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Background: Gut-derived bacterial and endotoxin translocation induce systemic inflammation, which exerts a pivotal pathogenetic role in all phases of atherosclerosis., Objectives: To investigate prospectively the gut barrier function, endotoxin translocation and inflammatory response in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary artery intervention (PPCI)., Methods: Twenty-seven patients with STEMI that underwent successful PPCI were subjected to peripheral blood sampling at 3-time points; before PPCI (day0), 24 h (day1) and 96 h (day4) after PPCI and were compared with 20 chronic coronary syndrome (CCS) patients and 11 healthy controls. Serum ZO-1, I-FABP and endotoxin concentrations were determined by ELISA. Concentrations of cytokines IL-1β, -6, -8, -10 and TNF-α were determined by flow cytometry., Results: Patients with STEMI before PPCI (day0) had increased serum ZO-1 and endotoxin, both at significantly higher levels compared to CCS patients. STEMI induced also significant increases of the cytokines IL-6, -8 and -10. After PPCI, a significant improvement of gut barrier integrity (ZO-1) and endotoxemia was observed from the first day. At day4 post PPCI, systemic endotoxin and cytokines IL-6, -8 and -10 levels were reduced to control levels. Serum ZO-1 levels were positively correlated with systemic IL-10 concentrations (r = 0.471)., Conclusion: STEMI is associated with gut barrier dysfunction, systemic endotoxemia and inflammatory response, which improve rapidly following successful PPCI., Competing Interests: Declaration of competing interest The following authors declare that they have no competing interests: Ioanna Oikonomou, MD, Angeliki Papageorgiou, MD, Anne-Lise de Lastic, MD, PhD, Athanasios Moulias, MD, PhD, Georgia-Andriana Georgopoulou, MD, Athanasia Mouzaki, MD, PhD, Eleni-Evangelia Koufou, MD, Grigorios Tsigkas, MD, PhD, Charalambos Gogos, MD, PhD, Periklis Davlouros, MD, PhD, Stelios F. Assimakopoulos, MD, PhD, (Copyright © 2024 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Background: In the experimental setting, obstructive jaundice induces oxidative stress in several extrahepatic tissues (systemic phenomenon), which is at least partly attributed to activation of the enzyme xathine oxidase. Very little is known on this important issue in patients with cholestasis. The present study was designed to (a) assess directly oxidative stress in the blood of patients with obstructive jaundice by measuring superoxide radical, and (b) investigate ex vivo whether xanthine oxidase (XO) is the source of this radical., Methods: Twelve patients with malignant obstructive jaundice and no signs of cholangitis, 12 nonjaundiced disease-controls with a localized gastrointestinal malignancy, and 12 healthy-controls were enrolled in the study. Superoxide radical levels were measured in the whole blood (plasma and cells) and in plasma previously separated. These measurements were also done in blood samples in the presence of the specific XO inhibitor allopurinol., Results: Superoxide radical levels were significantly increased in the plasma fraction of whole blood in jaundiced patients when compared with disease-controls (P < 0.001) and healthy-controls (P < 0.001), whereas disease-control patients presented significantly increased superoxide radical levels when compared with healthy-controls (P < 0.001). No differences in superoxide radical levels in the blood cells were detected between jaundiced patients and disease-controls. In jaundiced patients, superoxide radical levels in the plasma fraction of whole blood were positively correlated with the degree of cholestasis. The addition of allopurinol to whole blood samples decreased superoxide radical in the plasma fraction of jaundiced patients to the disease-control level (P < 0.001), whereas it had no effect on superoxide radical levels in the cell fraction. No superoxide radical was detected in fractionated plasma in all cases., Conclusions: These data show that increased superoxide radical in the plasma of jaundiced patients is possibly formed from a source in the cytoplasmic membrane of blood cells and secreted into plasma. The reversal of this phenomenon by allopurinol, ex vivo, indicates that a blood cell membranous XO might be the source of increased plasma superoxide radical in patients with extrahepatic cholestasis.

Patients with primary Sjögren syndrome frequently present hematologic abnormalities, consisting mainly of immune cytopenias. Pure red cell aplasia is a very rare complication of primary Sjögren syndrome. This is the first report in the literature describing the development of pure red cell aplasia combined with autoimmune hemolytic anemia in a 74-year-old woman with primary Sjögren syndrome. In our patient, despite administration of diverse therapeutic schemes, such as corticosteroids, immunomodulating agents (intravenous immune globulin), immunosuppressive drugs (cyclophosphamide), and novel treatment options (monoclonal antibody directed against the CD20 antigen), no response was achieved. The present case suggests that the possibility of comorbid connective tissue disease should be a diagnostic consideration in patients with acquired pure red cell aplasia and autoimmune hemolytic anemia. Although most of the hematologic abnormalities that occur in primary Sjögren syndrome are not clinically significant, serious and difficult-to-treat hematologic complications may also occur.

A potential complication of leptospirosis is cardiovascular involvement. Electrocardiographic abnormalities are frequent. Leptospirosis has been reported to be one of the infectious causes of relative bradycardia, but severe absolute sinus bradycardia has been rarely described as a potential electrocardiographic alteration. We present a case of marked sinus bradycardia (35 bpm) lasting for 4 days in a patient with anicteric leptospirosis and relative bradycardia on admission. Heart rate resolved spontaneously after control of infection by appropriate antibiotic therapy. This case points toward the need for close monitoring of vital signs and electrocardiogram in leptospirosis, especially when relative bradycardia is present on admission.