Objectives: Recently, the need for early diagnosis of modifiable risk factors involved in the etiology of stroke has been highlighted in the literature. Nesfatin-1 is a peptide expressed in the central nervous system and peripheral tissues and has been used as a biomarker in recent years. This study aimed to determine the association of ischemic stroke with internal carotid artery stenosis according to nesfatin-1 level and whether it could be used as a biomarker. Methods: A total of 118 patients were included in the study. Three groups were defined: acute stroke patients with symptomatic internal carotid artery stenosis, acute stroke patients without internal carotid artery stenosis, and a control group. Nesfatin-1 levels were measured and compared. Results: The median value was 22 pg/mL in acute stroke patients with internal carotid artery stenosis, 24.3 pg/mL in acute stroke patients without internal carotid artery stenosis, and 46.4 pg/mL in the control group. There is a difference between the median values of nesfatin-1 according to the stroke groups with the control group (p < 0.001). When a cut-off value of ≤30.62 was taken for nesfatin-1, an AUC value of 0.773 indicated statistical significance (p < 0.001). Sensitivity was 77.03%, specificity 83.33%, PPV 90.48%, and NPV 63.83%. The main limitations of our study are the small sample size and the fact that the function of nesfatin-1 is not completely known. Conclusions: Although we found that nesfatin-1 levels were lower in ischemic stroke patients compared to controls, its diagnostic potential indicates a moderate discriminatory ability with an AUC value of 0.773. Therefore, whether it is suitable for clinical use will be demonstrated by studies in larger and multicenter cohorts.

Objective: The thalamus is a control point that is a gateway for all sensory impulses except smell and contributes to regulating the sleep-wake process. Therefore, infarcts of the thalamus cause a diversity of symptoms along with a diversity of vascular anatomy. The fact that thalamic infarcts are mostly considered lacunar infarcts seems to create inadequacy in understanding the etiology. This study aimed to compare the etiologic, diagnostic, and therapeutic parameters of thalamic infarction. Materials and Methods: This retrospective study analyzed 230 patients with thalamic infarction among 820 stroke patients admitted between January 2019 and April 2022. Patients with hemorrhagic stroke, malignancy, or infection were excluded. Demographic data, comorbidities, imaging results, and treatments administered were evaluated. All these results were analyzed in two subgroups: isolated thalamic and extrathalamic involvement. Results: Bilateral thalamic involvement was 8.386 times more common in patients with extrathalamic participation. Patients using dual antiaggregants had 2.207 times higher isolated thalamic involvement, while those on oral anticoagulants had 2.378 times higher extrathalamic involvement. Pathologies in the basilar and vertebral arteries increased the risk of extrathalamic involvement by 2.660 times (p<0.001). Conclusion: Thalamic infarcts cannot be considered exclusively lacunar. Extrathalamic involvement has been associated with worse functional scores and arterial pathologies. The protective effects of dual antiaggregants and oral anticoagulants vary depending on whether the thalamic infarct is extrathalamic or not, emphasizing the need for individualized therapies.

We present a case of a 66-year-old female patient with partially compromised immunity due to diabetes mellitus, exhibiting progressive encephalopathy characterized by balance issues, cognitive decline, and hallucinations. Magnetic resonance imaging (MRI) revealed widespread cerebral and cerebellar atrophy, and John Cunningham virus (JCV) – DNA was detected in the cerebrospinal fluid. This case highlights JCV encephalopathy as a potential diagnosis even in patients with partially weakened immune systems, expanding the recognized spectrum of JCV-associated neurological conditions beyond progressive multifocal leukoencephalopathy.

Background/Aims: Pancreatic steatosis (PS) is characterized by fat accumulation within the pancreas and is associated with chronic low-grade inflammation. Migraine, the third most commonly seen disease worldwide, is an established risk factor for white matter lesions (WMLs). Given the shared inflammatory background of these conditions, it was hypothesized that the presence of PS in patients with migraine may contribute to the development of WMLs. Materials and Methods: This cross-sectional study included patients with migraine who attended the outpatient clinic and had undergone cranial magnetic resonance imaging (MRI) scan for any indication within the last 6 months. Following MRI, patients were referred to the radiology department for transabdominal ultrasonography to assess the presence of PS and hepatosteatosis. Results: Among the 78 patients with migraine included in the study, 35 (44.9%) had cranial WMLs. PS was significantly more prevalent among patients with WMLs than among those without WMLs (57.4% vs. 16.7%, P < .001). In multivariable logistic regression analysis adjusted for age, body mass index, and low-density lipoprotein/high-density lipoprotein ratio, PS remained independently associated with cranial WMLs (odds ratio (OR) 5.79, 95% CI 1.004-33.41; P = .049). Increasing age was also independently associated with WMLs (OR 1.095 per year, 95% CI 1.018-1.179; P = .015). Conclusion: This study demonstrated that the presence of PS may contribute to disease burden in patients with migraine. Evaluation of PS in this population may help identify a potentially modifiable metabolic condition and provide additional insight into the management of this common and debilitating disorder. Cite this article as: Alparslan AS, Ocal R, Buldukoglu OC, et al. Pancreatic steatosis: Innocent bystander or silent culprit? Turk J Gastroenterol. Published online July 20, 2026. doi:10.5152/tjg.2026.26091.