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    Can the reduction of cytokines stop the progression of sepsis?
    (Cureus, Inc., 2022) Koç, Suna; Çelebi, Serdar; Hanikoğlu, Ferhat; Polat, Yalçın; Börkü Uysal, Betül; Dokur, Mehmet; Özer, Türkan; Yavuzer, Serap; İslamoğlu, Mehmet Sami; Cengiz, Mahir; Vardar, Gökay; Küpeli, İlke
    Objective In this study, we aimed to analyze the laboratory and clinical results of cytokine hemadsorption as an immunomodulation therapy in ICU patients diagnosed with sepsis or septic shock. Methods The levels of procalcitonin (PCT) and C-reactive protein (CRP), determined to be indicators of infection/sepsis, and the levels of interleukins (IL-6, IL-8, and IL-10) and tumor necrosis factor α (TNFα), deemed as indicators of the cytokine storm, were compared among 32 patients before and after the hemadsorption procedure. Results The hemadsorption significantly reduced the levels of IL-6, IL-8, IL-10, TNFα, PCT, CRP, Acute Physiology and Chronic Health Evaluation (APACHE) scores, mortality rate, and Sequential Organ Failure Assessment (SOFA) scores (p<0.05). APACHE scores and the mean predicted mortality rate (PMR) of the non-survivors measured before the procedure was significantly higher than those of survivors (p=0.002 for both). IL-10, APACHE scores, and the mortality rates determined before the hemadsorption procedure were deemed significant parameters to predict the mortality among all ICU patients (p<0.05). IL-10 levels ≤125.3 ng/L, APACHE score >30, and PMR >70.33 were significantly associated with the mortality rates of all patients, indicating that these three parameters determined before the hemadsorption may be good predictors of mortality among ICU patients with sepsis. Conclusion The progression of sepsis in ICU patients may be prevented with cytokine hemadsorption applied as an immunomodulator therapy.
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    The role of Adenovirus-36 in adults with obesity-induced type 2 diabetes
    (Verlag Klinisches Labor GmbH, 2022) Tokman, Halit; Ergin, Sevgi; Sarıbaş, Suat; Dinç, Harika Öykü; Cengiz, Mahir; Yavuzer, Serap; Çizmecigil, Utku Yusuf; Önder, Nuri T.; Yılmaz, Hüseyin; Eryiğit, Önder Yüksel; Gareayaghi, Nesrin; Kocazeybek, Bekir Sami
    Background: Obesity may also develop due to a viral infection caused by adenovirus 36. We aimed to detect the presence of neutralizing antibodies against Ad-36 in adult patients who developed type 2 diabetes due to obesity (BMI ≥ 30 kg/m2). Methods: The patient group (PG) was composed of 80 obese people with type 2 diabetes, the patient control group (PCG) was composed of 40 non-obese people with type 2 diabetes, and the healthy control group (HCG) was composed of 40 non-obese people without type 1 or type 2 diabetes in this case-control study. The presence of Ad-36 neutralizing antibodies was studied by serum neutralization assay. Results: A significant difference was found between the PG and HCG in terms of Ad-36 antibody positivity (p < 0.0001) but no significant difference was detected between the PG and the PCG (p > 0.05). BMI, serum leptin, adiponectin, and triglyceride levels were significantly higher in the PG (p < 0.05). Conversely, TNF-α and IL-6 levels were significantly lower in the PG (p < 0.0001). When the two groups were compared, the mean levels of total cholesterol and LDL in the PG were found to be high, although not significant (p > 0.05). In type 2 diabetes patients (n = 120), age, BMI, HDL, LDL, triglyceride, total cholesterol, Ad-36 presence, leptin, adiponectin, TNF-α, and IL-6 parameters were taken as independent variables for logistic regression. While BMIs was found to be significant (odds ration [OR] = 2.358; p = 0.0001, 95% Cl 1.507 - 3.690, Ad-36 presence was found to be a significant (OR = 27.352; p = 0.003, 95% Cl 3.157 - 236.961). Our study showed that BMI and Ad-36 increase type 2 diabetes risk by 2.3 and 27.3-fold in the PG and PCG (type 2 diabetes patients) versus the HCG. There was also a significant difference between PCG and HCG. Conclusions: We suggest that Ad-36 seropositivity is also a risk factor for the development of type 2 diabetes independent of being obese. © 2022 Verlag Klinisches Labor GmbH. All rights reserved.