Li-Kai Wang, MD, MSc^1,2, Shu-Wei Liao, MD^1,3, Wei-Cheng Liu, MD^1,4, Yu-Li Pang, MD^1,5,6, Yao-Tsung Lin, MD, MSc⁷, Jen-Yin Chen, MD, PhD^1,8*

¹Department of Anesthesiology, Chi Mei Medical Center, Tainan, Taiwan

²School of Medicine, Chung Shan Medical University, Taichung, Taiwan

³Center of General Education, Chia Nan University of Pharmacy and Science, Tainan, Taiwan

⁴Department of Occupational Therapy, Shu-Zen Junior College of Medicine and Management, Kaohsiung, Taiwan

⁵Department of Nursing, Shu-Zen Junior College of Medicine and Management, Kaohsiung, Taiwan

⁶Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan

⁷Department of Anesthesiology, Chi Mei Medical Center, Chiali, Tainan, Taiwan

⁸School of Medicine, College of Medicine, National Sun Yat-sen University, Kaohsiung, Taiwan

^*Corresponding Author: Jen-Yin Chen, MD, PhD, Department of Anesthesiology, Chi Mei Medical Center, No. 901, Zhonghua Road, Yongkang District, Tainan 71004, Taiwan, Tel: +886-6-2812811; Fax: +886-6-2830122

Received: 29 March 2026; Accepted: 02 April 2026; Published: 01 May 2026

Article Information

Citation: Li-Kai Wang, Shu-Wei Liao, Wei- Cheng Liu, Yu-Li Pang, Yao-Tsung Lin, Jen-Yin Chen. Combined Intravenous Selenium, Zinc, and Magnesium Therapy for Refractory Chemotherapy- Induced Peripheral Neuropathy: A Case Report. Archives of Clinical and Medical Case Reports. 10 (2026): 96-99.

DOI: 10.26502/acmcr.96550757

Abstract

Keywords

Chemotherapy; Peripheral neuropathy; Selenium; Zinc; Magnesium

Article Details

1. Introduction

Chemotherapy-induced peripheral neuropathy (CIPN) is a common dose-limiting side effect of cancer treatment, resulting from damage to peripheral nerves. This condition manifests as numbness, tingling, and neuropathic pain in the distal extremities, which profoundly impacts the quality of life of cancer survivors. Duloxetine is the only agent currently recommended by the American Society of Clinical Oncology (ASCO) for the treatment of painful CIPN [1]; however, its clinical utility remains limited by modest efficacy and poor patient tolerability. Consequently, the management of established CIPN continues to be a significant therapeutic challenge.

Recent clinical evidence has highlighted the potential of high-dose intravenous selenium (2,000 µg), administered prior to each chemotherapy cycle with platinum-based regimens, in reducing the incidence and severity of CIPN in cancer patients [2,3]. Furthermore, zinc and magnesium sulfate have been investigated as promising adjunctive therapies for neuropathic pain [4-6]. In this report, we describe a case of severe, refractory CIPN following taxane-platinum therapy in a patient with non-small cell lung cancer (NSCLC). The introduction of a multimodal intravenous nutrient cocktail—consisting of selenium, zinc, and magnesium—was associated with substantial symptomatic relief and a near-complete restoration of physical function.

2. Case Presentation

A 68-year-old female (height 154 cm, weight 56 kg, BMI 23.6) with Anaplastic Lymphoma Kinase (ALK)-mutant NSCLC presented with progressive, debilitating CIPN following a complex oncological history. Her previous treatments included surgical resection followed by a four-year regimen involving nivolumab, paclitaxel, carboplatin, and bevacizumab, supplemented by concurrent chemoradiotherapy, pemetrexed, and crizotinib for her ALK-positive disease. During treatment, she developed severe neurotoxicity, manifesting as persistent erythema of the extremities, distal numbness, dysesthesia, hyperesthesia, and excruciating tingling and needling pain. Her pain was rated 9/10 on the numeric rating scale (NRS 0-10) and led to profound sleep disturbances.

The neurological impairment advanced to sensory ataxia, resulting in frequent dropping of objects and a complete inability to perform fine motor tasks such as using chopsticks or spoons, despite having discontinued paclitaxel and carboplatin several months earlier. Her symptoms remained refractory, with pain scores persisting at 7/10 for nearly eight months despite therapeutic trials of duloxetine, pregabalin, and morphine. These conventional agents were poorly tolerated due to significant adverse effects including dry mouth, dizziness, fatigue, and anorexia. She experienced three falls attributed to impaired proprioception and dizziness, necessitating supportive interventions. The patient subsequently presented to our pain clinic for further management.

Her clinical picture was consistent with cumulative neurotoxicity from taxane-platinum therapy, manifesting as a “coasting phenomenon” where neuropathic features persist or worsen after treatment cessation. In contrast, nivolumab, bevacizumab, pemetrexed, and crizotinib are not typically associated with CIPN. She had received nutrient supplementation, including Kentamin (a vitamin B complex preparation containing thiamine [B1] 50 mg, pyridoxine [B6] 50 mg, and cyanocobalamin [B12] 500 µg) at one capsule daily, together with vitamin C 1000 mg and vitamin D3 4000 IU daily for one year. Nutrient analysis demonstrated serum selenium (113 µg/L) and magnesium (1.9 mg/dL) concentrations at the lower limits of the reference range, alongside a definitive zinc deficiency (68 µg/dL). (Reference range: selenium 70-190 µg/L; magnesium 1.9-2.5 mg/dL; zinc 70-120 µg/dL.) An experimental intravenous nutrient cocktail was subsequently initiated, comprising 4 mL of sodium selenite (containing 50 µg/mL elemental selenium), 10 mL of zinc sulfate (containing 5 mg/mL elemental zinc), and 10 mL of magnesium sulfate (containing 98.6 mg/mL elemental magnesium), diluted in 250 mL of normal saline, administered twice weekly as a 2-hour infusion. After four weeks of treatment, pain intensity decreased from NRS 9/10 to 5/10. The area of numbness reduced from the entire palm to approximately half of the distal palm. The regimen was subsequently adjusted to once-weekly infusions of 2 mL of sodium selenite, 5 mL of zinc sulfate, and 10 mL of magnesium sulfate in 100 mL of normal saline, combined with oral supplementation of selenium (200 µg/day) and zinc (10 mg/day) for two months. Following this adjustment, pain intensity further decreased to 3/10, and numbness was localized to the distal metacarpal region. The intravenous infusion, combined with oral supplementation of selenium (100 µg/day) and zinc (10 mg/day), was subsequently reduced to once every two weeks for two months. Over five months, her pain gradually decreased from NRS 9/10 to 0/10, accompanied by a near-complete restoration of hand function and a significant reduction in fall risk. Serum nutrient levels normalized in parallel with clinical recovery: selenium rose to 218 µg/L, zinc to 98 µg/dL, and magnesium to 2.1 mg/dL.

3. Discussion

This case illustrates that targeted, multimodal intravenous nutrient therapy may effectively reverse established, refractory CIPN, offering a robust therapeutic alternative when conventional pharmacological interventions fail.

The diagnosis of CIPN is established from clinical history and symptom characterization [1]. In this case, the patient’s presentation was consistent with the known cumulative neurotoxicity of paclitaxel and carboplatin, further complicated by the coasting phenomenon. Paclitaxel, a taxane, stabilizes microtubules and disrupts axonal transport, resulting in mitochondrial dysfunction, glial activation, and ion channel changes that drive neuroinflammation and neuronal hyperexcitability [7-9]. Meanwhile, platinum agents such as oxaliplatin cause CIPN via DNA adducts formation, mitochondrial dysfunction, oxidative stress, and ion channel dysregulation, resulting in axonal degeneration and apoptosis of dorsal root ganglion neurons [9,10]. These effects of taxane-platinum regimens induce oxidative stress, energy depletion, and sensory dysfunction, leading to CIPN via distinct pathways [9].

Standard management strategies for CIPN remain inadequate. While duloxetine is the only agent recommended by ASCO [1], its benefit is limited in certain cases. Pregabalin was effective in relieving neuropathic pain in some studies [11,12], whereas morphine is not recommended [1]. In our case, the therapeutic effects of duloxetine, pregabalin, and morphine were limited, while their adverse effects proved intolerable. Consequently, non-pharmacological alternative approaches such as nutritional supplements are warranted [6]. Our findings suggest that correcting micronutrient deficiencies through intravenous administration can bypass gastrointestinal absorption barriers frequently seen in cancer patients, providing rapid therapeutic concentrations of neuroprotective elements. Clinical trials demonstrated efficacy and safety of high-dose intravenous selenium (2,000 µg/day) in CIPN [2,3]. However, transient adverse effects such as nausea and gastrointestinal upset were reported in some patients [13]. Current evidence indicates that multimodal nutritional strategies are more promising than single-agent monotherapy for preventing or mitigating CIPN [14]. To our knowledge, this is the first reported case in which intravenous nutrient cocktail therapy—including selenium, zinc, and magnesium—effectively managed CIPN.

In our case, nutrient analysis revealed low-normal selenium and magnesium with concurrent zinc deficiency. Cancer survivors with CIPN show lower intake of selenium [15] and magnesium [16], while peripheral neuropathy is linked to acute zinc deficiency in guinea pigs [17]. The synergistic effect of selenium, zinc, and magnesium addresses multiple pathogenic pathways. Mechanistically, selenium mitigates CIPN by stabilizing mitochondrial function, reducing apoptosis, and enhancing antioxidant defenses. It downregulates nuclear factor kappa B (NF-κB) and pro-inflammatory cytokines, limits calcium influx mediated by TRPV₁ (transient receptor potential vanilloid 1), and modulates ion channel activity, thereby decreasing neuroinflammation, neuronal hyperexcitability, and neuropathic pain [14,18]. Zinc inhibits N-methyl-D-aspartate (NMDA) receptors in the spinal dorsal horn and TRPV₁ channels in dorsal root ganglion neurons [4,19], both of which are key mediators of nociceptive signaling and neuropathic pain. Through zinc transporter-mediated inhibition of TRPV₁, zinc reduces calcium influx and paclitaxel-induced hypersensitivity [19]. In addition, zinc attenuates pro-inflammatory cytokine release, stabilizes neuronal membranes, and supports antioxidant defenses by serving as a cofactor for antioxidant enzymes, including superoxide dismutase, thereby limiting peripheral sensitization and oxidative stress-related axonal injury [14]. Magnesium mitigates CIPN by acting as a natural calcium antagonist, limiting NMDA receptor and voltage-gated calcium channel influx [20], thereby preserving mitochondrial integrity and preventing neuronal apoptosis. It supports ATP-dependent metabolism, suppresses NF-κB–mediated inflammation, and reduces oxidative stress, ultimately stabilizing sensory neuron excitability and alleviating neuropathic pain [14]. Our outcomes with a multi-nutrient approach are promising for mitigating CIPN, given its complex pathogenesis and the complementary mechanisms of action of these nutrients.

In conclusion, this case demonstrates that a multimodal intravenous nutrient cocktail consisting of selenium, zinc, and magnesium can provide rapid and durable symptomatic relief in patients with severe, refractory CIPN. By simultaneously targeting oxidative stress, mitochondrial stability, and NMDA-mediated excitotoxicity, this regimen successfully reversed sensory ataxia and excruciating pain where conventional pharmacotherapy failed. Given the excellent safety profile and measurable functional recovery observed, further clinical trials are warranted to validate this nutritional intervention as a viable adjunct in oncological supportive care, particularly for patients who are intolerant to guideline-recommended medications [2,3,14].

Conflicts of Interest

The authors declare no conflicts of interest.

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