Publications by authors named "Sargın Altunok"

3 Publications

  • Page 1 of 1

Performance of pneumonia severity index and CURB-65 in predicting 30-day mortality in patients with COVID-19.

Int J Infect Dis 2020 Sep 14;98:84-89. Epub 2020 Jun 14.

Department of Rheumatology, Gaziosmanpasa Research and Training Hospital, University of Health Sciences, Istanbul, Turkey. Electronic address:

Objective: The aim of the study was to analyze the usefulness of CURB-65 and the pneumonia severity index (PSI) in predicting 30-day mortality in patients with COVID-19, and to identify other factors associated with higher mortality.

Methods: A retrospective study was performed in a pandemic hospital in Istanbul, Turkey, which included 681 laboratory-confirmed patients with COVID-19. Data on characteristics, vital signs, and laboratory parameters were recorded from electronic medical records. Receiver operating characteristic analysis was used to quantify the discriminatory abilities of the prognostic scales. Univariate and multivariate logistic regression analyses were performed to identify other predictors of mortality.

Results: Higher CRP levels were associated with an increased risk for mortality (OR: 1.015, 95% CI: 1.008-1.021; p < 0.001). The PSI performed significantly better than CURB-65 (AUC: 0.91, 95% CI: 0.88-0.93 vs AUC: 0.88, 95% CI: 0.85-0.90; p = 0.01), and the addition of CRP levels to PSI did not improve the performance of PSI in predicting mortality (AUC: 0.91, 95% CI: 0.88-0.93 vs AUC: 0.92, 95% CI: 0.89-0.94; p = 0.29).

Conclusion: In a large group of hospitalized patients with COVID-19, we found that PSI performed better than CURB-65 in predicting mortality. Adding CRP levels to PSI did not improve the 30-day mortality prediction.
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September 2020

Protease Inhibitors Drug Resistance Mutations in Turkish Patients with Chronic Hepatitis C.

Int J Infect Dis 2016 Sep 9;50:1-5. Epub 2016 Jul 9.

Infectious Diseases and Clinical Microbiology, Okmeydanı Training and Research Hospital, İstanbul, Turkey.

Background: Drug resistance development is an expected problem during treatment with protease inhibitors (PIs), this is largely due to the fact that Pls are low-genetic barrier drugs. Resistance-associated variants (RAVs) however may also occur naturally, and prior to treatment with Pls, the clinical impact of this basal resistance remains unknown. In Turkey, there is yet to be an investigation into the hepatitis C (HCV) drug associated resistance to oral antivirals.

Materials And Methods: 178 antiviral-naïve patients infected with HCV genotype 1 were selected from 27 clinical centers of various geographical regions in Turkey and included in the current study. The basal NS3 Pls resistance mutations of these patients were analyzed.

Results: In 33 (18.5%) of the patients included in the study, at least one mutation pattern that can cause drug resistance was identified. The most frequently detected mutation pattern was T54S while R109K was the second most frequently detected. Following a more general examination of the patients studied, telaprevir (TVR) resistance in 27 patients (15.2%), boceprevir (BOC) resistance in 26 (14.6%) patients, simeprevir (SMV) resistance in 11 (6.2%) patients and faldaprevir resistance in 13 (7.3%) patients were detected. Our investigation also revealed that rebound developed in the presence of a Q80K mutation and amongst two V55A mutations following treatment with TVR, while no response to treatment was detected in a patient with a R55K mutation.

Conclusion: We are of the opinion that drug resistance analyses can be beneficial and necessary in revealing which variants are responsible for pre-treatment natural resistance and which mutations are responsible for the viral breakthrough that may develop during the treatment.
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September 2016

A case report: antiviral triple therapy with telaprevir in a haemodialysed HCV patient in Turkey.

Acta Clin Belg 2015 Dec;70(6):440-1

Infectious Diseases and Clinical Microbiology, Kocaeli University Faculty of Medicine , Turkey.

A 49-year-old woman was diagnosed with chronic hepatitis C 7 years ago. She began haemodialysis at the same time. She was on the waiting list for kidney transplantation (KTx). The real-time PCR technique revealed an HCV RNA viral load of 212,000 IU/ml, genotype 1a, IL28B the rs12979860 minor allele heterozygous CT (rs8099917 TT homozygous). She had a history of first antiviral treatment for 48 weeks of PEG-IFN-alpha 2a, 135 μg/week in 2011, but the HCV infection relapsed. Considering her relatively young age, candidacy for renal transplant, and the heterozygous pattern of IL28B, we decided to proceed with a second (and last) antiviral treatment using triple therapy with telaprevir at the regular dose of 750 mg every 8 hours+PEG-IFN-alpha 2a 135 μg/week sc+200 mg RBV three times a week. At the end of 6-month therapy, HCV RNA was found to be negative at months 3, 5, and 6.The patient has reached the sustained virological response (SVR) and is ready for KTx. All renal transplant candidates (dialysis-dependent, or not) with HCV should be assessed for antiviral treatment given the increased risk of progressive liver disease due to immunosuppressive therapy, increased life expectancy compared to other HCV-positive patients on dialysis, and the inability to receive interferon after transplantation.
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December 2015