinal repair are limited. In this study, we demonstrate that treatment with the microbial metabolite urolithin A (UroA) attenuates CDI-induced adverse effects on the colon epithelium in a preclinical model of CDI-induced colitis. Moreover, our analysis suggests that UroA treatment protects against C. difficile-induced inflammation, disruption of gut barrier integrity, and intestinal tight junction proteins in the colon of CDI mice. Importantly, UroA treatment significantly reduced the expression and release of toxins from C. difficile without inducing bacterial cell death. These results indicate the direct regulatory effects of UroA on bacterial gene regulation. Overall, our findings reveal a novel aspect of UroA activity, as it appears to act at both the bacterial and host levels to protect against CDI-induced colitis pathogenesis. This research sheds light on a promising avenue for the development of novel treatments for C. difficile infection.IMPORTANCETherapy for Clostridioides difficile infections includes the use of antibiotics, immunosuppressors, and fecal microbiota transplantation. However, these treatments have several drawbacks, including the loss of colonization resistance, the promotion of autoimmune disorders, and the potential for unknown pathogens in donor samples. To date, the potential benefits of microbial metabolites in CDI-induced colitis have not been fully investigated. Here, we report for the first time that the microbial metabolite urolithin A has the potential to block toxin production from C. difficile and enhance gut barrier function to mitigate CDI-induced colitis.