RARE DISEASE
Infantile mercury poisoning
Infantile mercury poisoning
Infantile mercury poisoning
Synonyms: Erythroedema polyneuritis, Feer disease, Infantile acrodynia, Infantile mercury intoxication, Pink disease, Swift disease, Swift-Feer disease
Synonyms: Erythroedema polyneuritis, Feer disease, Infantile acrodynia, Infantile mercury intoxication, Pink disease, Swift disease, Swift-Feer disease
Synonyms: Erythroedema polyneuritis, Feer disease, Infantile acrodynia, Infantile mercury intoxication, Pink disease, Swift disease, Swift-Feer disease
Drug discovery
0
drugs
With orphan designations
Overview
Infantile Mercury Poisoning is a rare neurotoxic disorder caused by exposure to elemental, organic, or inorganic mercury, primarily affecting infants and young children. It manifests with acrodynia (erythema, edema, and desquamation of extremities), autonomic dysfunction (hypertension, tachycardia), and neurological symptoms (irritability, muscle weakness, photophobia). Chronic exposure can lead to irreversible neurodevelopmental deficits [1][3][12].
Categories: rare disorders due to toxic effects
Research Papers
27 drug discovery papers about Infantile mercury poisoning, with 1 first-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
27 drug discovery papers about Infantile mercury poisoning, with 1 first-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
categories:
Small molecules
small molecules
2026-05-01 | Beyond acrodynia: infantile mercury vapor poisoning presenting with refractory hypoglycemia and persistent neurological damage.
Infantile elemental mercury poisoning is clinically rare and poses a severe long-term health threat. This report describes a rare case of non-accidental infantile elemental mercury poisoning, in which the infant was continuously exposed to mercury vapor for 20 days starting from postnatal day 15. The infant initially presented with feeding difficulties and respiratory symptoms, which rapidly progressed to respiratory distress and seizure-like episodes at 5 months of age; laboratory tests revealed severe hypoglycemia and metabolic acidosis. Despite 5 days of intravenous glucose infusion and comprehensive support involving mechanical ventilation, sedation, and corticosteroids, hypoglycemia and epileptic symptoms persisted. The diagnosis of mercury poisoning was confirmed by a blood mercury test and governmental investigation, followed by two courses of dimercaptopropane sulfonate (DMPS) chelation therapy, after which hypoglycemia, respiratory symptoms, and epilepsy were effectively managed. The patient was discharged 25 days after admission. CT images revealed no abnormalities in the head at admission, but subsequent MRI at discharge and thereafter indicated persistent brain damage, including signal abnormalities and cerebral atrophy. This case suggests that severe hypoglycemia can be a critical component of infantile elemental mercury poisoning and contributes to persistent neurological injury. It also highlights that the efficacy of chelation therapy is severely limited when treatment is delayed after prolonged exposure. Current chelators such as DMPS have poor blood-brain barrier penetration and cannot effectively remove accumulated inorganic mercury from the CNS, underscoring the urgent need for novel CNS-penetrating therapeutic strategies in delayed presentations.
2023-06-26 | Clinical Spectrum of Mercury Poisoning in India: Case-series from a Poison Control Center.
Mercury is a naturally occurring heavy metal that finds wide application in industrial and household settings. It exists in three chemical forms which include elemental (Hg0 ), inorganic mercurous (Hg+) or mercuric (Hg++) salts, and organic compounds. All forms are highly toxic, particularly to the nervous, gastrointestinal, and renal systems. Common circumstances of exposure include recreational substance use, suicide or homicide attempts, occupational hazards, traditional medicines, and endemic food ingestions as witnessed in the public health disasters in Minamata Bay, Japan and in Iraq. Poisoning can result in death or long-term disabilities. Clinical manifestations vary with chemical form, dose, rate, and route of exposure. To summarize the incidence of mercury poisoning encountered at an Indian Poison Center and use three cases to highlight the marked variations observed in clinical manifestations and long-term outcomes among poisoned patients based on differences in chemical forms and routes of exposure to mercury. A structured retrospective review of the enquiry-database of the Poison Information Center and medical records of patients admitted between August 2019 and August 2021 in a tertiary care referral center was performed. All patients with reported exposure to mercury were identified. We analyzed clinical data and laboratory investigations which included heavy metal (arsenic, mercury, and lead) estimation in whole blood and urine samples. Additionally, selected patients were screened for serum voltage-gated potassium ion channels (VGKC)- contactin-associated protein-like 2 (CASPR2) antibodies. Three cases with a classical presentation were selected for detailed case description. Twenty-two cases were identified between August 2019 and August 2021. Twenty (91%) were acute exposures while two (9%) were chronic. Of these, three representative cases have been discussed in detail. Case 1 is a 3.5-year-old girl who was ought to the emergency department with suspected elemental-mercury ingestion after biting a thermometer. Clinical examination was unremarkable. Chest and abdominal radiography revealed radiodense material in the stomach. Subsequent serial radiographs documented distal intestinal transit of the radiodense material. The child remained asymptomatic. This case exemplifies the largely nontoxic nature of elemental mercury ingestion as it is usually not absorbed from the gastrointestinal tract. Case 2 is a 27-year-old lady who presented with multiple linear nodules over both upper limbs after receiving a red intravenous injection for anemia. Imaging revealed metallic-density deposits in viscera and bones. Nodular biopsy was suggestive of mercury granulomas. A 24-hour urine mercury levels were elevated. She was advised chelation therapy with oral dimercaptosuccinic acid (DMSA). Case 3 is a 22-year-old lady who presented with acrodynia, neuromyotonia, tremulousness, postural giddiness, tachycardia, and hypertension for 2 months, associated with intractable, diffuse burning pain over the buttocks and both lower limbs, 1 month after completing a 3-week course of traditional medications for polycystic ovarian syndrome. A 24-hour urine normetanephrine levels and mercury levels were markedly elevated. Serum anti-VGKC antibodies were present. She was treated with glucocorticoids and oral DMSA with a favorable clinical response. The clinical manifestations of mercury toxicity are highly variable depending on the source, form, and route of mercury exposure and are related to its toxicokinetics.
2022-01-18 | Heavy Metal Mercury and its Toxicity – A Review
Mercury is a toxic heavy metal that naturally found in earth crust, air, water and food. The symbol of Mercury is Hg and atomic number is 80. It is also known as quick silver, liquid silver, para. Mercury is also known as parada. Parada has many blemishes like bhumija, girija, varija, nagaja, vangaja etc. If parada is consumed in this form, causes santapa, jadatwa, vata roga, kushta, murcha and even death, hence it is used after purification. After proper purification parada have been used in rasa aushadi preparation. It exist nature in three forms organic, inorganic and elemental. Organic compound of mercury is more toxic than inorganic compound. Elemental mercury is liquid at the room temperature and less toxic than the two other forms of mercury. Any form of mercury is toxic. The sign & symptoms of toxicity depend upon the type, route, dose and duration of exposure. Human exposed to mercury from breathing in contaminated air, seafood consumption, dental amalgam, gold mining, vaccines containing thiomersal etc. The chronic exposure of mercury damage CNS, lungs, kidney, heart and immune system etc. mercury toxicity can diagnosed by mercury level in hair, blood and urine. Beside the supportive measurement, BAL (british anti lewisite), diamercaprol, dimercaptopropanesulfoxid acid (DMPS), penicillamine and chelating agents are used in treatment for mercury toxicity.
2021-06-01 | Characteristics and treatment of elemental mercury intoxication: A case series
Abstract Background and aims Elemental mercury toxicity is a rare condition which can be difficult to diagnose due to its nonspecific signs and symptoms. The purpose of this investigation is to describe the presenting characteristics and treatment of adult and pediatric patients with elemental mercury poisoning. Methods A retrospective review was performed in six patients with elemental mercury exposure or intoxication who were treated in an outpatient medical toxicology clinic. Clinical signs and symptoms, laboratory assessments, and public health responses were reviewed. Results Headache, anorexia, rash, and personality changes were commonly reported symptoms in pediatric patients; the adult patients were asymptomatic or reported signs and symptoms included myalgias, tremors, and hypertension. Delays in diagnosis were common. Symptomatic patients had 24‐hour urine mercury concentrations greater than 20 mcg/L. Treatment, including removal from the exposure source as well as chelation with dimercaptosuccinic acid, resulted in resolution of signs and symptoms within 6 months of diagnosis. Conclusion The evaluation and treatment of patients with suspected elemental mercury poisoning frequently require a multidisciplinary approach including medical toxicologists and public health officials. A heightened awareness of the clinical presentations of this condition, as well as early identification and removal of patients from the source of exposure and consideration of chelation therapy, can result in accelerated patient recovery.
2018-02-16 | Protective Effect of Leaf Ethanolic Extract Etlingera hemisphaerica Blume Against Mercuric Chloride Toxicity in Blood of Mice.
This research was intended to investigate the protective effect of leaf ethanolic extract Etlingera hemisphaerica Blume (LE3H) against mercuric chloride (HgCl2) toxicity in blood of mice (Mus musculus). The experimental animals, 95 male M. musculus, received drink and food ad libitum. Three materials were tested: LE3H (0.13, 0.26, 0.39 mg/g body weight [bw]) was administered by gavage; HgCl2 (5 mg/kg bw) was administrated by gavage or intraperitoneal injection; and Imunos (the nutritional supplement to stimulate the immune system; 0.2 mg/g bw), as a positive control for LE3H treatment, was given by gavage. Blood samples were taken from the tails for determining number of blood cells. The animals were killed by cervical dislocation (CD), and then blood samples were collected from the hearts for protein electrophoresis. Results revealed the same number of leukocytes with LE3H (0.39 mg/g bw) treatment as with the Imunos treatment. HgCl2 administration increased leukocytes and decreased erythrocytes; HgCl2 administration followed by LE3H (0.39 mg/g bw) treatment protected the amount of blood cells as well as the control. HgCl2 administration showed a new 125 kDa protein and caused overexpression of 48 kDa protein; this protein profile could be protected by LE3H (0.39 mg/g bw) treatment as in the control condition. We conclude that LE3H provides a protective effect against HgCl2 toxicity in blood of M. musculus.
small molecules
2026-05-01 | Beyond acrodynia: infantile mercury vapor poisoning presenting with refractory hypoglycemia and persistent neurological damage.
Infantile elemental mercury poisoning is clinically rare and poses a severe long-term health threat. This report describes a rare case of non-accidental infantile elemental mercury poisoning, in which the infant was continuously exposed to mercury vapor for 20 days starting from postnatal day 15. The infant initially presented with feeding difficulties and respiratory symptoms, which rapidly progressed to respiratory distress and seizure-like episodes at 5 months of age; laboratory tests revealed severe hypoglycemia and metabolic acidosis. Despite 5 days of intravenous glucose infusion and comprehensive support involving mechanical ventilation, sedation, and corticosteroids, hypoglycemia and epileptic symptoms persisted. The diagnosis of mercury poisoning was confirmed by a blood mercury test and governmental investigation, followed by two courses of dimercaptopropane sulfonate (DMPS) chelation therapy, after which hypoglycemia, respiratory symptoms, and epilepsy were effectively managed. The patient was discharged 25 days after admission. CT images revealed no abnormalities in the head at admission, but subsequent MRI at discharge and thereafter indicated persistent brain damage, including signal abnormalities and cerebral atrophy. This case suggests that severe hypoglycemia can be a critical component of infantile elemental mercury poisoning and contributes to persistent neurological injury. It also highlights that the efficacy of chelation therapy is severely limited when treatment is delayed after prolonged exposure. Current chelators such as DMPS have poor blood-brain barrier penetration and cannot effectively remove accumulated inorganic mercury from the CNS, underscoring the urgent need for novel CNS-penetrating therapeutic strategies in delayed presentations.
2023-06-26 | Clinical Spectrum of Mercury Poisoning in India: Case-series from a Poison Control Center.
Mercury is a naturally occurring heavy metal that finds wide application in industrial and household settings. It exists in three chemical forms which include elemental (Hg0 ), inorganic mercurous (Hg+) or mercuric (Hg++) salts, and organic compounds. All forms are highly toxic, particularly to the nervous, gastrointestinal, and renal systems. Common circumstances of exposure include recreational substance use, suicide or homicide attempts, occupational hazards, traditional medicines, and endemic food ingestions as witnessed in the public health disasters in Minamata Bay, Japan and in Iraq. Poisoning can result in death or long-term disabilities. Clinical manifestations vary with chemical form, dose, rate, and route of exposure. To summarize the incidence of mercury poisoning encountered at an Indian Poison Center and use three cases to highlight the marked variations observed in clinical manifestations and long-term outcomes among poisoned patients based on differences in chemical forms and routes of exposure to mercury. A structured retrospective review of the enquiry-database of the Poison Information Center and medical records of patients admitted between August 2019 and August 2021 in a tertiary care referral center was performed. All patients with reported exposure to mercury were identified. We analyzed clinical data and laboratory investigations which included heavy metal (arsenic, mercury, and lead) estimation in whole blood and urine samples. Additionally, selected patients were screened for serum voltage-gated potassium ion channels (VGKC)- contactin-associated protein-like 2 (CASPR2) antibodies. Three cases with a classical presentation were selected for detailed case description. Twenty-two cases were identified between August 2019 and August 2021. Twenty (91%) were acute exposures while two (9%) were chronic. Of these, three representative cases have been discussed in detail. Case 1 is a 3.5-year-old girl who was ought to the emergency department with suspected elemental-mercury ingestion after biting a thermometer. Clinical examination was unremarkable. Chest and abdominal radiography revealed radiodense material in the stomach. Subsequent serial radiographs documented distal intestinal transit of the radiodense material. The child remained asymptomatic. This case exemplifies the largely nontoxic nature of elemental mercury ingestion as it is usually not absorbed from the gastrointestinal tract. Case 2 is a 27-year-old lady who presented with multiple linear nodules over both upper limbs after receiving a red intravenous injection for anemia. Imaging revealed metallic-density deposits in viscera and bones. Nodular biopsy was suggestive of mercury granulomas. A 24-hour urine mercury levels were elevated. She was advised chelation therapy with oral dimercaptosuccinic acid (DMSA). Case 3 is a 22-year-old lady who presented with acrodynia, neuromyotonia, tremulousness, postural giddiness, tachycardia, and hypertension for 2 months, associated with intractable, diffuse burning pain over the buttocks and both lower limbs, 1 month after completing a 3-week course of traditional medications for polycystic ovarian syndrome. A 24-hour urine normetanephrine levels and mercury levels were markedly elevated. Serum anti-VGKC antibodies were present. She was treated with glucocorticoids and oral DMSA with a favorable clinical response. The clinical manifestations of mercury toxicity are highly variable depending on the source, form, and route of mercury exposure and are related to its toxicokinetics.
2022-01-18 | Heavy Metal Mercury and its Toxicity – A Review
Mercury is a toxic heavy metal that naturally found in earth crust, air, water and food. The symbol of Mercury is Hg and atomic number is 80. It is also known as quick silver, liquid silver, para. Mercury is also known as parada. Parada has many blemishes like bhumija, girija, varija, nagaja, vangaja etc. If parada is consumed in this form, causes santapa, jadatwa, vata roga, kushta, murcha and even death, hence it is used after purification. After proper purification parada have been used in rasa aushadi preparation. It exist nature in three forms organic, inorganic and elemental. Organic compound of mercury is more toxic than inorganic compound. Elemental mercury is liquid at the room temperature and less toxic than the two other forms of mercury. Any form of mercury is toxic. The sign & symptoms of toxicity depend upon the type, route, dose and duration of exposure. Human exposed to mercury from breathing in contaminated air, seafood consumption, dental amalgam, gold mining, vaccines containing thiomersal etc. The chronic exposure of mercury damage CNS, lungs, kidney, heart and immune system etc. mercury toxicity can diagnosed by mercury level in hair, blood and urine. Beside the supportive measurement, BAL (british anti lewisite), diamercaprol, dimercaptopropanesulfoxid acid (DMPS), penicillamine and chelating agents are used in treatment for mercury toxicity.
2021-06-01 | Characteristics and treatment of elemental mercury intoxication: A case series
Abstract Background and aims Elemental mercury toxicity is a rare condition which can be difficult to diagnose due to its nonspecific signs and symptoms. The purpose of this investigation is to describe the presenting characteristics and treatment of adult and pediatric patients with elemental mercury poisoning. Methods A retrospective review was performed in six patients with elemental mercury exposure or intoxication who were treated in an outpatient medical toxicology clinic. Clinical signs and symptoms, laboratory assessments, and public health responses were reviewed. Results Headache, anorexia, rash, and personality changes were commonly reported symptoms in pediatric patients; the adult patients were asymptomatic or reported signs and symptoms included myalgias, tremors, and hypertension. Delays in diagnosis were common. Symptomatic patients had 24‐hour urine mercury concentrations greater than 20 mcg/L. Treatment, including removal from the exposure source as well as chelation with dimercaptosuccinic acid, resulted in resolution of signs and symptoms within 6 months of diagnosis. Conclusion The evaluation and treatment of patients with suspected elemental mercury poisoning frequently require a multidisciplinary approach including medical toxicologists and public health officials. A heightened awareness of the clinical presentations of this condition, as well as early identification and removal of patients from the source of exposure and consideration of chelation therapy, can result in accelerated patient recovery.
2018-02-16 | Protective Effect of Leaf Ethanolic Extract Etlingera hemisphaerica Blume Against Mercuric Chloride Toxicity in Blood of Mice.
This research was intended to investigate the protective effect of leaf ethanolic extract Etlingera hemisphaerica Blume (LE3H) against mercuric chloride (HgCl2) toxicity in blood of mice (Mus musculus). The experimental animals, 95 male M. musculus, received drink and food ad libitum. Three materials were tested: LE3H (0.13, 0.26, 0.39 mg/g body weight [bw]) was administered by gavage; HgCl2 (5 mg/kg bw) was administrated by gavage or intraperitoneal injection; and Imunos (the nutritional supplement to stimulate the immune system; 0.2 mg/g bw), as a positive control for LE3H treatment, was given by gavage. Blood samples were taken from the tails for determining number of blood cells. The animals were killed by cervical dislocation (CD), and then blood samples were collected from the hearts for protein electrophoresis. Results revealed the same number of leukocytes with LE3H (0.39 mg/g bw) treatment as with the Imunos treatment. HgCl2 administration increased leukocytes and decreased erythrocytes; HgCl2 administration followed by LE3H (0.39 mg/g bw) treatment protected the amount of blood cells as well as the control. HgCl2 administration showed a new 125 kDa protein and caused overexpression of 48 kDa protein; this protein profile could be protected by LE3H (0.39 mg/g bw) treatment as in the control condition. We conclude that LE3H provides a protective effect against HgCl2 toxicity in blood of M. musculus.
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