Description, Causes and Risk Factors:
A syndrome caused almost exclusively in the past by mercury poisoning: in children, characterized by erythema of the extremities, chest, and nose, gastrointestinal symptoms and by polyneuritis; in adults, characterized by anorexia, photophobia, sweating, and tachycardia.
Acrodynia was first recognized in France in 1828 (Hanson 1987), and the term was introduced in 1830 by Chardon (Chardon, 1830). The term is derived from Greek, denotes painful extremities (Gorlin et al, 1976).
This is a condition where high levels of mercury accumulate in the body. It can be caused by consuming foods or items contaminated with mercury. It can also be caused by chemicals found in paint, teething powders, and batteries. Accidental consumption of the mercury inside of traditional glass thermometers can also cause acrodynia.
Commonly affecting young children in the 1950s due to contaminated teething powders, the condition is noted to cause a pink discoloration in the body's extremities, sensitivity to light sources, irritability, and chronic nerve pain. It can result in severe damage to the nervous system if left untreated.
If the acrodynia is left untreated, then listlessness and fatigue will set in as the immune system tries to ward off the invading contaminant. Weakness and nerve pain in the extremities are hallmarks of a person being adversely affected with mercury poisoning. Prolonged exposure to mercury can cause excessive trembling, reduced cognitive ability, discoloration in the toes, and sleep disturbances.
Many of the toxic effects of mercury are partially or wholly reversible, either through specific therapy or through natural elimination of the metal after exposure has been discontinued. However, heavy or prolonged exposure can do irreversible damage, in particular in fetuses, infants, and young children. Young's syndrome is believed to be a long term consequence of early childhood mercury poisoning. Mercuric chloride may cause cancer as it has caused increases in several types of tumors in rats and mice, while methyl mercury has caused kidney tumors in male rats. The EPA has classified mercuric chloride and methyl mercury as possible human carcinogens (ATSDR, EPA).
Clinical manifestation may include several of the following symptoms which in the well established cases are so distinctive that there is practically no differential diagnosis, pink hands and feet, scarlet tip of nose and cheeks, extreme irritability and restlessness alternating with periods of apathy, insomnia, anorexia, pain in extremities, profuse perspiration, generalized skin rashes, photophobia, desquamation, itching, salivation, loss of teeth, hypotonia which permits the child to assume many different and bizarre positions. There may be albuminuria but no blood or CSF changes, and no characteristic urinary finding except an abnormally raised level of mercury.
Evidence of excess mercury in the urine of affected persons has been noted. A 24-hour urine collection is recommended because urinary elimination of mercury is unpredictable and may vary from day to day or from hour to hour.A value of less than 10 mcg/L is generally considered within reference range.Concentrations greater than 300 mcg/L are considered the threshold of toxicity, and symptoms rarely occur until mercury excretion rises to this level.
Mercury levels in the plasma may be elevated for prolonged periods because of slow release from erythrocytes after oxidation.
Mercury blocks the action of catechol methyltransferase, leading to increased amounts of vanillylmandelic and homovanillic acid in urine.
Excretion of 17-ketosteroid has also been shown to be increased in these patients.
Analysis of hair strands by means of x-ray fluorescence for mercury contamination also may be considered, but the results may be falsely elevated in persons residing in environments with increased ambient atmospheric concentrations or in populations consuming methylmercury-contaminated seafood.
Blood evaluation is recommended, particularly for acute intoxication.Normal levels rarely exceed 15 mcg/L.
Removal of the inciting agent is the goal of treatment. Correcting fluid and electrolyte losses and rectifying any nutritional imbalances (vitamin-rich diets, vitamin-B complex) are of utmost importance in the treatment of the disease.
Recently, the chelating agent meso 2,3-dimercaptosuccinic acid has been shown to be the preferred treatment modality. It can almost completely prevent methylmercury uptake by erythrocytes and hepatocytes.
In the past, dimercaprol (British anti-Lewisite; 2,3-dimer-capto-l-propanol) and D-penicillamine were the most popular treatment modalities. Disodium edetate (Versene) was also used.
N-acetyl-penicillamine has been successfully given to patients with mercury-induced neuropathies and chronic toxicity, although it is not approved for such uses. It has a less favorable adverse effect profile than meso 2,3-dimercaptosuccinic acid.
Hemodialysis with and without the addition of L-cysteine as a chelating agent has been used in some patients experiencing acute renal failure from mercury toxicity.
Peritoneal dialysis and plasma exchange also may be of benefit.
Tolazoline (Priscoline) has been shown to offer symptomatic relief from sympathetic overactivity.
Antibiotics are necessary when massive hyperhidrosis, which may rapidly lead to miliaria rubra, is present. This can easily progress to bacterial secondary infection with a tendency for ulcerating pyoderma.
Risks and benefits of the treatment must be carefully discussed with the physician.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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