Atherosclerosis is a chronic process characterized by inflammation and the progressive accumulation of inflammatory cells and lipids in the blood vessel wall, resulting in narrowing of the blood vessel’s circumference. Treatment of people with dyslipidemia aims to reduce the risk of developing atherosclerotic disease and prevent major adverse cardiovascular events (MACE). The results of previous studies indicated that lipoprotein(a) (Lp(a)) is a critical causal factor in the estimated risk of developing a cardiovascular (CV) incident even after achieving desirable low-density lipoprotein (LDL) cholesterol levels. Lp(a) is a low-density lipoprotein particle, like LDL cholesterol. The levels of Lp(a) in plasma are genetically determined. Lp(a) catabolism is still controversial. The pathogenic potential of Lp(a) can be divided into three categories: promotion of plaque formation, thrombogenicity, and proinflammatory effects. Lp(a) levels above the 75th percentile reduced the risk of aortic valve stenosis and myocardial infarction, whereas higher levels (above 90th percentile) were associated with an increased risk of heart failure. However, no hypolipidemic agents have been approved for targeted use in patients with high Lp(a) levels. There are insufficient randomized controlled trials assessing CV outcomes that would support the evidence that current treatment options, which effectively lower Lp(a) levels, also effectively prevent CV event. However, according to some studies, there is strong evidence that better CV outcome is one of the benefits of such therapy. The results of ongoing clinical trials are eagerly awaited.

Obesity is a significant health issue associated with increased cancer risks, including gynecological malignancies. The worldwide rise in obesity rates is significantly impacting both cancer development and treatment outcomes. Adipose tissue plays a crucial role in metabolism, secreting various substances that can influence cancer formation. In obese individuals, dysfunctional adipose tissue can contribute to cancer development through inflammation, insulin resistance, hormonal changes, and abnormal cholesterol metabolism. Studies have shown a strong correlation between obesity and gynecological cancers, particularly endometrial and breast cancers. Obesity not only increases the risk of developing these cancers but is also associated with poorer outcomes. Additionally, obesity affects the perioperative management of gynecological cancers, requiring specialized care due to increased complications and resistance to therapy. Treatment strategies for managing metabolic dysregulation in patients with gynecological cancers include weight management, statin therapy, and insulin-sensitizing medications. Emerging studies suggest that interventions like intermittent fasting and caloric restriction may enhance the effectiveness of cancer treatments. Furthermore, targeting cholesterol metabolism, such as with statins or proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, shows potential in cancer therapy. In conclusion, addressing metabolic issues, particularly obesity, is crucial in preventing and treating gynecological malignancies. Personalized approaches focusing on weight management and metabolic reprogramming may improve outcomes in these patients.

This review examines hormone replacement therapy (HRT) in cases of surgical menopause following gynecological malignancies. It aims to capture current knowledge, summarize recent findings, and provide recommendations for clinical settings. Unlike natural menopause, surgical menopause occurs abruptly, without an adjustment period, and is associated with a notably higher risk of fractures, arthritis, cognitive decline, dementia, Parkinson’s disease, and various metabolic disorders affecting glucose and lipid levels—all of which contribute to an increased risk of major cardiovascular events. In 2017, The North American Menopause Society recommended that, barring contraindications, HRT should be initiated in women who enter surgical menopause before age 45. If these women do not experience vasomotor symptoms or other issues, HRT should be maintained consistently at least until age 52. This guideline reflects contemporary knowledge and is the result of a multidisciplinary consensus, based on a review of existing literature and several randomized clinical trials focusing on women who have survived gynecological cancers and whose quality of life is significantly impacted by surgical or early menopause. Estrogen supplementation is particularly beneficial, as it is linked to marked improvements in quality of life, including delayed onset of chronic cardiovascular issues, reduced fracture risk, enhanced cognitive function, reduced inflammation, and improved self-esteem, as well as better social and work performance. Clinical implementation of HRT, however, requires a highly individualized approach. This approach must consider the type and stage of malignancy, histopathological characteristics, risk factors for recurrence (such as diet, concurrent medications, medical history, and genetic predispositions), and a thorough assessment of the potential benefits and risks of HRT, as well as the patient’s personal wishes and expectations.

Introduction. Obesity is a chronic metabolic disorder characterised by excess adiposity, persistent low-grade inflammation, and high frequency of musculoskeletal complications in both athletic and non-athletic populations. Body mass index and fat distribution, particularly visceral adiposity, are key determinants of metabolic and orthopaedic risk, including disorders of the knee tendons and ligaments. From adiposity to ligament pathology. In obesity, white adipose tissue undergoes phenotypic remodelling toward a pro-inflammatory state, marked by immune cell infiltration, increased secretion of cytokines and adipokines, and reduced adiponectin levels. These alternations promote lipotoxicity and ectopic fat deposition in skeletal muscle, ligaments, fat pads, and entheses, contributing to sarcopenic obesity, angiofibroblastic degeneration, and impaired ligament healing. Clinical implications. Elevated body mass index increases mechanical loading and alters lower-limb biomechanics, thereby promoting repetitive microtrauma, chronic inflammation, and higher incidence of tendinopathies, particularly of the extensor mechanism and pes anserinus. In individuals with body mass index above 25 kg/ m^{2} , published studies report a higher prevalence of multiligament knee injuries, a greater proportion of trauma-related anterior cruciate ligament ruptures, increased postoperative complications, and delayed functional recovery. However, heterogeneity in study design limits precise quantification of effect sizes. Conclusion. Excess adiposity likely increases anterior cruciate ligament injury risk through the combined effects of mechanical overload and obesity-related inflammation and is associated with more extensive ligament damage and a less favourable postoperative course. Integrated interventions targeting fat-mass reduction, metabolic optimisation, and neuromuscular conditioning may enhance recovery, reduce re-injury risk, and support long-term knee joint health. This conceptual framework is applicable across age groups in both recreational and competitive sports populations.

Introduction/Objective. Breastfeeding prevalence in Serbia remains low compared with global estimates. Breastfeeding self-efficacy scale - Short form (BSES-SF) is widely recognized as a key, modifiable determinant of breastfeeding outcomes, with growing evidence that improving it is associated with higher breastfeeding rates. This study aimed to translate and culturally adapt the scale for use in Serbian language, establish its psychometric adequacy within a population of breastfeeding mothers throughout the first postpartum year, and examine differences in scores by selected sociodemographic and obstetric characteristics. Methods. A total of 70 breastfeeding mothers who delivered at the Clinic for Gynecology and Obstetrics, University Clinical Center of Vojvodina participated in this cross-sectional study. The validated Croatian version served as the basis for the adaptation process, which followed standardized cross-cultural procedures. Internal consistency was evaluated using item-total statistics and Cronbach’s α. Group differences were compared using the Mann-Whitney Utest. Results. The participants' mean age was 32.19 years (SD = 5.17). The instrument showed strong internal consistency (Cronbach’s α = 0.81; 95% CI: 0.73-0.87). Corrected item-total correlation coefficients ranged from 0.13 to 0,73. The mean score was 54.11 ± 10.81, indicating high breastfeeding self-efficacy. Lower scores were observed among mothers with cesarean delivery, shorter intended breastfeeding duration, early cessation, lack of early initiation, and insufficient breastfeeding support. Conclusion. The Serbian version of the scale exhibited good internal consistency and preliminary validity as an instrument for assessing breastfeeding self-efficacy.

Obesity is characterized by chronic low-grade inflammation (meta-inflammation) and metabolic dysregulation. Adipose tissue acts as an immunometabolic organ, with macrophages playing a central role. This review examines inflammatory memory in adipose tissue, focusing on CD68+ macrophages and their role in cardiometabolic and cancer risk during weight cycling. (2) Narrative synthesis of evidence from immunology, obesitology, and oncology, with emphasis on macrophage polarization and signaling pathways. (3) Weight cycling induces persistent immune memory in adipose tissue, characterized by exaggerated macrophage responses upon weight regain. CD68+ macrophages contribute to extracellular matrix remodeling, tumor signaling, and metabolic dysfunction. Key mechanisms include PI3K/AKT/mTOR dysregulation, FOXO1/KLF10 axis impairment, and CREB-mediated transcription. This inflammatory memory promotes atherosclerosis progression, insulin resistance, and increased cancer risk, despite prior weight loss. (4) Macrophage-driven inflammatory memory represents a key mechanistic link between obesity, cardiometabolic disease, and cancer. Targeting meta-inflammation independent of body weight should be integral to future therapies.