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Lead Poisoning: Clinical Presentation, Diagnosis, and Treatment
abstract
This abstract is available on the publisher's site.
Access this abstract nowA 47-year-old man presented to the general medicine clinic with a 6-month history of wrist drop. He also reported a 3-year history of abdominal pain and constipation, a 14-month history of confusion, and a 1-year history of darkening of his tongue and gums. For the past 5 years, he had worked as a manual laborer in a lead–acid car battery factory. Physical examination was notable for tongue hyperpigmentation (Panel A) and gingival “lead lines” — bluish pigmentation along the gum line that is seen in patients with lead poisoning who have impaired dental hygiene (Panel B). Wrist drop of both arms (Panel C) plus impaired attention, working memory, and executive processing were observed on neurologic examination. Laboratory studies showed microcytic anemia, normal kidney function, a normal manganese level, and a blood lead level of 83 µg per deciliter (4.0 µmol per liter; reference value, <10 µg per deciliter [<0.5 µmol per liter]). A diagnosis of chronic lead poisoning was made. Chelation therapy was initiated. The patient stopped working in the factory, and the health care team reported the occupational exposure. At a 6-month follow-up visit, the blood lead level was 32 µg per deciliter (1.5 µmol per liter). The patient’s gastrointestinal and neurologic symptoms had abated, but the mucosal hyperpigmentation was unchanged.
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Lead Poisoning
N. Engl. J. Med 2023 May 04;388(18)e63, S Dhar, D GargFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
Lead is a bluish-gray nonessential heavy metal known to cause several preventable morbidity and fatal consequences. Children (due to “pica syndrome”) and individuals with occupational chronic exposure are particularly affected groups, especially in developing countries. On the other hand, in developed countries, lead poisoning is declining progressively due to increased industrial surveillance.
Human exposure is usually confirmed by blood lead concentrations (reference value, <10 μg/dL or <0.5 μmol/L). After absorption, lead is distributed to the brain, liver, kidneys, and bones, with teeth and bones being the storage compartments. As one image is worth more than a thousand words, describing the signs by images is a good approach to rapidly suspect a particular intoxication or exposure. Indeed, several previous studies have highlighted the relevance of images in clinical and forensic medicine for presumptive diagnosis.
This article describes a 47-year-old Indian man with a 6-month history of wrist drop and a 1-year history of darkening of his tongue and gums following occupational exposure to lead. Colic abdominal pain, nausea, vomiting, obstipation, anemia with basophilic stippling of red cells due to the inhibition of enzymes of heme synthesis, blue-purplish (ie, “Burton’s line”) gum deposits at the base of the teeth, renal tubulopathies, headaches, cognitive and memory disorders, and emotional impairment and motor neuropathies with muscle weakness are the common findings related to lead poisoning. In particular, the “Burton’s line” represents a typical clinical sign related to lead exposure, suggested to be due to a reaction between the circulating lead and sulfur ions released during oral bacterial activity, which leaves lead sulfide deposits. Differential diagnosis is needed for “bismuth line,” which has a similar appearance but is a much rarer and less toxic condition. Lead neuropathy includes weakness of the wrist and finger extensors and may cause bilateral wrist drops (also known as radial nerve palsy or lead palsy), as evidenced by this case report. This peripheral neuropathy is caused by degenerative changes in motor neurons and their axons with myelin sheaths as a side effect. It involves the upper extremities more than the lower extremities, and it usually manifests as a symmetrical or asymmetrical wrist drop.
Following chelation (most commonly, D-penicillamine, ethylenediaminetetraacetic acid, or dimercaprol) and stopping working at the factory, blood lead concentrations declined and gastrointestinal and neurologic symptoms decreased, while mucosal hyperpigmentation persisted.