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Introduction Coeliac disease (CeD) is a chronic, immune-mediated enteropathy triggered by the ingestion of gluten peptides in genetically susceptible individuals, with environmental and epigenetic factors also contributing to its pathogenesis. These peptides are modified via deamidation by tissue transglutaminase (tTG), thereby enhancing their immunogenicity. Although strict adherence to a gluten-free diet (GFD) remains the standard treatment, up to 30–40% of patients experience persistent symptoms and/or on-going mucosal inflammation and/or disruption leading to long-term complications. We aimed to assess compliance to GFD and correlate this to tTG level, histopathology, micronutrients and vitamins deficiencies.Methods In this observational prospective cohort study we selected 120 adult patients with coeliac disease for GFD diet assessment with a specialist coeliac service. We analysed tTG level, histopathology Marsh classification, vitamin D, vitamin B12, folate and ferritin levels at baseline and after 1 year from enrolment. We hypothesised that tTG level was correlated with inflammatory enteropathy but not with the severity of intestinal damage or the extent of nutrient absorption.Results We identified 49 patients (40.8%) out of 120 with non-responsive coeliac disease (NRCD). Four out of 49 (8.2%) were intentionally not compliant with GFD. Twenty-three patients (46.9%) had normal range of micronutrients absorption. Fourteen patients out of twenty- three (60.9%) demonstrated persistently elevated tTG 10 times upper limit of normal (ULN) despite normal range of micronutrients absorption.Conclusions These preliminary results indicate that, in clinical practice, tTG alone might be insufficient to monitor disease response to a GFD and should be interpreted alongside clinical biomarkers and histological parameters. Raised follow up tTG values, in the context of normal micronutrient absorption, indicates that the immune response is still ongoing leading to possible long-standing complications in coeliac disease. Understanding of the full pathophysiological mechanisms underlying this disorder is key for new developing diagnostic modalities and therapeutic targets.