Palmoplantar eruption in a patient with mercury poisoning.

Mercury poisoning is a rare event that can present with a variety of nonspecific systemic symptoms, making it difficult to diagnose. Dermatologic manifestations of mercury exposure may be variable and include pink disease (acrodynia), mercury exanthem, contact dermatitis, and cutaneous granulomas. We present the case of an 18-year-old woman with a palmoplantar eruption associated with tachycardia, hyperhidrosis, myalgia, paresthesia, and muscle fasciculations. Physical examination demonstrated poorly demarcated pink macules coalescing into patches on the left palm, right wrist, and soles. A punch biopsy was nonspecific, showing acanthosis and orthokeratosis with mild inflammation. Elevated urine and serum mercury levels confirmed a diagnosis of mercury poisoning. This case highlights the importance of consideration of mercury poisoning in the differential diagnosis for acral eruptions, especially in the presence of systemic symptoms and known risk factors.

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.

Microbial Protein Produced from Brown Seaweed and Spruce Wood as a Feed Ingredient.

The conversion of nonedible biomass to protein for use in feed is an attractive strategy toward improved sustainability in aquaculture. We have studied the possibility to produce protein-rich yeast Candida utilis on a medium consisting of enzymatically hydrolyzed sulphite-pulped spruce wood, mainly providing glucose, and enzymatically hydrolyzed brown seaweed, supplemented with ammonium sulfate. The results show that this blend constitutes a complete fermentation medium that enables good growth rates and cell yields. Results from a salmon feeding trial showed that the yeast can replace parts of a traditional fishmeal diet without harmful effects, although the apparent protein digestibility coefficient for the yeast was suboptimal. While further optimization of both the fermentation process and downstream processing is needed, the present proof-of-concept study shows a path to the production of microbial protein based on a simple, local and sustainable fermentation medium.

Mercury toxicity presenting as acrodynia and a papulovesicular eruption in a 5-year-old girl.

Acrodynia is a reaction that occurs in children who have been exposed to mercury. Mercury toxicity has systemic manifestations as well as cutaneous manifestations, which can appear similar to those found in a number of other diseases. We present a case of acrodynia caused by mercury exposure in a previously healthy 5-year-old girl who developed hypertension, palmoplantar pruritus, and a papulovesicular eruption.

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.

ITPKC susceptibility in Kawasaki syndrome as a sensitizing factor for autoimmunity and coronary arterial wall relaxation induced by thimerosal's effects on calcium signaling via IP3.

Recently, a single nucleotide polymorphism (SNP) of the inositol 1,4,5-triphosphate kinase C (ITPKC), rs28493229, was found to passively confer susceptibility for Kawasaki syndrome (KS) and subsequent coronary arterial lesions. This association is believed to be the result of defective phosphorylation of inositol 1,4,5-triphosphate (IP3), which releases calcium from intracellular stores, resulting from reduced genetic expression of ITPKC in carriers of the SNP. Reduced ITPKC activity would increase IP3 levels, and thus, increase calcium release. We hypothesized that an environmental agent which influences IP3-mediated calcium release is potentiated by the ITPKC SNP. This led us to an attractive candidate, thimerosal, an organomercurial medical preservative still used in several pediatric vaccines. Thimerosal is well-known to sensitize IP3 receptors via its induction of oxidative stress, resulting in enhanced release of intracellular calcium with distinctive consequences for various cell types. Dysregulated calcium signaling in T cells and other immune cells can result in autoimmunity, while hyperpolarization of vascular smooth muscle cells secondary to the stimulation of calcium-activated potassium channels can result in increased vascular permeability and arterial relaxation. We propose that ITPKC susceptibility in KS is related to its synergy with environmental triggers, such as thimerosal, which alter calcium homeostasis and promote oxidative stress. Therefore, carriers of the ITPKC SNP are more susceptible to thimerosal-induced autoimmunity and coronary arterial lesions observed in KS. This would explain why only a susceptible subset of children develops KS although pediatric thimerosal exposure is nearly universal due to vaccination. As was experienced with the infantile acrodynia epidemic, only 1 in 500 children developed the disease although pediatric mercury exposure was nearly ubiquitous due to the use calomel teething powders. This hypothesis also mirrors the current leading theory for KS in which a widespread infection only induces the disease in susceptible children. We conclude that KS may be the acute febrile form of acrodynia.

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.

Metal mercury poisoning in two boys initially treated for brucellosis in Mashhad, Iran.

Elemental mercury (Hg) is the only metal which evaporates in room temperature and its inhalation may cause toxicity. Hg poisoning may occur by mishandling the metal, particularly in children who play with it. Wide-spectrum of the clinical presentations of chronic Hg poisoning may cause misdiagnosis, particularly when history of exposure is unknown. We report two cases of accidental Hg poisoning, which initially had been diagnosed and treated for brucellosis. The patients were two brothers (7 and 14 years old) who presented with pain in their lower extremities, sweating, salivation, weight loss, anorexia and mood changes on admission. Meticulous history taking revealed that they had played with a ball of Hg since 3 months before admission. The level of urinary Hg was 125.9 and 54.2 9 g/L in the younger and older brother, respectively (normal ≤25 g/L). The patients were successfully treated by dimercaprol and discharged in good condition 24 days after admission. These cases are being reported to emphasize the importance of acrodynia as a differential diagnosis for brucellosis in endemic areas.

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.

Ancestry of pink disease (infantile acrodynia) identified as a risk factor for autism spectrum disorders.

Pink disease (infantile acrodynia) was especially prevalent in the first half of the 20th century. Primarily attributed to exposure to mercury (Hg) commonly found in teething powders, the condition was developed by approximately 1 in 500 exposed children. The differential risk factor was identified as an idiosyncratic sensitivity to Hg. Autism spectrum disorders (ASD) have also been postulated to be produced by Hg. Analogous to the pink disease experience, Hg exposure is widespread yet only a fraction of exposed children develop an ASD, suggesting sensitivity to Hg may also be present in children with an ASD. The objective of this study was to test the hypothesis that individuals with a known hypersensitivity to Hg (pink disease survivors) may be more likely to have descendants with an ASD. Five hundred and twenty-two participants who had previously been diagnosed with pink disease completed a survey on the health outcomes of their descendants. The prevalence rates of ASD and a variety of other clinical conditions diagnosed in childhood (attention deficit hyperactivity disorder, epilepsy, Fragile X syndrome, and Down syndrome) were compared to well-established general population prevalence rates. The results showed the prevalence rate of ASD among the grandchildren of pink disease survivors (1 in 22) to be significantly higher than the comparable general population prevalence rate (1 in 160). The results support the hypothesis that Hg sensitivity may be a heritable/genetic risk factor for ASD.

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.

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.

Mercury intoxication in a 2-year-old girl: a diagnostic challenge for the physician.

A 2-year-old girl presented with hypertension, anorexia and vomiting, restlessness, insomnia and acrodynia. Her blood pressure upon arrival was 145/98 mmHg. Ultrasound of the abdomen, CT scan of chest, abdomen and pelvis, and echocardiogram, were normal. Urinary levels of catecholamines were elevated, urine level of mercury was found to be high (33.2 microg/g creatinine), although blood level was normal (>0.5 microg/dl, reference value 0-4 microg/dl). Following a 1-month course of oral treatment with dimercaptosuccinic acid (DMSA) the child's symptoms and signs resolved, and urinary mercury and catecholamines levels normalized. Mercury intoxication should be suspected in a patient with severe hypertension, personality changes and acrodynia. Normal blood levels of mercury do not exclude this diagnosis, and catecholamine levels may serve as a surrogate marker for confirmation of the diagnosis and to evaluate response to treatment.

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.

Mercury intoxication: it still exists.

A3-year-old boy presented to the Hospital for Sick Children with systemic symptoms and oropharyngeal and peripheral extremity changes suggestive of Kawasaki disease. He was found to have severe hypertension. Investigation for a catecholamine-secreting tumor was negative. Toxins were considered when the patient's 20-month-old brother presented with similar symptoms, and the boys were subsequently diagnosed with elemental mercury poisoning. We review the literature on mercury intoxication and discuss the historical context, clinical syndrome (acrodynia), treatment, and radiologic findings of this unusual diagnosis.

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.