Cobalt-chromium toxicity and late-onset disease conversion in LHON - is there a causal link?

Lebers hereditary optic neuropathy (LHON, OMIM 535000) is the most common primary mitochondrial DNA disease in the population with the marked gender bias (male predominance) and the peak age of onset is in the second and third decades of life. However, presentation has been reported in patients from 2 to 87 years of age. There is increasing evidence that mitochondrial dysfunction can be influenced by environmental factors such as smoking, heavy drinking and particular drug agents. In addition, cobalt has been linked to mitochondrial dysfunction and ocular cobalt toxicity has been reported in the context of cobalt-chromium ions released from a metal hip prosthesis. The measurement of cobalt-chromium ions blood level is helpful in confirming the diagnosis, but there are challenges related to the laboratory methods used and the threshold level deemed to be toxic. We report a case, where cobalt-chromium ions leak possibly have contributed to disease conversion in late-onset LHON.