Neurotoxicity of cobalt

Catalani, Simona; Rizzetti, M. Cristina; Padovani, Alessandro; Apostoli, Pietro

doi:10.1177/0960327111414280

Cited by 155 publications

(115 citation statements)

References 112 publications

(189 reference statements)

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“…Mercury's irreversible damage to both the peripheral and central auditory systems following acute and long-term exposures does not appear to be dose-dependent [15]. Previously, patients receiving cobalt chloride as a therapeutic to treat refractory anemia experienced tinnitus and deafness [16]. Currently, cobalt ototoxicity has been suggested in patients with cobalt chromium alloy prosthetic joint implants.…”

Section: What Is the Differential Diagnosis Of Sensorineural Hearing mentioning

confidence: 99%

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Oxymorphone Insufflation Associated with Acute Sensorineural Hearing Loss: Case Files of the University of Massachusetts Medical Toxicology Fellowship

Boyle

Rosenbaum

2013

J. Med. Toxicol.

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Section: What Is the Differential Diagnosis Of Sensorineural Hearing mentioning

confidence: 99%

“…Currently, cobalt ototoxicity has been suggested in patients with cobalt chromium alloy prosthetic joint implants. These patients may suffer from a release of metal ions due to deterioration of the prosthesis leading to progressive hearing loss and tinnitus [16].…”

Section: What Is the Differential Diagnosis Of Sensorineural Hearing mentioning

confidence: 99%

Oxymorphone Insufflation Associated with Acute Sensorineural Hearing Loss: Case Files of the University of Massachusetts Medical Toxicology Fellowship

Boyle

Rosenbaum

2013

J. Med. Toxicol.

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“…Interestingly, in a patient with sensory polyneuropathy identified by our search, sural nerve biopsy revealed "moderate axonal degeneration with no inflammatory changes," suggesting that inflammation of nerves may not completely explain neurotoxicity [8]. Another patient identified by our search exhibited hyperintense lesions on brain magnetic resonance imaging (MRI) suggesting demyelination [7,27]. Comprehensive reviews of cobalt's pathologic mechanisms are available elsewhere [27,28,33,34,36].…”

Section: Proposed Mechanisms Of Toxicitymentioning

confidence: 93%

“…Proposed mechanisms include disruption of mitochondrial oxidative phosphorylation, neurotransmitter modulation, and direct neuron cytotoxicity [27].…”

Section: Neurological Dysfunctionmentioning

confidence: 99%

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Clinical Features, Testing, and Management of Patients with Suspected Prosthetic Hip-Associated Cobalt Toxicity: a Systematic Review of Cases

et al. 2013

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Safety concerns regarding cobalt-containing metal alloy hip prosthetics (Co-HP) have resulted in product recalls, a medical device alert, and issuance of guidance for clinicians. Recently, cases of suspected prosthetic hip-associated cobalt toxicity (PHACT) from Co-HP have been reported. Although little is known about suspected PHACT, these patients may be referred to medical toxicologists for evaluation and management recommendations. We searched MEDLINE, EMBASE, and unpublished abstracts from toxicology scientific meetings for references relevant to PHACT. Authors independently screened publications for inclusion criteria: publication in English, human study population, subject(s) are symptomatic (except for isolated hip pain), and cobalt values in any matrix (blood, serum, urine, CSF, synovial fluid) available for review. Data from 10 cases are reviewed. Patients with suspected PHACT had findings consistent with cobalt toxicity, including thyroid, cardiac, and neurologic dysfunction.Signs and symptoms appeared between 3 and 72 months after arthroplasty (median 19 months). Neurologic symptoms were most common. Ancillary testing varied considerably. All patients had elevated cobalt levels in one or more matrices. Enhanced elimination was attempted in 27 % of patients. At this time, the information currently available regarding patients with suspected PHACT is inadequate to guide clinical decision making. No consensus has been reached regarding the management of Co-HP patients with systemic symptoms. Indications for chelation have not been established and require further study. Improved case definitions, improved surveillance, and controlled studies are needed to elucidate the scope of this problem and guide future investigations.

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Prevalence of Cobalturia Among Adults With Joint Replacements

et al. 2021

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Twenty million North Americans have cobalt-chrome arthroprosthetic components, and 1 million have metal-on-metal hip replacements. 1 Cobalt is a mitochondrial toxin-encephalopathy and cardiomyopathy (cobaltism) may occur from iatrogenic, industrial, dietary, or arthroprosthetic cobalt exposure. 2,3 In unexposed populations, the 95th percentile of cobalt levels in urine and blood are 1 part per billion (ppb) and 0.4 ppb, respectively. 3 Wear and corrosion of cobalt-chrome joint implantations can result in periprosthetic tissue inflammation or necrosis, also known clinically as adverse reactions to metallic debris. 1,4 Periprosthetic cobalt-chrome metallosis is disseminated systemically and may result in arthroprosthetic cobaltism. 1,3,4 Systemic cobalt dissemination can result in brain hypometabolism and atrophy; patients with levels of cobalt in blood as low as 1.1 ppb and in urine as low as 4.1 ppb are reported as having cobalt encephalopathy. 5,6 MethodsThis cohort study analyzed redacted data from 1 orthopedic clinic. The institutional review board at the University of Alaska Anchorage designated the study to be exempt, and patients provided written informed consent for this study. Patients with a suspected hip, knee, or shoulder replacement containing cobalt-chrome were screened with a spot screening of cobalt in urine. Levels of cobalt in blood were then determined for patients with cobalt levels in urine 1 ppb or higher. Patients were designated as cobalt-positive if cobalt levels in urine were 1 ppb or higher or if levels in blood were 0.4 ppb or higher. The reference laboratory test results threshold for reporting cobalt in urine and blood are generally 1 ppb and 0.5 ppb, respectively. Patients with cobalt levels below the reporting threshold in either were assigned half the threshold value. All P values were from 2-sided tests and results were deemed statistically significant at P < .05. Analysis was conducted using Prism version 9.1.1 (GraphPad). This study followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guideline. ResultsA total of 241 patients were screened (mean [SD] age at time of cobalt determination, 68.1 [9.3] years; median duration of exposure to any cobalt-chrome implantation, 11.6 years [range, 2.0-33.2 years]; 117 [48.5%] women); 138 (57%) tested cobalt-positive (mean cobalt level in urine, 12.6 ppb; median, 1.2 ppb). Eleven subjects had no cobalt-chrome implantation (because zirconia and cobaltchrome femoral-heads are indistinguishable radiographically), none of whom were cobalt-positive.Paired cobalt levels in urine and blood (144 patients) correlated significantly (cobalt in blood = 0.25 × cobalt in urine; P < .001). Paired joint-fluid and urine cobalt (57 patients) correlated significantly (joint fluid = 20 × cobalt in urine; P < .001). Patients were classified by type, location, number, and brand of their implantation (Table ). These classes were risk-grouped based on mean cobalt levels in urine (ie, extreme, greater than 20 ppb; high...

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Neurotoxicity of cobalt

Cited by 155 publications

References 112 publications

Oxymorphone Insufflation Associated with Acute Sensorineural Hearing Loss: Case Files of the University of Massachusetts Medical Toxicology Fellowship

Oxymorphone Insufflation Associated with Acute Sensorineural Hearing Loss: Case Files of the University of Massachusetts Medical Toxicology Fellowship

Clinical Features, Testing, and Management of Patients with Suspected Prosthetic Hip-Associated Cobalt Toxicity: a Systematic Review of Cases

Prevalence of Cobalturia Among Adults With Joint Replacements

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