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    Evaluation of personalized methylprednisolone therapy in critically ill COVID-19 patients: an observational comparative study using real-life data
    (Verduci Publisher, 2022) Duman, I; Celik, J. B.; Iyisoy, M. S.; Degirmencioglu, S.; Korkmaz, A.; Duman, A.
    OBJECTIVE: Methylprednisolone is commonly used to attenuate the cytokine storm and prevent mortality in COVID-19 pneumonia. However, the optimal methylprednisolone dose and duration are unclear. Additional data are required on the effectiveness of methylprednisolone in reducing mortality in COVID-19. This real-life retrospective study aimed to analyze the data of a COVID-19 dedicated ICU and compare the mortality rates of standard care, low-dose, and pulse-dose met hylprednisolone in patients requiring mechanical ventilatory support. PATIENTS AND METHODS: Methylprednisolone's indication. dose. and duration were determined according to the severity of COVID-19 pneumonia based on the patient's demographic parameters, comorbidities. laboratory data. radiology, and arterial blood gas analysis results. 867 patients were grouped as: no methylprednisolone (standard care), low-dose (0.5-1 mg/kg/day) methylprednisolone or pulse-dose (250-1,000 mg/day) met hylprednisolone. RESULTS: The overall mortality rate was 63.78%. Adjusting the dose of methylprednisolone according to the severity of the disease resulted in statistically similar mortality rates despite the increase in disease severity. Mortality was 62.71% in standard treatment. 65.76% in low-dose, and 62.10% in pulse-dose methylprednisolone groups (p = 0.633). Invasive mechanical ventilation at admission was associated with increased mortality (HR: 1.826 [95% CI: 1.542-2.161]; p < 0.001). Hematologic disorders and malignancies, arterial blood pH and HCO3, neutrophil count, and NLR at admission were also associated with mortality. CONCLUSIONS: Personalizing the dose and duration of methylprednisolone according to the patient's disease severity assessed with demographic, clinical, and laboratory results may benefit mortality in severe COVID-19 patients receiving ventilatory support in the ICU. Hematologic disorders and malignancies, arterial blood pH and HCO3, neutrophil count, and NLR at admission were associated with mortality in our patient cohort.
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    In vitro vasoactive effects of dexmedetomidine on isolated human umbilical arteries
    (Comenius Univ, 2019) Arun, O.; Taylan, S. B.; Duman, I; Oc, B.; Yilmaz, S. A.; Tekin, A.; Celik, C.
    OBJECTIVE: We aimed to investigate the vasoactive effects of dexmedetomidine on isolated human umbilical arteries and possible mechanisms involved. METHODS: Human umbilical artery strips were suspended in Krebs-Henseleit solution and dose-response curves were obtained for cumulative dexmedetomidine before and after incubation with different agents; propranolol, atropine, yohimbine, prazosin, indomethacin, verapamil. Effects of calcium on cumulative dexmedetomidine-induced contractions were also studied. RESULTS: Cumulative dexmedetomidine resulted in dose dependent contraction responses. Incubation with propranolol (Emax: 93.3 +/- 3.26 %), atropine (Emax: 92.0 +/- 6.54 %), or indomethacin (Emax: 94.25 +/- 2.62 %), did not attenuate dexmedetomidine-elicited contractions (p > 0.05). There were significant decreases in the contraction responses of cumulative dexmedetomidine with yohimbine (Emax: 12.1 +/- 11.9 %), prazosin (Emax: 28.8 +/- 4.6 %) and verapamil (Emax: 11.2 +/- 13.6 %) (p < 0.05). In Ca+2 free medium contraction responses to cumulative dexmedetomidine was insignificant (Emax: 5.20 +/- 3.42 %). Addition of cumulative calcium to the Ca+2 free medium resulted in concentration dependent increase in contractions (Emax: 64.83 +/- 37.7 %) (p < 0.05). CONCLUSION: Dexmedetomidine induces vasoconstriction in endothelial-free umbilical arteries via both, alpha(1)- and alpha(2)-adrenergic receptors and also extracellular Ca+2 concentrations play a major role. beta-adrenergic receptors, muscarinic cholinergic receptors, and inhibition of cyclooxygenase enzyme are not involved in this vasoconstriction (Fig. 3, Ref. 36). Text in PDF www.elis.sk.