Merve Ateş

Background/Objectives: Reflex testing may improve laboratory stewardship by limiting downstream analyses to situations in which additional testing is supported by the result of an initial test. This study evaluated the projected impact of predefined reflex testing algorithms on thyroid function and prostate-specific antigen (PSA) test utilization and laboratory expenditure. Methods: This observational modelling study included clinician-initiated thyroid function and PSA testing sessions recorded at a tertiary-care hospital in Türkiye during 2022. Clinician-requested tests and corresponding laboratory results were compared with predefined reflex algorithms applied retrospectively at the testing-session level. For thyroid testing, thyroid-stimulating hormone (TSH) was used as the initial test; free thyroxine (FT4) was projected for elevated TSH, and both FT4 and free triiodothyronine (FT3) for decreased TSH. For PSA testing, free PSA was projected only when total PSA was 4.0–10.0 ng/mL. Observed clinician-initiated testing was compared descriptively with projected algorithm-based testing, including downstream test utilization and laboratory expenditure. Results: The thyroid cohort comprised 60,656 testing sessions from 43,839 patients, and the PSA cohort comprised 4583 sessions from 3631 patients. In the thyroid cohort, clinicians requested 49,858 FT4 and 19,899 FT3 measurements. Under the predefined algorithm, these numbers were projected to decrease to 6205 and 2478, respectively, reducing total thyroid test volume from 130,413 to 69,339 tests, a projected reduction of 61,074 tests (46.8%). In the PSA cohort, free PSA testing was projected to decrease from 2133 to 642 measurements, reducing total PSA-related test volume from 6716 to 5225 tests (22.2%). Projected laboratory expenditure decreased from US dollars (USD) 73,579.01 to USD 39,121.06 for thyroid testing and from USD 6468.78 to USD 4560.73 for PSA testing. Across both pathways, the projected saving was USD 36,366.00, corresponding to a 45.4% reduction in expenditure. Conclusions: Retrospective application of predefined reflex testing algorithms to clinician-initiated thyroid function and PSA requests projected substantial reductions in downstream test utilization and laboratory expenditure. Prospective implementation studies incorporating patient-specific clinical information are needed to determine whether these projected reductions can be achieved safely in routine clinical practice without limiting clinically appropriate testing.

Aim: This study aimed to determine the incidence of contrast-induced acute kidney injury (CI-AKI) and to identify the clinical factors associated with it in patients undergoing contrast-enhanced computed tomography (CECT) in the emergency department (ED).Material and Methods: This prospective observational study, reported in accordance with the STROBE statement, enrolled 125 consecutive adults (≥18 years) who underwent CECT in the ED between October 2023 and May 2024. The sample size was estimated a priori. CI-AKI was defined as an increase in serum creatinine of ≥0.5 mg/dL or ≥25% at 48–120 hours after contrast administration. Demographic, clinical, and laboratory variables were compared between patients who did and did not develop CI-AKI.Results: CI-AKI developed in 17 of 125 patients (13.6%, 95% confidence interval [CI] 8.7–20.7%). CI-AKI was not associated with age, sex, hemoglobin, diabetes, hypertension, coronary artery disease, heart failure, or contrast volume. Pre-procedural hypotension (p=0.001) and atrial fibrillation (p=0.031) were significantly associated with CI-AKI, and CI-AKI was more frequent among patients requiring intensive care unit (ICU) admission (31.6% vs 5.7%; risk difference 25.8%, 95% CI 11.5–42.0%; p=0.001), interpreted as a marker of illness severity rather than a pre-procedural predictor.Conclusion: CI-AKI occurred in 13.6% of ED patients undergoing CECT; pre-procedural hypotension and atrial fibrillation were significantly associated with its development.

Tiroid bezi, hormon sentezi ve metabolik homeostazın sürdürülmesinde merkezi rol oynayan bir endokrin organdır. Tiroid hormonlarının sentezi, aktivasyonu ve hücresel etkileri; yalnızca iyot varlığına değil, aynı zamanda çeşitli eser elementlerin biyokimyasal ve moleküler düzeydeki katkılarına bağlıdır. Bu bölümde, tiroid fonksiyonlarının düzenlenmesinde rol alan başlıca eser elementler; iyot, selenyum, demir, çinko, bakır, manganez, magnezyum ve molibden güncel literatür ışığında ele alınmıştır. Her bir elementin tiroid hormon biyosentezi, periferal dönüşüm mekanizmaları, redoks dengesi ve immünomodülasyon üzerindeki etkileri detaylandırılmıştır. Ayrıca bu elementlerin eksiklik veya fazlalık durumlarında ortaya çıkan biyokimyasal bozukluklar ve tiroid hastalıklarıyla ilişkileri tartışılmıştır. Tiroid fizyolojisinin eser elementler üzerinden değerlendirilmesi, hem hastalık patogenezinin anlaşılması hem de hedefe yönelik tedavi stratejilerinin geliştirilmesi açısından önemli bilgiler sunmaktadır. Bu bölüm, tiroid biyokimyası ile eser element metabolizması arasındaki karmaşık ilişkiye bütüncül bir bakış açısı sağlamayı amaçlamaktadır. The thyroid gland is a central endocrine organ responsible for hormone synthesis and metabolic homeostasis. The synthesis, activation, and cellular actions of thyroid hormones depend not only on iodine but also on the biochemical and molecular contributions of several trace elements. This chapter discusses the major trace elements involved in thyroid function, including iodine, selenium, iron, zinc, copper, manganese, magnesium, and molybdenum, in the light of current literature. The role of each element in thyroid hormone biosynthesis, peripheral conversion mechanisms, redox balance, and immunomodulation is comprehensively reviewed. In addition, the biochemical disturbances associated with deficiency or excess of these elements and their relationship with thyroid disorders are highlighted. Evaluating thyroid physiology through the perspective of trace elements provides important insights into both disease pathogenesis and the development of targeted therapeutic strategies. This chapter aims to provide a comprehensive overview of the complex interaction between thyroid biochemistry and trace element metabolism.

Background: The genes mutated in monogenic diabetes vary across populations, and different clinical outcomes are observed depending on the affected gene. GCK-MODY, which develops as a result of a glucokinase gene mutation, is the most common subtype in Türkiye. This review aims to summarize the clinical presentations, mutations, and diagnostic and therapeutic approaches observed in MODY studies conducted in Türkiye.Review Text: Twelve studies conducted in Türkiye between 2015 and 2024 were analyzed for demographic, clinical, and molecular data. Additionally, one case compatible with GCK-MODY was evaluated. GCK-MODY was found to be the predominant MODY subtype in Türkiye, and GCK gene mutation rates ranged from 20% to 70% depending on study design and inclusion criteria. Patients with GCK-MODY were found to exhibit typical clinical features, including mild fasting hyperglycemia, HbA1c levels below 7%, negative autoantibodies, and preserved C-peptide levels. The presented 22-year-old female case demonstrated clinical and genetic features consistent with GCK-MODY.Conclusion: Data from studies in Türkiye indicate that GCK-MODY is the most common monogenic diabetes subtype, with the expected clinical features. Accurate clinical and molecular diagnosis is crucial for preventing unnecessary pharmacological treatment, providing appropriate treatment, and providing appropriate genetic counseling in special circumstances such as pregnancy.

Objective: Expression of mammalian target of rapamycin (mTOR), which plays a key role in coordinating the balance between cell growth and autophagy, is elevated in thyroid tissues of patients with Hashimoto’s disease. Sestrins are an evolutionarily conserved, stress-inducible protein family that reduces oxidative stress and regulates the adenosine monophosphate-dependent protein kinase (AMPK)-mTOR signaling pathway. The aim of this study was to investigate the potential role and significance of sestrin 2 (SESN2), a member of the sestrin family, in Hashimoto’s disease. Methods: This cross-sectional study included patients with Hashimoto’s disease and healthy volunteers. Thyroid autoantibodies, free T4, TSH, and sestrin 2 were measured from blood samples. Sestrin 2 was analyzed by an ELISA kit. Results: One hundred ten patients and 64 healthy volunteers were included in the study. Median SESN2 levels in the patient group (1.36 ng/mL (1.10–2.03)) were significantly lower than in the control group (1.83 ng/mL (1.34–2.64)) (P = 0.002). There was no significant difference in SESN2 levels between euthyroid and subclinical hypothyroidism subgroups of patients (P > 0.05). Conclusion: In this study, serum SESN2 levels were found to be lower in patients with Hashimoto’s disease than in healthy adults, suggesting that SESN2 may have a role in the pathophysiology of Hashimoto’s disease. These results indicate that further research is needed to better understand the effect of regulation of SESN2 in Hashimoto’s disease on the course and pathological processes of the disease.