A Pilot Study on the Effect of Acetyl-L-Carnitine in Paclitaxel-And Cisplatin-Induced Peripheral Neuropathy

2005 ◽  
Vol 91 (2) ◽  
pp. 135-138 ◽  
Author(s):  
Antonio Maestri ◽  
Adolfo De Pasquale Ceratti ◽  
Sante Cundari ◽  
Claudio Zanna ◽  
Enrico Cortesi ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Exploratory Study ◽  
Renal Toxicity ◽  
Chemotherapeutic Agents ◽  
Bone Marrow Suppression ◽  
Antitumor Therapy ◽  
Therapy Discontinuation ◽  
Double Blind ◽  
Who Grade ◽  
Regimen Modification

Aims and background In addition to bone marrow suppression and renal toxicity, neurotoxicity is a commonly occurring side effect of widely used chemotherapeutic agents like taxanes, cisplatin and vinca alkaloids. Neurotoxicity can cause antitumor therapy discontinuation or dose regimen modification. The aim of the present exploratory study was to investigate the activity of acetyl-L-carnitine in reversing peripheral neuropathy in patients with chemotherapy-induced peripheral neuropathy. Methods and study design Twenty-seven patients (16 males and 11 females) with paclitaxel and/or cisplatin-induced neuropathy (according to WHO recommendations for the grading of acute and subacute toxic effects) were enrolled. Patients received at least one cisplatin- (n = 5) or one paclitaxel- (n = 11) based regimen, or a combination of both (n = 11). Patients with chemotherapy-induced peripheral neuropathy were treated with acetyl-L-carnitine 1 g/die iv infusion over 1-2 h for at least 10 days. Results Twenty-six patients were evaluated for response having completed at least 10 days of acetyl-L-carnitine therapy (median, 14 days; range, 10-20). At least one WHO grade improvement in the peripheral neuropathy severity was shown in 73% of the patients. A case of insomnia related to ALC treatment was reported in one patient. Acetyl-L-carnitine seems to be an effective and well-tolerated agent for the treatment of chemotherapy-induced peripheral neuropathy. Conclusions Our preliminary results should be confirmed in double-blind, placebo controlled studies.

The Therapeutic Potential of Chemokines in the Treatment of Chemotherapy- Induced Peripheral Neuropathy

2020 ◽  
Vol 21 (3) ◽  
pp. 288-301 ◽  
Author(s):  
Lin Zhou ◽  
Luyao Ao ◽  
Yunyi Yan ◽  
Wanting Li ◽  
Anqi Ye ◽  
...  
Keyword(s):  
Nervous System ◽  
Neuropathic Pain ◽  
Immune System ◽  
Peripheral Neuropathy ◽  
Immune Cell ◽  
Therapeutic Potential ◽  
Chemotherapeutic Agents ◽  
Cell Trafficking ◽  
Mediated Communication ◽  
Novel Therapeutic Strategies

Background: Some of the current challenges and complications of cancer therapy are chemotherapy- induced peripheral neuropathy (CIPN) and the neuropathic pain that are associated with this condition. Many major chemotherapeutic agents can cause neurotoxicity, significantly modulate the immune system and are always accompanied by various adverse effects. Recent evidence suggests that cross-talk occurs between the nervous system and the immune system during treatment with chemotherapeutic agents; thus, an emerging concept is that neuroinflammation is one of the major mechanisms underlying CIPN, as demonstrated by the upregulation of chemokines. Chemokines were originally identified as regulators of peripheral immune cell trafficking, and chemokines are also expressed on neurons and glial cells in the central nervous system. Objective: In this review, we collected evidence demonstrating that chemokines are potential mediators and contributors to pain signalling in CIPN. The expression of chemokines and their receptors, such as CX3CL1/CX3CR1, CCL2/CCR2, CXCL1/CXCR2, CXCL12/CXCR4 and CCL3/CCR5, is altered in the pathological conditions of CIPN, and chemokine receptor antagonists attenuate neuropathic pain behaviour. Conclusion: By understanding the mechanisms of chemokine-mediated communication, we may reveal chemokine targets that can be used as novel therapeutic strategies for the treatment of CIPN.

scholarly journals Melittin, a honeybee venom derived peptide for the treatment of chemotherapy-induced peripheral neuropathy

2021 ◽  
Vol 38 (5) ◽  
Author(s):  
Tenzin Tender ◽  
Rakesh Ravishankar Rahangdale ◽  
Sridevi Balireddy ◽  
Madhavan Nampoothiri ◽  
K. Krishna Sharma ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Motor Nerve ◽  
Symptomatic Relief ◽  
Neurological Complication ◽  
Treatment Protocol ◽  
Chemotherapeutic Agents ◽  
Lens Protein ◽  
Active Constituent ◽  
Honeybee Venom ◽  
Eye Lens Protein

Abstract Chemotherapy-induced peripheral neuropathy (CIPN) is the most prevalent neurological complication of cancer treatment which involves sensory and motor nerve dysfunction. Severe CIPN has been reported in around 5% of patients treated with single and up to 38% of patients treated with multiple chemotherapeutic agents. Present medications available for CIPN are the use of opioids, nonsteroidal anti-inflammatory agents, and tricyclic antidepressants, which are only marginally effective in treating neuropathic symptoms. In reality, symptom reappears after these drugs are discontinued. The pathogenesis of CIPN has not been sufficiently recognized and methods for the prevention and treatment of CIPN remain vulnerable to therapeutic problems. It has witnessed that the present medicines available for the disease offer only symptomatic relief for the short term and have severe adverse side effects. There is no standard treatment protocol for preventing, reducing, and treating CIPN. Therefore, there is a need to develop curative therapy that can be used to treat this complication. Melittin is the main pharmacological active constituent of honeybee venom and has therapeutic values including in chemotherapeutic-induced peripheral neuropathy. It has been shown that melittin and whole honey bee venom are effective in treating paclitaxel and oxaliplatin-induced peripheral neuropathy. The use of melittin against peripheral neuropathy caused by chemotherapy has been limited despite having strong therapeutic efficacy against the disease. Melittin mediated haemolysis is the key reason to restrict its use. In our study, it is found that α-Crystallin (an eye lens protein) is capable of inhibiting melittin-induced haemolysis which gives hope of using an appropriate combination of melittin and α-Crystallin in the treatment of CIPN. The review summarizes the efforts made by different research groups to address the concern with melittin in the treatment of chemotherapeutic-induced neuropathy. It also focuses on the possible approaches to overcome melittin-induced haemolysis. Graphic Abstract

Efficacy of topical Citrullus colocynthis (bitter apple) extract oil in chemotherapy‐induced peripheral neuropathy: A pilot double‐blind randomized placebo‐controlled clinical trial

2019 ◽  
Vol 33 (10) ◽  
pp. 2685-2691 ◽  
Author(s):  
Nematollah Rostami ◽  
Seyed Hamdollah Mosavat ◽  
Ghazaleh Heydarirad ◽  
Roya Arbab Tafti ◽  
Mojtaba Heydari
Keyword(s):  
Clinical Trial ◽  
Peripheral Neuropathy ◽  
Controlled Clinical Trial ◽  
Citrullus Colocynthis ◽  
Double Blind

scholarly journals Herbal Medicine Goshajinkigan Prevents Paclitaxel-Induced Mechanical Allodynia without Impairing Antitumor Activity of Paclitaxel

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Muh. Akbar Bahar ◽  
Tsugunobu Andoh ◽  
Keisuke Ogura ◽  
Yoshihiro Hayakawa ◽  
Ikuo Saiki ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Herbal Medicine ◽  
Tumor Growth ◽  
Mechanical Allodynia ◽  
Chemotherapeutic Agents ◽  
Antitumor Action ◽  
Effective Strategies ◽  
Anti Cancer ◽  
Mammary Fat Pad ◽  
4T1 Cells

Chemotherapy-induced peripheral neuropathy is a major dose-limiting side effect of commonly used chemotherapeutic agents. However, there are no effective strategies to treat the neuropathy. We examined whether Goshajinkigan, a herbal medicine, would prevent paclitaxel-induced allodynia without affecting the anticancer action in mice. Murine breast cancer 4T1 cells were inoculated into the mammary fat pad. Paclitaxel (10 and 20 mg/kg, intraperitoneal, alternate day from day 7 postinoculation) inhibited the tumor growth, and Goshajinkigan (1 g/kg, oral, daily from day 2 postinoculation) did not affect the antitumor action of paclitaxel. Mechanical allodynia developed in the inoculated region due to tumor growth and in the hind paw due to paclitaxel-induced neuropathy. Paclitaxel-induced allodynia was markedly prevented by Goshajinkigan, although tumor-associated allodynia was not inhibited by Goshajinkigan. These results suggest that Goshajinkigan prevents paclitaxel-induced peripheral neuropathy without interfering with the anti-cancer action of paclitaxel.

scholarly journals Chronic inflammatory demyelinating polyradiculoneuropathy induced by paclitaxel

2021 ◽  
Author(s):  
Isabella Sabião Borges ◽  
João Victor Aguiar Moreira ◽  
Eustaquio Costa Damasceno Junior ◽  
Alencar Pereira dos Santos ◽  
Gabriela Tomás Alves ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Glial Cells ◽  
Conduction Block ◽  
Chemotherapeutic Agents ◽  
Chronic Inflammatory Demyelinating Polyradiculoneuropathy ◽  
Microtubule Stabilization ◽  
Progressive Muscle Weakness ◽  
History Of ◽  
Secondary Demyelination ◽  
Distal Axonal Degeneration

Background: Peripheral neuropathies in cancer are most often due to neurotoxic chemotherapeutic agents. Approximately 30% of patients receiving neurotoxic chemotherapy (CTX) will suffer from chemotherapy-induced peripheral neuropathy (CIPN). Paclitaxel is an extremely effective chemotherapeutic agent for the treatment of breast, ovarian, and lung cancer. However, paclitaxel-induced peripheral neuropathy occurs in 59-87% of patients who receive this drug. Paclitaxel is an anti-tubulin drug that causes microtubule stabilization, resulting in distal axonal degeneration, secondary demyelination and nerve fiber loss. Case: We present a case of a 68-year-old female patient with history of breast cancer who presented sensorial ataxia and progressive muscle weakness two months after starting CTX with paclitaxel. The physical examination showed tetraparesis with proximal predominance, areflexia, severe hypopalesthesia and postural instability. Electroneuromyography showed the existence of asymmetric demyelinating polyradiculoneuropathy, with conduction block and temporal dispersion in practically all evaluated nerves. The cerebrospinal fluid confirmed the albumin-cytological dissociation. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) was confirmed and patient underwent monthly treatment with methylprednisolone with good response. Discussion: Evidences has implicated neuroinflammation in the development of PIPN. While most CTX drugs do not cross the blood-brain-barrier, they readily penetrate the blood-nerve-barrier and bind to and accumulate in dorsal root ganglia and peripheral axons. CTX can induce neuroinflammation through activation of immune and immune- like glial cells. In fact, immune cells (e.g., macrophages, lymphocytes) and glial cells (e.g., Schwann cells) in the peripheral nervous system play important role in the induction and maintenance of neuropathy. Conclusion: CIDP should be included in the spectrum of CIPN.

Sign in / Sign up

Export Citation Format

Share Document