Xian Qiao

Acute abdominal pathologies can cause electrocardiogram (ECG) changes mimicking an acute coronary syndrome (ACS), resulting in diagnostic uncertainty and delay. We report a 65-year-old male with multiple risk factors for ACS who presented with four hours of progressive epigastric and chest pain that resolved in the emergency department. ECG findings were concerning for new deeply inverted T-waves with normal troponins, raising concerns for Wellens Syndrome. Emergent heart catheterization was negative but abdominal computed tomography angiography showed occlusion of the superior mesenteric vessels. Subsequent exploratory laparotomy revealed a small bowel volvulus with extensive necrosis, resulting in a 430 cm resection.

Purpose of Review: SARS-CoV-2 infection, the culprit of the COVID-19 pandemic, has been associated with significant long-term effects on various organ systems, including bone health. This review explores the current understanding of the impacts of SARS-CoV-2 infection on bone health and its potential long-term consequences. Recent Findings: As part of the post-acute sequelae of SARS-CoV-2 infection, bone health changes are affected by COVID-19 both directly and indirectly, with multiple potential mechanisms and risk factors involved. In vitro and preclinical studies suggest that SARS-CoV-2 may directly infect bone marrow cells, leading to alterations in bone structure and osteoclast numbers. The virus can also trigger a robust inflammatory response, often referred to as a "cytokine storm", which can stimulate osteoclast activity and contribute to bone loss. Clinical evidence suggests that SARS-CoV-2 may lead to hypocalcemia, altered bone turnover markers, and a high prevalence of vertebral fractures. Furthermore, disease severity has been correlated with a decrease in bone mineral density. Indirect effects of SARS-CoV-2 on bone health, mediated through muscle weakness, mechanical unloading, nutritional deficiencies, and corticosteroid use, also contribute to the long-term consequences. The interplay of concurrent conditions such as diabetes, obesity, and kidney dysfunction with SARS-CoV-2 infection further complicates the disease's impact on bone health. Summary: SARS-CoV-2 infection directly and indirectly affects bone health, leading to potential long-term consequences. This review article is part of a series of multiple manuscripts designed to determine the utility of using artificial intelligence for writing scientific reviews.

(1) Background: The disease-modifying mechanisms of high-dose intravenous vitamin C (HDIVC) in sepsis induced acute respiratory distress syndrome (ARDS) is unclear. (2) Methods: We performed a post hoc study of plasma biomarkers from subjects enrolled in the randomized placebo-controlled trial CITRIS-ALI. We explored the effects of HDIVC on cell-free DNA (cfDNA) and syndecan-1, surrogates for neutrophil extracellular trap (NET) formation and degradation of the endothelial glycocalyx, respectively. (3) Results: In 167 study subjects, baseline cfDNA levels in HDIVC (84 subjects) and placebo (83 subjects) were 2.18 ng/µL (SD 4.20 ng/µL) and 2.65 ng/µL (SD 3.87 ng/µL), respectively, p = 0.45. At 48-h, the cfDNA reduction was 1.02 ng/µL greater in HDIVC than placebo, p = 0.05. Mean baseline syndecan-1 levels in HDIVC and placebo were 9.49 ng/mL (SD 5.57 ng/mL) and 10.83 ng/mL (SD 5.95 ng/mL), respectively, p = 0.14. At 48 h, placebo subjects exhibited a 1.53 ng/mL (95% CI, 0.96 to 2.11) increase in syndecan-1 vs. 0.75 ng/mL (95% CI, 0.21 to 1.29, p = 0.05), in HDIVC subjects. (4) Conclusions: HDIVC infusion attenuated cell-free DNA and syndecan-1, biomarkers associated with sepsis-induced ARDS. Improvement of these biomarkers suggests amelioration of NETosis and shedding of the vascular endothelial glycocalyx, respectively.

Background: Vitamin C is a water-soluble antioxidant vitamin. Oxidative stress and its markers, along with inflammatory markers, are high during critical illness. Due to conflicting results of the published literature regarding the efficacy of vitamin C in critically ill patients, and especially the concerns for nephrotoxicity raised by some case reports, this meta-analysis was carried out to appraise the evidence and affirmation regarding the role of vitamin C in critically ill patients. Methods: We searched the database thoroughly to collect relevant studies that assessed intravenous vitamin C use in critically ill patients published until 25 February 2021. We included randomized controlled trials and observational studies with 20 or more critically ill patients who have received intravenous ascorbic acid (vitamin C). After screening 18,312 studies from different databases, 53 were included in our narrative synthesis, and 48 were included in the meta-analysis. We used the Covidence software for screening of the retrieved literature. Review Manager (RevMan) 5.4 was used for the pooling of data and Odds Ratios (OR) and Mean difference (MD) as measures of effects with a 95% confidence interval to assess for explanatory variables. Results: Pooling data from 33 studies for overall hospital mortality outcomes using a random-effect model showed a 19% reduction in odds of mortality among the vitamin C group (OR, 0.81; 95% CI, 0.66–0.98). Length of hospital stay (LOS), mortality at 28/30 days, ICU mortality, new-onset AKI and Renal Replacement Therapy (RRT) for AKI did not differ significantly across the two groups. Analysis of data from 30 studies reporting ICU stay disclosed 0.76 fewer ICU days in the vitamin C group than the placebo/standard of care (SOC) group (95% CI, −1.34 to −0.19). This significance for shortening ICU stay persisted even when considering RCTs only in the analysis (MD, −0.70; 95% CI, −1.39 to −0.02). Conclusion: Treatment of critically ill patients with intravenous vitamin C was relatively safe with no significant difference in adverse renal events and decreased in-hospital mortality. The use of vitamin C showed a significant reduction in the length of ICU stays in critically ill patients.

Intestinal pacing (IP) has been previously shown to delay gastric emptying and reduce food intake in animals. The aims of this study were to investigate the effect and mechanism of IP on nutrient absorption in healthy volunteers. Twelve healthy volunteers (six men, six women) were involved in a two-session (one session without IP and one with IP) study. At the beginning of each session, a nasal-duodenal feeding tube, with two ring electrodes (used for IP) on the tip of the tube, was incubated into the duodenum under endoscopy. After a complete recovery from the incubation, the duodenum was infused via the feeding tube with 150 ml 30% intralipid + 25 g D-xylose within 30 min, and the stool was collected for 24 h for the analysis of fecal lipid during which a controlled meal was taken. Then 100 ml 1mCi⁹⁹Tc-labeled non-absorbable solution was infused within 3 min. The subject was asked to lie under a γ camera for at least 1 h for the measurement of small bowel transit. The movement of isotopes was monitored by γ camera at an interval of 10 s. The first appearance of isotopes in the cecum was considered as small intestinal transit time. The order of the two sessions was randomized and 1 week apart. In the IP session, intestinal pacing was performed via the pair of the ring electrodes for 2 h initiated at the beginning of infusion with a pacing frequency of 13 pulses/min, pulse width of 300 ms and amplitude of 5 mA. (1) IP significantly reduced lipid and D-xylose absorption. The fecal lipid was 6.6 ± 4.6 g without IP and almost doubled with IP (11.1 ± 6.5 g, P = 0.047). Similarly, the D-xylose in urine was 3.46 ± 2.22 g with IP, which was significantly lower than that without IP (6.63 ± 5.06 g, p = 0.049). (2) IP accelerated intestinal transit. The transit time was 39 ± 17 min in the control session and reduced to 28 ± 10 min in the IP session (p < 0.03). (3) Diarrhea was reported in one subject without IP but in six subjects with IP (p < 0.05). The increased fecal lipid and induction of diarrhea with intestinal pacing suggest that intestinal pacing is capable of inducing malabsorption. This effect maybe contributed to the acceleration of intestinal transit.