Effect of high‐dosed thiamine hydrochloride and S‐benzoyl‐thiamine‐O‐monophosphate on thiamine‐status after chronic ethanol administration

Netzel, M.; Ziems, M.; Jung, Kristina; Noll, E.; Borsch, Christian; Bitsch, I.

doi:10.1002/biof.5520110133

Cited by 8 publications

(9 citation statements)

References 6 publications

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“…In an animal study, it has been found that chronic alcohol consumption in rats resulted in a significant depletion in thiamine diphosphate (TDP), the active coenzyme form of thiamine. Supplementation with benfotiamine significantly increased concentrations of TDP and total thiamine compared with supplementation with thiamine HCl [96]. An 8 week, randomized, multicentre, placebo‐controlled, double‐blind study compared the effect of benfotiamine alone with a benfotiamine complex (Milgamma‐N) or placebo in 84 alcoholic patients.…”

Section: Clinical Management Of Alcoholic Neuropathymentioning

confidence: 99%

Alcoholic neuropathy: possible mechanisms and future treatment possibilities

Chopra

Tiwari

2012

Brit J Clinical Pharma

199

103

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Chronic alcohol consumption produces painful peripheral neuropathy for which there is no reliable successful therapy, mainly due to lack of understanding of its pathobiology. Alcoholic neuropathy involves coasting caused by damage to nerves that results from long term excessive drinking of alcohol and is characterized by spontaneous burning pain, hyperalgesia and allodynia. The mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed. These include activation of spinal cord microglia after chronic alcohol consumption, oxidative stress leading to free radical damage to nerves, activation of mGlu5 receptors in the spinal cord and activation of the sympathoadrenal and hypothalamo-pituitary-adrenal (HPA) axis. Nutritional deficiency (especially thiamine deficiency) and/or the direct toxic effect of alcohol or both have also been implicated in alcohol-induced neuropathic pain. Treatment is directed towards halting further damage to the peripheral nerves and restoring their normal functioning. This can be achieved by alcohol abstinence and a nutritionally balanced diet supplemented by all B vitamins. However, in the setting of ongoing alcohol use, vitamin supplementation alone has not been convincingly shown to be sufficient for improvement in most patients. The present review is focused around the multiple pathways involved in the development of peripheral neuropathy associated with chronic alcohol intake and the different therapeutic agents which may find a place in the therapeutic armamentarium for both prevention and management of alcoholic neuropathy.

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Section: Clinical Management Of Alcoholic Neuropathymentioning

confidence: 99%

Alcoholic neuropathy: possible mechanisms and future treatment possibilities

Chopra

Tiwari

2012

Brit J Clinical Pharma

199

103

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“…For example, one group claims benfotiamine increases brain thiamine (Pan et al, 2010a), whereas others claim it does not (Volvert et al, 2008). Another report found slight increases after six months (Netzel et al, 2000). Others report that both benfotiamine and fursultiamine increase brain thiamine, but not thiamine esters, and only benfotiamine diminishes plaques (Pan et al, 2010a).…”

Section: Introductionmentioning

confidence: 97%

“…Neither show increases in the thiamine esters. One study showed a 90% increase in thiamine diphosphate levels in brain of rats that received benfotiamine in their diet for 6 months followed by 6 months of thiamine (Netzel et al, 2000). In the paper in which plaque levels were diminished (see below) (Pan et al, 2010b), the treatment was over an eight-week period.…”

Section: Introductionmentioning

confidence: 99%

Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes

Gibson

Hirsch

Cirio

et al. 2013

Molecular and Cellular Neuroscience

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Reduced glucose metabolism is an invariant feature of Alzheimer’s Disease (AD) and an outstanding biomarker of disease progression. Glucose metabolism may be an attractive therapeutic target, whether the decline initiates AD pathophysiology or is a critical component of a cascade. The cause of cerebral regional glucose hypometabolism remains unclear. Thiamine-dependent processes are critical in glucose metabolism and are diminished in brains of AD patients at autopsy. Further, the reductions in thiamine-dependent processes are highly correlated to the decline in clinical dementia rating scales. In animal models, thiamine deficiency exacerbates plaque formation, promotes phosphorylation of tau and impairs memory. In contrast, treatment of mouse models of AD with the thiamine derivative benfotiamine diminishes plaques, decreases phosphorylation of tau and reverses memory deficits. Diabetes predisposes to AD, which suggests they may share some common mechanisms. Benfotiamine diminishes peripheral neuropathy in diabetic humans and animals. In diabetes, benfotiamine induces key thiamine-dependent enzymes of the pentose shunt to reduce accumulation of toxic metabolites including advanced glycation end products (AGE). Related mechanisms may lead to reversal of plaque formation by benfotiamine in animals. If so, the use of benfotiamine could provide a safe intervention to reverse biological and clinical processes of AD progression.

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“…Multifaceted beneficial effects of benfotiamine have been reported such as the reduction of glucose toxicity, alleviation of diabetes‐induced cerebral oxidative damage, acceleration of the healing of ischemic diabetic limbs in mice, and rescue of cardiomyocyte contractile dysfunction in experimental diabetes mellitus . Many studies show that administration of benfotiamine leads to higher thiamine blood concentrations than administration of water‐soluble thiamine . It was revealed that high TDP concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfotiamine …”

mentioning

confidence: 99%

“…19 Many studies show that administration of benfotiamine leads to higher thiamine blood concentrations than administration of water-soluble thiamine. [9][10][11]20,21 It was revealed that high TDP concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfotiamine. 22 In recent years, most of studies about benfotiamine were focused on pharmacological utilities, while its clinical pharmacokinetic data were inadequate.…”

mentioning

confidence: 99%

Pharmacokinetic study of benfotiamine and the bioavailability assessment compared to thiamine hydrochloride

Xie

Zhang

et al. 2014

The Journal of Clinical Pharma

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Benfotiamine is a lipid-soluble thiamine precursor which can transform to thiamine in vivo and subsequently be metabolized to thiamine monophosphate (TMP) and thiamine diphosphate (TDP). This study investigated the pharmacokinetic profiles of thiamine and its phosphorylated metabolites after single- and multiple-dose administration of benfotiamine in healthy Chinese volunteers, and assessed the bioavailability of orally benfotiamine administration compared to thiamine hydrochloride. In addition, concentration of hippuric acid in urine which is produced in the transformation process of benfotiamine was determined. The results showed that thiamine and its phosphorylated metabolites exhibited different pharmacokinetic characteristics in plasma, blood and erythrocyte, and one-compartment model provided the best fit for pharmacokinetic profiles of thiamine. The transformation process of benfotiamine to thiamine produced large amount of hippuric acid. No accumulation of hippuric acid was observed after multiple-dose of benfotiamine. Compared to thiamine hydrochloride, the bioavailability of thiamine in plasma and TDP in erythrocyte after oral administration of benfotiamine were 1147.3 ± 490.3% and 195.8 ± 33.8%, respectively. The absorption rate and extent of benfotiamine systemic availability of thiamine were significantly increased indicating higher bioavailability of thiamine from oral dose of benfotiamine compared to oral dose of thiamine hydrochloride.

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Effect of high‐dosed thiamine hydrochloride and S‐benzoyl‐thiamine‐O‐monophosphate on thiamine‐status after chronic ethanol administration

Cited by 8 publications

References 6 publications

Alcoholic neuropathy: possible mechanisms and future treatment possibilities

Alcoholic neuropathy: possible mechanisms and future treatment possibilities

Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes

Pharmacokinetic study of benfotiamine and the bioavailability assessment compared to thiamine hydrochloride

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