Manifestation Of Thiamine Deficiency Research Articles

Beriberi in Brazil: A Disease That Affects Indigenous People.

Beriberi is the clinical manifestation of thiamine deficiency. It is multicausal and typically associated with poverty and food insecurity among vulnerable populations, such as indigenous people. The objective of this study was to carry out a spatial analysis of reported cases of beriberi among indigenous people in Brazil. Cross-sectional study using time series data on suspected cases of beriberi reported to the Ministry of Health via the FormSUS between July 2013 and September 2018. Indigenous villages were georeferenced, and Kernel density estimation was used to identify patterns of the spatial distribution of beriberi cases. A total of 414 cases of beriberi were reported in the country of which 210 (50.7%) were indigenous people. All the cases in indigenous people occurred in states located in the Legal Amazon (Maranhão, Roraima, and Tocantins). Kernel density estimation showed high-density areas in Tocantins and Roraima. This is the first nationwide study of reported cases of beriberi. The findings can be used to guide actions that contribute to the monitoring and prevention of beriberi among indigenous people.

Serum growth differentiation factor 15 levels and clinical manifestations in patients with thiamine deficiency

AbstractBackgroundThiamine deficiency can cause a broad range of symptoms affecting the central nervous system. Although the precise mechanisms underlying these effects remain unclear, research suggests that mitochondrial dysfunction is involved. Some studies have reported that growth differentiation factor 15 (GDF15) is a useful biomarker for diagnosing mitochondrial disorder.AimIn the present study, we investigated the clinical associations between GDF15 and thiamine deficiency.MethodsWe measured serum GDF15 levels in four patients with thiamine deficiency, 28 healthy controls, five patients with mitochondrial disorder, three patients with neuromyelitis optica spectrum disorder, and one patient who presented with thiamine deficiency‐like symptoms despite normal blood levels of thiamine. GDF15 concentrations were measured via enzyme‐linked immunosorbent assay. Serum GDF15 levels were evaluated in consideration of clinical parameters including age, sex, and body mass index.ResultsMean GDF15 levels were significantly higher in the thiamine deficiency (3990.5 pg/mL) and mitochondrial disorder groups (3363.2 pg/mL) than in the healthy control group (1062.0 pg/mL). Multiple regression analysis revealed that serum GDF15 levels were significantly associated with age and cognitive function in the healthy control group. The patient with thiamine deficiency‐like symptoms exhibited elevated serum GDF15 levels. In one patient with thiamine deficiency, GDF15 levels gradually decreased after initiating thiamine supplementation.ConclusionThe present study demonstrates that serum GDF15 levels may be useful in the diagnosis and evaluation of patients with various manifestations of thiamine deficiency.

Shoshin syndrome: report of a treatable disaster

Shoshin syndrome is a rare fulminating heart failure caused by thiamine deficiency. In Japanese “sho” means acute damage and “shin” means heart. It consists of a rare and hyperacute manifestation of beriberi that was first described in polished white rice-eating communities in various locations across Asia including China, Japan and Indonesia. In a totally different context, ‘Shoshin’ is a word from Zen Buddhism meaning “beginner’s mind”, which is considered the necessary attitude to approach the Zen practice. This case report is a prime example of clinical manifestations of thiamine deficiency for the presence of both cardiological and neurological disorders, for hyperacute onset of cardiac failure (shoshin syndrome), for the simultaneous involvement of peripheral and central nervous system, and for the dramatic global recovery after thiamine replacement therapy. We therefore explain why the physician should adopt a beginner’s mind in clinical practice.

Thiamine and Fatigue in Inflammatory Bowel Diseases: An Open-label Pilot Study

To demonstrate that fatigue and other disorders related to ulcerative colitis and Crohn's disease are the manifestation of an intracellular mild thiamine deficiency and not due to malabsorbtion, augmented requirements, or nutritional factors, and that this dysfunction is curable with high doses of thiamine administered orally or parenterally. In this pilot study, we treated fatigue in eight patients with ulcerative colitis and four patients affected by Crohn's disease from January to April 2011. The patients were recruited through general practitioners' surveys and among personnel and affiliated personnel of the clinic Villa Immacolata. Fatigue was measured using the chronic fatigue syndrome scale, and the determination of thiamine and thiamine pyrophosphate levels in the blood was carried out through blood tests. The levels of thiamine and thiamine pyrophosphate in the blood were normal. All patients were assigned to receive high doses of thiamine orally. Depending upon the body weight of each patient, dosage ranged from 600 mg/day (60 kg) to 1,500 mg/day (90 kg). The chronic fatigue syndrome scale as well as thiamine and thiamine pyrophosphate levels in the blood were measured 20 days after the beginning of the therapy. Ten patients out of twelve showed complete regression of fatigue, while the remaining two patients showed nearly complete regression of fatigue compared to the chronic fatigue syndrome scale scores before therapy. The absence of blood thiamine deficiency and the efficacy of high-dose thiamine in our patients suggest that fatigue is the manifestation of a thiamine deficiency, likely due to a dysfunction of the active transport of thiamine inside the cells, or due to structural enzymatic abnormalities. The administration of large quantities of thiamine increases the concentration in the blood to levels in which the passive transport restores the normal glucose metabolism in all cells and leads to a complete regression of fatigue.

Aging potentiates the acute and chronic neurological symptoms of pyrithiamine-induced thiamine deficiency in the rodent

The present study aimed to assess the role of advanced age in the development and manifestation of thiamine deficiency using an animal model of Wernicke-Korsakoff syndrome (WKS). Interactions between pyrithiamine-induced thiamine deficiency (PTD) and age were examined relative to working memory impairment and neuropathology in Fischer 344 rats. Young (2–3 months) and aged (22–23 months) F344 rats were assigned to one of two treatment conditions: PTD or pair-fed control (PF). Rats in the former group were further divided into three groups according to duration of PTD treatment. Working memory was assessed with an operant matching-to-position (MTP) task; after testing, animals were sacrificed and both gross and immunocytochemical measures of brain pathology were obtained. Aged rats exhibited acute neurological disturbances during the PTD treatment regime earlier than did young rats, and also developed more extensive neuropathology with a shorter duration of PTD. Aged rats displayed increased brain shrinkage (smaller frontal cortical and callosal thickness) as well as enhanced astrocytic activity in the thalamus and a decrease in ChAT-positive cell numbers in the medial septum; the latter two measures of neuropathology were potentiated by PTD. In both young and aged rats, and to a greater degree in the latter group, PTD reduced thalamic volume. Behaviorally, aged rats displayed impaired choice accuracy on the delayed MTP task. Regardless of age, rats with lesions centered on the internal medullary lamina of the thalamus also displayed impaired choice accuracy. Moreover, increased PTD treatment duration led to increased response times on the delayed MTP task. These results suggest that aging does indeed potentiate the neuropathology associated with experimental thiamine deficiency, supporting an age coupling hypothesis of alcohol-related neurological disorders.