Candida-Associated Gut Biofilm–Driven Refractory Dysglycaemia: A Rare Phenotype with Threshold-Triggered Glucose Collapse Proposing a Candidate Syndrome (CGB-RDS)

Background: Interactions between the intestinal mycobiome and systemic metabolic regulation remain insufficiently characterised. While fungal colonisation is common in diabetes, its role in dynamic, event-driven dysglycaemia has not been defined. In particular, the impact of fungal morphological plasticity and biofilm formation under hyperglycaemic conditions remains unclear. Case Presentation: We report a 43-year-old female with a 25-year history of autoimmune insulin-dependent diabetes mellitus, characterised by refractory hyperglycaemia and chronic passage of high-volume, gelatinous, mucus-dominant intestinal material. Microbiological analysis confirmed Candida albicans with both yeast and hyphal forms. Episodes of evacuation were consistently preceded by extreme hyperglycaemia (>500 mg/dL) and followed by rapid declines to hypoglycaemic levels (<60 mg/dL). A 7-day observational log demonstrated reproducible glucose reductions ranging from 247 to >465 mg/dL per episode. Despite insulin therapy, glycaemic control remained unstable and was associated with systemic manifestations including pruritus, dehydration, and neuroenteric symptoms. Mechanistic Interpretation: We propose that chronic intestinal accumulation of a mucus-integrated fungal biofilm functions as a dynamic immunometabolic compartment. Hyperglycaemic conditions likely promote Candida albicans yeast-to-hypha transition via glucose-sensitive pathways, including cAMP–PKA and MAPK signalling, facilitating biofilm formation and persistence. Biofilm-associated β-glucans and mannans activate pattern recognition receptors such as Dectin-1 and Toll-like receptors, driving NF-κB and JNK-mediated inflammatory signalling. This results in inhibitory serine phosphorylation of IRS-1, impaired PI3K–AKT signalling, and functional insulin resistance. Accumulation of the biofilm amplifies this state, while threshold-triggered evacuation abruptly reduces inflammatory signalling, restores insulin sensitivity, and unmasks the pharmacodynamic effect of circulating insulin, resulting in rapid glucose decline.Conclusion: This case supports the proposal of a candidate syndrome, Candida-Associated Gut Biofilm–Driven Refractory Dysglycaemia Syndrome (CGB-RDS), characterised by reversible, compartment-driven insulin resistance and threshold-dependent metabolic switching. These findings highlight a previously unrecognised gut–mycobiome–metabolic axis and warrant further investigation into biofilm-mediated regulation of systemic glucose homeostasis.