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Sun Exposure and Amyotrophic Lateral Sclerosis
- Israel Steiner, MD;
- Bettina Birmanns, MD; and
- Amos Panet, PhD
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TO THE EDITOR:
Recently, mutations in the gene for Cu/Zn superoxide dismutase, an enzyme that scavenges the toxic free-radical superoxide anion (O2-), were reported in patients with familial amyotrophic lateral sclerosis [1]. This defective dismutase could be responsible for progressive motor neuron damage in amyotrophic lateral sclerosis. Although the familial version of the disorder has several unique features distinguishing it from the sporadic disease, the clinical and pathologic similarities [2] suggest a common pathogenesis. If free radicals play a role in the sporadic disease, one would expect a higher disease incidence in populations exposed to environmental factors, such as solar energy, associated with increased production of O2-[3].
We therefore examined the records of the Hadassah University Hospital and identified 69 hospitalized patients who developed sporadic amyotrophic lateral sclerosis between 1979 and 1992. From 1979 to 1985, 31 patients developed the disease, and 38 developed it during the next 7 years. The patients included 50 men (72.4%; mean age at disease onset, 54 years) and 19 women (mean age at onset, 57 years). Mean age at onset for the entire group was 54.5 years. These sex and age distributions are in accord with other studies [2], including data on patients with the disease in Israel [4]. Twenty-seven patients (39%), all men, were either farmers or building construction workers. This observation was remarkable because the percentage of people who work in agriculture and building construction in Israel was no more than 12% between 1980 and 1990 [5].
The interpretation of this observation requires caution because we were unable to obtain information on length of exposure to solar energy and because ours is a referral hospital and therefore represents a highly selected patient population. In addition, we did not have an appropriate control group.
Nonetheless, our findings indicate the possibility of an increased incidence of sporadic amyotrophic lateral sclerosis among persons chronically exposed to sunlight. If this is true, we suggest the following hypothesis: The disease, both sporadic and familial, results from free-radical-induced motor neuron cellular damage. In the familial disease, a partially functional, mutated superoxide dismutase fails to protect from O (2)--induced damage during many decades of incompletely effective scavenging. In some sporadic cases, the motor neuron damage is caused by the increased load of free radicals in the presence of environmental factors that produce them in excess.
Israel Steiner, MD
Bettina Birmanns, MD
Amos Panet, PhD
Hadassah University Hospital; Jerusalem, 91120
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
