RESUMO
The use of antibiotics has increased drastically over the last few decades. Many antibiotics can target the commensal microbiota and promote gut dysbiosis. These alterations contribute to disease onset and exacerbation. Although the etiology of inflammatory bowel disease (IBD) is mostly unknown, it involves a complex interaction among host genetics, microbiota, environmental factors, and aberrant immune responses. Studies have shown a relationship between very-early-onset inflammatory bowel disease (VEO-IBD) and microbiota alterations. The case discussed in this report endorses the current clinical evidence for this interaction. This is an anonymous record review with no identifiers involving a 23-month-old female patient who was brought to the emergency department by her parents due to persistent bloody diarrhea. Eight days before the presentation, she had experienced watery diarrhea that progressed to bloody stools. The patient had a history of acute otitis media, acute enteritis, and right-arm cutaneous abscess, for which she had received multiple antibiotic therapies. Strategies to manipulate the microbiome through diet, probiotics, antibiotics, or fecal microbiota transplantation (FMT) may be used therapeutically to modulate disease activity. A high index of clinical suspicion for VEO-IBD should be maintained for patients with a history of multiple, recurrent antibiotic use. We believe this case report will raise awareness about the issue of early anaerobic antibiotic exposure and help prevent its unnecessary use and, consequently, prevent gut microbiota dysbiosis that can lead to VEO-IBD. Also, our literature review will hopefully prompt clinicians to consider alternative therapeutic options for this patient population, such as rebuilding intestinal microbiota composition to improve VEO-IBD activity.
RESUMO
OBJECTIVE: The objective of this study was to assess the clinical response and safety of mirtazapine in the pediatric population with a diagnosis of functional nausea and nausea associated with functional dyspepsia postprandial distress syndrome. METHODS: This was a retrospective chart review to evaluate the safety and efficacy of mirtazapine for pediatric nausea and nausea associated with functional dyspepsia postprandial distress syndrome. Clinical response was classified as complete response, partial response, and no response. We also identified the prescribed doses, side effects, and weight changes during mirtazapine therapy. RESULTS: Among the 57 total patients, 67% were females and ages ranged from 7 to 19 years with a mean of 14 ± 3 years. Clinical (complete and partial) response was reported in 82% of patients. Nausea resolved in 82% and insomnia in 77% of the patients. Eighty-four percent gained weight with a mean of 4 ± 7 kg. Sixty-five percent did not report adverse effects. The most common adverse effects were undesired weight gain (16%) and dysphoria (9%). Two patients discontinued the medicine after the first dose because of adverse effects. There was a significant correlation between the initial dose and weight (rs = 0.478; p = 0.0002). The median initial and final doses were 15 mg, respectively. CONCLUSIONS: Mirtazapine is an option for treating children and adolescents with functional nausea and nausea associated with functional dyspepsia post-prandial distress syndrome, especially for a select group of patients with concurrent weight loss, anxiety, and insomnia.