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Correspondence to:

ARTICLES:
Alvaro Alonso, Luis A. García Rodríguez, Giancarlo Logroscino, and Miguel A. Hernán
Gout and risk of Parkinson disease: A prospective study
Neurology 2007; 69: 1696-1700 [Abstract] [Full text] [PDF]
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Correspondence published:

[Read Correspondence] Gout and risk of Parkinson disease: A prospective study
Yasuo Iwasaki, Osamu Kano,Ken Ikeda   (24 January 2008)
[Read Correspondence] Gout and risk of Parkinson disease: A prospective study
Ilana Schlesinger, MD, Naomi Schlesinger, MD, Robert Wood Johnson Medical School, New Brunskwick, NJ   (24 January 2008)
[Read Correspondence] Reply from the authors
Alvaro Alonso, Miguel A. Hernan, Department of Epidemiology, Harvard School of Public Health   (24 January 2008)

Gout and risk of Parkinson disease: A prospective study 24 January 2008
 Next Correspondence Top
Yasuo Iwasaki,
Toho University Omori Hospital
6-11-1,Omorinishi,Ota-ku,Tokyo ,Japan,
Osamu Kano,Ken Ikeda

Send Correspondence to journal:
Re: Gout and risk of Parkinson disease: A prospective study

yaso{at}med.toho-u.ac.jp Yasuo Iwasaki, et al.

We read the article by Alonso et al with great interest. [1] They conclude the initiation of anti-gout medication is associated with a lower risk of developing Parkinson Disease (PD).

We have determined an association between serum uric acid (UA) in neurodegenerative disorders such as PD, ALS, and AD. In our research of 100 cases with PD, there are no significant differences in the serum level of PD and controls. Correlation coefficients in the PD group showed no significant relationships between the variable age, sex, duration, and clinical characteristics of PD. There is no past history of gout in our PD patients. UA is product of purine metabolism in mammals. UA is an important natural antioxidant and acts as a scavenger of free radicals. [2]

We would like the authors to clarify several points. Firstly, were all patients with high levels of UA treated with anti-gout drugs? In addition, was there any possibility that the anti-gout medicine possessed neuroprotective action to reduce the occurrence of developing PD? We would also like to know whether there were any cases of overdoses of anti-gout medicine and if so, were there subsequent lower levels of UA and still the risk of developing PD?

Finally, is there a possibility that anti-gout medicines could prevent the reduction of nigral neuronal loss; and is it possible to take a medicine to raise the level of UA and not developing PD?

Chronological serological changes or measurement of cerebrospinal fluid level of UA may be needed to determine whether metabolism of UA may influence neuronal loss in the substantia nigra in PD.

References

1.Alonso A, Rodriguez LAG, Logroscino G,Hernan MA. Gout and risk of Parkinson disease. Neurology 2007;69:1696-1700.

2.Davies KJ,Sevanian A,Muakkassah-Kellf SF,Hochstein P.Uric acid-iron complex. A new aspect of the antioxidant functins of uric acid. Biochem J 1986;235:747-754.

Disclosure: The authors report no conflicts of interest.

Gout and risk of Parkinson disease: A prospective study 24 January 2008
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Ilana Schlesinger, MD,
Department of Neurolgy Rambam Health Care Campus
Haifa, Israel,
Naomi Schlesinger, MD, Robert Wood Johnson Medical School, New Brunskwick, NJ

Send Correspondence to journal:
Re: Gout and risk of Parkinson disease: A prospective study

i_schles{at}rambam.health.gov.il Ilana Schlesinger, MD, et al.

The data presented by Alonso et al. on gout and the risk of Parkinson disease (PD) are interesting. [1] However, a weakness in the design of the study is the reliance on the General Practice Research Database, a large population-based database in the UK.

The gold standard for establishing a definite diagnosis of gout has been demonstrating the presence of monosodium urate crystals in aspirated joint fluid or tophus. [3] However, physicians do not routinely perform synovial fluid analysis opting instead to reach a diagnosis based on clinical features and demonstration of hyperuricemia. [4] There are many limitations to this diagnostic approach.

Of 9,108 consecutive new patients seen in an outpatient rheumatology clinic, 155 (1.7%) were diagnosed as having gout. However, a higher number (164/1.8%) had been incorrectly diagnosed as having gout in the community. [5]

A recent study of the validity of gout diagnoses in administrative data [6] found that there was low concordance between physician assessments and established gout criteria including American College of Rheumatology, Rome, and New York criteria [4] and that the use of administrative data alone in epidemiologic research on gout may lead to misclassification and provide an inadequate standard to confirm gout diagnoses.

References

3.McCarty DJ, Hollander JL. Identification of urate crystals in gouty synovial fluid. Ann Intern Med 1961;54:452-460.

4.Schlesinger N. Diagnosis of gout: clinical, laboratory, and radiologic findings Am J Manag Care 2005;11:S443-S450.

5.Wolfe F Cathy MA. The misdiagnosis of gout and hyperuricemia. J Rheumatol 1991;18:1232-1234.

6.Harrold LR, Saag KG, Yood RA et al. Validity of gout diagnoses in administrative data. Arthritis Rheum 2007;57:103-108.

Disclosure: The authors report no conflicts of interest.

Reply from the authors 24 January 2008
Previous Correspondence  Top
Alvaro Alonso,
Division of Epidemiology and Community Health, School of Public Health, University of Minnesota
1300 S 2nd St, Suite 300. Minneapolis, MN 55454,
Miguel A. Hernan, Department of Epidemiology, Harvard School of Public Health

Send Correspondence to journal:
Re: Reply from the authors

aalogut{at}alumni.unav.es Alvaro Alonso, et al.

We studied the association between gout and PD in the General Practice Research Database (GPRD).[1] Iwasaki et al inquire about data on uric acid levels and overdoses of anti-gout medication in our study. The GPRD does not record this information.

Schlesinger and Schlesinger point out that diagnoses of gout may be misclassified in our study. We agree but this misclassification is likely small because the incidence of gout in the GPRD is similar to that in other populations.[7]

In addition, because misclassification of gout is most likely non-differential, we could presume that the true association between gout and PD risk is even stronger than the observed association.

References

7. Mikuls TR, Farrar JT, Bilker WB, Fernandes S, Schumacher HR, Jr., Saag KG. Gout epidemiology: results from the UK General Practice Research Database, 1990-1999. Ann Rheum Dis 2005;64:267-272.

Disclosure: The authors report no conficts of interest.


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