
Type 2 diabetes mellitus (DM2) and depression are chronic non-communicable diseases that affect millions of people worldwide. The interaction of these two diseases is complex and has a huge clinical significance. The association between DM2 and depression was recognized decades ago; however, the cause of the high prevalence of this comorbidity is not fully understood. It is assumed that shared genetic and environmental risk factors play a role, such as certain gene polymorphisms related to the secretion and effects of cortisol, obesity and others. Pathophysiological mechanisms underlying depression, such as HPA axis dysregulation and inflammation, impair insulin resistance and contribute to the development of DM2, while on the other hand, chronic stress linked to DM2 may cause depression. This relationship, which is often described as bidirectional, leads to the formation of the so-called “vicious cycle” that results in poor health outcomes of both conditions. Patients with DM2 and comorbid depression have a higher incidence of long-term complications, primarily macrovascular, lower quality of life and a higher mortality rate. Therefore, the prevention, early detection and treatment of depression in DM2 is extremely important. The treatment of comorbidity of these diseases includes a multidisciplinary approach aimed at the simultaneous improvement of mental and physical health. Treatment involves pharmacotherapy, psychotherapy and psychosocial interventions, with the main goal of reducing the incidence of DM2 complications and improving the quality of life of affected individuals.
Total laryngectomy presents the standard therapeutic protocol in the treatment of advanced laryngeal cancer. There is not enough research in this area to indicate the necessity of performing thyroidectomy in patients with advanced squamous cell carcinoma of the larynx, although some studies indicate that unilateral thyroidectomy is performed routinely in some centers. The National Comprehensive Cancer Network (NCCN) recommends ipsilateral hemithyroidectomy with laryngectomy for advanced squamous cell carcinoma of the larynx. However, in these cases, the risk of hypothyroidism and hypoparathyroidism is significantly higher, which requires postoperative monitoring of hormone status and thyroid replacement therapy. Invasion of the thyroid gland can occur due to direct or lymphovascular spread of advanced squamous cell carcinoma of the larynx, and the risk of locoregional recurrence and distant metastases in these cases increases significantly. The incidence of thyroid gland invasion in patients with advanced laryngeal squamous carcinoma is relatively low, and the most common predictors for infiltration are subglottic and transglottic extension of the laryngeal tumor, as well as direct invasion of the thyroid cartilage. Preservation of thyroid tissue during laryngectomy significantly reduces postoperative morbidity, however, thyroidectomy may be indicated if the presence of risk factors for thyroid invasion is assessed based on clinical, radiological and intraoperative findings. A careful assessment of risk factors is necessary to avoid the occurrence of locoregional recurrence, and thus a significantly worse prognosis.
Introduction: Coarctation of the aorta (CoA) is a narrowing of the thoracic aorta, most often localized at the junction of the ductus arteriosus. Data on risk factors for the development of recoarctation remain contradictory in the literature. Aim: To determine the frequency of recoarctation and to identify risk factors for recoarctation after surgical correction of CoA. Material and methods: The research included 94 patients who underwent surgery for coarctation of the aorta from 2012 to 2017. Demographic and clinical characteristics, preoperative, intraoperative, postoperative and echocardiographic parameters were observed. Pressure gradient over 25 mm Hg immediately after operation is considered predictor for recoarctation of the aorta. The data was processed using methods of descriptive and analytical statistics. Results: The median age at the time of surgery was 2 months (4 days - 19 years). The dominant technique was extended end-to-end anastomosis (90.4%). Kaplan Meier survival analysis showed a higher incidence of recoarctation in the group of patients with immediate postoperative gradient > 25 mm Hg (p < 0.001). Also, Cox logistic regression showed higher immediate postoperative gradient to be a predictor (HR 4.57, p = 0.009, 95% CI 1.47 - 14.22). After correction for other cofactors, including sex, genetic syndrome, small body weight, administration of prostaglandine E1, presence of bicuspid aortic valve, surgical technique, it was shown that the group of patients with higher immediate postoperative gradient has 4-fold higher probability for recoarctation (HR 4.37, p = 0.035, 95% CI 1,11 - 17,16) . Conclusion: Immediate postoperative pressure gradient > 25 mm Hg is an independent predictor for recoarctation after surgical correction of the coarctation of the aorta.
Obesity represents a multifactorial, systemic disorder strongly associated with adverse health outcomes, including cardiometabolic syndrome. Beyond caloric imbalance between caloric intake and expenditure, recent evidence highlights the essential role of gut microbiota in the development and progression of obesity and related metabolic dysfunctions. The gut microbiota, composed of diverse bacterial species, archaea, fungi, and viruses, influences host metabolism through the production of low-molecular-weight metabolites and gastrointestinal hormones, significantly modulating energy homeostasis, appetite regulation, and insulin sensitivity. Specific bacterial taxa are implicated in either promoting metabolic health or contributing to obesity through mechanisms involving chronic systemic low-grade inflammation, increased intestinal permeability, and altered energy harvest. Dysbiosis - marked by reduced microbial diversity and compositional imbalance is consistently linked to enhanced adiposity and systemic inflammation. Dietary patterns are key modulators of gut microbial composition and function. This review underscores the complex interplay between dietary patterns, gut microbiota-derived metabolites and host endocrine responses that contribute to dysregulation of gut-brain axis communication observed in obesity.
Introduction: Anxiety disorders are among the leading types of disorders in the general population, with symptoms that often have a significant impact on people's daily lives. Additionally, anxiety symptoms have been shown in studies conducted worldwide to be a significant factor influencing the course of diabetes, as well as the development of potential complications of the disease itself. Aim: The aim of this study was to examine the level of anxiety in patients with type 2 diabetes mellitus depending on the presence of diabetic foot. Material and methods: This study is a retrospective-prospective analysis conducted between October 15, 2023, and February 15, 2024. A total of 87 patients were included, who were categorized into three groups based on the presence of diabetic foot. All participants were treated at the Clinic for Endocrinology, Diabetes and Metabolic Diseases of the University Clinical Center of Serbia (UCCS) and the Institute of Orthopedic Surgery and Traumatology, UCCS. Anxiety levels among the subjects were assessed using the Generalized Anxiety Disorder-7 (GAD-7) questionnaire. Results: The highest scores on the GAD-7 scale were observed in patients with diabetic foot who underwent amputation, while significantly lower scores were found in patients with diabetic foot treated with conservative methods. Conclusion: A possible factor contributing to the higher scores on the GAD-7 test may have been the severity of the disease, as well as the complex interaction between anxiety, diabetes, and diabetic foot. This underscores the importance of considering mental health in the comprehensive care of individuals with diabetes.
Introduction: Mammoplasty is a surgical procedure of placement of breast implants for aesthetic reasons or due to breast reconstruction after mastectomy for cancer. As the implant represents a foreign body, there is an inflammatory reaction and complications (most often capsule contractures, most rarely anaplastic large cell lymphoma), with different histopathological presentations (synovial metaplasia, chronic inflammation, dystrophic calcifications, granulomas around a foreign body type). Clinically, these complications are presented as tumor-like changes. Aim: The aim of the paper is to show the most significant histopathological parameters, age of the patients at the time of the complications, period that passed from the placement of the implant to the onset of complications and the existence of previous cancer. Material and methods: This study included patients with breast implants in the period of January 2019 to December 2023. Evaluating data from medical records, a retrospective study was performed, which included age of the patient at the time of complications, reasons for performing mammoplasty and the period that passed from mammoplasty to the appearance of complications. Archived material was used (paraffin molds and histopathological material stained with the hematoxylin-eosin method, as well as immunochistochemical stainings). Descriptive statistics methods (Fisher’s exact probability test) were used for data analysis. Results: Average age of the patients was 50.1 years, and the period that passed from the placement of the implant to the appearence of complications was 16.7 years. The breast cancer rate previously was 22%. Most common histopathological parameters were synovial metaplasia (100%) followed by chronic inflammation (76%), foreign material (52%) and granuloma around a foreign body (32%). The breast surgery was performed for cosmetic reasons in 88% of the patients. Conclusion: This study proved that the patients were older and that more time passed before complications occurred than was shown in literature. A large percentage of patients had the procedure only due to cosmetic reasons.
Antibiotics have fundamentally transformed modern medicine, however, their widespread use and misuse have led to the escalating crisis of antimicrobial resistance (AMR) in bacteria. Today, bacterial AMR represents a critical global health threat with severe medical and economic consequences. It is estimated that nearly five million deaths worldwide are linked to bacterial AMR each year. While vital for maintaining host health, the human gut microbiome also harbors a collection of antibiotic resistance genes (ARGs), collectively known as the gut resistome. Numerous studies have shown that the gut resistome serves as a reservoir for ARGs, which can be mobilized and transferred to both commensal and pathogenic bacteria through horizontal gene transfer. Antibiotic exposure is a major factor that disrupts the diversity and function of the gut microbiome, leading to the proliferation of resistant bacteria and the accumulation of ARGs. These changes, in turn, facilitate the further spread of resistance among bacterial populations. Conversely, one of the gut microbiome's key functions is to prevent the colonization and proliferation of both external pathogens and resident pathobionts, including bacteria resistant to antibiotics. This protection is mediated through mechanisms such as resource competition, metabolic interactions, and modulation of the host immune response. By limiting the colonization and expansion of resistant bacteria, the gut microbiome helps reduce the incidence of related infections and may contribute to lowering the overall burden of AMR. This review explores the dual role of gut microbiome in the dynamics of bacterial AMR, both as a reservoir for the emergence of AMR and a critical line of defense against its spread. The review also highlights key research gaps that need to be addressed to promote the development of targeted microbiome-based strategies for combating bacterial AMR effectively.
Clubfoot is recognized as one of the most frequent musculoskeletal deformities. Being characterized by equinus and varus hindfoot, adduction and inversion of the forefoot, cavus and calf muscles’ atrophy, it occurs in 1 to 2 per 1000 newborns. The concrete etiology of the deformity is not completely known but different studies suggest multifactorial pathogenesis, including numerous genetic and environmental risk factors. The most frequent clubfoot clinical presentation is isolated while it may also be associated with other neurologic conditions as part of a syndrome. The disease is easy seen at birth and its degree may vary from mild to an extremely rigid foot that is not reducible to manipulation. The challenge of identifyng the best clubfoot treatment method has become less demanding as Ponseti invented his method that is today thought to be the gold standard, including weekly stretching and casting while following tenotomy of the Achilles tendon is mandatory for rigid equinus. Foot abduction brace treatment for four to five years is indicated to prevent relapse. Surgical soft-tissue releases might be necessary for those resistant clubfeet, where conservative treatment is not sufficient. If untreated, clubfoot leads to lifelong disability, so it is essential to aware parents of the importance of persistent and patient commitment and compliance during the treatment period. This paper aims to show the significance of multifactorial clubfoot etiology as well as different clubfoot therapeutic modalities.
Introduction: Metabolic syndrome is a disorder that encompasses a range of symptoms such as central obesity, insulin resistance, dyslipidemia, hypertension, and is associated with a stronger predisposition to the development of cardiovascular diseases and type 2 diabetes (T2D). The occurrence of metabolic syndrome depends on both environmental factors and genetic influences. Changes in the expression of the gene for peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) are among the factors that may influence the development of insulin resistance, obesity, dyslipidemia, and consequently, metabolic syndrome and T2D. Aim: The aim of this study was to examine the association of the Gly482Ser polymorphism in the PGC-1α gene with lipid status and the occurrence of obesity, T2D, and metabolic syndrome in the postmenopausal period. Material and methods: The study included 112 postmenopausal women, aged 65.01 ± 6.16 years. Demographic and anthropometric (height, body mass index, waist-to-hip ratio) data, as well as biochemical analysis results (lipid status, glucose levels) were collected for all participants. Genotyping was performed using real-time polymerase chain reaction (PCR) with a standardized TaqMan assay. Results: The study found a statistically significant difference in the mean total cholesterol levels based on the participants’ genotypes. Women with the AA genotype had significantly higher total cholesterol levels (p = 0.030). No statistically significant association was found between the Gly482Ser genotype and other parameters. Conclusion: This study found an association between the AA genotype of the Gly482Ser polymorphism in the PGC-1α gene and higher total cholesterol levels in postmenopausal women.
Introduction: Endothelin-1 is a vasoconstrictor peptide primarily synthesized by endothelial and smooth muscle cells. Increased expression of this peptide has been observed in inflammation, hypoxia, ischemia, various cardiovascular diseases and various types of cancer. In addition to vasoconstrictive, significant mitogenic, proangiogenic and anti-apoptotic effects have also been proven. Aim: To examine the expression of endothelin-1 in the unaffected mucosa 10 cm and 20 cm away from the colon adenocarcinoma and the lamina propria of the colon mucosa of healthy subjects. Material and methods: The samples were obtained by biopsy at the Center for Gastroenterology, Clinical Hospital Center “Dr. Dragiša Mišović-Dedinje” in Belgrade from patients with malignant colon tumors. During the diagnostic colonoscopy, colon mucosa samples were taken 10 cm and 20 cm distal to the primary tumor lesion (n = 10). A control group of samples (n = 10) was obtained by endoscopic biopsy of the healthy subjects in the same institution. Immunohistochemical staining on paraffin samples was performed according to the established protocol. For statistical analysis of frequency, Fisher’s exact probability test was used, using 2 x 2 contingency tables. Results: Statistically significant difference in the frequency of endothelin-1 expression was detected neither in the surface epithelium nor in the endothelial cells of the lamina propria of the colon mucosa at a distance of 10 cm (p = 0.38) or 20 cm (p = 0.67) from the tumor compared to the lamina propria of colon mucosa of healthy subjects. Also, no statistically significant difference was detected in the frequency of high and low expression of endothelin-1 in the epithelium and blood vessels of the lamina propria of the colon mucosa at a distance of 10 cm and 20 cm from the tumor (p = 0.82). Conclusion: Endothelin-1 is variably expressed in the colon mucosa, predominantly by epithelial and endothelial cells. A statistically significant difference in the frequency of high and low expression of endothelin-1 between the groups was not detected.
Multiple sclerosis (MS) is an immune-mediated disorder of central nervous system. It most frequently occurs in young female adults, and the prevalence increases with latitude. So far, over 200 genes, loci and single nucleotide polymorphisms (SNPs) have been linked with MS, although each one contributing only slightly in the overall etiology of the disease. The HLA-DRB1*15:01 haplotype has been shown to have the strongest association with MS occurrence risk in genome-wide association studies (GWAS), while HLA-A*02 has been shown to have a protective effect. The exact etiology of MS is still unclear, but there seems to exist an interplay between genetic burden of an individual, and environmental factors which contribute to MS occurrence such as Epstein-Barr virus (EBV) infection, vitamin D levels, smoking status, and early life obesity. An interaction between HLA-DRB1*15:01 and EBV infection, the strongest environmental risk factor for MS, has been observed. It has been suggested that this interaction is a result of HLA-DRB1*15:01 acting as a coreceptor for EBV, thus providing a pathophysiological explanation connecting environmental with genetic MS risk factors. A recent study including participants from two case-control studies with over 13.000 individuals showed that an interaction exists between sun exposure, vitamin D levels, and HLA-DRB*15:01 carrier status, leading to increased risk of MS in individuals with lower sun exposure, vitamin D deficient, and HLA-DRB*15:01 positive. The interaction of HLA-DRB1*15:01 with smoking has been observed in a meta-analysis, while the same study only showed an interaction of smoking with the absence of HLA-A*02 in a subset of studies. The risk of MS has been shown to vary in obese individuals, with obese individuals with the susceptible genotype (HLA-DRB1*15:01+, HLA-A*02-) having 16x higher odds of having MS compared with non-obese persons with a non-susceptible genotype.
Coronary microvascular dysfunction (CMD) is encountered in up to 50% of patients presenting with ST-segment elevation acute myocardial infarction (STEMI) and treated with primary percutaneous coronary intervention (PCI). The current reference standard to diagnose microvascular injury in this setting is cardiac magnetic resonance (CMR) imaging. The extent of microvascular injury, termed microvascular obstruction (MVO) on CMR, increases over time after recanalization of the infarct-related artery (IRA), until it reaches its peak around day 3, and it subsides by day 10. Most of the current research evaluated MVO on CMR on days 2 - 7 after primary PCI, and showed its association with cardiac death and heart failure independently of the infarct size. As microvascular injury becomes a new therapeutic target in STEMI, given the plateauing mortality curves despite widespread access to timely reperfusion, the question of early diagnosis of CMD grows in importance. To this end, invasive coronary microcirculation assessment in the recanalized IRA immediately after primary PCI, has been tested in terms of its association with MVO and infarct size on CMR, as well as its ability to predict adverse clinical outcomes. Both invasive thermodilutionand Doppler wire-derived indices of microvascular resistance were successful in stratifying patients according to the risk of cardiac death and heart failure in the follow-up. Recently, a coronary angiography-based method, which unlike thermodilution and Doppler derives indices of microvascular resistance from a computational dynamics software and does not require additional wiring of the epicardial artery, has demonstrated the ability to predict adverse clinical outcomes. The described diagnostic tools for stratification of patients according to the risk of CMD and consequently impaired prognosis after STEMI, still remain a subject of ongoing research, in terms of both the most relevant cut offs for different indices and the optimal time point of assessment.
Infective endocarditis is a rare disease with an increasing incidence and an unchanged high mortality rate, despite the rapid medical development. Imaging plays integrative part in diagnosis of IE, with echocardiography as main diagnostic test. Rising research data in utility of Cardiac Computed Tomography (CCT) in diagnostic algorithm of IE, indicates its importance in detection of IE-related lesion along with the exclusion of coronary artery disease. The latest 2023 European Society of Cardiology Guidelines in management of IE classified CCT as class of recommendation I and level of evidence B in detection of both valvular and paravalvular lesions in native and prosthetic valve endocarditis. This review article provides comprehensive and contemporary review of role of CCT in diagnosis of IE, optimization of acquisition protocols, morphology characteristics of IE-related lesions, published data of diagnostic performance of CCT in comparison to echocardiography as the state-of-art method, limitation and future possibilities.
Muscarinic acetylcholine receptors (mAChRs) are a subfamily of G protein-coupled receptors that have been identified as promising targets for drug development. Five different mAChR subtypes regulate various fundamental functions. In the central nervous system (CNS), they play a crucial role in regulating numerous cognitive, behavioral, and autonomic functions. Outside the CNS, they facilitate the effects of acetylcholine in organs and tissues innervated by parasympathetic nerves, participating in various vegetative functions such as regulating heart rate, smooth muscle contraction, and glandular secretion. The disruption in cholinergic signalling contributes to several pathophysiological conditions and diseases. Thus, muscarinic agonists and antagonists have a wide therapeutic potential in the treatment of neuropsychiatric disorders, such as Alzheimer's disease, schizophrenia or pain, and also in diseases like COPD and incontinence. Activation of different mAChR with selective ligands could be beneficial for treating the above-mentioned diseases while avoiding side effects. Clinical trials targeting mAChRs have shown promising results, with several compounds demonstrating efficacy and better tolerability profiles. However, developing drugs targeting mAChR still presents challenges, primarily due to the high homology in the structure of the orthosteric binding site. The recent insights into the physiology, pharmacology, and structure of mAChRs have provided opportunities for the development of novel drugs targeting these receptors, including allosteric modulators. Allosteric modulators offer the advantage of selective binding mAChR, potentially enhancing therapeutic efficacy while minimizing off-target effects. In conclusion, mAChRs represent promising targets for drug development. Further research and clinical trials are needed to develop effective therapies targeting muscarinic receptors for various diseases.
The gut microbiota plays a crucial role in maintaining gastrointestinal balance and regulating immune system activity. Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are changes associated with significant alterations in both the composition and activity of the gut microbiota, a condition known as dysbiosis. Dysbiosis can lead to compromised mucosal barrier integrity, increased inflammation, and irregular immune system activity. Microbiota influences the development of IBD through altered short-chain fatty acid levels, lower microbial diversity, and an imbalance between protective and harmful bacterial populations. Current research continues to explore how interactions between the microbiota and immune cells contribute to the onset and persistence of inflammation. Therapies designed to adjust the gut microbiota, such as the use of probiotics, prebiotics, dietary modifications, and fecal microbiota transplantation, have shown encouraging results for symptom relief and longer remission in individuals with IBD. Enhanced knowledge of the complex microbiota role facilitates the development of tailored medical interventions and new treatment strategies for inflammatory bowel diseases.
Neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and other cognitive and behavioral impairments, are increasing globally, placing significant burdens on individuals and healthcare systems. Traditional therapeutic strategies, primarily pharmacologic and behavioral, offer limited efficacy and often fail to address the multifactorial etiology of these conditions. Recent advances in microbiome research highlight the gut microbiota as a potential modulator of brain function via the microbiota-gut-brain axis (MGBA). This bidirectional network influences neurodevelopment through neural, immune, endocrine, and metabolic pathways. Dysbiosis, or microbial imbalance, has been consistently reported in individuals with NDDs, particularly in ASD and ADHD, correlating with symptom severity and gastrointestinal comorbidities. Emerging interventions aimed at restoring microbial balance, such as probiotics, prebiotics, synbiotics, faecal microbiota transplantation (FMT), and dietary modifications – demonstrate potential in modulating behaviour and cognition. However, the current evidence is limited by small sample sizes, heterogeneous methodologies, and a lack of long-term follow-up. This mini-review synthesizes current findings on the role of gut microbiome modulation in NDDs, evaluates the therapeutic efficacy of microbiome-based interventions, and discusses future directions, including personalized microbiome-targeted strategies and the need for robust randomized controlled trials.
Introduction: Chronic inflammatory bowel diseases (IBD) include ulcerative colitis (UC) and Crohn's disease (CD), characterized by relapses and an insufficiently clarified etiology. The enteric nervous system (ENS) consists of neuronal cells distributed along the gastrointestinal tract, organized into the submucosal Meissner's plexus and myenteric Auerbach's plexus. The glial cell index (GCI) represents the ratio of the number of glial cells to ganglion cells within the ganglia of the ENS. Aim: The aim of this study is a morphometric analysis of the ENS in intestinal samples from surgically treated pediatric patients with CD and UC. Material and methods: Histological slides from the archives of the Institute of Pathology, Faculty of Medicine, University of Belgrade, were analyzed. In the study groups of UC and CD, there were five participants in each group, while the control group included four participants. The study included an analysis of intestinal wall sections from pediatric patients with IBD (experimental group) and those with uncomplicated familial adenomatous polyposis syndrome (control group). Using the ImageJ software, five microphotographs of submucosal and myenteric nerve plexuses stained with Masson trichrome and captured with an Olympus DP70 digital camera at x400 magnification were analyzed. Results: A significant difference in the GCI value in the myenteric plexus of the colon was observed between the experimental and control groups. No significant difference in the GCI value in the submucosal plexus of the colon was found between the two groups. A minimal difference in the GCI value within the experimental group was observed in the submucosal plexus sections. Conclusion: This study presents a unique analysis of glial cells in CD, UC, and the control group in the submucosal and myenteric plexuses. The results indicate a disruption of GCI in the ENS in IBD, which likely represents the morphological substrate for intestinal motility disorders in these conditions.
Pregnancy induces intricate physiological changes, including alterations in lipid profiles crucial for fetal development. The transition from an anabolic to a catabolic phase in the third trimester reflects increasing insulin resistance, facilitating lipid breakdown for fetal energy. Physiological pregnancy exhibits significant lipid profile changes, with dyslipidemia linked to negative effects on maternal and fetal health. Dyslipidemia in pregnancy correlates strongly with cases of pregnancy-related high blood pressure and diabetes. Gestational diabetes mellitus (GDM) introduces distinctive lipid alterations, including elevated triglycerides (TG) and low-density lipoprotein particles. Mixed dyslipidemia in GDM, exceptionally high TG, and reduced levels of high-density lipoprotein cholesterol (HDL-C) are linked to negative perinatal outcomes, emphasizing the importance of lipid profile assessment. Evaluating lipid profiles, especially TG levels, in early pregnancy proves valuable in predicting GDM. The ratio of triglycerides to high-density lipoprotein cholesterol (TG/HDL-C) shows potential as a predictive marker for GDM, demonstrating commendable sensitivity and specificity. Elevated TG levels, even before 28 weeks, increase GDM risk, emphasizing the role of lipid markers in early detection. Early predictions of GDM through plasma lipid profiling offer a promising avenue for enhancing antenatal care. While standardized markers and thresholds require further research, integrating lipid profiles into routine screenings may optimize GDM management, ultimately benefiting both the mother and fetus.
Introduction: Sjögren’s syndrome (SS) is a chronic systemic autoimmune disease. The disease spectrum extends from sicca syndrome to systemic involvement and extraglandular manifestations. Patients with SS present a broad spectrum of serologic features. Certain serological findings are highly correlated with specific clinical features and can be used as prognostic markers. Aim: This paper aimed to analyze glandular and extraglandular clinical manifestations of primary SS (pSS) and their association with laboratory findings. Material and methods: The research was conducted as a retrospective cross-sectional study involving 30 patients with pSS hospitalized at the Clinic for Allergology and Immunology, University Clinical Center of Serbia in Belgrade. Demographic, clinical and laboratory characteristics of patients were analyzed, as well as the association between them. Results: Dry eyes and mouth were experienced by all subjects included in the study. Arthralgia and/or myalgia were the most common extraglandular manifestations of pSS, which were present in all patients. This was followed by: chronic fatigue (83.3%), skin manifestations (66.67%), psychiatric manifestations (60%), Raynaud’s phenomenon (40%), gastrointestinal manifestations (33.3%), thyroid (26.67%), and respiratory disorders (23.3%). Paraprotein was identified in 13.33%, and proteinuria in 10% of patients. Antinuclear antibodies (ANA) were positive in 80%, anti-Ro/SSA in 76.67%, anti-La/SSB in 20%, and RF in 16.67% of patients. Raynaud’s phenomenon was associated with the presence of chronic fatigue (p=0.047), gastrointestinal symptoms with psychiatric manifestations (p=0.017), and chronic fatigue associated with involvement of exocrine glands of other locations (except lacrimal and salivary glands). Thyroid dysfunction was inversely associated with SSB antibody findings (p=0.024). Conclusion: Dry eyes and mouth, arthralgia and/or myalgia were the most common manifestations of pSS. Both ANA and SSA antibodies were the most common immunoserological findings. There was no statistically significant association of any examined immunoserological findings with the presence of glandular and extraglandular manifestations of pSS.