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.

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.

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.

[False erythermalgia]. / Les fausses erythermalgies.

The differential diagnosis of erythermalgia is sometimes complicated by the absence of consensus on proposed diagnostic criteria. Unwarranted diagnosis can result from any clinical situation leading to burning sensations in the limbs. This can occurs in patients with peripheral neuropathies who often experience dysesthesia when going to bed when the legs are under the covers; in such cases, redness and local warmth are missing. Venous insufficiency can also produce sensations of warm feet, often at retiring, together with edema and an increase in local heat. Algodystrophy, during the inflammatory phase can also mimic erythermalgia with intense pain and local modifications. Nevertheless, the unilateral aspect and persistence of the symptoms together with the post-traumatic situation usually directs the diagnosis. Acrodynia is a rare disease caused by excessive mercury intake and should be discussed in children. Vasomotor impairment in the limbs is the main sign. The red color of the hands and feet is accompanied by intense paroxysmal burn-type pain. The diagnosis is confirmed by high mercury levels in urine. Fabry's disease is a hereditary sphingolipidosis transmitted on chromosome X and occurs predominantly in men, often starting early in childhood with burning sensation in the limbs. The diagnosis should be entertained in children with pseudo-erythermalgia and is confirmed by chromatographic search for abnormal sphingolipids in the urine.

[Morvan's fibrillary chorea and acrodynic syndrome following mercury treatment]. / Chorée fibrillaire de Morvan et syndrome acrodynique après un traitement mercuriel.

A 31 year-old inhabitant of French Guiana was prescribed mercuric iodide per os for two and a half months. Shortly before the end of the treatment he developed fasciculations in the trunk and particularly the lower limb muscles, distal painful paresthesias with vasomotor disorders, episodes of excessive perspiration and palmoplantar erythema, moderate fluctuating hypertension, progressive loss of weight and irritability with insomnia. Clinical and electrical signs of neuropathy were lacking. The clinical picture was that of Morvan's fibrillary chorea with acrodynia, the conditions of onset strongly suggesting a mercurial intoxication. Blood and particularly urine mercury levels were elevated. Administration of dimercaprol (BAL) considerably increased urinary excretion of mercury and there was progressive improvement and finally recovery after two months of BAL treatment. This case exemplifies the possible co-existence of fibrillary chorea and acrodynia. Whereas in many cases of fibrillary chorea a precise etiology cannot be determined, the affection can be induced by mercury as by gold administration. The fact that cases of fibrillary chorea due to mercury poisoning are rarely reported may be the result of individual patient hypersensitivity or particular metabolic absorption and excretion features of mercury. This case cannot be included within the continuous activity syndrome of muscle fibers described by Isaacs, since muscle contractures were absent and there was associated acrodynia. Moreover, there was no latent polyneuropathy, in spite of the intense fasciculations. It must be concluded, therefore, that in spite of its rarity fibrillary chorea should keep its semiologic autonomy.

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.

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.

Acute mercury poisoning (acrodynia) mimicking pheochromocytoma in an adolescent.

A 14-year-old boy was seen because of irritability, insomnia, lethargy, and profuse sweating, together with hypertension (blood pressure: 160/120 mm Hg), tachycardia, and a diffuse erythematous rash with desquamation of the palms and soles. Initial biochemical investigation suggested a diagnosis of pheochromocytoma, but subsequently a history of exposure to mercury vapor was obtained. This case emphasizes the clinical and biochemical similarities between mercury poisoning (acrodynia) and pheochromocytoma.