Abstract

ABSTRACTA healthy 15-year-old male spilled elemental mercury contaminating his garage and bedroom. The patient developed new onset hypertension, significant weight loss, pain (muscular, testicular, and abdominal), insomnia, delusions, hallucinations, tachycardia, palmar desquamation, diaphoresis, tremor, and ataxia leading to two consecutive hospitalizations. Blood and urine mercury were 23 and 330 µg/L, respectively. He received 21 days of chelation with 2,3-Dimercaptosuccinic acid during his second hospital stay. He continued to deteriorate. Three weeks post-chelation, he was transferred to our facility and his exam was unchanged. He could not stand or feed himself unassisted. He was started on selenium 500 mcg/day and N-acetylcysteine (NAC) 50 mg/kg/day. By day 3 of Se and NAC, he showed noticeable improvement, and by day 11, delusions, delirium, tachycardia, and abdominal pain resolved. Muscle strength, weight gain, speech, unassisted ambulation, and emotional liability improved. After five months with Se and NAC (1) he had regained 45 pounds, (2) restored to premorbid emotional, academic, and athletic performance, and (3) tachycardia, hypertension, rash, palmar skin changes, tremor, and insomnia had resolved. Features of this case include (1) improvement after selenium and NAC supplementation (2) contrasted with continued deterioration after DMSA chelation.

Highlights

  • In recent years, there has been an important shift in the understanding of the mechanisms of toxicity of mercury (Hg) both at the cellular and organism level

  • Recent evidence suggests that the mechanism of toxicity of mercury is the selenium-based proteins thioredoxin reductase and glutathione peroxidase [1,2]

  • We report a case of severe mercury poisoning unchanged by chelation who later achieved significant improvement related to selenium and N-acetylcysteine (NAC) supplementation

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Summary

Introduction

There has been an important shift in the understanding of the mechanisms of toxicity of mercury (Hg) both at the cellular and organism level. He was started on lisinopril and clonidine, evaluated by psychiatry, and discharged home with no clear diagnosis One week later, he was admitted to a second hospital for worsening abdominal pain, continued weight loss, auditory hallucinations, persistent tachycardia, hypertension, palmar desquamation, diaphoresis, tremor of his hands, ataxia, constipation, and dyschezia. He was admitted to a second hospital for worsening abdominal pain, continued weight loss, auditory hallucinations, persistent tachycardia, hypertension, palmar desquamation, diaphoresis, tremor of his hands, ataxia, constipation, and dyschezia His weight had declined to 52.45 kg (115.4 lb). On arrival to our facility, his exam was unchanged with muscle pain, muscle weakness, testicular pain, persistent sinus tachycardia, diaphoresis, palmar desquamation, rash on trunk and arms, tremor of his hands, ataxia, mood changes, and insomnia He could not stand or feed himself unassisted.

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