International Journal of Medical Science and Public Health Research

Perforated Colonic Peritonitis As A Source Of Surgical Sepsis

Okhunov Alisher Oripovich — Wed, 21 Jan 2026 00:00:00 +0000

Background. Perforated colonic peritonitis remains one of the most severe conditions in emergency abdominal surgery and is frequently complicated by surgical sepsis. Despite radical elimination of the perforation source, systemic deterioration may develop rapidly or follow a subacute course, particularly in patients with significant comorbidity.

Methods. A retrospective cohort study included 118 patients operated on for perforated colonic peritonitis of malignant and non-malignant etiology. Surgical sepsis was defined according to Sepsis-3 criteria. Clinical course, comorbid conditions, surgical strategy, need for intensive care, progression to septic shock and multiple organ failure, and in-hospital mortality were analyzed.

Results. Surgical sepsis was identified in a substantial proportion of patients either at admission or during early postoperative period. Patients with pronounced comorbidity more often demonstrated fulminant septic progression with early development of septic shock, multiple organ failure, and high mortality, despite radical surgical source control. In patients without severe comorbidities, septic complications frequently evolved in a subacute manner, with transient postoperative stabilization that could mask ongoing systemic infection. Requirement for intensive care treatment and progression to septic shock were strongly associated with adverse outcomes.

Conclusion. Perforated colonic peritonitis should be regarded as a condition with an inherent risk of surgical sepsis regardless of the apparent adequacy of operative management. Apparent postoperative stabilization does not exclude systemic progression. Continuous assessment for septic manifestations and timely escalation of anti-septic therapy are essential to improve outcomes in this high-risk patient population.

Serotonergic Mechanisms Of Central Nervous System Dysfunction In Eating Disorders In School-Aged Children

Farangisbonu Alisher qizi Doniyorova, Moxinur Shomahmudovna Abduaxadova — Thu, 15 Jan 2026 00:00:00 +0000

Eating disorders in school-aged children represent a significant medical and social problem due to their close association with neuropsychiatric dysfunctions and long-term consequences for physical and mental development. Increasing evidence indicates that serotonergic neurotransmission plays a key role in the regulation of appetite, emotional stability, cognitive functions, and stress responsiveness. Disruption of serotonin metabolism, receptor sensitivity, and synaptic signaling may contribute to the development and persistence of maladaptive eating behaviors in childhood. This abstract highlights the serotonergic mechanisms underlying central nervous system dysfunction in children with eating disorders. Alterations in central serotonin levels are associated with impaired hypothalamic regulation of hunger and satiety, dysregulation of limbic structures involved in anxiety and mood control, and reduced cortical modulation of impulse control and decision-making. Neurochemical imbalance within serotonergic pathways may lead to heightened anxiety, obsessive behaviors, emotional lability, and disturbed reward processing, which together form a neurobiological basis for restrictive, compulsive, or dysregulated eating patterns.

Understanding serotonergic dysfunction in the context of eating disorders provides important insights into the pathogenesis of these conditions and supports the development of targeted diagnostic and therapeutic strategies. Early identification of serotonergic imbalance may improve prognostic assessment and enable personalized interventions aimed at restoring neurochemical homeostasis, optimizing cognitive-emotional regulation, and improving long-term outcomes in school-aged children with eating disorders.

Antenatal Care Utilization, Maternal Knowledge, And Adverse Birth Outcomes: A Comprehensive Multilevel Analysis Of Determinants, Pathways, And Implications In Low- And Middle-Income Contexts

Dr. Amanuel Bekele Tesfahun — Thu, 01 Jan 2026 00:00:00 +0000

Antenatal care (ANC) remains one of the most critical pillars of maternal and child health, serving as a primary preventive and promotive intervention to reduce adverse birth outcomes and maternal mortality. Despite global progress in improving maternal health indicators, delayed initiation, irregular attendance, and suboptimal quality of antenatal care persist across low- and middle-income countries, particularly in Sub-Saharan Africa and parts of South and Southeast Asia. This research article provides a comprehensive, theory-driven synthesis and original analytical interpretation of existing empirical evidence on antenatal care utilization, maternal knowledge of pregnancy danger signs, socio-demographic determinants, and their relationship with adverse birth outcomes. Drawing strictly on the provided references, this study integrates findings from cross-sectional studies, systematic reviews, meta-analyses, demographic health surveys, and institutional health profiles to construct a multilayered explanatory framework. The article explores how structural factors such as food security, health system accessibility, urban–rural disparities, and policy environments interact with individual-level determinants including maternal education, pregnancy intention, spousal support, and exposure to mass media. Furthermore, it examines the mediating role of maternal knowledge, early risk detection, and continuity of care in shaping maternal and neonatal outcomes. By moving beyond descriptive summaries, this paper elaborates on causal pathways, theoretical implications, contextual variations, and countervailing explanations. The findings underscore that antenatal care utilization is not merely a behavioral choice but a socially embedded practice shaped by intersecting economic, cultural, informational, and institutional forces. The article concludes with a critical discussion of methodological limitations in existing studies and proposes future research and policy directions aimed at strengthening equitable, timely, and effective antenatal care systems.

Early Diagnosis Of Oral Leukoplakia As A Key Factor In The Prevention Of Malignant Transformation

Yusupjanova Munira Abdukhamid qizi — Thu, 15 Jan 2026 00:00:00 +0000

Oral leukoplakia is recognized as the most common potentially malignant disorder of the oral cavity and remains a major concern in preventive dentistry and oral medicine. Despite its often asymptomatic nature, oral leukoplakia carries a significant risk of malignant transformation into oral squamous cell carcinoma, particularly when diagnosis is delayed or clinical monitoring is insufficient. Early diagnosis plays a decisive role in reducing this risk, enabling timely intervention, elimination of etiological factors, and appropriate clinical management. This paper explores the importance of early detection of oral leukoplakia as a preventive strategy against malignant transformation. Emphasis is placed on epidemiological relevance, etiological factors, clinical and histopathological characteristics, diagnostic approaches, and the prognostic value of early identification. The paper also discusses the role of dental practitioners in screening, patient education, and long-term follow-up. By integrating clinical vigilance with modern diagnostic tools, early diagnosis can significantly reduce morbidity and mortality associated with oral cancer. Strengthening early detection strategies is therefore essential for improving patient outcomes and advancing oral cancer prevention.

Cytokine Dysregulation As A Key Mechanism Of Dic Syndrome Formation In Children With Severe Pneumonia: Clinical And Immunological Analysis

Wed, 07 Jan 2026 00:00:00 +0000

The aim of the study: To determine the clinical and immunological characteristics and elucidate the role of cytokine dysregulation in the development of DIC syndrome in children aged 1–3 years with severe pneumonia in order to improve early diagnosis and prognosis of complications.

Materials and methods. The study was conducted in 2024–2025 at the Intensive Care and Pediatric Pulmonology Department of the Multidisciplinary Clinic of TSMU. Thirty-nine children aged 1–3 years diagnosed with severe pneumonia were observed. To elucidate the role of cytokine dysregulation in the development of DIC syndrome, the patients were divided into two groups. The first group consisted of 17 children (43.6%) who developed DIC syndrome against a background of severe pneumonia. Among them, there were 10 boys (58.8%) and 7 girls (41.2%). The second group consisted of 22 children (56.4%) who did not have hemostasis disorders. Of these, 12 were boys (54.5%) and 10 were girls (45.5%).

Results and discussion. The analysis of the examined children revealed significant differences in clinical and laboratory parameters between the group with DIC and patients without coagulopathic complications. Already at admission, children with DIC demonstrated a more pronounced inflammatory response: their C-reactive protein levels averaged 118.4 mg/L (95% CI: 103–132 mg/L), which was statistically significantly higher than those in the second group, where the average values were 62.7 mg/L (95% CI: 52–73 mg/L; p < 0.01).

Conclusions. In children aged 1–3 years with severe pneumonia, the development of DIC syndrome is accompanied by more pronounced systemic inflammation, as evidenced by significantly elevated levels of C-reactive protein and procalcitonin compared to patients without DIC. The development of DIC is associated with pronounced cytokine dysregulation: IL-6 concentrations in children with DIC were more than twice as high, while IL-10 levels were significantly lower, indicating an insufficient anti-inflammatory response.