Case Review

Journal of

CLINICAL NEUROMUSCULAR DISEASE

161

Volume 15, Number 4 June 2014

Peripheral Neuropathy After Hair Dye Exposure: A Case Report Wissam Deeb, MD,* David Cachia, MD,† Colin Quinn, MD,* and Johnny Salameh, MD* Abstract We present a case of length-dependent sensory axonal polyneuropathy due to lead exposure from a cosmetic product. Serial follow-ups showed a direct relationship between the lead level, clinical symptoms, and the polyneuropathy. Our patient had a relatively short-term exposure to lead after misusing a hair dye on his beard. Nerve conduction studies showed a predominantly axonal sensory neuropathy that correlated with lead blood levels and reached 3 times the upper limit of normal. The patient had an unexpected sensory predominant neuropathy. He had a full recovery after stopping the leadcontaining product. Blood lead levels were noted to be below previously reported toxic levels. No other systemic signs of lead toxicity were noted. This could be related to the mucosal route of absorption inducing a reversible injury at lower than previously reported lead levels and after a shorter duration of exposure. Key Words: neuropathy, lead toxicity, electrophysiology, cosmetic product, hair dye

( J Clin Neuromusc Dis 2014;15:161–163)

INTRODUCTION The incidence of lead intoxication has decreased in developed countries with stricter regulations in place to decrease exposure to lead, especially industrial exposure.1 The main routes of exposure are by ingestion, inhalation, or absorption through the skin. A hidden source of lead is increasingly reported in cosmetic products.2,3 We present here a case of lead toxicity due to a cosmetic product at a much lower concentration than previously reported.

CASE REPORT A 52-year-old man presented with a 7-month history of numbness and tingling sensation affecting both feet and hands

bilaterally. Symptoms initially started in his feet with the hands getting involved at a later stage. Over months, the numbness progressed proximally to reach the level of the ankle in his feet, whereas in the arms, he felt this altered sensation up to the wrists bilaterally. He denied weakness in the upper or lower extremities. He had stopped drinking alcohol more than 6 months before the onset of his symptoms. Up to that point, he was drinking about a bottle of wine daily, which was his daily alcohol intake since age 20. Examination showed decreased sensation to light touch and pinprick up to the wrist on the right and up to about midforearm on the left. In the lower extremities, sensation was decreased to the ankle on the right and up to the mid-shin area on the left. Vibration sense was decreased over the first metatarsophalangeal joint and normal over the medial malleolus bilaterally. Joint position sense was normal bilaterally. Romberg test was negative. Reflexes were 1+ at the biceps, triceps, and brachioradialis bilaterally. In the lower extremities, reflexes were 1+ at the knee and absent at the ankle. The rest of the neurological examination was normal. Laboratory studies showed normal blood sugar and glycosylated hemoglobin (HbA1C), normal inflammatory markers, and slightly elevated bilirubin at 1.69 mg/dL. Serum protein electrophoresis with immunofixation, vitamins D, B1, B6, and B12, parathyroid levels, and Lyme screen were all normal. A complete blood count showed a mean corpuscular volume of 98 fL. No basophilic stippling was seen on peripheral smear. A heavy metal screen showed a blood

From the *Department of Neurology, University of Massachusetts, Worcester, MA; and †Department of Neurooncology, MD Anderson Cancer Center, Houston, TX. The authors report no conflicts of interest. Reprints: Wissam Deeb, MD, Department of Neurology, University of Massachusetts, 55 Lake Avenue North, Worcester, MA 01655 (e-mail: wissam.deeb@ umassmemorial.org). Copyright © 2014 by Lippincott Williams & Wilkins

162

Journal of

CLINICAL NEUROMUSCULAR DISEASE

Volume 15, Number 4 June 2014

Deeb et al

lead level of 17.3 mg/dL, which is more than 3 times the upper limit of normal. Electromyography (EMG) performed at the initial presentation revealed moderately reduced amplitudes with slow conduction velocities of sensory and motor responses in both lower extremities suggestive of a predominantly axonal polyneuropathy. On further questioning, the patient had been using a hair dye product to dye his hair and beard. He had started using this product a month before the onset of symptoms applying it about 20 times to his beard. Reviewing the product contents, it was found to contain lead acetate. The patient at this point was strongly advised to stop using this product. Lead levels were sequentially monitored, and over a period of 6 months, the lead levels decreased gradually to within normal limits. At the last clinic visit, 12 months after stopping using the hair dye product, the patient reported dramatic improvement of his symptoms with complete resolution of the symptoms in both the upper and lower extremities. On neurologic examination, sensation in the upper and lower extremities was now normal to light touch and pinprick, with normal vibratory sense. His ankle reflexes were still absent. The rest of the neurological examination was unchanged and nonfocal. A repeat EMG, during the last clinic visit, was normal with no evidence of a largefiber peripheral neuropathy.

DISCUSSION It has been noted that neuropathy occurs mainly after exposure to inorganic lead, with the clinical presentation dependent on the duration and level of lead exposure. Two major forms are described1: one form called “classic” subacute lead neuropathy and is characterized by a motor neuropathy with early and severe involvement of the wrist and finger extensors. The second form is due to “chronic” lead exposure. In this case, the lead levels are usually lower than those leading to subacute neuropathy. This presents with © 2014 Lippincott Williams & Wilkins

a predominant sensory length-dependent neuropathy. It has been noted that the latter form has a poorer recovery rate.1 According to the US Environmental Protection Agency,1,2,4 it has been accepted that a blood lead level of 40 mg/dL is considered to be a “safe” level in adults. A review of literature indicates cases of neuropathy at even lower concentrations (as low as 30 mg/dL),1,4 although these tended to occur after long-term exposure, which might explain the neurologic manifestations at usually safe blood lead levels. Our patient presented with a predominantly sensory polyneuropathy identified both clinically and electrophysiologically after exposure of several months, rather than years, to lead.1 One can postulate that this relatively short exposure to lead might have been enough to cause symptoms due to our patient’s history of chronic alcohol abuse. We hypothesize that the patient’s previous alcohol abuse might have lowered the threshold for nerve damage due to the lead exposure even at levels that are now considered safe secondary to an additive effect from multiple neurotoxins. However, we excluded an alcohol-induced neuropathy as the sole cause of the patient’s symptoms, as we would not have expected the repeat EMG to be completely normal just 1 and a half years after discontinuing alcohol intake. The relatively short-term exposure at a lower cumulative dose might have induced a more reversible injury allowing the neurons to recover after a relatively short exposure to this neurotoxin. It is known that the subacute form of lead exposure is associated with a better prognosis of full recovery unlike the more chronic form. This has been speculated to be related to porphyrin-induced intoxication in the subacute form. Interestingly, our patient had a subacute period of lead exposure but had a predominantly sensory presentation, which usually suggests a chronic exposure. Previous reports of a mixed sensorimotor presentation after subacute exposure to lead exist, but to the best of our knowledge, this is the first

Peripheral Neuropathy After Hair Dye Exposure

reported case of a predominantly sensory axonal neuropathy that correlates with subacute lead exposure.1 The timeline both clinically and electrophysiologically mirrors the levels of lead with complete resolution of symptoms soon after normalization of the lead levels. No causal relationship could be established. Other nonmeasured chemicals or elements could have induced similar symptoms and presentation. While considering these limitations, there is a temporal relationship between the lead level, the patient’s symptoms, and the clinical findings. F. Fluri in Neurology2,3 reported 4 criteria to diagnose lead-induced neuropathy. 1. Presence of a neuropathy demonstrated on both clinical and electrophysiologic basis. 2. Evidence of involvement of other systems. 3. Suitable exposure corresponding to the disease progression and removal of lead exposure resulting in an improvement of the neuropathy. 4. Increased blood lead level and urine levels. Our patient lacks systemic manifestations of lead toxicity, which could have been due to the relatively short exposure time but matches the rest of the criteria. Indeed, the correlation between the blood levels and other serum or blood markers is not established.5

CONCLUSIONS This is the first case report of a patient with neuropathy that was temporally linked to lead acetate exposure from a cosmetic product (hair dye) at blood levels lower than what is considered safe. With the limitations of a case report, blood lead levels at much lower limit than what is considered safe can be associated with neuropathy, particularly in individuals at higher risk of developing neuropathy such as a previous exposure to a neurotoxin in our case alcohol. It also emphasizes the importance to search for unexpected lead sources and to question the pattern of use.6 REFERENCES 1. Thomson RM, Parry GJ. Neuropathies associated with excessive exposure to lead. Muscle Nerve. 2006;33: 732–741. 2. Fluri F, Lyrer P, Gratwohl A, et al. Lead poisoning from the beauty case: neurologic manifestations in an elderly woman. Neurology. 2007;69:929–930. 3. Pischik E, Kauppinen R. Lead poisoning from the beauty case: neurologic manifestations in an elderly woman. Neurology. 2008;71:302–303. 4. Chia SE, Chia HP, Ong CN, et al. Cumulative blood levels and nerve conduction parameters. Occup Med (Lond). 1996;46:59–64. 5. Carton JA, Maradona JA, Arribas JM. Acute-Subacute lead poisoning. Clinical findings and comparative study of diagnostic tests. Arch Intern Med. 1987;147:697–703. 6. Marzulli FN, Watlington PM, Maibach HI. Exploratory skin penetration findings relating to the use of lead acetate hair dyes. Hair as a test tissue for monitoring uptake of systemic lead. Curr Probl Dermatol. 1978; 7:196–204. [Abstract].

www.jcnmd.com

Journal of

CLINICAL NEUROMUSCULAR DISEASE Volume 15, Number 4 June 2014

163

Peripheral neuropathy after hair dye exposure: a case report.

We present a case of length-dependent sensory axonal polyneuropathy due to lead exposure from a cosmetic product. Serial follow-ups showed a direct re...
80KB Sizes 3 Downloads 2 Views