ArticleCureus2026
Duodenal Lymphocytosis and B1 Deficiency: Unveiling the Overlap Between Gut and Brain.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.