UIUmut İlHan

Umut İlHan

*This is an algorithmically generated author record based on publicly available information.

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Umut İlHan has a total of 29 co-authors. Here are the top co-authors by number of shared publications:


Latest Publications

  • Real-world effectiveness and safety of nintedanib in connective tissue disease– associated interstitial lung disease: Retrospective cohort study

    by Ayşenur YILMAZ, Erdem Bektaş, Barış DEMİRKOL, Ramazan Eren, Umut İlHan, Erdoğan ÇETİNKAYA, Cemal Bes

  • Hidden granulomatous-lymphocytic interstitial lung disease (GLILD): A missed diagnosis in granulomatous and interstitial lung diseases

    by Şeyma Özden, Burcu Babaoğlu Elkhatroushi̇, Umut İlHan, Barış DEMİRKOL, Erdoğan ÇETİNKAYA, Fatma Merve Tepetam, Nur Dilek Bakan

  • Open Access

    Diagnostic value of CD4, CD8 and CD68 immunohistochemical profiling in EBUS-TBNA samples for differentiating sarcoidosis and tuberculosis

    by Zehra Büşra Özbolat, Mediha Gönenç Ortaköylü, Halide Nur Ürer, Mehmet Atilla Uysal, Belma Akbaba Bağcı, Esma Seda Akalın, Mehmet Akif Parlar, Umut İlHan

    Differentiating sarcoidosis from tuberculosis in patients with mediastinal and/or hilar granulomatous lymphadenopathy remains challenging due to overlappin

  • Open Access

    Diagnostic value of biochemical ratios in the differential diagnosis of tuberculous and malignant pleural effusions

    by Umut İlHan, Zeynep Güney, Ayşe Özçelik, Helin Su Kaya, Erdogan Cetinkaya, Mustafa Çörtük

    Background and objective: The differential diagnosis between tuberculous pleural effusion (TPE) and malignant pleural effusion (MPE) in patients with pleural effusion (PE) continues to pose significant clinical challenges. While conventional pleural fluid cytology has limited sensitivity, invasive diagnostic procedures are often costly or inaccessible, particularly in resource-limited settings. In this study, we investigated the diagnostic contribution of ratios derived from pleural fluid adenosine deaminase (ADA), total protein, serum lactate dehydrogenase (S-LDH), and pleural effusion lactate dehydrogenase (PE-LDH) levels in patients with histopathological confirmed pleural effusion etiology. Specifically, the diagnostic performance of biochemical and hematological parameters, particularly the ADA/serum protein, S-LDH/ADA and PE-LDH/ADA ratios were evaluated for their ability to discriminate between TPE and MPE. Methods: This retrospective cross-sectional study was conducted among patients who underwent diagnostic evaluation and treatment for pleural effusion at a tertiary referral hospital between 1 November 2014 and 1 November 2024. A total of 1,003 patients with pleural effusion (397 TPE and 606 MPE: 409 primary, 133 metastatic, and 64 mesothelioma) were included, whose etiologies were determined using a composite reference standard based on clinical, radiological, microbiological, and histopathological findings, with multidisciplinary team (MDT) evaluation applied in selected cases where appropriate. Receiver operating characteristic (ROC) curve analyses were performed to determine diagnostic accuracy, sensitivity, specificity, and optimal cut-off values. Results: Patients with TPE were significantly younger than those with MPE (median age: 32 vs. 65 years, p < .001). Overall, 62.9% of the study population were male. ADA levels were significantly higher in the TPE group, whereas S-LDH levels were higher in the malignant effusion group. When ratio-based parameters were evaluated, the S-LDH/ADA ratio was markedly higher in patients with malignant pleural effusion and emerged as the most powerful discriminatory marker, with an area under the curve (AUC) of 0.938, sensitivity of 89.5%, and specificity of 91.3%. The ADA/serum protein ratio also demonstrated high diagnostic accuracy for differentiating TPE, with an AUC of 0.929, sensitivity of 89.9%, and specificity of 93.3%. In multivariate analysis, the S-LDH/ADA ratio, ADA/serum protein ratio, and PE-LDH/ADA ratio remained independently associated with diagnostic discrimination between TPE and MPE. Conclusions: Biochemical ratios particularly the S-LDH/ADA and PE-ADA/serum protein ratios are reliable, minimally invasive diagnostic tools for distinguishing TPE from MPE. These ratios are especially useful in guiding clinical decision-making in settings where access to invasive diagnostic procedures is limited.

  • Clinical Reflection of Pre- and Post-COVID-19 Symptoms in COVID-19 Patients

    by Barış Demirkol, Şule Gül, Mustafa Çörtük, Aysu Sinem Koç, Umut İlhan, Kürşad Nuri Baydili, Erdoğan Çetinkaya

  • Open Access

    Frequency of alpha-1 antitrypsin deficiency and unexpected results in COPD patients in Turkey; rare variants are common

    by Mustafa Çörtük, Bariş Demi̇rKol, Meli̇h Akay Arslan, Umut İlHan, Yunus Emre Kalkan, Demet Turan, Şule Gül, Hali̇t Çinarka, Kürşad Nuri̇ Baydi̇lİ, Erdoğan Çeti̇nKaya

    Background/aim: Alpha-1 antitrypsin (?1-AT) is a protease inhibitor that is largely released from liver cells. It inhibits neutrophil elastase and its deficiency increases the risk of developing chronic obstructive pulmonary disease (COPD). The frequency of ?1-AT deficiency has been reported with different prevalence rates in different parts of the world. The most common ?1-AT variant causing ?1-AT deficiency is the Pi*Z allele. In this study, we aimed to determine the frequency of the ?1-AT genotypic variant in COPD patients in our country. Materials and methods: In this study, 196 consecutive COPD patients admitted to our clinic were included. In addition to recording the demographic data of the volunteers, a dry drop of blood sample was taken from the fingertip for the SERPINA1 genotype study. Results: One hundred and fifty-eight (80.6%) of the patients were male and the mean age was 56.92 ± 9.84 years. A variant in the SERPINA1 gene was detected in a total of 14 (7.1%) COPD patients. Pi*ZZ homozygous variant was detected in only 1 (0.51%) patient, while Pi*MZ was detected in 3 (1.53%) patients. The Pi*S variant was never detected. Various rare heterozygous variants were detected in 9 (4.6%) patients and a single point mutation was found in one (0.51%) patient. Serum ?1-AT levels were significantly lower in patients with variants compared to the Pi*MM group (p < 0.001). Conclusion: In this study, which investigated the genotypic ?1-AT variant frequency in COPD patients for the first time in our country, we found that the percentage of homozygous Pi*ZZ patients was 0.51%, but when heterozygous ?1-AT gene variant and single point mutation were included, the frequency was 7.1%. At the same time, while the Pi*S variant was never detected, rare variants were found more frequently than expected.