Duodenal Lymphocytosis and B1 Deficiency: Unveiling the Overlap Between Gut and Brain

Thiamine (vitamin B1) deficiency is a reversible, yet potentially fatal condition that affects both the central and peripheral nervous systems. Although commonly linked to chronic alcoholism, non-alcoholic causes, including malabsorption syndromes, are increasingly being recognized. We report the case of a 22-year-old woman who presented with progressive lower limb weakness, gait disturbances, and confusional symptoms, following a history of intermittent diarrhea and vomiting. Neurological examination revealed ascending motor deficits, areflexia, cerebellar syndrome, and internuclear ophthalmoplegia. Brain magnetic resonance imaging (MRI) showed bilateral symmetrical lesions in the caudate nuclei and periaqueductal area, suggesting Gayet-Wernicke encephalopathy (GWE). The electroneuromyography (ENMG) revealed axonal sensorimotor polyneuropathy. Cerebrospinal fluid (CSF) analysis showed mild hyperproteinorachia mimicking acute inflammatory demyelinating polyneuropathy (AIDP). A profound thiamine deficiency (22.4 nmol/L) was identified alongside duodenal lymphocytosis without villous atrophy or celiac-specific antibodies. High-dose intravenous (IV) thiamine therapy led to rapid improvement in neuropsychiatric symptoms, with partial motor recovery over two months and near-complete resolution on follow-up MRI at six months. This case highlights the diagnostic complexity of non-alcoholic thiamine deficiency, in which Gayet-Wernicke encephalopathy and dry beriberi may present atypically. MRI findings and clinical response to thiamine are key to early diagnosis. Duodenal lymphocytosis may suggest an underlying malabsorption process even in the absence of definitive celiac disease. Clinicians must maintain a high index of suspicion for thiamine deficiency in patients with neurological and gastrointestinal (GI) symptoms regardless of alcohol use. Prompt thiamine supplementation is crucial to prevent irreversible neurological damage.