In recent years, there has been a noticeable increase in the incidence of inflammatory bowel diseases in the pediatric population. Entry observations demonstrate anemia, malabsorption, deficiencies in vitamin D and calcium. These aspects, together with the systemic action of pro-inflammatory cytokines and steroid therapy are widely recognized as factors influencing bone metabolism. Presently, however, there are very few studies that can be found in the scientific literature on metabolic disorders in patients with IBD, especially in the pediatric population as the coexistence has not been sufficiently examined and understood. This review aims to summarize the currently available literature, as well as assess which areas have information gaps and need further research.

Background: Inflammatory bowel diseases (IBD), such as Crohn’s disease (CD) and ulcerative colitis (UC), may impair bone metabolism, particularly in children. The RANKL/OPG axis, as a key regulator of bone turnover, may contribute to these disturbances. However, data in the pediatric population remain limited. Methods: A single-center, prospective observational study included 100 children aged 4–18 years, with a comparable number of girls and boys. Among them, 72 had IBD (27 CD, 45 UC) and 28 were healthy controls. Anthropometric, biochemical, and densitometric assessments were performed, including serum levels of RANKL and OPG, and markers of inflammation and bone turnover. Results: Children with CD had significantly lower height and weight percentiles compared to UC and controls. Serum RANKL and the RANKL/OPG ratio were significantly elevated in IBD patients, particularly in CD (p < 0.01). Total body BMD Z-scores were lower in IBD compared to controls (p = 0.03). Low BMD was found in 14.7% of UC and 26.3% of CD patients. In both groups, over 30% had values in the “gray zone” (−1.0 to −2.0). A positive correlation was observed between height and weight and bone density (p < 0.01). Higher OPG was associated with lower body weight (p < 0.001), while increased RANKL correlated with osteocalcin (p = 0.03). Patients receiving biological therapy had significantly lower BMD. Conclusions: Pediatric IBD is associated with significant alterations in the RANKL/OPG axis and reduced bone density. These findings support early screening and suggest RANKL/OPG as a potential biomarker of skeletal health.

Background: Inflammatory bowel disease (IBD) is associated with multiple factors that influence bone metabolism. This study aimed to compare the clinical manifestations and diagnostic parameters of patients with Crohn’s disease (CD) and ulcerative colitis (UC) at the time of diagnosis, as well as to assess their relationship with subsequent bone disorders. Methods: Blood tests (including calcium–phosphate metabolism) and fecal tests (including calprotectin) were performed in eighty children recently diagnosed with IBD. Additionally, the bone densitometry results were evaluated in 25 of them. Results: Diarrhea (p = 0.02) and bloody stools (p < 0.001) were more frequent in patients with UC, whereas fever was more common in patients with CD (p = 0.003). Laboratory tests revealed anemia in 62.5% (50/80) and thrombocytosis in 36.3% (29/80). Higher calprotectin levels in the feces were found in girls at the time of diagnosis (p = 0.02). Osteopenia was detected in almost half of the examined patients (12/25), and 20% (5/25) met the criteria for osteoporosis. Low calcium levels at diagnosis were correlated with subsequent bone disorders (p = 0.005). Insufficient levels of vitamin D were detected in 77.8% (56/80). Conclusions: Early disease detection and the appropriate monitoring of children with IBD may decrease the risk of serious consequences, including osteoporosis.

Background: Noonan syndrome is a rare genetic disorder from the group of RASopathies, characterized by facial dysmorphism, congenital heart defects, hematologic abnormalities, and growth impairment. Case Presentation: We report the case of an 8-year-old girl with Noonan syndrome admitted for evaluation of abdominal pain and failure to thrive. Hematological evaluation before EGD did not identify contraindications to biopsy, and initial laboratory tests, including coagulation parameters, were normal. Several hours after upper gastrointestinal endoscopy, the patient developed abdominal pain and coffee-ground vomiting. Abdominal ultrasonography revealed an intramural duodenal hematoma (58 × 37 mm), which was confirmed and further characterized by computed tomography as an extensive, long-segment lesion involving the duodenum. Progressive anemia required transfusion of blood products. Conservative management, including nasogastric decompression, parenteral nutrition, and pharmacological treatment, was implemented. Despite the severity and prolonged clinical course, gradual clinical and radiological improvement was achieved, and the patient was discharged in good general condition after one month. Conclusions: Intramural duodenal hematoma is an extremely rare complication of upper gastrointestinal endoscopy with duodenal biopsy. This case highlights the importance of individualized assessment and close monitoring in patients with Noonan syndrome, and indicates that this complication should be considered early when abdominal pain, vomiting, or progressive anemia develops after the procedure, even when hematological evaluation and baseline coagulation parameters are reassuring.