Article Text

Download PDFPDF

Mercury poisoning in a bodybuilder
  1. Marc Edwards1,
  2. Rob Powell2
  1. 1 Neurology Department, Swansea Bay University Health Board, Swansea, UK
  2. 2 Neurology, Morriston Hospital, Swansea, UK
  1. Correspondence to Dr Marc Edwards, Neurology Department, Swansea Bay University Health Board, Swansea SA6 6NL, UK; marc.edwards{at}wales.nhs.uk

Abstract

A 64-year-old man had progressive unsteadiness over several years, with tingling in his feet. He was a longstanding bodybuilding enthusiast. Clinical assessment and neurophysiology confirmed a cerebellar ataxia and axonal peripheral neuropathy. His serum mercury concentration was significantly raised. We diagnosed chronic mercury toxicity secondary to excessive tuna consumption. We advised him to stop eating tuna and prescribed dimercaptosuccinic acid, after which his serum mercury concentrations subsequently fell. This case report highlights the importance of considering dietary and nutritional causes of neurological disease. We also discuss the mechanisms, diagnosis and treatment of mercury toxicity.

  • CEREBELLAR ATAXIA
  • TOXICOLOGY
  • PHARMACOLOGY
  • NEUROPATHY

Data availability statement

All data relevant to the study are included in the article.

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Case report

A 64-year-old man presented with 3 years of progressive unsteadiness when walking, and tingling sensations in his feet. He had not fallen. He also had longstanding reduced dexterity in both hands. There were no problems with vision, swallowing, bladder or bowel function.

He had a history of right ulnar neuropathy treated several years before by cubital tunnel decompression, hypertension, asthma and an aortic valve replacement. He had been an enthusiastic bodybuilder for his entire adult life and continued to train for this. He had competed in many international competitions and had taken regular anabolic steroids since his 20s. He had previously worked in an office, was a non-smoker and rarely drank alcohol.

On examination, he had a broad-based gait, a positive Romberg’s test, and had difficulty with tandem walking. There was mild dysarthria, dysmetria and a left-sided intention tremor. There was muscle wasting in his right hand. There was mild weakness of finger abduction but full strength in all other muscle groups. Muscle tone was normal in all four limbs. His reflexes were generally diminished and plantar reflexes were downgoing. Pin-prick sensation was reduced to the knees and there was also reduced joint-position and vibration sense at the toes only.

The clinical impression was of a combination of cerebellar ataxia and peripheral neuropathy. Initial investigations were normal, including renal function, thyroid function, a vasculitic screen, immunoglobulin profile, HIV, hepatitis B and C, copper, antineuronal antibodies and vitamin A, vitamin B12 and vitamin E. Liver function tests were deranged with a raised serum alanine transaminase, and he had a consistently raised haemoglobin. Genetic testing for an array of spinocerebellar ataxias (1, 2, 3, 6, 7, 17) was normal. An MR scan of brain showed generalised cerebellar atrophy (figure 1). MR imaging of the spine showed multilevel degenerative disc disease in the cervical and lumbar spine but without significant compression or cord signal change.

Figure 1

MR scan of brain (T1 weighted sagittal) showing cerebellar atrophy.

Nerve conduction studies confirmed a length-dependent axonal polyneuropathy with reduced or absent sensory responses. There was evidence of a severe right ulnar neuropathy and a less severe left ulnar neuropathy, as well as bilateral carpal tunnel syndrome.

Further targeted history taking identified that he had consumed four cans of blended tuna every day for the past 25 years. This was intended as a high protein diet to maximise his muscle growth. With this added information, we requested serum zinc and mercury concentrations. Serum mercury was significantly raised at 256 nmol/L (normal<25). We diagnosed chronic mercury toxicity causing peripheral neuropathy and cerebellar ataxia. We advised him to stop eating tuna. After seeking toxicology advice, we prescribed dimercaptosuccinic acid (DMSA). After 3 months, his serum mercury concentration had dropped to 48 nmol/L; after a further course of DMSA, the serum concentration was within normal limits at 13 nmol/L.

Discussion

Mercury is a toxic heavy metal found throughout the environment. It is released from coal-burning power plants and industrial factories but also released naturally during volcanic eruptions. It can then settle in bodies of water through atmospheric deposition.

Human exposure to mercury can occur in various ways depending on its form—organic, inorganic or elemental.

Elemental mercury (liquid mercury) is found in glass thermometers and dental fillings. It becomes a vapour at room temperature and acute exposure through its inhalation can cause neurological and respiratory damage as well as bleeding gums. The neuropsychiatric symptoms that occur in felt hatmakers (who used mercury to stabilise wool) led to the term ‘mad as a hatter’.

Inorganic mercury is used in several industries and exposure to it can arise through occupation. Its ingestion can cause severe gastrointestinal disturbance and renal failure but it may also be deposited in the nervous system.

Organic mercury (methylmercury) was the explanation in this case, since mercury may be found in contaminated fish. Mercury can enter water naturally (in several ways) but also through contamination from burning fossil fuels, mining and waste incineration. Mercury in water is converted into organic mercury by aquatic microorganisms; this is ingested by smaller fish, which in turn are consumed by larger fish. Tuna and other fish such as swordfish and sharks may accumulate high concentrations of mercury due to biomagnification as they ingest large quantities of mercury-containing organisms from lower in the food chain. Humans who regularly eat tuna and other fish in excessive quantities risk developing chronic mercury toxicity.

Chronic mercury toxicity presents in various ways due to its deposition in different organs (kidneys, liver, brain). Long-term mercury exposure can lead to paraesthesia, headache, fatigue, tremor, dysarthria, ataxia, visual and hearing impairment. Chronic inorganic mercury toxicity may give neuropsychiatric manifestations including behavioural change, irritability and pathological shyness.1 In this case, excessive exposure to organic mercury in tinned tuna fish led to a peripheral neuropathy and cerebellar ataxia.

There are several historic examples of public health emergencies related to mercury exposure. In Minamata, Japan during the 1940s, industrial waste from factories contaminated local water sources.2 Organic mercury ingested by microorganisms worked its way up the food chain to the fish farmed by local communities. Several thousand people developed neurological complications such as neuropathy, ataxia, seizures and cognitive decline. In Iraq in 1971, many people unintentionally consumed seed grain treated with a methylmercury fungicide resulting in similar neurological problems as well hundreds of deaths.3 More recently, many lakes across North America have been closed to fishing due to concerns of high mercury concentrations. The current UK online NHS advice is for children to avoid eating shark, swordfish and marlin due to mercury contamination in these species. With respect to tuna, the only advice relates to pregnancy, when women should limit tuna consumption to four cans a week.

Mercury concentrations can be measured on whole blood for organic mercury but urine measurement is preferred for inorganic mercury. We recommend seeking local specialist toxicology guidance to advise on treatment and further monitoring. Chelating agents such as DMSA and dimercaptopropane sulfate can be effective in acute poisoning but they do not reverse the neurological damage from long-term exposure.

Key points

  • This case shows the importance of a full dietary and nutritional history.

  • Chronic mercury toxicity may cause various neurological problems, including an axonal polyneuropathy and cerebellar ataxia.

  • It can be very helpful to involve the local toxicology team (or the National Poisons Information Service) to guide management.

  • Chelation may not reverse neurological damage but aims to prevent further deterioration.

Data availability statement

All data relevant to the study are included in the article.

Ethics statements

Patient consent for publication

Ethics approval

Not applicable.

References

Footnotes

  • Twitter @hwrpowell

  • Contributors ME was the primary author of the case report. RP reviewed and edited the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned. Externally peer reviewed by Freddie Vonberg, London, UK.