The emergence of anti-TNF agents has revolutionized the management of inflammatory bowel disease, yet a significant proportion of patients experience primary non-response or secondary loss of response due to immunogenicity. As the field of precision medicine advances, genetic predictors such as human leukocyte antigen (HLA) variants are gaining increasing attention. This review provides a comprehensive synthesis of current evidence on the role of HLA genotypes in inflammatory bowel disease susceptibility and disease behavior, with a focus on their mechanistic and clinical relevance in anti-TNF therapy. Special emphasis is placed on HLA-DQA1*05, a validated predictor of anti-drug antibody formation and reduced therapeutic durability. We explore the immunological basis of HLA-mediated immunogenicity, summarize pharmacogenetic and biomarker findings, and discuss how HLA typing may be integrated into treatment algorithms to improve patient stratification and long-term outcomes. As immunogenetics continues to inform clinical decision-making, understanding the interplay between HLA polymorphisms and therapeutic response offers new opportunities for biomarker-guided, personalized care in inflammatory bowel disease.

Background/Objectives: Chronic idiopathic thrombocytopenic purpura (chITP) is an autoimmune disease which develops in 10–30% of patients with newly diagnosed idiopathic thrombocytopenic purpura (ndITP). It is defined as thrombocytopenia which lasts longer than 12 months, with extremely diverse clinical expressions. The aim is to present the most significant clinical and laboratory characteristics of children with chITP. Methods: This is retrospective, observational research, which included children between 2–18 years with chITP who were treated in the Republic of Serbia for 25 years. We analyzed clinical data from personal and family medical histories and different laboratory analyses. Results: The total number of respondents was 152, with female predominance (F:M = 1.27:1) and mild predominance of adolescents. Of the patients, 15% were asymptomatic, but 15% had periodically life-threatening bleeding. Transfusion was not required for 70% of patients. Thirty-five percent of patients had chITP alone, and 45% had high titer levels of autoantibodies. The most frequent comorbidity was Hashimoto thyroiditis (15%). The same percentage (45%) of family members were reported with and without autoimmune diseases. Twenty-five percent of patients were resistant to initial therapy. Helicobacter pylori was detected in 20%, 70% had higher levels of lactate dehydrogenase (LDH), three patients had sufficient serum vitamin D levels, splenomegaly was found in 25%, and accessory spleen in 14% of patients. Around 50% of patients had a platelet count between 20–50 × 10⁹/L, and 40% below 20 × 10⁹/L. Mean platelet volume (MPV) was 10.6 ± 1.4 fL. No dysplastic changes were noted in bone marrow aspirate. Initial first-line therapy was sufficient for 45% of patients, second-line therapy was administered in 25%, splenectomy was performed in 20%, and 10% received all available treatments. Conclusions: The severe clinical form of pediatric chITP is accompanied by a low platelet count, the presence of autoimmune comorbidities, a positive family medical history, resistance to initial therapy, hypovitaminosis D, and rare megakaryocytes in the bone marrow.

Background/Objectives: The assessment of platelet kinetics (APK) is recommended for patients with chronic idiopathic thrombocytopenic purpura (chITP). The aim of this study was to examine the importance of APK as a prognostic instrument in the selection of therapy in children with chITP. Methods: Retrospective, observational research, which included chITP children who were treated and subjected to APK in Serbia for 25 years (total number was 152). Results: In the acute phase of the disease, 15% of patients had life-threatening bleeding, 15% were asymptomatic, and there were no cases of fatal bleeding. Mean platelet life was 0.89 ± 0.47 days. A total of 45% of patients had normal platelet production, and 35% had very low production. Among the patients, 55% exhibited splenic platelet sequestration, 35% had mixed sequestration, and 10% showed hepatic platelet sequestration. Platelet lifespan and production indices were less reliable parameters, due to numerous contradictory results, especially when compared with the location of platelet sequestration. Distribution of bleeding and therapy-resistant patients was dominant with mixed sequestration. Good therapy responders had dominant splenic sequestration. In the chronic phase of the disease, initial therapy was sufficient for 40–45% of patients, while another 25% required second-line therapy, regardless of platelet sequestration location. A total of 25% percent of patients had undergone splenectomy, and all of them were in stable remission. The remaining 10%, which represented the most severe cases, required all available therapies, had equally mixed and liver sequestration, and splenectomy showed no effect. Conclusions: APK may be a determining factor for the selection of splenectomy as a therapeutic option in case of predominantly splenic sequestration. Although the platelet production index has been explored in several studies, its clinical relevance remains controversial. In our findings, it did not contribute to therapeutic decision-making and may even lead to misinterpretation. The factors distinguishing the minority of bleeding and therapy-resistant patients with similar laboratory profiles remain unclear.

Background: Ventilator-associated pneumonia (VAP) is a leading cause of nosocomial infections in neonatal intensive care units (NICUs) and is associated with significant morbidity, mortality, and prolonged hospitalization, particularly in preterm neonates. Management is complicated by the emergence of multidrug-resistant (MDR) and extensively drug-resistant (XDR) pathogens, with very limited evidence supporting the use of reserve antibiotics in this population. Case Presentation: We report a male neonate born at 25 weeks of gestation (birth weight 740 g) who developed severe VAP caused by XDR Acinetobacter calcoaceticus-baumannii complex and Pseudomonas aeruginosa. After failure of multiple antibiotic regimens, including ampicillin, amikacin, meropenem, vancomycin, cefepime with inhaled colistin, tigecycline, and ceftazidime-avibactam combined with fosfomycin, the infant was treated with sulbactam–durlobactam (25 mg/kg/dose every 6 h) in combination with ceftazidime-avibactam. After 12 days of this regimen, the neonate was successfully extubated. Conclusions: This case highlights the therapeutic challenges of XDR infections in extremely preterm neonates and suggests that sulbactam–durlobactam may represent a viable salvage treatment option. Further pharmacokinetic and clinical studies are needed to establish optimal dosing and safety in the neonatal population.