Case PresentationĪ 23-year-old man presented with diarrhea, vomiting, numbness and tingling of the fingers, weakness, ataxic gait, hearing loss, concentric vision loss, and psychomotor slowing. For the first time, we present serial magnetic resonance imaging (MRI) of the patient’s brain as well as data on immunotoxicologic and hemostaseologic response in acute MeHg poisoning. We here report the case of a young man with severe MeHg poisoning of unknown etiology and unfavorable outcome despite chelator and erythrocyte apheresis therapy. To the best of our knowledge, little data are available on the additive effects of acute MeHg toxicity on human immune and coagulation systems and our case provides new insights. However, the exact mechanisms of MeHg neurotoxicity are not fully understood so far.īesides its neurotoxicity, MeHg can also affect human immune cells ( 7) and platelet function due to its known high affinity to sulfhydryl (SH) groups ( 8). The extent of neurological damage can be associated with the toxic increase of reactive oxygen species ( 6). In both cases, brain tissue loss caused by necrosis of neurons and gliosis was mainly found in the cerebral cortex, especially in the calcarine cortex, parietal cortex, and cerebellar folia. The organic compound methyl mercury (MeHg) is particularly poisonous due to its known ability to cause neurological alterations as shown in the cases of a chemistry professor and a family who died as a consequence of brain damage caused by MeHg ( 3, 4). The severity of its toxicity depends on the type of mercury and the route of exposure together with the dosage of administration. Mercury poisoning can be especially harmful to the nervous and immune systems and can even be fatal in extreme cases ( 1– 5). Since the Minamata disaster in the 1950s, the worldwide recognition of mercury toxicity led to strict preventive measures making severe mercury intoxication very rare in western countries ( 1). Data on immune-cell and thrombocyte function as well as on coagulation in mercury poisoning reveal potential implications for anticoagulation and immunomodulatory treatment. This case illustrates the neurotoxicity of MeHg following severe intoxication for the first time by serial MRI. Despite the successful reduction of the MeHg concentration in the patient’s blood with erythrocyte apheresis and chelator therapy, his condition did not improve and led to a persistent vegetative state. Moreover, the ex vivo analyses display alterations of thrombocyte function and coagulation, as well as an immunological milieu facilitating autoimmunity. Together with the clinical history, our findings show the progressive neuronal degeneration accompanying the deterioration of the patient. We show serial magnetic resonance imaging (MRI) of the patient’s brain, as well as ex vivo analyses of blood and cerebrospinal fluid including multicolor flow cytometric measurements, functional assays of hemostaseologic efficacy, and evaluation of regulatory effector molecules. Here, we describe the dramatic physical and cognitive decline of a 23-year-old patient caused by a severe methyl mercury (MeHg) intoxication of unknown origin. Severe mercury intoxication is very rare in developed countries, but still occurs as the result of volatile substance abuse, suicide attempts, occupational hazards, or endemic food ingestion as reported in the cases of public health disasters in Iraq and in Minamata Bay, Japan. 3Institute for Clinical Radiology, University Hospital Muenster, Muenster, Germany.2Department of Anesthesiology, Intensive Care and Pain Medicine, Experimental and Clinical Haemostasis, University of Muenster, Muenster, Germany.1Department of Neurology, University of Muenster, Muenster, Germany.Gross 1 Kerstin Göbel 1 Heinz Wiendl 1 Beate E. Ilka Kleffner 1* † Susann Eichler 1† Tobias Ruck 1† Lisa Schüngel 2 Steffen Pfeuffer 1 Philipp Polzer 3 Ralf Dittrich 1 Rainer Dziewas 1 Catharina C.
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