Acrodynia and hypertension in a young girl secondary to elemental mercury toxicity acquired in the home.

Acrodynia, also known as pink disease, erythredema polyneuropathy, Feer syndrome, and raw-beef hands and feet, is thought to be a toxic reaction to elemental mercury and less commonly to organic and inorganic forms. Occurring commonly in the early 20th century, acrodynia is now a seemingly extinct disease in the modern world because of regulations to eliminate mercury from personal care products, household items, medications, and vaccinations. We present a case of a 3-year-old girl with acrodynia secondary to toxic exposure to elemental mercury in the home environment.

Elemental mercury poisoning presenting as hypertension in a young child.

Mercury intoxication is an uncommon cause of hypertension in children and can mimic several other diseases, such as pheochromocytoma and vasculitis. Mercury intoxication can present as a diagnostic challenge because levels of catecholamines may be elevated, suggesting that the etiology is a catecholamine-secreting tumor. Once acrodynia is identified as a primary symptom, a 24-hour urine mercury level can confirm the diagnosis. Inclusion of mercury intoxication in the differential diagnosis early on can help avoid unnecessary and invasive diagnostic tests and therapeutic interventions. We discuss a case of mercury intoxication in a 3-year-old girl presenting with hypertension and acrodynia, without a known history of exposure. Chelation therapy successfully treated our patient's mercury intoxication. However, it was also necessary to concurrently treat her hypertension and the pain associated with her acrodynia. Because there were no known risk factors for mercury poisoning in this case, and because ritual use of mercury is common in much of the United States, we recommend high clinical suspicion and subsequent testing in all cases of acrodynia.

Metallic mercury vapour poisoning revisited.

Mercury poisoning was once common in the 19th century. With its declining use, now clinicians and the public in general are often unaware and unsuspecting of mercury toxicity. A 40-year-old woman and her two children were hospitalized with a 1-week history of a generalized lichenoid eruption. Clinical improvement occurred without a diagnosis; however, on returning home, features of acrodynia with digital gangrene developed in the woman, leading to suspicion of heavy metal poisoning. There was no recurrence after moving from their contaminated house.

Mercury poisoning: a rare but treatable cause of failure to thrive and developmental regression in an infant.

An infant presented with failure to thrive and developmental regression. Physical examination revealed an irritable child with swollen, erythematous extremities, and elevated blood pressure. Extensive investigations, including a metabolic work-up and neuroimaging, were unrevealing. Exposure to self-purchased medication was initially denied. The physical signs were suggestive of acrodynia. Mercury poisoning was ultimately established by measuring paired blood and urine mercury levels. On further enquiry, it was revealed that the child had been given a Chinese medicinal product for 4 months. He responded well to a chelating agent. Acrodynia is a childhood disease considered to be of historical interest only, but making a diagnosis of mercury poisoning is rewarding because the response to treatment is good. This case highlights the common misconception that alternative medicines are safe and benign.

Elemental mercury intoxication in 7 patients admitted to a pediatric rheumatology clinic.

Paç Kisaarslan A, Sözeri B, Bastug F, Gündüz Z, Yel S, Nalçacioglu H, Sahin N, Özdemir Çiçek S, Poyrazoglu H, Düsünsel R. Elemental mercury intoxication in 7 patients admitted to a pediatric rheumatology clinic. Turk J Pediatr 2019; 61: 786-790. Mercury (Hg) is a toxic heavy metal that can be classified into three groups; organic (methyl), inorganic (mercuric), and elemental (metallic) mercury(Hg0). Mercury intoxication occurs mostly with the elemental form which can potentially damage the function of any organ, or any subcellular structure. The target organ of mercury is the brain, but peripheral nerve function, renal function, immune function, endocrine and muscle function, and several types of dermatitis have been described. We present 7 patients admitted to a pediatric rheumatology clinic with severe extremity pain. One of the patients had acrodynia, two of them had hypertension, two of them had tubulopathy, and three of them had neuropathy. The treatments were Dimercaptosuccinic acid and metalcaptase. In this report, we emphasize that mercury intoxication should be kept in mind with unexplained extremity pain. Timely diagnosis and treatment may prevent severe morbidity and mortality.

Kawasaki's disease, acrodynia, and mercury.

A superantigen or autoimmunity has been hypothesized to be the main cause of the Kawasaki's Disease but the etiology is unknown. Medical literature, epidemiological findings, and some case reports have suggested that mercury may play a pathogenic role. Several patients with Kawasaki's Disease have presented with elevated urine mercury levels compared to matched controls. Most symptoms and diagnostic criteria which are seen in children with acrodynia, known to be caused by mercury, are similar to those seen in Kawasaki's Disease. Genetic depletion of glutathione S-transferase , a susceptibility marker for Kawasaki's Disease, is known to be also a risk factor for acrodynia and may also increase susceptibility to mercury . Coinciding with the largest increase (1985-1990) of thimerosal (49.6% ethyl mercury) in vaccines, routinely given to infants in the U.S. by 6 months of age (from 75microg to 187.5microg), the rates of Kawasaki's Disease increased ten times, and, later (1985-1997), by 20 times. Since 1990 88 cases of patients developing Kawasaki's Disease some days after vaccination have been reported to the Centers of Disease Control (CDC) including 19% manifesting symptoms the same day. The presented pathogenetic model may lead to new preventive- and therapeutic strategies for Kawasaki's disease.

A Child with elemental mercury poisoning and unusual brain MRI findings.

Mercury vapor poisoning is a serious and potentially fatal problem. Neurological manifestations involving the central nervous system are seen with chronic mercury intoxication. We present the case of a 10-year-old child who demonstrated acrodynia, seizures, and visual impairment following 20 days of exposure to elemental mercury at home. The initial blood mercury concentration was 27.7 microg/L (normal <2 microg/L) and the initial 24-hour urine mercury concentration was 34.4 microg/L (normal =10 microg/L). After 9 months of treatment with D-penicillamine, the patient's clinical condition, biochemical laboratory parameters, and mercury concentrations all returned to normal. The T2-weighted MRI images of the patient's brain initially showed multiple hyperintense lesions in cerebral white matter, left globus pallidus, and putamen, which also improved.

Pyridoxine deficiency and antagonism produce increased ground substance viscosity with resulting seborrheic dermatitis and increased tumor resistance.

Pyridoxine deficiency and 4'-deoxypyridoxine produce acrodynia in rats and seborrheic dermatitis in man. They also produce tumor inhibition in man and animals. Pyridoxine is extensively involved in metabolism and its relationship to the inhibitor 4'-deoxypyridoxine is complex. Pyridoxine deficiency and antagonism increases ground substance viscosity. This increase the inflammatory reactivity of the skin to produce acrodynia in rats and seborrheic dermatitis in man. The increase in ground substance viscosity would explain the increased resistance to tumors in man and animals. Pyridoxine is important in protein metabolism. The protein moiety of glycosaminoglycans in ground substance is small but plays a major role in tissue viscosity. Pyridoxine deficiency or antagonism by itself does not offer a definitive answer for tumors. Combined with substances that stimulate fibroblast or glycosaminoglycans production it may have a significant additive effect.

[What is left of Morvan's fibrillary chorea?]. / Que reste-t-il de la chorée fibrillaire de Morvan?

In 1890, Morvan described a syndrome of myokimia associated with muscle pain, excessive sweating and sleep disorders. The course was severe and the patient died five weeks after the onset. Several cases were published after this first report in the French literature. The last for 10 years the disease seems to have disappeared. In fact, it seems that the progress in electromyography introduced clear definitions of spontaneous muscle discharges (myokimia, neuromyotonic discharges, fibrillations, fasciculations) allowing recognition of a disease characterized by a syndrome of spontaneous and continuous muscle fiber activity associated with cramping, slow relaxation (pseudomyotonia), excessive sweating and stiffness. Different terms have been used to describe this entity: neuromyotonia (Mertens and Zschocke, 1965) or continuous muscle fibre activity (Isaacs, 1961). Classification of these syndromes has to distinguish inherited from acquired forms, idiopathic cases from cases where neuromyotonia is associated with a peripheral neuropathy, a cancer or an immunological disease. Moreover, the frequent occurrence of this later association and recent reports of improvement after plasma exchanges suggest a possible autoimmune aetiology for this group. Finally, we suggest that the term of "Maladie de Morvan" must be used instead of chorée fibrillaire but only concerning patients who exhibit central disorders including insomnia, hallucinations and altered behaviour.

Mercury exposure and early effects: an overview.

OBJECTIVES: This paper was given as a keynote address at the conference on The Assessment of the Effects Due to Low Doses of Inorganic Mercury following Environmental and Occupational Exposures: Human and in vitro Studies on the Specific Mechanisms of Toxicity in Gargnano, Italy, in September 2001. METHODS: The most relevant literature over the past 40 years has been reviewed, and in particular, the proceedings of the World Health Organisation conferences on the health effects of inorganic and organic mercury exposure have been considered. RESULTS: In an uncontaminated environment the general population is exposed to mercury vapour from the atmosphere and from dental amalgam, while the diet, mainly from fish, is the principal source for methyl mercury absorption. Mercury vapour release from amalgam fillings increases with chewing, with absorption and uptake by the brain and kidneys. Infants exposed to phenyl mercury from treated diapers and young children ingesting mercurous chloride in teething powders have developed acrodynia (pink disease), and Kawasaki disease and the use of mercurial skin lightening creams has been followed by the development of the nephrotic syndrome. Both mercury compounds and mercury vapour have given rise to contact dermatitis in the general population. Epidemics of mercury poisoning have followed release of mercury into the environment from industrial activity, with uptake of methyl mercury from fish eating in Minamata Bay and uptake of both inorganic and methyl mercury following release of mercury vapour and deposition into waterways from gold recovery procedures in the Amazon basin. The ingestion of wheat and barley seed treated with an alkyl mercury fungicide for sowing, by a largely illiterate population in Iraq, led to a major outbreak of poisoning with a high fatality rate. Following exposure to mercury vapour, the earliest clinically observed adverse effects at urine mercury levels of the order of 30-100 mg/g creatinine, are objectively detectable tremor, psychological disorder and impaired nerve conduction velocity in sensitive subjects, with subjective symptoms of irritability, fatigue and anorexia. At these and at lower levels, proteinuria has also been observed. Both glomerular and tubular damage may occur at exposure levels lower than those giving rise to central nervous system effects. An immunological effect has also been observed in studies on clinically asymptomatic workers with low level exposure. CONCLUSIONS: As mercury can give rise to allergic and immunotoxic reactions which may be genetically regulated, in the absence of adequate dose-response studies for immunologically sensitive individuals, it has not been possible to set a level for mercury in blood or urine below which mercury related symptoms will not occur.