Mercury poisoning in a bodybuilder.

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.

Pathology of human organic mercury poisoning: Lessons from an autopsy case.

We had an opportunity to perform a general autopsy of a case with chronic organic mercury toxicosis in 2017. He had been engaged in synthesizing a variety of organic mercury compounds throughout the four years from 1966 and developed chronic organic mercury poisoning in 1969. Almost forty years on, he still remained to complain of persistent paresthesia at finger tips and tongue, and of narrowed visual field. Neurological examinations clarified a rise of two-point discrimination thresholds, a systemic increase of touch thresholds, constriction of the visual field caused by general visual depression, and sensorineural hearing loss while primary modalities of his somatic, visual, and auditory sensations were preserved. These symptoms and signs are characteristic of human organic mercury poisoning. Furthermore, he had difficulty in processing a lot of visual and auditory information at a time. His two-point discrimination thresholds and systemic elevation of touch thresholds were comparable to those of mild organic mercury poisoning cases. He had slight sensory ataxia, but not cerebellar ataxia. Brain [18F]-2-fluorodeoxyglucose positron emission tomography analysis exhibited marked hypometabolism at bilateral postcentral gyrus, striate cortex, and superior temporal gyrus, but not the cerebellum. Histopathological studies revealed considerable decrease of granular neurons and neuronal networks in bilateral primary somatosensory, visual, and auditory cortices. Those characteristic brain lesions fairly explain increase of thresholds of somatic, visual, and auditory sensations, and degradation of integrating sensory information. It is noted that damages to the peripheral nervous system and the cerebellum were not detected and that his intellectual faculties were preserved.

Suicidal intoxication with mercury chloride.

PURPOSE: Poisoning with elemental metals and metallic compounds was much more frequent in the past, and was related, among other things, to lifestyle and the lack of appropriate toxicological diagnostics. One example is mercury, which is being gradually eliminated but still has many different applications as a pure metal or in the form of various compounds. The paper presents a case of suicidal poisoning with mercury chloride (corrosive sublimate). METHODS: Forensic and toxicological tests including inductively coupled plasma mass spectrometry (ICP-MS) were at the Department of Forensic Medicine, PMU in Szczecin. RESULTS: The patient before death had a range of symptoms such as epigastric pain, vomiting of the stomach contents, central cyanosis with tachycardia, tremors, severe shortness of breath with wheezing, difficulty swallowing, slurred speech, rales in the lungs, and diarrhea. The concentration of mercury measured by ICP-MS was 191 mg/L for a blood sample collected antemortem, and 147 mg/L for a blood sample collected at autopsy. Both concentrations of mercury are regarded as lethal. The post-mortem examination revealed signs of extensive thrombotic necrosis in some internal organs. CONCLUSIONS: Mercuric chloride has an estimated human fatal dose of between 1 and 4 g. It can produce a range of toxic effects, including corrosive injury, severe gastrointestinal disturbances, acute renal failure, circulatory collapse, and eventual death. The presented case of fatal poisoning with mercury chloride, due to the type of agent used, is now interesting in toxicological practice.

Nephrotic syndrome of minimal change disease following exposure to mercury-containing skin lightening cream: A case report and literature review.

Long-term exposure to mercury-containing skin lightening cream can cause mercury-related nephropathy, among which, membranous nephropathy (MN) and minimal change disease (MCD) are the main pathological types. In contrast to these two conditions, MCD with IgA deposition is not a common disease. In the present study, we report a 65-year-old Asian woman who developed nephrotic syndrome following long-term use of mercury-containing skin lightening cream. The urine mercury level of the patient was significantly increased, and the results of the renal biopsy indicated diagnosis of MCD with IgA deposition. Following three courses of treatment with sodium dimercaptopropane sulfonate (DMPS) alone and discontinuation of the skin cream, the symptoms of the patient were relieved without use of glucocorticoids, with proteinuria turning negative and a significant reduction in urine mercury levels. During the 6-month follow-up period, routine urinalysis remained normal. By reviewing relevant published literature, we summarized the pathological characteristics, possible mechanism of action, and treatment strategies of mercury poisoning-related MCD. The possibility of mercury poisoning should be considered for patients with nephropathy and history of use of skin lightening cosmetics. In these patients, the urine mercury levels should be measured in time so that mercury removal therapy can be implemented early.

Comprehensive Review Regarding Mercury Poisoning and Its Complex Involvement in Alzheimer's Disease.

Mercury (Hg) is considered one of the most widespread toxic environmental pollutants, which seems to have multiple effects on organisms even at low concentrations. It has a critical role in many health problems with harmful consequences, with Hg primarily targeting the brain and its components, such as the central nervous system (CNS). Hg exposure was associated with numerous CNS disorders that frequently trigger Alzheimer's disease (AD). Patients with AD have higher concentrations of Hg in blood and brain tissue. This paper aims to emphasize a correlation between Hg and AD based on the known literature in the occupational field. The outcome shows that all these concerning elements could get attributed to Hg. However, recent studies did not investigate the molecular level of Hg exposure in AD. The present review highlights the interactions between Hg and AD in neuronal degenerations, apoptosis, autophagy, oxidative stress (OS), mitochondrial malfunctions, gastrointestinal (GI) microflora, infertility and altering gene expression.

Mercury poisoning complicated by acquired neuromyotonia syndrome: A case report.

RATIONALE: Acquired neuromyotonia syndrome is a rare form of peripheral nerve hyperexcitability syndrome. It is characterized by spontaneous and continuous muscle contractions. Acquired neuromyotonia syndrome is mainly observed in patients with autoimmune diseases or tumors, but it is a rare neurological clinical manifestation in patients with mercury poisoning. PATIENT CONCERNS: A 56-year-old woman presented with continuous and involuntary muscle twitching in her legs for 2 months; it was accompanied by a burning sensation in the lower limbs, insomnia, fatigue, and night sweats. These symptoms did not disappear during sleep. DIAGNOSES: Toxicological blood analysis via atomic fluorescence spectrometry revealed that the level of mercury was 0.07 µmol/L (normal level: <0.05 µmol/L). Her urinary mercury level measured using the cold atomic absorption method was 217.50 µmol/mol creatinine, which was considerably higher than the reference range (0-2.25 µmol/mol creatinine for people not in contact with mercury, 0-20 µmol/mol creatinine following long-term exposure). Upon further testing, a high level of mercury (10,572 mg/kg) was detected in the patient's cream. Accordingly, this patient was diagnosed with mercury poisoning. INTERVENTIONS: Treatment with 2,3-dimercapto-1-propanesulfonic acid (DMPS) was initiated. Her urinary mercury level decreased to 9.67 µmol/mol creatinine, and her neuromyotonia syndrome and hyponatremia were relieved, with urine protein completely disappearing after 3 months of treatment. OUTCOMES: After DMPS treatment, the clinical manifestations of the nervous system disappeared and electrolyte parameters returned to normal levels. LESSONS: Acquired neuromyotonia syndrome is a rare disorder caused by the hyperexcitability of peripheral nerves, resulting in spontaneous and continuous muscle contraction. Mercury poisoning should be considered in patients with neuromyotonia syndrome. Early detection of mercury poisoning can prevent unnecessary examinations and treatments.

Acute intranasal intoxication with mercuric chloride taken accidently instead of cocaine - A case report.

CONTEXT: Mercuric chloride (mercury (II) chloride) belongs to inorganic mercury compounds characterized by good water solubility and associated high toxicity. The paper describes an unusual case of intranasal intoxication with corrosive sublimate confused with cocaine by a young male. CASE REPORT: Intranasal administration of corrosive sublimate caused severe local symptoms of chemical burn within the nasal cavity. From the 2nd day the patient developed symptoms of renal dysfunction with transient polyuria and serum retention of nitrogen metabolites. The patient was undergoing chelation therapy with DMPS, N-acetylcysteine and d-penicyllamine. Four procedures of haemodialysis were performed with simultaneous DMPS and N-acetylcysteine treatment. The urine mercury level on the first day of hospitalization was 1989 µg/L, and after 26 days of treatment returned to the physiological level. During treatment renal function was normalized, the patient was discharged in general good condition. DISCUSSION: Mercuric chloride is readily absorbed from the nasal cavity. Its administration may cause intoxication manifested by both chemical burn at the exposure site and systemic symptoms, particularly renal impairment. Even in case of renal dysfunction the use of DMPS seems safe, if haemodialysis is performed at the same time. Simultaneous haemodialysis and chelation therapy may accelerate elimination of mercury from the organism.

Acute Elemental Mercury Poisoning Masquerading as Fever and Rash.

This is a case series of 3 children from a single family who developed symptomatic elemental mercury poisoning requiring hospitalization and chelation. The mercury exposure primarily occurred in the home but the mercury was also tracked to one of their schools requiring environmental cleanup at both the home and school. The clinical assessment and management, as well as public health investigation and response, are discussed. There are many lessons learned in this difficult, often delayed, diagnosis. Early recognition of this environmental toxic exposure is essential. Communication between the clinicians and public health officials played a critical role. Public education prevented panic. Proper environmental sampling, and assessment and management of those exposed, were a few of the many challenges faced in this complicated case series.

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.

The Association Between Mercury Exposure and Atopic Dermatitis in Early Childhood: A Mothers and Children's Environmental Health Study.

BACKGROUND: Atopic dermatitis is a chronic and relapsing inflammatory skin disease. Although mercury has been suggested as a risk factor, the underlying mechanism and the relationship between mercury and atopic dermatitis remains unclear. The objective of the present study was to investigate the relationship between mercury exposure and the presence of atopic dermatitis in early childhood. METHODS: This study is part of the prospective Mothers and Children's Environmental Health cohort study. A total of 1,751 pregnant women were enrolled in Mothers and Children's Environmental Health. After delivery, children were followed up. Blood samples were collected and mothers were asked about the presence of atopic dermatitis in their children via a questionnaire at 6, 12, 24, 36, and 60 months of age. RESULTS: After excluding participants who did not meet the inclusion criteria, a total of 1,061 mother-children pairs were included in the analysis. The geometric mean of mercury concentrations in cord blood was 5.1 µg/L. In adjusted models, cord blood mercury exposure (odds ratio [OR] = 1.1; 95% confidence interval [CI] = 1.0, 1.2 at 12-24 months) and postnatal mercury exposure (OR = 1.2; 95% CI = 1.0, 1.5 at 24-36 months, OR = 1.4; 95% CI = 1.1, 1.8 at 48-60 months) were associated with the presence of atopic dermatitis in children. CONCLUSIONS: Postnatal mercury exposure at 24 months of age increases the risk of atopic dermatitis in children.

[Clinical characteristics, treatment and outcome of chronic mercury-related nephrotic syndrome].

Objective: To investigate the etiology, clinical features, treatment and outcome of nephrotic syndrome associated with chronic mercury poisoning. Methods: From June 2013 to April 2018, Beijing Chaoyang Hospital, Capital Medical University received 33 patients with chronic mercury-neutral nephrotic syndrome. The clinical manifestations, laboratory tests, treatment methods, and outcomes were analyzed. Results: Among the 33 patients, 27 patients had mercury exposure due to daily-life contact and the other 6 patients were caused by iatrogenic mercury. The symptom was characterized by typical nephrotic syndrome such as lower extremity edema and proteinuria at first onset. The treatment was based on mercury-removing treatment, 19 cases were treated with mercury removal alone, 16 cases were completely relieved; 10 cases were treated with mercury removal and glucocorticoids, all of which were completely relieved; 4 cases were treated with mercury removal, glucocorticoids and immunosuppressive agents, all complete remission; clinical complete remission rate is about 90.9% (30 cases in total) . Urinary mercury levels decreased the fastest between the first and second courses of mercury treatment, but the total amount of urine protein increased. As the amount of urinary mercury excreted increased, the total amount of urine protein decreased gradually (Z=2.86, P<0.01) . Conclusion: The clinical features of chronic mercury-induced nephrotic syndrome are non-specific, easy to be misdiagnosed and missed. The treatment is mainly treated with mercury removal treatment. The prognosis is good. In severe cases, glucocorticoid therapy can be supplemented.

The life-threatening rash of poisoning.

Dermatology is frequently viewed by physician and surgical colleagues as a specialty with few emergencies. Although the majority of dermatology practice is in the office setting, cutaneous emergencies do occur through referrals from primary care and as ward consults. Even though cutaneous signs of poisoning would be an uncommon emergency consultation, it is important for dermatologists to be aware of the clinical presentations so as to be able instigate appropriate time critical treatments.

Effects of Chronic Exposure to Mercury on Angiotensin-Converting Enzyme Activity and Oxidative Stress in Normotensive and Hypertensive Rats / Efeitos da Exposição Crônica ao Mercúrio sobre a Atividade da Enzima Conversora de Angiotensina e Estresse Oxidativo em Ratos Normotensos e Hipertensos

Abstract Background: Mercury's deleterious effects are associated with increased cardiovascular risk. Objective: To determine whether chronic exposure to inorganic mercury increases the activity of angiotensin-converting enzyme and its relationship with oxidative stress in several organs and tissues. Methods: We studied male Wistar and spontaneously hypertensive rats (SHR) (3-month-old) exposed or not to HgCl2 for 30 days. At the end of treatment, we investigated the following: changes in body weight, hemodynamic parameters, angiotensin-converting enzyme (ACE) activity and oxidative stress in the heart, aorta, lung, brain and kidney in hypertensive compared to normotensive animals. A value of p < 0.05 was considered significant. Results: Chronic exposure to HgCl2 did not affect weight gain in either group. Systolic blood pressure, measured weekly, did not increase in Wistar rats but showed a small increase in SHR rats. We also observed increases in left ventricular end-diastolic pressure and ACE activity in the plasma and hearts of normotensive rats. In the SHR+Hg group, ACE activity increased in plasma but decreased in kidney, lung, heart, brain and aorta. Oxidative stress was assessed indirectly by malondialdehyde (MDA) production, which increased in Hg-treated rats in both plasma and heart. In the SHR+Hg group, MDA increased in heart and aorta and decreased in lungs and brain. Conclusion: These results suggest that chronic exposure to inorganic mercury aggravates hypertension and produces more expressive changes in ACE activity and oxidative stress in SHRs. Such exposure affects the cardiovascular system, representing a risk factor for the development of cardiovascular disorders in normotensive rats and worsening of pre-existing risks for hypertension.

Resumo Fundamento: Os efeitos deletérios do mercúrio estão associados ao risco cardiovascular aumentado. Objetivo: Determinar se a exposição crônica ao mercúrio inorgânico aumenta a atividade da enzima conversora de angiotensina e sua relação com o estresse oxidativo em vários órgãos e tecidos. Métodos: Estudamos ratos Wistar e ratos espontaneamente hipertensos (SHR) (3 meses de idade) expostos ou não a HgCl2 por 30 dias. Ao final do tratamento, investigamos: alterações de peso, parâmetros hemodinâmicos, atividade da enzima conversora de angiotensina (ECA) e estresse oxidativo no coração, aorta, pulmão, cérebro e rim de animais hipertensos comparados a animais normotensos. Um valor de p < 0,05 foi considerado significativo. Resultados: A exposição crônica ao HgCl2 não afetou o ganho de peso em nenhum dos grupos. A pressão arterial sistólica, medida semanalmente, não aumentou em ratos Wistar, mas mostrou um pequeno aumento nos ratos SHR. Também observamos aumentos na pressão diastólica final do ventrículo esquerdo e na atividade da ECA no plasma e no coração de ratos normotensos. No grupo SHR + Hg, a atividade da ECA aumentou no plasma, mas diminuiu no rim, pulmão, coração, cérebro e aorta. O estresse oxidativo foi avaliado indiretamente pela produção de MDA, que aumentou nos ratos tratados com Hg tanto no plasma quanto no coração. No grupo SHR + Hg, o MDA aumentou no coração e na aorta e diminuiu nos pulmões e no cérebro. Conclusão: Estes resultados sugerem que a exposição crônica ao mercúrio inorgânico agrava a hipertensão e produz mudanças mais expressivas na atividade da ECA e no estresse oxidativo em SHRs. Essa exposição afeta o sistema cardiovascular, representando um fator de risco para o desenvolvimento de distúrbios cardiovasculares em ratos normotensos e para piorar riscos pré-existentes para hipertensão.

Unusual complication of an Alaskan cruise: thinking outside the box.

A 69-year-old man with a medical history of hypertension and diabetes presented with altered mental status once he returned from a 14-day Alaskan cruise. An extensive workup for stroke was negative. His physical examination was normal without any focal motor deficits, but he had developed memory loss and paresthesia. He admitted to eating a lot of fish when he was in Alaska. The whole-blood mercury level was found to be elevated. He was managed conservatively and his symptoms resolved completely in a few days. This led to a diagnosis of organic mercury toxicity.