Jakub Jurica

Polish Archives of Internal Medicine is an international, peer-reviewed, online-only periodical issued monthly in English as an official journal of the Polish Society of Internal Medicine. The journal is designed to publish articles related to all aspects of internal medicine, both clinical and basic science, provided they have practical implications.

Introduction: The prevalence of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is rapidly increasing, possibly becoming the leading cause of chronic liver disease (CLD) in the coming years. Samaglutide (a long-acting glucagon-like peptide receptor agonist 1—GLP-1RA) therapy might be connected with an improved liver function. The aim of the presented study was to assess the impact of semaglutide administered at submaximal doses on biopsy-free scoring systems in patients with obesity and MASLD. Methods: We performed an observational, prospective, post-marketing study. The research included 30 patients (21 being women, mean age 47 ± 14 years) with obesity (Body mass index/BMI/39.7 ± 5.78 kg/m²) and known MASLD. All patients received semaglutide dosed initially 0.25 mg s.c. weekly, which was uptitrated (to a maximal dose of 1.5 mg) over 6 months. MASLD biopsy-free scoring systems (BFSS: SAFE, Fib-4, BARD, NAFLD Fibrosis Score, Fatty Liver Index—FLI, and Hepatic Steatosis Index—HSI) were assessed before and after 6 months of therapy. Results: In this study, a significant change (decrease) in FLI (92.4 ± 9.85 vs. 75.3 ± 21.0, p < 0.001), HSI (50.7 ± 6.78 vs. 45.0 ± 6.42, p < 0.001) and SAFE score (30.8 ± 80.7 vs. 11.2 ± 81.6, p < 0.033) was observed. The changes in the remaining BFSS (BARD, Fib-4 and NAFLD Fibrosis Score) were nonsignificant (p = 0.501; p = 0.303; p = 0.503). Conclusions: In our study, administration of sub-maximally dosed semaglutide was connected with improved FLI, HIS, and SAFE BFSS, suggesting the efficacy of submaximal semaglutide for improvement in MASLD.

Background: Obesity is closely linked to metabolic dysfunction and systemic low-grade inflammation. Glucagon-like peptide-1 receptor agonists (GLP-1RA) are increasingly utilized for obesity treatment due to their significant metabolic benefits, including weight loss and improved glycemic control. The aim of the study was to evaluate the effect of submaximal doses of long-lasting GLP-1RA semaglutide on selected biomarkers of obesity-related inflammation, adipocytokines levels and metabolism in a real-world population of obese patients. Methods: We performed a prospective, observational study involving 32 adult patients (11 men, 21 women; mean age 49 ± 12 years; BMI 40.5 ± 7.3 kg/m²) treated with submaximal doses of semaglutide over 12 weeks, together with hypocaloric diet and increased physical activity based. We analyzed selected biomarkers including insulin, leptin, ferritin, resistin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and plasminogen activator inhibitor-1 (PAI-1) before and after three months of treatment. Results: We observed significant reductions in weight, BMI, waist circumference, insulin and leptin levels (all p < 0.001). On the other hand, no significant changes were recorded in ferritin (p = 0.806), IL-6 (p = 0.607), TNF-α (p = 0.633), resistin (p = 0.250) or PAI-1 (p = 0.134) levels. Correlation analyses revealed the correlation between IL-6 and adiposity indices (BMI, waist circumference) both before and after treatment. Ferritin and PAI-1 levels positively correlated with waist circumference, while resistin showed a negative correlation with central obesity. Conclusions: Submaximal-dose GLP-1 RA therapy was associated with significant improvements in metabolic parameters and adipokine regulation, but did not affect systemic inflammatory markers within 12 weeks. Future studies with larger cohorts and longer follow-ups are needed to clarify the associations.

Rationale: Aortic stenosis (AS) is currently the most frequent valve disorder. In addition, the angiodysplasias are the most common vascular malformations of the gastrointestinal tract. Heyde syndrome (HS) is a rare disease which links these 2 pathological conditions. Patient concerns: Currently, there are no clearly defined guidelines for the confirmation of HS diagnosis and for timing of aortic valve replacement in patients with confirmed HS, despite the fact that HS is connected with increased mortality and the need for numerous rehospitalizations and multiple blood transfusions. Therefore, the aim of this study was to report (our) first experiences with novel diagnostic method for acquired von Willebrand (vW) syndrome and transcatheter aortic valve replacement (TAVR) for treatment of HS. Diagnoses: We report a case of a 68-year-old man who was diagnosed with HS with the use of semiautomatic vW factor multimer analysis. Interventions: A successful TAVR was used for treatment of AS. Outcomes: After the interventional treatment of AS, the patient did not have a recurrence of the anemic syndrome. Lessons: This is a unique case of a patient with HS in whom semiautomatic vW factor multimer analysis was used for diagnosis of acquired vW syndrome together with TAVR procedure for HS treatment.

Background/Objectives: Cardiovascular diseases are the most prevalent comorbidities in patients with acromegaly (APs). Acromegalic cardiomyopathy is the leading cause of mortality in APs. This study aimed to assess changes in morphology and function of the left heart in naïve APs 12 months after the beginning of acromegaly treatment and to explore the effects of disease activity and body composition parameters on changes in the left heart. Methods: This prospective study involved 34 APs and 34 healthy controls (CON) matched for age, gender, and BMI. DXA and 2D echocardiography were performed at diagnosis and 12 months after the beginning of the treatment. Results: In APs, the prevalence of left ventricular (LV) hypertrophy was 70%. LV mass index (LVMI) was greater in APs compared to CON (124 vs. 86 ± g/m², p < 0.001), but with no difference in size and systolic function of the LV. APs presented with increased left atrium volume (LAVI) and with diastolic dysfunction of the LV. Twelve months after the beginning of acromegaly treatment, IGF-1 levels decreased significantly (p < 0.001), and biochemical control of disease was achieved in 73.52% of APs. We found that in all APs, LAVI and LVMI decreased (all p < 0.05), and diastolic function of the LV improved without changes in systolic function. In multiple analyses, the changes in body surface area (β = −0.444, p < 0.001) and in lean body mass (β = −0.298, p = 0.027) were independent predictors of reverse remodelling of LVMI after the treatment. Conclusions: This study confirmed remodelling reversal of the left heart structure, followed by an improvement in diastolic function in naïve APs 12 months after the beginning of acromegaly treatment.

Background: Impaired endothelial function has been associated with vascular complications in type 2 diabetes (T2D), but its role in T2D-related heart failure (HF) remains indeterminate. The aim of this study was to assess selected markers of endothelial function in T2D patients with acute decompensated HF. Methods: A pilot prospective study on patients with acute decompensated HF requiring in-hospital admission was carried out. The vascular endothelial growth factor (VEGF), intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) were assessed at admission and after decongestion. Subsequently, differences in these markers between T2D and non-diabetic (ND) patients were studied. Results: In total, 39 patients (21 with T2D and 18 ND patients) were enrolled. Twenty-eight patients presented with preserved ejection fraction (EF), and 11 presented with reduced EF. Looking at the VEGF levels in T2D patients, on admission, a median of 233.0 pg/mL (1.7–598 pg/mL) was found compared to 106.0 pg/mL (1.7–888 pg/mL) in ND individuals; the differences reached statistical significance (p = 0.04). There were no significant differences in VEGF levels after decongestion, and in VCAM-1 (2237 ± 1195 vs. 2699 ± 1093 ng/mL, p = 0.37) and ICAM-1 (596 ± 268 vs. 638 ± 437 ng/mL, p = 0.79) levels between T2D and ND patients upon admission and after decongestion. The value of EF (preserved or reduced) affected the VEGF levels upon admission. Conclusions: This study identified significantly higher VEGF levels upon admission due to acute decompensated HF in T2D patients.

Aims: The aims of this study were to compare global longitudinal strain of the left ventricle (LV-GLS) and reservoir strain of the left atrium (R-LAS) values between patients with acute decompensation of chronic heart failure (HF) and a control group. Methods: Sixteen patients admitted to our ward for acute decompensation of HF were enrolled in this study. Transthoracic echocardiography (TTE) with two-dimensional speckle-tracking analysis (2D ST) was performed in each patient. The patients were divided into two subgroups according to the value of left ventricular ejection fraction (EF) using a cut-off value of ≤40% to distinguish heart failure with reduced ejection fraction (HFrEF) from heart failure with preserved ejection fraction (HFpEF). The control group consisted of 16 individuals without a history of cardiovascular disease, each of whom underwent 2D ST analysis as well. Results: We found that LV-GLS and R-LAS were significantly lower in both the HFrEF and HFpEF subgroups in comparison with the control group (LV-GLS: −13.4 ± 4.7% vs. −19.7 ± 2.5%, p ˂ 0.05; R-LAS: +12.2 ± 6.9% vs. +40.3 ± 7.4%, p ˂ 0.05). Furthermore, there was a significant difference in LV-GLS (−9.6 ± 3.2% vs. −15.2 ± 4.3%, p ˂ 0.05) but not in R-LAS (+13.7 ± 8.6% vs. +11.4 ± 6.2%) between the HFrEF and HFpEF subgroups. Conclusions: Our study demonstrated a significant difference in LV-GLS and R-LAS in all enrolled HF patients compared to the control group. There was also a significant difference in LV-GLS between the HFrEF and HFpEF subgroups.

Transarterial chemoembolization (TACE) is a minimally invasive treatment for liver cancer, often employed as a bridging therapy or destination treatment for non-operable cases. This case report discusses an 82-year-old woman with a large hepatocellular carcinoma (HCC) who underwent elective TACE due to the high surgical risk associated with her tumor size. Unexpectedly, the patient experienced liver rupture 20 h post-procedure, leading to acute surgical intervention. Despite successful hemostasis during surgery, the patient succumbed to progressive multi-organ failure. We aimed to search the PubMed database for documented cases of ruptured HCC after TACE. This study highlights risk factors for spontaneous HCC rupture and specific factors associated with TACE-induced rupture. Transarterial embolization (TAE) is currently favored as the treatment method for spontaneous ruptures, while the optimal therapy for TACE-induced ruptures remains unclear. In conclusion, this case underscores the importance of recognizing the rare complication of HCC rupture post-TACE and the need for personalized risk assessment. While TAE emerges as a primary treatment choice, the lack of consensus necessitates further studies to establish evidence-based approaches for managing this uncommon yet life-threatening complication.

Ciele: Dvojrozmern? „speckle tracking“ (2D ST) anal?za umo??uje zhodnotenie deform?cie myokardu a m??e by? vyu?it? v determin?cii funkcie ?avej komory (?K) a ?avej predsiene (?P). Cie?om na?ej ?t?die bolo porovna? v?sledky glob?lne... Ciele: Dvojrozmern? „speckle tracking“ (2D ST) anal?za umo??uje zhodnotenie deform?cie myokardu a m??e by? vyu?it? v determin?cii funkcie ?avej komory (?K) a ?avej predsiene (?P). Cie?om na?ej ?t?die bolo porovna? v?sledky glob?lne...

Atherosclerosis is the primary process that underlies cardiovascular disease. The connection between LDL cholesterol and the formation of atherosclerotic plaques is established by solid evidence. PCSK9 inhibitors have proven to be a valuable and practical resource for lowering the LDL cholesterol of many patients in recent years. Their inhibitory effect on atherosclerosis progression seems to be driven not just by lipid metabolism modification but also by LDL-independent mechanisms. We review the effect of PCSK9 inhibitors on various mechanisms involving platelet activation, inflammation, endothelial dysfunction, and the resultant clot formation. The main effectors of PCSK9 activation of platelets are CD36 receptors, lipoprotein(a), oxidised LDL particles, tissue factor, and factor VIII. Many more molecules are under investigation, and this area of research is growing rapidly.