Background: Migraine is a highly prevalent and disabling primary headache disorder frequently accompanied by gastrointestinal symptoms and comorbid gastrointestinal diseases. Increasing evidence suggests that alterations in the gut microbiota and dysregulation of the microbiome–gut–brain axis may contribute to migraine pathophysiology through immune activation, oxidative stress, impaired intestinal barrier function, and neuroinflammatory signaling. Objectives: This narrative review aims to summarize current mechanistic and clinical evidence linking the gut–brain axis to migraine, with a particular focus on the potential roles of probiotics, prebiotics, and postbiotics as adjunctive strategies in migraine management. Methods: A narrative synthesis of experimental, translational, and clinical studies was performed, focusing on microbiome composition, gut barrier integrity, immune and oxidative pathways, and interventional trials evaluating probiotics, prebiotics, synbiotics, and microbiota-derived metabolites in adult and pediatric migraine populations. Results: Migraine has been associated with intestinal dysbiosis, increased gut permeability, and low-grade systemic inflammation. Probiotics, most commonly strains of Lactobacillus and Bifidobacterium, may modulate inflammatory cytokine profiles, enhance tight junction integrity, reduce oxidative stress, and influence neurotransmitter-related pathways along the gut–brain axis. Clinical trials evaluating probiotic supplementation report heterogeneous but promising signals, including reductions in migraine frequency, severity, disability scores, and analgesic use, particularly in chronic migraine and pediatric populations. Emerging evidence also supports a potential role for prebiotics (e.g., inulin-type fructans) and microbiota-derived metabolites such as short-chain fatty acids, although direct clinical data remain limited. Conclusions: Modulation of the microbiome–gut–brain axis represents a biologically plausible adjunct approach in migraine management. While probiotics, prebiotics, and postbiotics show potential benefits with favorable safety profiles, current evidence of their strain-, formulation-, and population-specific characteristics is lacking. Well-powered, placebo-controlled trials with standardized migraine endpoints and integrated microbiome and metabolomic analyses are needed to define responders, optimal interventions, and clinical relevance.

Purpose: Clostridioides difficile infection (CDI) represents a major healthcare associated infection with potentially life-threatening complications. While gastrointestinal and systemic manifestations are well recognized, severe micronutrient deficiencies, particularly vitamin K deficiency are rarely described. We aimed to report a unique case of CDI-and antibiotic-associated dysbiosis and malabsorption leading to profound vitamin K deficiency and coagulopathy, thereby highlighting the clinical intersection between infection, microbiome disruption, and hemostasis. Methods: We report the clinical course, diagnostic work-up, and therapeutic management of an elderly female patient with CDI complicated by life-threatening coagulopathy. In addition, a narrative review of published case reports of antibiotic-associated vitamin K deficiency was performed to contextualize our findings. Results: The patient developed extensive subcutaneous hematomas with a severely deranged coagulation profile (PT > 100 s, INR > 8, markedly reduced activities of vitamin K–dependent factors). Normal liver function and preserved platelet count excluded disseminated intravascular coagulation and hepatic failure. The findings were consistent with severe vitamin K deficiency secondary to antibiotic-induced dysbiosis, malnutrition, and persistent diarrhea. High-dose intravenous vitamin K supplementation resulted in rapid normalization of coagulation parameters within 24 h, with subsequent clinical stabilization and resolution of bleeding manifestations. Conclusion: This case illustrates a rare but clinically significant complication of CDI: profound vitamin K deficiency–associated coagulopathy. Clinicians should maintain a high index of suspicion for vitamin K deficiency in elderly, malnourished, and antibiotic-exposed patients with CDI who present with unexplained coagulopathy or bleeding.