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Chlorine Level as a Predictive Factor for Oxaliplatin-induced Peripheral Neuropathy  [PDF]
Shamim Hossain,Shahedur Rahman,Ashrafuzzaman Zahid
Journal of Medical Sciences , 2011,
Abstract: Peripheral neuropathy is a major adverse event associated with oxaliplatin-based chemotherapy and is a major dose-limiting adverse event in clinical practice. However, some patients treated with oxaliplatin may show no or minimal peripheral neuropathy. These differences are still poorly understood. This study was carried out as a retrospective analysis of 77 patients data that had been treated with oxaliplatin-based regimens at the South Dhaka Medical Center between January 2005 and June 2010. Among them 51 patients data were selected and factor analysis was performed. The serum Chlorine (Cl) level at baseline was significantly higher in patients with a high frequency of peripheral neuropathy (106; range 104-107 vs. 104; range 101-104 mEq L-1, p = 0.02). Principal component analysis showed the variables Cl, body mass index, status of liver metastasis and status of lymph node metastasis were related to the incidence of peripheral neuropathy. Discriminant analysis showed the model had predicted 72.5% of peripheral neuropathy. An understanding of the patients characteristics could be useful for preventing or predicting oxaliplatin-induced peripheral neuropathy.
Efficacy of Goshajinkigan for Oxaliplatin-Induced Peripheral Neuropathy in Colorectal Cancer Patients  [PDF]
Naohisa Yoshida,Toyoshi Hosokawa,Takeshi Ishikawa,Nobuaki Yagi,Satoshi Kokura,Yuji Naito,Masayoshi Nakanishi,Yukihito Kokuba,Eigo Otsuji,Haruo Kuroboshi,Masafumi Taniwaki,Tetsuya Taguchi,Hajime Hosoi,Terukazu Nakamura,Tsuneharu Miki
Journal of Oncology , 2013, DOI: 10.1155/2013/139740
Abstract: Objective. To evaluate the efficacy of Goshajinkigan for oxaliplatin-induced peripheral neuropathy in colorectal cancer patients. Patients. Colorectal cancer patients ( ) who received ≥4 weeks of Goshajinkigan for oxaliplatin-induced peripheral neuropathy during chemotherapy at Kyoto Prefectural University of Medicine were (Goshajinkigan group) compared to 44 patients who had not received Goshajinkigan during the same period (non-Goshajinkigan group). Main Outcome Measures. The effect of Goshajinkigan was graded as curative, effective, stabilizing, or deleterious. The relationships between the grade of peripheral neuropathy and the dose of oxaliplatin in the Goshajinkigan and non-Goshajinkigan groups were evaluated. Results. The effect of Goshajinkigan on peripheral neuropathy in the Goshajinkigan group was curative, effective, stabilizing, and deleterious in 3.4, 20.7, 69.0, and 6.9% of patients, compared to the effect in the non-Goshajinkigan group (4.5, 15.9, 45.5, and 34.1%). The ratio of deleterious effects was significantly different between these two groups ( ). A Kaplan-Meier analysis in relation to the cumulative dose of oxaliplatin showed that the incidence of grade 3 peripheral neuropathy tended to be less in the Goshajinkigan group ( ). There were no significant differences in time to treatment failure and severe adverse events between these two groups. Conclusions. Goshajinkigan prevented exacerbation of oxaliplatin-induced peripheral neuropathy. This trial is registered with UMIN000009956 1. Introduction Oxaliplatin-based chemotherapy regimens such as XELOX (CapeOX) and FOLFOX have gained acceptance worldwide as first-line therapies in advanced or recurrent colorectal cancer; subsequently, the incidence of the often intractable oxaliplatin-induced peripheral neuropathy also continues to rapidly increase [1]. Peripheral neuropathy occurs in approximately 80% of the patients receiving oxaliplatin-based chemotherapy. Grade 3 peripheral neuropathy affects approximately 15% of the patients after a cumulative dose of 800?mg/m2 and requires discontinuation of therapy [2]. The unique direct effect of oxaliplatin on nerve excitability has been attributed to one of its metabolites, oxalate, which is a calcium chelator that alters voltage-gated Na+ channels. In experimental models, acute dysfunction of Na+ channels is correlated with axonal loss and degeneration [3]. Furthermore, cumulative neurotoxicity may be related to direct toxicity of the dorsal root ganglia [4]. The hallmarks of oxaliplatin-induced peripheral neuropathy are paresthesia and
Self-Management of Oxaliplatin-Related Peripheral Neuropathy in Colorectal Cancer Survivors  [PDF]
Cindy Tofthagen,Laura Gonzalez,Constance Visovsky,Alex Akers
Chemotherapy Research and Practice , 2013, DOI: 10.1155/2013/547932
Abstract: Purpose. The purpose of this study was to evaluate medications that cancer survivors with oxaliplatin-induced peripheral neuropathy take to control neuropathic symptom, and to explore self-management techniques used at home to provide temporary relief of painful neuropathy. This was a mixed methods, descriptive, cross-sectional study using self-reported data from colorectal cancer survivors previously treated with oxaliplatin. We analyzed demographic and medication data obtained from participants, along with written comments from an open-ended question regarding methods participants had tried to self-manage symptoms of neuropathy. Results. Twenty-nine percent of the sample reported taking some type of nutritional supplement with potential neuroprotective qualities. Opioids were being taken by 10% of the sample, and nonsteroidal anti-inflammatory and over-the-counter medications were taken by 15% of participants. Twelve percent of participants were taking antidepressants and 10% were taking anticonvulsants, primarily gabapentin. Recurrent themes for nonpharmacologic treatment included avoiding the cold/keeping warm, keeping moving, massaging or rubbing the affected area, and living with it. Conclusions. Patients treated with oxaliplatin for colorectal cancer utilize a variety of traditional pharmacologic agents and nutritional supplements in an effort to self-manage neuropathic symptoms. Patients also employ a variety of home-based therapies to provide temporary relief of peripheral neuropathy symptoms. 1. Introduction Oxaliplatin is a highly neurotoxic chemotherapy drug routinely used to treat colorectal cancer in the adjuvant and metastatic disease settings [1]. Among the approximately 100,000 persons diagnosed with colon cancer each year, approximately 60% will be candidates to receive oxaliplatin-based chemotherapy [2]. At least 48% of patients who receive oxaliplatin will develop chronic peripheral neuropathy that arises during treatment, and still more patients will go on to develop chronic neuropathy after cessation of treatment, a phenomenon known as “coasting” [3–6]. Few evidence-based interventions exist for treatment of oxaliplatin-related neuropathy [7–9]. Supportive care for peripheral neuropathy includes pain management, fall prevention, home safety education, provision of psychological support, measures to enhance or maintain physical functioning, and recommendations for assistive devices to help with daily activities [10]. In clinical practice, the focus of management of peripheral neuropathy is primarily aimed at control of neuropathic
Effect of green tea extracts on oxaliplatin-induced peripheral neuropathy in rats  [cached]
Lee Jung,Kim Yoon,Jeon Eun,Won Hye
BMC Complementary and Alternative Medicine , 2012, DOI: 10.1186/1472-6882-12-124
Abstract: Background A common side effect of oxaliplatin is peripheral neurotoxicity. Oxidative stress to dorsal root ganglion (DRG) may be one of important pathogenic mechanisms. Green tea contains four polyphenol catechins, which are known to be potent antioxidants. The present work is aimed to determine whether green tea extracts have neuroproective or palliative effects on neurotoxicity symptoms induced by oxaliplatin. Methods We conducted behavioral tests including sensory and thermal thresholds, an electrophysiological study, and TUNEL staining to assess neurotoxicity during the experimental period using animal models. Results A total of 14 adult rats were randomly allocated into two groups. Oxaliplatin (4 mg/kg) with or without green tea (300 mg/kg orally once daily) was administered intraperitoneally twice per week for 6 weeks. At 4 and 6 weeks after oxaliplatin administration, sensory threshold values were significantly decreased and at 6 weeks after oxaliplatin administration, thermal threshold values were significantly increased in oxaliplatin-treated rats compared with those in rat treated with oxaliplatin and green tea extracts. The electrophysiological assessment, including sensory nerve conduction and H-reflex-related sensory nerve conduction velocity, revealed no significant changes in the two groups. TUNEL staining showed no significant difference in the number of apoptotic-featured cells between the two experimental groups in the DRG or peripheral nerves, but the number of apoptotic-featured cells in DRG was higher than that in sciatic nerves within each group. Conclusions Green tea extracts may be a useful adjuvant to alleviate sensory symptoms after oxaliplatin administration, such as allodynia, but did not prevent morphometric or electrophysiological alterations induced by oxaliplatin.
Multimodal assessment of painful peripheral neuropathy induced by chronic oxaliplatin-based chemotherapy in mice
Cynthia L Renn, Valentina A Carozzi, Peter Rhee, Danisha Gallop, Susan G Dorsey, Guido Cavaletti
Molecular Pain , 2011, DOI: 10.1186/1744-8069-7-29
Abstract: We found significantly decreased NCV and action potential amplitude after oxaliplatin treatment along with neuronal atrophy and multinucleolated DRG neurons that have eccentric nucleoli. Oxaliplatin also induced significant mechanical allodynia and cold hyperalgesia, starting from the first week of treatment, and a significant increase in the activity of wide dynamic range neurons in the SDH.Our findings demonstrate that chronic treatment with oxaliplatin produces neurotoxic changes in BALB/c mice, confirming that this model is a suitable tool to conduct further mechanistic studies of oxaliplatin-related antineoplastic activity, peripheral neurotoxicity and pain. Further, this model can be used for the preclinical discovery of new neuroprotective and analgesic compounds.Oxaliplatin is an effective platinum-based drug used as first line chemotherapy for metastatic colorectal cancer [1]. Moreover it has been used to treat some cisplatin-resistant cancers, including those of the stomach [2], pancreas [3], ovary [4], breast and lung [5]. Oxaliplatin induces DNA crosslinks that cause apoptotic death of dividing cells [6] and reduced tumor growth. Unfortunately, the platinum derivative drugs have a molecular affinity for the peripheral nervous system [7,8], leading to severe peripheral neurotoxicity that affects most cancer patients treated with oxaliplatin-based chemotherapy. Oxaliplatin-induced peripheral neuropathy is clinically characterized by two different types of neurological symptoms [9]. One type, occurring in 90% of patients, is an acute, transient syndrome characterized by cramps, paresthesias and dysesthesias that are triggered or enhanced by exposure to cold. The second type is a chronic [9] and more severe syndrome that is characterized by the loss of sensory perception and frequently associated with painful sensations that generally occur after repeated drug administration. The mechanisms underlying the development of oxaliplatin-induced neurotoxicity rema
The slipping slipper sign: a simple test with high specificity and positive predictive value for peripheral neuropathy among diabetic patients  [cached]
Krystal A.T. Gayle,Marshall K. Tulloch-Reid,Rainford J. Wilks,Trevor S. Ferguson
Clinics and Practice , 2012, DOI: 10.4081/cp.2012.e51
Abstract: This study evaluated the ability of the slipping slipper sign (defined as unknowingly losing a slipper while walking) to identify diabetic neuropathy in Jamaican patients. A single question was used to ascertain the presence of the slipping slipper sign (SSS) among 69 patients attending a diabetes clinic. Nurses assessed pain, vibration and pressure perception among the same patients in order to detect diabetic neuropathy. The sensitivity, specificity and positive predictive value for the SSS were calculated. Eight participants (men=5, women=3) reported positive SSS. The SSS had a sensitivity of 28.6%, specificity of 100% and positive predictive value (PPV) 100% for neuropathy on at least one of the three tests. These findings indicate that the SSS has high specificity and PPV for diabetic neuropathy but the sensitivity is low. The sign may be a useful adjuvant to conventional methods of screening for severe neuropathy
Oxaliplatin-Induced Neuropathy in Colorectal Cancer  [PDF]
Andrew Weickhardt,Keith Wells,Wells Messersmith
Journal of Oncology , 2011, DOI: 10.1155/2011/201593
Abstract: Oxaliplatin use in palliative and adjuvant treatment of colon cancer is frequently limited by cumulative neurotoxicity, leading to reduced quality of life and decreased dose. The mechanism of this neurotoxicity is unclear, but may relate to neuronal voltage-gated sodium channels involving calcium chelation by a metabolite of the drug. Various preventative measures have been tested to reduce the incidence of neurotoxicity, including calcium and magnesium infusions, dose interruption of the drug, and prophylactic neuromodulatory agents. Despite the promising efficacy of these measures, they are not universally accepted. Less is known about the best way to treat established neurotoxicity, which is permanent in some patients, although venlafaxine has shown promise in small clinical trials. This paper analyzes the extent, cause and risk factors for neuropathy, and the potential preventative and therapeutic treatments for oxaliplatin-induced neuropathy. 1. Introduction Oxaliplatin is a 3rd-generation platinum-based chemotherapeutic, possessing the 1,2 diaminocyclohexane-containing carrier ligand, useful in treating advanced colorectal cancer. It is often used in combination regimens with 5-flourouracil [1], capecitabine [2], or 5-flourouracil/irinotecan [3] for the treatment of colorectal cancer. Oxaliplatin has also been studied in clinical trials for the treatment of other cancers but has found the most success in gastrointestinal neoplasms including gastric, esophageal, and pancreatic cancers [4]. Platinum-based chemotherapeutics have effect via cell phase nonspecific mechanisms causing the formation of cross-linking DNA adducts, leading to strand breaks and inhibition of DNA replication [5]. Oxaliplatin produces common side effects of cytopenias, peripheral neuropathy, diarrhea, and nausea [4]. Oxaliplatin-induced neurotoxicity (OXIN) is a recognized dose-limiting complication [6]. This paper analyzes the extent, cause and risk factors for neuropathy, and the potential preventative and therapeutic treatments for OXIN. 2. Extent of Problem OXIN demonstrates two clinically significant types: acute and chronic. Neither type has its mechanism of action fully elucidated. Acute OXIN usually begins with paresthesias and dysesthesias of the hands and feet, but may include the mouth or throat [7]. Its onset may begin during the initial infusion or up to 1-2 days following the administered dose and is often triggered by cold. Typically, the symptoms will resolve spontaneously within days, but often return upon subsequent oxaliplatin administration. It is associated
Mice with cisplatin and oxaliplatin-induced painful neuropathy develop distinct early responses to thermal stimuli
Lauren E Ta, Philip A Low, Anthony J Windebank
Molecular Pain , 2009, DOI: 10.1186/1744-8069-5-9
Abstract: We have established mouse models of cisplatin and oxaliplatin-induced neuropathy using doses similar to those used in patients. Adult male C57BL6J mice were treated with daily intraperitoneal injection for 5 days, followed by 5 days of rest, for two cycles. Total cumulative doses of 23 mg/kg cisplatin and 30 mg/kg oxaliplatin were used. Behavioral evaluations included cold plate, von Frey, radiant heat, tail immersion, grip strength and exploratory behavior at baseline and at weekly intervals for 8 weeks. Following two treatment cycles, mice in the cisplatin and oxaliplatin treatment groups demonstrated significant mechanical allodynia compared to control mice. In addition, the cisplatin group exhibited significant thermal hyperalgesia in hind paws and tail, and the oxaliplatin group developed significant cold hyperalgesia in hind paws.We have therefore established a model of platinum drug-induced painful peripheral neuropathy that reflects the differences in early thermal pain responses that are observed in patients treated with either cisplatin or oxaliplatin. This model should be useful in studying the molecular basis for these different pain responses and in designing protective therapeutic strategies.Cisplatin has had a central role in cancer chemotherapy for the last 40 years [1,2] and continues to be among the most widely-used antineoplastic drugs in clinical use [3,4]. Cisplatin displays therapeutic efficacy in a broad range of solid tumors especially against testicular, ovarian, and bladder cancers [5,6]. It exerts its antitumor activity by binding to DNA and distorting the helical structure in a way that inhibits transcription [7] and induces apoptotic cell death through DNA damage recognition pathways [8,9]. Peripheral neuropathy remains the most common dose limiting toxicity of cisplatin and limits its clinical use [10,11]. Currently, no effective treatment is available to prevent or treat chemotherapy-induced neuropathy [12].Significant cisplatin neurot
Efficacy of Goshajinkigan for Peripheral Neurotoxicity of Oxaliplatin in Patients with Advanced or Recurrent Colorectal Cancer
Toru Kono,Noriaki Mamiya,Naoyuki Chisato,Yosiaki Ebisawa,Hirotaka Yamazaki,Jiro Watari,Yasuhiro Yamamoto,Shigetaka Suzuki,Toshiyuki Asama,Kazunori Kamiya
Evidence-Based Complementary and Alternative Medicine , 2011, DOI: 10.1093/ecam/nep200
Abstract: Peripheral neurotoxicity is the major limiting factor for oxaliplatin therapy. Goshajinkigan (GJG), a traditional Japanese herbal medicine, was recently shown to be effective in protecting against the neurotoxicity of taxanes in Japan. We retrospectively investigated the effect of GJG on peripheral neurotoxicity associated with oxaliplatin therapy. Ninety patients with metastatic colorectal cancer that received FOLFOX4 or modified FOLFOX6 therapy were assigned to receive one of the following adjuncts: oral GJG at 7.5 g day−1 (Group A, =11), intravenous supplementation of calcium gluconate and magnesium sulfate (1 g each before and after FOLFOX) (Group B, =14), combined GJG and calcium gluconate and magnesium sulfate therapies (Group C, =21), or no concomitant therapy (Group D, =44). The incidence of peripheral neurotoxicity was investigated when the cumulative dose of oxaliplatin exceeded 500 mg m−2. When the cumulative dose of oxaliplatin exceeded 500 mg m−2, the incidence of neuropathy (all grades) in Groups A–D was 50.0%, 100%, 78.9%, and 91.7%, respectively. It was lowest in the group that received GJG alone. Concomitant administration of GJG reduced the neurotoxicity of oxaliplatin in patients that received chemotherapy for colorectal cancer.
Propylthiouracil and peripheral neuropathy
Boekel, Valentina Van;Godoy, José Maurício;Lamy, Luiz A.;Assuf, Samira;Meyer Neto, Jo?o G. Corrêa;Balassiano, Salim L.;Prata, Luiz E.;
Arquivos de Neuro-Psiquiatria , 1992, DOI: 10.1590/S0004-282X1992000200021
Abstract: peripheral neuropathy is a rare manifestation in hyperthyroidism. we describe the neurological manifestations of a 38 year old female with graves' disease who developed peripheral neuropathy in the course of her treatment with propylthiouracil. after the drug was tapered off, the neurological signs disappeared. therefore, we call attention for a possible toxic effect on peripheral nervous system caused by this drug.
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