RESUMEN
Extracellular vesicles (EVs), exhibiting their functional activity after internalization by recipient cells, are involved in the pathogenesis of drug-induced polyneuropathy (DIPN), a common complication of antitumor therapy. In this work, the internalization of EVs obtained from colorectal cancer patients undergoing polychemotherapy and its relationship with neurotoxicity were assessed using a model system of mononuclear leukocytes. Circulating EVs were isolated from 8 colorectal cancer patients who received antitumor therapy according to the FOLFOX or XELOX regimens before the start of chemotherapy (point 1) and after 3-4 courses (point 2). Mononuclear leukocytes of a healthy donor served as a cellular model system for EV internalization in vitro. EV internalization was assessed using fluorescence microscopy. It was shown that internalization of EVs obtained from colorectal cancer patients with high neurotoxicity was higher than in the group with low neurotoxicity. The ability of CD11b-positive (CD11bâº) and CD11b-negative (CD11bâ») mononuclear leukocytes of a healthy donor to internalize EVs obtained from patients before and after chemotherapy did not reveal significant differences. A direct relationship was found between the relative number of CD11bâ» cells with internalized EVs and the integral index of neurotoxicity according to the NRS scale at the peak of its manifestation (point 2) (r=0.675, p.
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Protocolos de Quimioterapia Combinada Antineoplásica , Vesículas Extracelulares , Leucocitos Mononucleares , Humanos , Leucocitos Mononucleares/metabolismo , Leucocitos Mononucleares/efectos de los fármacos , Vesículas Extracelulares/metabolismo , Vesículas Extracelulares/efectos de los fármacos , Masculino , Femenino , Persona de Mediana Edad , Anciano , Protocolos de Quimioterapia Combinada Antineoplásica/efectos adversos , Protocolos de Quimioterapia Combinada Antineoplásica/farmacología , Neoplasias Colorrectales/tratamiento farmacológico , Neoplasias Colorrectales/patología , Neoplasias Colorrectales/metabolismo , Fluorouracilo/efectos adversos , Fluorouracilo/farmacología , Capecitabina/efectos adversos , Capecitabina/farmacología , Antígeno CD11b/metabolismo , Compuestos Organoplatinos/efectos adversos , Compuestos Organoplatinos/farmacología , Leucovorina/farmacología , Oxaloacetatos , Adulto , Polineuropatías/inducido químicamente , Polineuropatías/metabolismo , Polineuropatías/patologíaAsunto(s)
Antibacterianos , Humanos , Antibacterianos/efectos adversos , Fluoroquinolonas/efectos adversos , Polineuropatías/inducido químicamente , Masculino , Enfermedades Desmielinizantes/inducido químicamente , Femenino , Persona de Mediana Edad , Anciano , Conducción Nerviosa/efectos de los fármacosRESUMEN
Immune checkpoint inhibitors (ICIs) have significantly improved the clinical outcome in multiple types of advanced or metastatic malignancies and are prescribed increasingly. However, immune-related adverse events (irAEs) occur frequently. Here, we present a patient with multifocal motor neuropathy and melanoma, with worsening of muscle weakness upon ICI therapy and concomitant use of steroids for the treatment of hepatitis, which was considered an irAE. Upon treatment with highly dosed immunoglobulins and steroid tapering, the patients' muscular symptoms improved while hepatitis resolved. This case highlights the importance of careful evaluation of patients with multifocal motor neuropathy treated with ICIs, highlights the risks of treatment with steroids in multifocal motor neuropathy patients and suggests an alternative treatment of irAEs with intravenous immunoglobulins.
[Box: see text].
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Inhibidores de Puntos de Control Inmunológico , Melanoma , Humanos , Inhibidores de Puntos de Control Inmunológico/efectos adversos , Inhibidores de Puntos de Control Inmunológico/uso terapéutico , Melanoma/tratamiento farmacológico , Melanoma/inmunología , Masculino , Inmunoglobulinas Intravenosas/uso terapéutico , Inmunoglobulinas Intravenosas/efectos adversos , Persona de Mediana Edad , Polineuropatías/inducido químicamente , FemeninoRESUMEN
BACKGROUND AND PURPOSE: The role of high-resolution nerve ultrasound (HRUS) and corneal confocal microscopy (CCM) in the early detection of taxane-induced polyneuropathy (TIPN) is unclear. The present prospective longitudinal controlled observational pilot study estimates the role of HRUS and CCM in the early diagnosis of TIPN in breast cancer patients. METHODS: Fifteen breast cancer patients receiving paclitaxel and 15 healthy age matched controls were included. Visits before and 3 weeks, 8 weeks and 6 months after treatment included clinical examination, the total neuropathy score, nerve conduction studies (NCS), monocular CCM including corneal nerve fibre length, density and branching and HRUS of bilateral median, ulnar, radial, tibial, peroneal and sural nerves. Patients were compared between different visits and to healthy controls. RESULTS: Total neuropathy score increased from 2.2 at baseline to 5.8 (p < 0.001) at week 8. NCS showed a decreased sensory amplitude in the sural, radial, ulnar and median nerve after 6 months (p < 0.001). HRUS revealed a significant increase of cross-sectional area in the sural nerve (p = 0.004), the median nerve (p = 0.003) at the carpal tunnel and the ulnar nerve in the forearm (p = 0.006) after 6 months. CCM showed no changes at different visits. CONCLUSIONS: Corneal confocal microscopy and HRUS do not detect early signs of TIPN during the paclitaxel treatment period. HRUS and NCS might detect congruent signs of an axonal, predominantly sensory polyneuropathy after 6 months. The clinical examination remains the most sensitive tool in the early detection of TIPN in breast cancer patients.
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Neoplasias de la Mama , Neuropatías Diabéticas , Enfermedades del Sistema Nervioso Periférico , Polineuropatías , Femenino , Humanos , Neoplasias de la Mama/tratamiento farmacológico , Neuropatías Diabéticas/diagnóstico , Microscopía Confocal , Conducción Nerviosa/fisiología , Paclitaxel , Enfermedades del Sistema Nervioso Periférico/inducido químicamente , Enfermedades del Sistema Nervioso Periférico/diagnóstico por imagen , Polineuropatías/inducido químicamente , Polineuropatías/diagnóstico por imagen , Estudios Prospectivos , Taxoides/efectos adversos , Proyectos PilotoRESUMEN
BACKGROUND AND PURPOSE: Nitrous oxide (N2 O) induced neurological symptoms are increasingly encountered. Our aim is to provide clinical and diagnostic characteristics with a focus on electrodiagnostic studies. METHODS: Patients with neurological sequelae due to N2 O presenting in our hospital between November 2018 and December 2021 reporting clinical and diagnostic data were retrospectively reviewed. RESULTS: Seventy patients (median 22 years) were included. Median N2 O usage was 4 kg/week during 12 months. Patients' history revealed a higher rate of sensory symptoms compared to motor (97% vs. 57%) and 77% walking difficulties. Clinical diagnosis was polyneuropathy (PNP) in 44%, subacute combined degeneration (SCD) of the spine in 19%, both in 37%. Median vitamin B12 level was low (159 pmol/L), normal in 16%. The median methylmalonic acid was increased (2.66 µmol/L). Electrodiagnostic abnormalities were observed in 91%, with 72% fulfilling axonal PNP criteria, 20% showing mild to intermediate slowing. One patient fulfilled demyelinating PNP criteria not related to N2 O abuse (Charcot-Marie-Tooth type 1a). More prominent motor nerve conduction abnormalities were found; lower limbs were more affected. In 64% with normal conduction, myography showed signs of axonal loss. Magnetic resonance imaging showed cervical myelopathy in 58% involving generally five to six segments. CONCLUSIONS: Nitrous oxide (N2 O) leads to neurological symptoms by causing PNP and/or SCD primarily involving the legs. Distinguishing PNP and SCD clinically was shown to be insufficient. Electrodiagnostic studies showed axonal PNP. Demyelinating PNP due to N2 O abuse was not present in our cohort. Therefore, further diagnostic work-up is warranted if demyelinating features are present.
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Enfermedad de Charcot-Marie-Tooth , Polineuropatías , Degeneración Combinada Subaguda , Humanos , Degeneración Combinada Subaguda/diagnóstico , Degeneración Combinada Subaguda/inducido químicamente , Degeneración Combinada Subaguda/complicaciones , Óxido Nitroso/efectos adversos , Estudios Retrospectivos , Polineuropatías/inducido químicamente , Polineuropatías/diagnóstico , Polineuropatías/complicaciones , Enfermedad de Charcot-Marie-Tooth/complicacionesAsunto(s)
Enfermedad de Parkinson , Polineuropatías , Humanos , Carbidopa/uso terapéutico , Levodopa/efectos adversos , Antiparkinsonianos/uso terapéutico , Enfermedad de Parkinson/tratamiento farmacológico , Combinación de Medicamentos , Polineuropatías/inducido químicamente , Polineuropatías/tratamiento farmacológicoRESUMEN
Chemoinduced polyneuropathy (CIPNP) is a common side-effect of chemotherapy, significantly impairing quality of life in patients treated for cancer. Platinum preparations are the most commonly used chemotherapeutic agents used in the treatment of ovarian, testicular, breast, lung and colon cancers. Clinical examination reveals restrictions on the motor, sensory and autonomic functions of the upper and lower extremities, which occur at different stages of antitumor treatment, seriously complicating the treatment of the underlying disease. Pain and sensory disturbances may persist for months or even years after chemotherapy is completed. Thus, CIPNP is a major problem because it is impossible to predict which patients will develop neurological symptoms, to estimate their timing of manifestation, which can occur at any time during the course of chemotherapy, there is no early indication to reduce the dose of the cytotoxic drug, and there are no drugs that effectively prevent or alleviate the course of neuropathy. This review focuses on neurotoxicity with the use of platinum drugs, including the frequency of occurrence, risk factors, cumulative doses, various pathogenetic mechanisms for the development of CIPNP, clinical features and variants of the neurophysiological picture.
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Antineoplásicos , Neoplasias , Enfermedades del Sistema Nervioso Periférico , Polineuropatías , Humanos , Platino (Metal)/efectos adversos , Calidad de Vida , Antineoplásicos/efectos adversos , Enfermedades del Sistema Nervioso Periférico/inducido químicamente , Enfermedades del Sistema Nervioso Periférico/diagnóstico , Enfermedades del Sistema Nervioso Periférico/tratamiento farmacológico , Neoplasias/complicaciones , Neoplasias/tratamiento farmacológico , Polineuropatías/inducido químicamenteAsunto(s)
Vacunas contra la COVID-19 , COVID-19 , Síndrome de Guillain-Barré , Polineuropatías , Polirradiculoneuropatía Crónica Inflamatoria Desmielinizante , Humanos , COVID-19/prevención & control , Vacunas contra la COVID-19/efectos adversos , Síndrome de Guillain-Barré/etiología , Polineuropatías/inducido químicamente , SARS-CoV-2RESUMEN
OBJECTIVE: Antibody- and complement-mediated peripheral nerve inflammation are central in the pathogenesis of MMN. Here, we studied innate immune responses to endotoxin in patients with MMN and controls to further our understanding of MMN risk factors and disease modifiers. METHODS: We stimulated whole blood of 52 patients with MMN and 24 controls with endotoxin and collected plasma. With a multiplex assay, we determined levels of the immunoregulating proteins IL-1RA, IL-1ß, IL-6, IL-10, IL-21, TNF-α, IL-8 and CD40L in unstimulated and LPS-stimulated plasma. We compared baseline and stimulated protein levels between patients and controls and correlated concentrations to clinical parameters. RESULTS: Protein level changes after stimulation were comparable between groups (p > 0.05). IL-1RA, IL-1ß, IL-6 and IL-21 baseline concentrations showed a positive correlation with monthly IVIg dosage (all corrected p-values < 0.016). Patients with anti-GM1 IgM antibodies showed a more pronounced IL-21 increase after stimulation (p 0.048). CONCLUSIONS: Altered endotoxin-induced innate immune responses are unlikely to be a susceptibility factor for MMN.
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Endotoxinas , Polineuropatías , Humanos , Endotoxinas/toxicidad , Proteína Antagonista del Receptor de Interleucina 1 , Interleucina-6 , Anticuerpos , Polineuropatías/inducido químicamente , Inmunidad InnataRESUMEN
Polyneuropathy (PNP) is a known complication of levodopa-carbidopa intestinal gel (LCIG) therapy of advanced Parkinson's Disease (PD). The overall prevalence of PNP in PD is estimated to be 42.1% (as shown in a review by Romagnolo et al. 2018), and the most common type is chronic axonal polyneuropathy. There is a group of acute/subacute onset demyelinating polyneuropathies, which is far less common, although it seems to be an important factor leading to the rapid discontinuation of LCIG treatment. In this systematic review, we present data on demyelinating polyneuropathy with acute/subacute onset; we identified nine papers including prospective assessments and case reports, with detailed information on 15 patients. In all patients, despite treatment with corticosteroids, intravenous immunoglobulins (IVIG) or plasma exchange (PE), the LCIG therapy was terminated. We also present a case of subacute demyelinating polyneuropathy with effective treatment and continuation of LCIG therapy.
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Enfermedad de Parkinson , Polineuropatías , Humanos , Carbidopa/efectos adversos , Levodopa/efectos adversos , Enfermedad de Parkinson/tratamiento farmacológico , Enfermedad de Parkinson/complicaciones , Antiparkinsonianos/efectos adversos , Estudios Prospectivos , Polineuropatías/inducido químicamente , Combinación de Medicamentos , GelesRESUMEN
We present a case of a 53-year-old male who presented with functionally limiting bilateral lower extremity neuropathic pain secondary to multiple subtypes of small fiber neuropathy. He had failed management with multiple conservative measures including oral medications, physical therapy and desensitization techniques. He ultimately underwent placement of a spinal cord stimulator and continued to experience 80% improvement of his pain, as well as improved function and quality of life at 5 month follow-up. To our knowledge, this is the first reported case of successful treatment of multiple subtypes of small fiber neuropathy with spinal cord stimulator.
We report a case of a 53-year-old male who presented with multiple subtypes of small fiber neuropathy, characterized by abnormal sensation and nerve pain in his distal lower extremities, which was making performing his activities of daily living challenging. He had failed multiple conservative measures including oral medications, physical therapy and desensitization techniques. The patient then underwent a trial with a spinal cord stimulator, which includes placing a device in the spinal canal that can alleviate pain by providing low levels of electrical current. At the 5 month follow-up, he continued to report 80% improvement of his pain as well as improved function and quality of life. This is the first reported use of spinal cord stimulator in a patient with multiple subtypes of small fiber neuropathy.
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Antineoplásicos , Infecciones por VIH , Neuralgia , Polineuropatías , Neuropatía de Fibras Pequeñas , Estimulación de la Médula Espinal , Infecciones por VIH/complicaciones , Infecciones por VIH/tratamiento farmacológico , Humanos , Masculino , Persona de Mediana Edad , Neuralgia/inducido químicamente , Neuralgia/complicaciones , Neuralgia/terapia , Polineuropatías/inducido químicamente , Polineuropatías/complicaciones , Polineuropatías/terapia , Calidad de Vida , Neuropatía de Fibras Pequeñas/complicaciones , Médula Espinal , Estimulación de la Médula Espinal/métodosRESUMEN
OBJECTIVE: The objective was to analyze the clinical characteristics and pathological characteristics of sural biopsy in nitrous oxide (N2O) -induced peripheral neuropathy. METHODS: We recruited 18 patients with N2O abuse-induced neurological disorders and reported their demographic data, clinical manifestations, laboratory examinations, and nerve conduction studies. Seven patients underwent sural nerve biopsy pathologic examination. RESULTS: All 18 patients had polyneuropathy, the nerve conduction results showed significant reductions in motor and sensory amplitudes, slowing of conduction velocities, and prolongation of latencies in most tested nerves compared to the controls. Toluidine blue staining of semi-thin sections of sural nerve biopsy showed decreased myelinated nerve fiber density, increased thin myelinated nerve fiber density, and axonal regeneration. Electron microscopy showed axonal degeneration and nerve regeneration. CONCLUSION: The main manifestations of peripheral nerve damage caused by the abuse of N2O are lower limb weakness and distal sensory disorder. The nerve conduction study results demonstrated that mixed axonal and demyelinating neuropathy was the most common type of neuropathy. Sural biopsy showed the main pathological change was chronic axonal degeneration.
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Traumatismos de los Nervios Periféricos , Polineuropatías , Biopsia , Humanos , Óxido Nitroso/efectos adversos , Traumatismos de los Nervios Periféricos/patología , Polineuropatías/inducido químicamente , Polineuropatías/patología , Nervio Sural/patología , Cloruro de TolonioRESUMEN
RATIONALE: Nitrous oxide (NO) is a commonly used drug in medical practice, restoration, and the automobile industry. Recreational abuse is an emerging public health problem owing to its accessibility and drug properties. PATIENT CONCERNS: A 25-year-old male was hospitalized with acute psychosis and lower-extremity sensorimotor proprioceptive ataxia due to nitrous oxide abuse. DIAGNOSIS: Laboratory studies confirmed a vitamin B12 deficiency. Magnetic resonance imaging of the spinal cord showed normal findings. Electrophysiological testing confirmed length-dependent sensorimotor polyneuropathy, with a predominant motor component and axonal degeneration. INTERVENTION AND OUTCOMES: Abstinence from toxic substances was suggested, and vitamin B12 substitution was introduced. The patient was lost to follow up. LESSONS: Nitrous oxide toxicity is multisystemic and is thought to result from vitamin B12 inactivation. Recent case reports postulated direct paranodal lesions resulting from nitrous oxide consumption. Neurological, neuropsychiatric, and hematological toxicities are among those explored in this case report. Correction of the functional vitamin B12 status and nitrous oxide abstinence are essential in the treatment process.
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Enfermedad Injerto contra Huésped , Polineuropatías , Trastornos Psicóticos , Deficiencia de Vitamina B 12 , Adulto , Enfermedad Injerto contra Huésped/tratamiento farmacológico , Humanos , Masculino , Óxido Nitroso/uso terapéutico , Polineuropatías/inducido químicamente , Polineuropatías/tratamiento farmacológico , Trastornos Psicóticos/tratamiento farmacológico , Trastornos Psicóticos/etiología , Vitamina B 12/uso terapéutico , Deficiencia de Vitamina B 12/inducido químicamente , Deficiencia de Vitamina B 12/complicaciones , Deficiencia de Vitamina B 12/tratamiento farmacológicoRESUMEN
Reports suggested the potential occurrence of peripheral neuropathies (PN) in patients treated with BRAF (BRAFi) and/or MEK inhibitors (MEKi) for BRAF-activated tumours. We aimed to better characterize these PN. We queried the French pharmacovigilance database for all cases of PN attributed to BRAFi and/or MEKi. Fifteen patients were identified. Two main clinical PN phenotypes were seen. Six patients presented a length-dependent, axonal polyneuropathy: symptoms were mostly sensory and affecting the lower limbs; management and outcome were variable. Nine patients developed a demyelinating polyradiculoneuropathy: symptoms affected the four limbs and included hypoesthesia, weakness and ataxia; cranial nerves were involved in four cases; most patients received intravenous immunoglobulins or glucocorticoids, with variable outcome; one patient was rechallenged with a different BRAFi/MEKi combination with a rapid relapse in symptoms. In conclusion, patients under BRAFi/MEKi therapy may develop treatment-induced PN. Two main phenotypes can occur: a symmetric, axonal, length-dependent polyneuropathy and a demyelinating polyradiculoneuropathy.
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Enfermedades del Sistema Nervioso Periférico , Polineuropatías , Polirradiculoneuropatía , Glucocorticoides/uso terapéutico , Humanos , Inmunoglobulinas Intravenosas , Quinasas de Proteína Quinasa Activadas por Mitógenos , Recurrencia Local de Neoplasia/tratamiento farmacológico , Enfermedades del Sistema Nervioso Periférico/inducido químicamente , Farmacovigilancia , Polineuropatías/inducido químicamente , Polineuropatías/tratamiento farmacológico , Polirradiculoneuropatía/inducido químicamente , Polirradiculoneuropatía/tratamiento farmacológico , Inhibidores de Proteínas Quinasas/efectos adversos , Inhibidores de Proteínas Quinasas/farmacología , Proteínas Proto-Oncogénicas B-raf/antagonistas & inhibidoresRESUMEN
Multifocal motor neuropathy (MMN) is an immune-mediated and acquired demyelinating motor polyneuropathy. Several cases of polyneuropathy associated with severe acquired respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination have been reported. However, MMN has not been reported as a complication of SARS-CoV-2 vaccination. In this study, we report a case of MMN with progressive muscle weakness following the second dose of the Pfizer-BioNTech mRNA vaccine. It was diagnosed by clinical evaluation and electroneuromyography. SARS-CoV-2 vaccination is increasing rapidly all over the world. Some cases of polyneuropathy, especially Guillain-Barré syndrome, have been reported after vaccination. This is the first case report of MMN after SARS-CoV-2 vaccination.
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Vacuna BNT162 , COVID-19 , Polineuropatías , Vacuna BNT162/efectos adversos , COVID-19/prevención & control , Humanos , Polineuropatías/inducido químicamente , SARS-CoV-2 , Vacunación/efectos adversosRESUMEN
INTRODUCTION: Cadmium is an important heavy metal in neurobiology, with potential neurotoxic effects, often in the form of polyneuropathy (PNP). CASE REPORT: We present an exceptional case of PNP due to cadmium of toxic-occupational origin, specifically a 47-year-old man, aeronautical mechanic, with a 5-year clinical picture, consisting of a tingling sensation having a 'glove and stocking' distribution of symptoms and bimanual manipulative clumsiness. The neurological examination revealed bilateral achilles hyporeflexia and protopathic-thermal-algesic exteroceptive hypoesthesia in hands and feet. The following complementary rests were requested: toxic-metabolic-infectious-vitamin profile, full craniospinal MRI, electroneurographic-electromyographic study (ENG-EMG) of the upper and lower limbs, PET-CT body and 24-hour video-electroencephalogram. The results were consistent with an axonal, distal, symmetric sensory-motor PNP, of moderate intensity, chronic evolution, with active denervation, of toxic-occupational origin due to cadmium. The patient continued on sick leave to cease exposure to cadmium, initiating intensive multimodal neurorehabilitation program, with serial analytical determinations of toxins and new ENG-EMG studies every 6 months. With normalization of the altered values ??and complete clinical restitution at one-year follow-up. CONCLUSIONS: This case highlights the importance of including the toxicological determination of cadmium in case of suspicion of a PNP of toxic-occupational origin, once ruled out other etiologies, in order to early interrupt occupational exposure, as it is a potentially reversible cause of peripheral neuropathy. Currently there is no specific pharmacological treatment against cadmium tested in humans. Randomized clinical trials carried out in these patients are warranted to develop an anti-cadmium drug in refractory cases despite the end of exposure.
TITLE: Polineuropatía por cadmio: una causa infrecuente, pero no menos importante, de neuropatía periférica.Introducción. El cadmio es un metal pesado importante en neurobiología, con potenciales efectos neurotóxicos, frecuentemente en forma de polineuropatía. Caso clínico. Presentamos un caso excepcional de polineuropatía por cadmio de origen tóxico-ocupacional, en concreto, un varón de 47 años, mecánico aeronáutico, con un cuadro de cinco años de evolución, consistente en sensación de hormigueo 'en guante y calcetín' y torpeza manipulativa bimanual. En la exploración destacaba una hiporreflexia aquílea bilateral, y una hipoestesia exteroceptiva protopático-térmico-algésica en las manos y los pies. Se solicitó analítica general completa con perfil tóxico-metabólico-infeccioso-vitamínico, resonancia magnética craneomedular completa, estudio electroneurográfico-electromiográfico de los miembros superiores e inferiores, tomografía por emisión de positrones-tomografía axial computarizada body y videoelectroencefalograma de 24 horas. Los resultados fueron compatibles con una polineuropatía sensitivomotora axonal, distal, simétrica, de intensidad moderada, de evolución crónica y desnervación activa, de origen tóxico-ocupacional por cadmio. El paciente prosiguió la baja laboral para cesar la exposición al cadmio, iniciando neurorrehabilitación intensiva multimodal, y determinaciones analíticas seriadas de tóxicos y nuevos estudios electroneurográficos-electromiográficos cada seis meses, con normalización de los valores alterados y restitución clínica ad integrum al año. Conclusiones. Este caso enfatiza la importancia de incluir la determinación toxicológica del cadmio ante la sospecha de una polineuropatía de origen tóxico-ocupacional, descartadas otras etiologías, para interrumpir precozmente dicha exposición laboral, al ser una causa potencialmente reversible de neuropatía periférica. Actualmente no existe un tratamiento farmacológico específico frente al cadmio demostrado en seres humanos. Urgen ensayos clínicos aleatorizados en estos pacientes, para desarrollar un fármaco frente al cadmio en casos refractarios pese a finalizar la exposición.
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Exposición Profesional , Enfermedades del Sistema Nervioso Periférico , Polineuropatías , Cadmio/toxicidad , Humanos , Masculino , Persona de Mediana Edad , Enfermedades del Sistema Nervioso Periférico/inducido químicamente , Polineuropatías/inducido químicamente , Polineuropatías/complicaciones , Tomografía Computarizada por Tomografía de Emisión de Positrones/efectos adversosRESUMEN
ABSTRACT: We present the case of a 37-year-old woman with alcohol use disorder, who developed leg cramping, bilateral foot drop, and hand weakness 3 months after starting disulfiram. This was accompanied by an 18-pound involuntary weight loss. Electrophysiologic findings showed a motor predominant axonal neuropathy. Neuromuscular ultrasound showed normal to small cross-sectional area of all nerves studied. This case is discussed, and the ultrasound findings are compared with another reported case.