Browsing by Author "Dusanovic Pjevic, Marija (57208618251)"

Objectives: Inflammatory cytokines like tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 can cause brain injury, slow recovery, and adverse effects (ADEs) in ischemic stroke (IS) patients treated with recombinant tissue plasminogen activator (rtPA). We explored the relationship between selected polymorphisms within TNF-α, IL-1β and IL-6 genes, and post-IS outcome and ADEs in patients treated with rtPA. Methods: One hundred and sixty-six patients with IS treated with rtPA were included in this study. The modified Rankin Scale (mRS) was used to assess functional recovery 3 months after IS likewise thrombolytic therapy efficacy. Patients were classified into groups with favorable (0–1) or poor recovery based on their mRS score at the ninetieth day post-IS. During hospitalization, ADEs following rtPA were monitored. TNF-α-308 G/A (rs1800629), IL-1β-511 G/A (rs16944), and IL-6-174 G/C (rs1800795) polymorphisms were genotyped using Real-Time PCR. SPSS software version 22.0 was used for statistical analyses. Results: Patients with the TNF-α-308 G/A GG genotype had a higher mean NIHSS value at admission (12.75 ± 5.176) than those carrying A-allele (10.56 ± 3.979;p = 0.016). Individuals with the CC genotype of the IL-6-174 G/C polymorphism had significantly lower NIHSS scores (8.79 ± 5.053) than those with G-allele (12.06 ± 6.562) 24 hours after rtPA (p = 0.050). Patients with the GG genotype of the IL-6-174 G/C polymorphism had a significantly poorer outcome (p = 0.024; OR = 2.339; 95%CI 1.121–4.880), while patients who were G-allele carriers of the Il-6–174 G/C polymorphism and had the AA genotype of the IL-1β-511 G/A polymorphism were statistically significantly more likely to experience hemorrhagic transformation (p = 0.046; OR = 2.7273; 95%CI 1.0414–7.1426). Conclusion: GG genotype of the IL-6-174G/C polymorphism is associated with poor recovery after IS treated with rtPA therapy. © 2023 Informa UK Limited, trading as Taylor & Francis Group.

Objectives: Inflammatory cytokines like tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 can cause brain injury, slow recovery, and adverse effects (ADEs) in ischemic stroke (IS) patients treated with recombinant tissue plasminogen activator (rtPA). We explored the relationship between selected polymorphisms within TNF-α, IL-1β and IL-6 genes, and post-IS outcome and ADEs in patients treated with rtPA. Methods: One hundred and sixty-six patients with IS treated with rtPA were included in this study. The modified Rankin Scale (mRS) was used to assess functional recovery 3 months after IS likewise thrombolytic therapy efficacy. Patients were classified into groups with favorable (0–1) or poor recovery based on their mRS score at the ninetieth day post-IS. During hospitalization, ADEs following rtPA were monitored. TNF-α-308 G/A (rs1800629), IL-1β-511 G/A (rs16944), and IL-6-174 G/C (rs1800795) polymorphisms were genotyped using Real-Time PCR. SPSS software version 22.0 was used for statistical analyses. Results: Patients with the TNF-α-308 G/A GG genotype had a higher mean NIHSS value at admission (12.75 ± 5.176) than those carrying A-allele (10.56 ± 3.979;p = 0.016). Individuals with the CC genotype of the IL-6-174 G/C polymorphism had significantly lower NIHSS scores (8.79 ± 5.053) than those with G-allele (12.06 ± 6.562) 24 hours after rtPA (p = 0.050). Patients with the GG genotype of the IL-6-174 G/C polymorphism had a significantly poorer outcome (p = 0.024; OR = 2.339; 95%CI 1.121–4.880), while patients who were G-allele carriers of the Il-6–174 G/C polymorphism and had the AA genotype of the IL-1β-511 G/A polymorphism were statistically significantly more likely to experience hemorrhagic transformation (p = 0.046; OR = 2.7273; 95%CI 1.0414–7.1426). Conclusion: GG genotype of the IL-6-174G/C polymorphism is associated with poor recovery after IS treated with rtPA therapy. © 2023 Informa UK Limited, trading as Taylor & Francis Group.

In the context of rheumatoid arthritis (RA) treatment, Methotrexate (MTX) plays a crucial role in preventing joint damage and bone erosion (BE). RA is characterized by elevated levels of matrix metalloproteinase 2 (MMP2), an enzyme responsible for extracellular matrix degradation, which contributes to joint damage and inflammation. Tissue inhibitor of metalloproteinase 2 (TIMP2) counteracts MMP2, and an imbalance between the two can exacerbate BE. Inosine triphosphatase (ITPA) is an enzyme involved in regulating inosine triphosphate levels, potentially linked to RA susceptibility. Genetic variations in ITPA, MMP2, and TIMP2 genes can influence MTX's efficacy. A study of 122 RA patients on MTX monotherapy assessed its effectiveness using Disease Activity Score (DAS28) changes over 6 months following EULAR response criteria. Genotyping, including MMP2 (rs243866, rs2285053), TIMP2 (rs2277698), and ITPA (rs1127354) polymorphisms, was performed. Among the patients, 87.7% were responders, 63.9% experienced BE, and 24.6% encountered adverse events. Notably, patients with the MMP2 (rs243866) GG genotype were the only ones reporting nausea (p=0.025). Patients with both the MMP2 (rs2285053) CC and TIMP2 (rs2277698) CT genotypes had a lower incidence of BE compared to those lacking this combination (p=0.048). The TIMP2 (rs2277698) CC genotype was associated with a higher baseline DAS28 score (p=0.035). In summary, this study suggests that specific MMP2/TIMP2 genotype combinations may serve as predictors for BE development in RA patients undergoing MTX monotherapy. © 2024 Marmara University Press.

In the context of rheumatoid arthritis (RA) treatment, Methotrexate (MTX) plays a crucial role in preventing joint damage and bone erosion (BE). RA is characterized by elevated levels of matrix metalloproteinase 2 (MMP2), an enzyme responsible for extracellular matrix degradation, which contributes to joint damage and inflammation. Tissue inhibitor of metalloproteinase 2 (TIMP2) counteracts MMP2, and an imbalance between the two can exacerbate BE. Inosine triphosphatase (ITPA) is an enzyme involved in regulating inosine triphosphate levels, potentially linked to RA susceptibility. Genetic variations in ITPA, MMP2, and TIMP2 genes can influence MTX's efficacy. A study of 122 RA patients on MTX monotherapy assessed its effectiveness using Disease Activity Score (DAS28) changes over 6 months following EULAR response criteria. Genotyping, including MMP2 (rs243866, rs2285053), TIMP2 (rs2277698), and ITPA (rs1127354) polymorphisms, was performed. Among the patients, 87.7% were responders, 63.9% experienced BE, and 24.6% encountered adverse events. Notably, patients with the MMP2 (rs243866) GG genotype were the only ones reporting nausea (p=0.025). Patients with both the MMP2 (rs2285053) CC and TIMP2 (rs2277698) CT genotypes had a lower incidence of BE compared to those lacking this combination (p=0.048). The TIMP2 (rs2277698) CC genotype was associated with a higher baseline DAS28 score (p=0.035). In summary, this study suggests that specific MMP2/TIMP2 genotype combinations may serve as predictors for BE development in RA patients undergoing MTX monotherapy. © 2024 Marmara University Press.

Objective Fetuses with abnormal karyotypes often exhibit distinctive ultrasonographic markers, including major anomalies and "soft" markers, indicating potential chromosomal issues. A crucial consideration arises when a single fetal anomaly is detected, raising the question of whether karyotyping is warranted, given the associated procedural risks. Our objective was to establish correlations between single fetal anomalies identified through ultrasound and chromosomal abnormalities. Methods A cross-sectional study analyzed the karyotype of 1493 fetuses and detected a single ultrasonographic anomaly over a 16-year period. Karyotyping was performed using the standard karyotype technique. Moreover, data regarding the type of anomaly detected ultrasonographically, karyotype results, and outcomes following interventions were collected. Among other methods, the use of positive likelihood ratios (LR+) was used to evaluate the diagnostic accuracy of ultrasound compared to karyotyping. Results In total, an aberrant karyotype was identified in 99 fetuses (6.6%). This was most commonly observed in cases involving a "soft" marker, occurring in 27 out of 218 fetuses (12.4%). The most frequently detected aberrant karyotype resulted from aneuploidies (80.6% of cases), notably trisomy 21 (50.5%). "Soft" markers predicted chromosomal issues (LR+ = 1.9; OR = 2.4), and isolated polyhydramnios (LR+ = 1.54; OR = 1.6) showed significance in predicting fetal chromosomal aberrations. Conclusion When assessing the necessity for karyotyping in fetuses with single major anomalies or "soft" markers, it is crucial to consider individual risks for chromosomopathies, including the LR+ of the detected marker. In cases where fetuses exhibit isolated anomalies with a normal karyotype, additional diagnostic measures, such as molecular cytogenetic and molecular genetics techniques, may become necessary. © 2024 Lippincott Williams and Wilkins. All rights reserved.