Constipation affects around 30% of children and in 95% of cases is functional (FC), a consequence of alterations in digestive tract peristalsis, modulated by the immune and nervous systems, bile acid metabolism, and the gut microbiota. The aim of this review was to assess the role of gut microbiota and the use of probiotics in children with constipation. The current treatment involves education, toilet training, and oral laxatives, effective in only 50% of patients. In chronic FC, the composition of the microbiota is altered, with increased abundance of Bacteroidetes, Enterobacteriaceae, and Firmicutes and decreases in Prevotella, Bifidobacteria, Faecalibacterium prausnitzii, and Clostridium leptum. Probiotics replenish lacking beneficial resident bacteria, downregulate mucosal inflammation, or produce short-chain fatty acids (SCFAs). Probiotics like Bifidobacterium breve and Bifidobacterium longum increase the defecation frequency and decrease the episodes of both fecal incontinence and abdominal pain. Bifidobacterium animalis subsp. lactis XLTG11 improves the gut microbiota by upregulating SCFA genes and downregulating those related to methane metabolism. Lactobacilli produce organic acids that stimulate bowel peristalsis and augment fecal bolus moisture. The heterogeneity of the current studies involving pediatric subjects thus far hinders the use of probiotics as a standard in the management of children with constipation.

Introduction: Cytomegalovirus (CMV) infection is present in a latent state in 70–90% of the immunocompetent population, and its reactivation might be triggered by inflammatory conditions such as post-COVID multisystem inflammatory syndrome (MIS-C) or by immunosuppression induced by steroids. The aim of this paper was to highlight the unexpected complications associated with SARS-CoV-2 infection that require a complex clinical approach for accurate diagnosis. Materials and Methods: We present the case of a 4-year-old male patient who, during an initially favorable course of PIMS, experienced symptoms of respiratory failure. Results: The patient initially presented with clinical and paraclinical signs of PIMS with cardiac involvement, for which high-dose corticosteroid therapy was initiated, followed by gradual tapering, along with immunoglobulins, anticoagulants, antiplatelet agents, and symptomatic treatment. After 10 days of favorable progress, the patient’s general condition deteriorated, showing tachypnea, desaturation, and a ground-glass appearance on thoracic CT. Negative inflammatory markers and favorable cardiac lesion evolution ruled out MIS-C relapse. The presence of anti-CMV IgM antibodies and viral DNA in the blood confirmed acute CMV infection, likely triggered by prior severe-acute-respiratory-syndrome-related coronavirus 2 (SARS-CoV-2) infection and secondary immunosuppression due to steroids. Non-specific immunomodulatory treatment was initiated but led to worsening of pulmonary lesions, prompting the initiation of specific antiviral treatment with ganciclovir, resulting in rapid clinical and imaging improvement. Conclusions: CMV infection can be reactivated by immunosuppression induced by corticosteroid therapy for MIS-C and may require specific etiological treatment.