Efficacy of lafutidine, a histamine H2-receptor antagonist, for taxane-induced peripheral neuropathy in patients with gynecological malignancies

Nagano, Hiroaki; Sanai, Hideomi; Muraoka, Mitsue; Takagi, Kimiyo

doi:10.1016/j.ygyno.2012.06.029

Cited by 11 publications

(4 citation statements)

References 11 publications

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“…Other RCTs evaluating the efficacy of recombinant human leukemia inhibitory factor (AM424), acetyl‐l‐carnitine, pregabalin, omega‐3, retinoic acid, minocycline, lafudine, and vitamin B complexes failed to demonstrate the efficacy of these agents in preventing neurotoxicity caused by paclitaxel‐based chemotherapeutic regimens …”

Section: Introductionmentioning

confidence: 99%

Taxane and epothilone‐induced peripheral neurotoxicity: From pathogenesis to treatment

Tamburin

Park

Alberti

et al. 2019

J Peripheral Nervous Sys

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Taxane-induced peripheral neurotoxicity (TIPN) is the most common nonhematological side effect of taxane-based chemotherapy, and may result in dose reductions and discontinuations, having as such a detrimental effect on patients' overall survival. Epothilones share similar mechanism of action with taxanes. The typical TIPN clinical presentation is mainly comprised of numbness and paresthesia, in a stocking-and-glove distribution and may progress more proximally over time, with paclitaxel being more neurotoxic than docetaxel. Motor and autonomic involvement is less common, whereas an acute taxane-induced acute pain syndrome is frequent. Patient reported outcomes questionnaires, clinical evaluation, and instrumental tools offer complementary information in TIPN. Its electrodiagnostic features include reduced/abolished sensory action potentials, and less prominent motor involvement, in keeping with a length-dependent, axonal dying back predominately sensory neuropathy. TIPN is dose-dependent and may be reversible within months after the end of chemotherapy. The single and cumulative delivered dose of taxanes is considered the main risk factor of TIPN development. Apart from the cumulative dose, other risk factors for TIPN include demographic, clinical, and pharmacogenetic features with several single-nucleotide polymorphisms potentially linked with increased susceptibility of TIPN. There are currently no neuroprotective strategies to reduce the risk of TIPN, and symptomatic treatments are very limited. This review critically examines the pathogenesis, incidence, risk factors (both clinical and pharmacogenetic), clinical phenotype and management of TIPN. K E Y W O R D S assessment, chemotherapy, docetaxel, ixabepilone, neurotoxicity, paclitaxel, prevention 1 | INTRODUCTION Taxanes (paclitaxel, docetaxel, cabazitaxel) were among the most important new chemotherapy agents in the late 20th century. 1 Paclitaxel is a natural compound with potent anticancer properties, which was originally isolated from the bark of the Pacific yew tree (Taxus brevifolia) in 1967, but low natural availability and insolubility in water hindered its diffusion since the 1980s. 2 Paclitaxel and docetaxel are currently obtained through a semisynthetic process from a precursor contained in the needles of the European yew tree (Taxus baccata),which is more widely available worldwide. 2 Nanoparticle albuminbound paclitaxel (nab-paclitaxel) is a novel formulation containing human serum albumin to encapsulate hydrophobic paclitaxel molecules to increase tumor uptake and reduce hypersensitivity

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Section: Introductionmentioning

confidence: 99%

Taxane and epothilone‐induced peripheral neurotoxicity: From pathogenesis to treatment

Tamburin

Park

Alberti

et al. 2019

J Peripheral Nervous Sys

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“…The incidence of sensory peripheral neuropathy in TC therapy was 78% [5], and worsens the rate of treatment completion and reduces quality of life (QOL) of patients. Many attempts using NSAIDs, steroids, antihistamines, tryptophan-N-formylated gramicidin (NFG), glial cell-line derived neurotrophic factor (GDNF), amifostine, gabapentin, and carbamazepine [6][7][8] have been conducted aiming to attenuate the drug-induced peripheral neuropathy, however, no methods have been established thus far.…”

Section: Introductionmentioning

confidence: 99%

The Prophylactic Effects of a Traditional Japanese Medicine, Goshajinkigan, on Paclitaxel-Induced Peripheral Neuropathy and its Mechanism of Action

et al. 2014

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BackgroundThis study aimed to evaluate the prophylactic effect of goshajinkigan (GJG) on paclitaxel (PTX)-induced neuropathy and to elucidate the mechanism of action.ResultsThere was a time-dependent irreversible decrease in pain threshold in PTX group. In PTX/GJG group, pain threshold showed changes in the same level as control. Electron microscope showed that although the ganglion cells of control and PTX/GJG groups were normal, degeneration of the nucleus and swelling of the mitochondria were observed in PTX group. Expression of transient receptor potential vanilloid 4 (TRPV4) gene in PTX group significantly increased compared with that in control and PTX/GJG groups. In TRPV4 knock-out mice, no PTX-induced hyperalgesia was observed, and there was no significant difference in pain threshold between the 3 groups.ConclusionsThese results showed that PTX induced hyperalgesia by enhancing TRPV4 expression, and suggested that GJG might alleviate hyperalgesia by preventing degeneration of the ganglion cells and suppressing TRPV4 expression.

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“…In the above mentioned reports,20,23,24 lafutidine was administered after developing PN and it improved PN, whereas in our study, it was administered before PN and was thought to protect against the progression of severe PN. The discrepancy between these previous studies and our study appears to depend on the timing of administration of lafutidine.…”

Section: Discussionmentioning

confidence: 48%

“…Lafutidine appears to function in a similar manner to capsaicin via the same neurons 15–17. There are some reports that lafutidine improves glossodynia20,23 and taxane induced PN 24. In these reports, it was assumed that lafutidine works in a similar manner to capsaicin via capsaicin sensitive afferent neurons and lafutidine increases local blood flow.…”

Section: Discussionmentioning

confidence: 99%

The protective effects of lafutidine for bortezomib induced peripheral neuropathy

Tsukaguchi¹,

Shibano²,

Matsuura³

et al. 2013

JBM

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Peripheral neuropathy (PN) caused by bortezomib is an important complication of multiple myeloma. Subcutaneous injection of bortezomib reduced PN, but 24% of cases were grade 2 PN and 6% of cases were grade 3 PN. PN higher than grade 2 was not resolved by subcutaneous injection. PN higher than grade 3 has serious dose limiting toxicity and is the cause of discontinuing bortezomib treatment. Lafutidine is an H2-blocker with gastroprotective activity and is thought to function by increasing mucosal blood flow via capsaicin sensitive neurons. The same activity of lafutidine is considered to improve glossodynia and taxane induced PN. We hypothesized that lafutidine prevents or improves PN that is caused by bortezomib. In the current study, bortezomib was administered in the usual manner (intravenous administration of bortezomib 1.3 mg/m2, twice a week for 2 weeks, followed by 1 week without treatment) for up to four cycles to compare our data with other studies. Lafutidine was administered orally at a dose of 10 mg twice daily. In our eight evaluated cases, the total occurrence of PN was four out of eight patients (50%). There were only grade 1 PN (4 out of 8) cases, and no cases higher than grade 2. We conclude that (1) the total occurrence of PN was not improved, (2) there was no PN after the first course, (3) there were only grade 1 cases and there were no cases higher than grade 2, and (4) no cases discontinued bortezomib treatment because of PN. This is the first report showing that lafutidine is useful for the amelioration of bortezomib induced PN.

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Efficacy of lafutidine, a histamine H2-receptor antagonist, for taxane-induced peripheral neuropathy in patients with gynecological malignancies

Cited by 11 publications

References 11 publications

Taxane and epothilone‐induced peripheral neurotoxicity: From pathogenesis to treatment

Taxane and epothilone‐induced peripheral neurotoxicity: From pathogenesis to treatment

The Prophylactic Effects of a Traditional Japanese Medicine, Goshajinkigan, on Paclitaxel-Induced Peripheral Neuropathy and its Mechanism of Action

The protective effects of lafutidine for bortezomib induced peripheral neuropathy

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