BackgroundThe pathogenesis of portal vein thrombosis (PVT) in cirrhosis is multifactorial, with altered hemodynamics being proposed as a possible contributor. The present systematic review was conducted to study the role of assessment of portal hemodynamics for the prediction of PVT in patients with cirrhosis.MethodsThree databases (Medline, Embase, and Scopus) were searched from inception to February 2023 for studies comparing portal venous system parameters in patients with cirrhosis developing PVT with those not. Results were presented as mean difference (MD) or odds ratio (OR) with their 95% confidence intervals (CIs).ResultsA total of 31 studies (patients with cirrhosis: 19 studies, patients with cirrhosis undergoing splenectomy: 12 studies) were included. On pooling the data from multivariable analyses of the included studies, a larger portal vein diameter was a significant predictor of PVT in patients with cirrhosis without or with splenectomy with OR 1.74 (1.12–2.69) and OR 1.55 (1.26–1.92), respectively. On the other hand, a lower portal vein velocity (PVV) was a significant predictor of PVT in cirrhotics without or with splenectomy with OR 0.93 (0.91–0.96) and OR 0.71 (0.61–0.83), respectively. A PVV of <15 cm/s was the most commonly used cut‐off for the prediction of PVT. Patients developing PVT also had a significantly higher splenic length, thickness, and splenic vein velocity.ConclusionThe assessment of portal hemodynamic parameters at baseline evaluation in patients with cirrhosis may predict the development of PVT. Further studies are required to determine the optimal cut‐offs for various parameters.

BackgroundThe disease COVID-19, caused by SARS-CoV-2 infection, has a systemic effect and is associated with a number of pathophysiological mechanisms that mobilize a wide range of biomolecules. Cytokines and growth factors (GFs) are critical regulators of tissue damage or repair in osteoarthritis (OA) and are being recognized as key players in the pathogenesis of COVID-19. A clear understanding of the long-term consequences of SARS-CoV-2 infection, especially in patients with concomitant chronic diseases, is limited and needs to be elucidated. The study aimed to evaluate the degree of inflammation and levels of pro-angiogenic and hypoxic factors, as well as heat shock proteins HSP60 and HSP70 in plasma, of patients with OA after recovery from COVID-19.MethodsThe research involved patients of an orthopedic specialty clinic aged 39 to 80 diagnosed with knee OA. All examined patients were divided into three groups: the Control group included conditionally healthy donors, group OA included patients with knee OA mainly stage II or III and the group of OA and COVID-19 included patients with OA who had COVID-19. The plasma levels of pro-inflammatory molecules IL-1β, IL-6, TNF-α, NF-κB, angiogenic factors VEGF, FGF-2, PDGF, hypoxic factor HIF-1α and molecular chaperones HSP60 and HSP70 were measured by enzyme-linked immunosorbent assay.ResultsThe study showed that in both groups of patients, with OA and convalescent COVID-19, there was an increase in the plasma level of IL-1β and a decrease in TNF-α and NF-κB levels when compared to healthy controls. Systemic deregulation of the cytokine profile was accompanied by reduction in plasma levels of pro-angiogenic growth factors, most pronounced in cases of VEGF and PDGF. This analysis did not reveal any significant difference in the plasma level of HIF-1α. A decrease in the level of stress protein HSP60 in the blood of patients with OA, as well as those patients who have had SARS-CoV-2 infection, has been established.ConclusionThe results suggest the potential role pro-inflammatory cytokines and angiogenesis-related growth factors in pathogenesis of both joint pathologies and long-term systemic post-COVID-19 disorders.

Background and Objectives: Coronary artery disease (CAD) is the foremost cause of adult disability and mortality. There is an urgent need to focus on the research of new approaches for the prevention and treatment of CAD. Materials and Methods: The effects of peptides isolated from the blood plasma of CAD patients on endothelial cell secretion using the in vitro model have been tested. Human endothelial progenitor cells (HEPCs) were incubated for 24 h with peptides isolated from the plasma of healthy subjects or patients with stable angina, progressive unstable angina, and myocardial infarction. The contents of some soluble anticoagulant as well as procoagulant mediators in HEPC culture treated with peptide pools were then compared. Results and Conclusion: The results show that peptides from the plasma of patients with myocardial infarction promote endothelial cells to release both von Willebrand factor and endothelin-1, increasing vasoconstriction and shifting hemostatic balance toward a prothrombotic state. In contrast, peptides from the plasma of patients with progressive unstable angina suppress the secretion of endothelin-1 by HEPCs, while the secretion of both von Willebrand factor and tissue plasminogen activator was increased. As can be seen from the results obtained, disease derived peptides may contribute to the homeostasis of living organisms or the progression of pathological processes.

An 84-year male patient with a past medical history of coronary artery disease, heart failure with preserved ejection fraction, hypertension, and chronic dysphagia status post percutaneous gastrostomy tube (PEG) placement presented for worsening hemoglobin levels on laboratories. The patient was asymptomatic on admission.The patient denied any melena, hematochezia, diarrhea, constipation, vomiting, hematemesis, and abdominal pain. His hemoglobin was 7 (reference range 13.8-17.2) g/dL on admission; therefore, he received 1 unit of packed red blood cells. The patient was scheduled for colonoscopy because of suspicion of iron deficiency anemia secondary to chronic blood loss. The total procedure time of colonoscopy was 92 min due to dense diverticular disease in the left colon, extremely difficult cecal intubation, and a large polyp in a difficult/unstable position, requiring scope exchange for completion of polypectomy. PEG tube shaft was noted going through the transverse colon (Figure 1). The PEG tube was placed 6 months prior to colonoscopy. Gastrocolic fistula was diagnosed clinically and confirmed on the CT scan of the abdomen. The definitive treatment for misplaced PEG tube includes surgical removal or endoscopic removal of PEG tube; however, the patient refused any further interventions. | DISCUSSION AND CONCLUSIONPEG is a favorable route of feeding and nutritional support in patients with a functional gastrointestinal system who require long term enteral nutrition, generally beyond 4 weeks. Feeding tubes designed for long term include gastrostomy

A seven-year-old male presented with complaints of food refusal, dysphagia, and odynophagia for three weeks. He also had a history of caustic ingestion six months prior to the presentation. Diagnostic esophagogastroduodenoscopy (EGD) revealed post-burn esophageal stricture, and biopsy confirmed eosinophilic esophagitis (EoE). In this report, we discuss the diagnosis and management of these pathologies. We suspect that the damage sustained from caustic ingestion laid the groundwork for the development of EoE in this patient.