To the Editor: Two cutaneous signs of mercury toxicity have recently been postulated. One consists of scattered or localized small erythematous spongiotic papules usually seen in people under 501 and the other is transient acantholytic dermatitis (Grover’s Disease) which consists of small erythematous, often pruritic, scaly or crusted papules, usually seen in people over 50 and often favoring sun damaged skin. Both of these signs have been linked to macular degeneration and may help to identify mercury as the causative agent of that disease.2 There have been numerous attempts at linking Parkinson disease to environmental factors but to date, nothing has been conclusively determined and the cause of Parkinson disease remains elusive.3
Materials and Methods
Fourteen patients with Parkinson disease were randomly selected and examined for signs of mercury toxicity. After obtaining informed consent, all patients had a physical examination, a 2 mm skin biopsy and a blood specimen for mercury which was measured by inductively coupled spectometry. As a control group, 14 patients with no signs of Parkinson disease were randomly selected and examined for signs of mercury toxicity.
Results
None of the patients with Parkinson disease were aware of or complained of any skin problems prior to examination. Of the 14 patients, 13 had 1–2 mm erythematous scaly papules of chest, abdomen, or back (#2–40) which showed characteristic Grover’s disease on biopsy and 13 of the 14 had measurable blood mercury levels (mean 5.2 micrograms/Liter). The fact that both skin signs and blood levels can fluctuate means that the one discrepancy in each series could represent a false negative. In the control group, none of the patients had any cutaneous signs of mercury toxicity and only 2 had measurable blood mercury levels (10 and 16 micrograms/Liter).
Comment
These results are strikingly similar to those obtained with macular degeneration and suggest that both diseases may represent part of the spectrum of chronic low levels of mercury poisoning in susceptible individuals. As part of this study, electron microscopy was performed on 3 patients and showed thinning and gaps in the basement membrane of the skin which could possibly represent a portal of entry of mercury into the epidermis and if Grover’s disease is proven to be a cutaneous component of Parkinson disease and macular degeneration, explain why some patients are afflicted by these diseases and why there seems to be some genetic susceptibility. Finally, recent studies have shown that mitochondrial dysfunction may play a role in the pathogenesis of Parkinson disease.3 In Grover’s disease, the epidermal cell’s inability to manufacture intracellular adhesion proteins also suggests a similar pathogenesis4 and mercury which has affinity for the sulfide bonds in the mitochondria,5 could represent the toxin in both diseases.
While these series are relatively small, the evidence suggests that Parkinson disease, macular degeneration and Grover’s disease may have a common etiology and further studies on the role of mercury in their etiologies is warranted. If these findings can be confirmed, then Grover’s disease might represent an important predictive sign for people at risk to develop Parkinson disease and macular degeneration and these diseases might be greatly reduced or even eradicated through strict and prompt environmental measures.
Paul I Dantzig, MD
Columbia University
New York, New York
References
1. Dantzig PI. A New Cutaneous Sign of Mercury Poisoning?
J Am Acad Dermatol. 2003;49:1109–1111.
2. Dantzig PI. Age Related Macular Degeneration and Cutaneous Signs of Mercury Toxicity.
Cutan Ocul Toxicol. 2005;24:1–7.
3. Steece-Collier K, Maries E, Kordower J. Etiology of Parkinson’s Disease: Genetics and Environment revisited.
Proc Natl Acad Sci. 2002;99:13972–19374.
4. Hashimoto K, Fujiwara K, Tada J, Harada M, Setoyama M, Eto H. Desmosomal Dissolution in Grover’s Disease, Hailey-Hailey Disease and Darier’s Disease.
J Cutan Pathol. 1979;22:488–501.
5. Shenker BJ, Guo TL, Shapiro IM. Low-level Mercury Exposure Causes Human T-cells to undergo Apoptosis: Evidence of Mitochondrial Dysfunction.
Environ Res. 1998;77:149–159.
