Long-Term Clinical and Toxicological Follow-up of Severe Cobalt and Chromium Intoxication - a Case Report

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Long-Term Clinical and Toxicological Follow-up of Severe Cobalt and Chromium Intoxication - a Case Report. / Preisser, Alexandra Marita; Scheit, Lorenz; Kraft, Alexander Michael; Thieme, Olaf; Harth, Volker.

in: SN Comprehensive Clinical Medicine, Jahrgang 5, 2023, S. 58.

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@article{b0d9927f118848119907479f9aa85926,
title = "Long-Term Clinical and Toxicological Follow-up of Severe Cobalt and Chromium Intoxication - a Case Report",
abstract = "Cobalt intoxications from fractured hip endoprostheses have been described since the early 2000s. Typical symptoms include cardiomyopathy, neurological symptoms with visual and hearing loss and hypothyroidism. Less is known about long-term progression of these pathologies. This case report shows the long-term course of complications caused by cobalt and chromium exposure after substantial elimination of the source of intoxication. We report here a 63-year-old male Caucasian with severe cobalt and chromium intoxication. He presented 1 month after 2nd revision surgery of a broken hip endoprosthesis in a reduced general condition with signs of heart failure, pale skin and diminished hearing and vision. Blood analyses showed a cobalt concentration of 600 μg/L (reference value < 0.45 μg/L). Because the blood cobalt concentration decreased rapidly after surgery and symptoms improved, chelation therapy was not applied. Close clinical and toxicological monitoring was performed. The intoxication was not diagnosed until 6 years after the faulty hip joint revision and 3 years of clear signs of intoxication during a 2nd revision of the prosthesis. The patient{\textquoteright}s ordeal could have been much shorter if his cobalt intoxication with neurologic, cardiac and thyroid symptoms had been detected earlier by toxicological blood tests. After the elimination of the source of poisoning, the long-term course showed constant excretion of cobalt and chromium over several years without chelation. Specific symptoms such as cardiomyopathy and neurological symptoms were declining. However, due to the continuous release of metal ions from the tissue, complete recovery did not occur.",
author = "Preisser, {Alexandra Marita} and Lorenz Scheit and Kraft, {Alexander Michael} and Olaf Thieme and Volker Harth",
year = "2023",
doi = "10.1007/s42399-023-01393-4",
language = "English",
volume = "5",
pages = "58",
journal = "SN Comprehensive Clinical Medicine",
issn = "2523-8973",
publisher = "Springer",

}

RIS

TY - JOUR

T1 - Long-Term Clinical and Toxicological Follow-up of Severe Cobalt and Chromium Intoxication - a Case Report

AU - Preisser, Alexandra Marita

AU - Scheit, Lorenz

AU - Kraft, Alexander Michael

AU - Thieme, Olaf

AU - Harth, Volker

PY - 2023

Y1 - 2023

N2 - Cobalt intoxications from fractured hip endoprostheses have been described since the early 2000s. Typical symptoms include cardiomyopathy, neurological symptoms with visual and hearing loss and hypothyroidism. Less is known about long-term progression of these pathologies. This case report shows the long-term course of complications caused by cobalt and chromium exposure after substantial elimination of the source of intoxication. We report here a 63-year-old male Caucasian with severe cobalt and chromium intoxication. He presented 1 month after 2nd revision surgery of a broken hip endoprosthesis in a reduced general condition with signs of heart failure, pale skin and diminished hearing and vision. Blood analyses showed a cobalt concentration of 600 μg/L (reference value < 0.45 μg/L). Because the blood cobalt concentration decreased rapidly after surgery and symptoms improved, chelation therapy was not applied. Close clinical and toxicological monitoring was performed. The intoxication was not diagnosed until 6 years after the faulty hip joint revision and 3 years of clear signs of intoxication during a 2nd revision of the prosthesis. The patient’s ordeal could have been much shorter if his cobalt intoxication with neurologic, cardiac and thyroid symptoms had been detected earlier by toxicological blood tests. After the elimination of the source of poisoning, the long-term course showed constant excretion of cobalt and chromium over several years without chelation. Specific symptoms such as cardiomyopathy and neurological symptoms were declining. However, due to the continuous release of metal ions from the tissue, complete recovery did not occur.

AB - Cobalt intoxications from fractured hip endoprostheses have been described since the early 2000s. Typical symptoms include cardiomyopathy, neurological symptoms with visual and hearing loss and hypothyroidism. Less is known about long-term progression of these pathologies. This case report shows the long-term course of complications caused by cobalt and chromium exposure after substantial elimination of the source of intoxication. We report here a 63-year-old male Caucasian with severe cobalt and chromium intoxication. He presented 1 month after 2nd revision surgery of a broken hip endoprosthesis in a reduced general condition with signs of heart failure, pale skin and diminished hearing and vision. Blood analyses showed a cobalt concentration of 600 μg/L (reference value < 0.45 μg/L). Because the blood cobalt concentration decreased rapidly after surgery and symptoms improved, chelation therapy was not applied. Close clinical and toxicological monitoring was performed. The intoxication was not diagnosed until 6 years after the faulty hip joint revision and 3 years of clear signs of intoxication during a 2nd revision of the prosthesis. The patient’s ordeal could have been much shorter if his cobalt intoxication with neurologic, cardiac and thyroid symptoms had been detected earlier by toxicological blood tests. After the elimination of the source of poisoning, the long-term course showed constant excretion of cobalt and chromium over several years without chelation. Specific symptoms such as cardiomyopathy and neurological symptoms were declining. However, due to the continuous release of metal ions from the tissue, complete recovery did not occur.

U2 - 10.1007/s42399-023-01393-4

DO - 10.1007/s42399-023-01393-4

M3 - Case report

VL - 5

SP - 58

JO - SN Comprehensive Clinical Medicine

JF - SN Comprehensive Clinical Medicine

SN - 2523-8973

ER -