Motivation: Lately, I have been meeting too many people with Parkinson's Disease - one of those random streaks of fate. Controllable at first, the disease is pretty disabling as it progresses. I was wondering about causes of this "idiopathic" disease and whether there are protective factors like say eating a salmon each day. During this search, I came across some rumors that calcium channel blockers may be protective against Parkinson's Disease. And, the data?
Paper: Ritz, B. et. al. "L-Type Calcium Channel Blockers and Parkinson Disease in Denmark." Ann. Neurol. (2010) 67: 600-606.
Methods: A case-control study in Denmark using the Denmark National Health Service registry that covers medical service for all citizens. Authors identified initial diagnoses of Parkinson's Disease (PD) between 2001-2006. Cases were identified either by first coded diagnosis of PD or first prescription of PD medication. Controls were chosen after matching for birth year and sex. Patients with any type of dementia or cerebrovascular disease before diagnosis of PD were excluded (along with matched controls). Also excluded were patients with PD who were not prescribed any PD drugs.
Results:
Subjects: In total, the authors identified 1931 cases of PD with 9651 matched controls. Five years prior to the index date of PD, the general health of cases and matched controls as measured by the Charson index was similar.
Non-dihydropyridine Calcium Channel Blockers: Authors looked at prescription drug use two years prior to diagnosis of PD to account for the pre-clinical phase and risk factors for developing PD. For non-dihydropyridine calcium channel blockers (verapamil and diltiazem), no association with PD was found.
Dihydropyridine CCB: For dihydropyridine calcium channel blockers (such as amlodipine or felodipine), authors separated analysis for amlodipine, which has low central nervous system penetrance, and other members of this class, which have higher CNS availability. For amlodipine, no protective effects were found. For other members of dihydropyridine CCB, use was associated with protective effects: odds ratio of 0.70, adjusted confidence interval (0.52-0.94). Of note, there were 55 patients with PD and 368 controls using medications of this class.
Discussion: The paper shows that use of non-hydropyridine calcium channel blockers (excepting amlodipine) was associated with about 30% decreased risk of PD diagnosis. While this paper is a case-control study, the results have some biological plausability. Non-CNS penetrant drugs did not show any effect while CNS penetrant calcium channel blockers had some protective effects. It is plausible that blocking calcium influx into oxidatively stressed cells may provide some degree of protection. On the other hand, the association observed may be indirect indicators of some other condition that is protective. In the study, not much information was provided about details of comorbidities and how comorbidities were different between cases and controls. This study is suggestive but far from definitive in using calcium channel blockers in the clinic. As usual, more rigorous study is needed.
Paper: Ritz, B. et. al. "L-Type Calcium Channel Blockers and Parkinson Disease in Denmark." Ann. Neurol. (2010) 67: 600-606.
Methods: A case-control study in Denmark using the Denmark National Health Service registry that covers medical service for all citizens. Authors identified initial diagnoses of Parkinson's Disease (PD) between 2001-2006. Cases were identified either by first coded diagnosis of PD or first prescription of PD medication. Controls were chosen after matching for birth year and sex. Patients with any type of dementia or cerebrovascular disease before diagnosis of PD were excluded (along with matched controls). Also excluded were patients with PD who were not prescribed any PD drugs.
Results:
Subjects: In total, the authors identified 1931 cases of PD with 9651 matched controls. Five years prior to the index date of PD, the general health of cases and matched controls as measured by the Charson index was similar.
Non-dihydropyridine Calcium Channel Blockers: Authors looked at prescription drug use two years prior to diagnosis of PD to account for the pre-clinical phase and risk factors for developing PD. For non-dihydropyridine calcium channel blockers (verapamil and diltiazem), no association with PD was found.
Dihydropyridine CCB: For dihydropyridine calcium channel blockers (such as amlodipine or felodipine), authors separated analysis for amlodipine, which has low central nervous system penetrance, and other members of this class, which have higher CNS availability. For amlodipine, no protective effects were found. For other members of dihydropyridine CCB, use was associated with protective effects: odds ratio of 0.70, adjusted confidence interval (0.52-0.94). Of note, there were 55 patients with PD and 368 controls using medications of this class.
Discussion: The paper shows that use of non-hydropyridine calcium channel blockers (excepting amlodipine) was associated with about 30% decreased risk of PD diagnosis. While this paper is a case-control study, the results have some biological plausability. Non-CNS penetrant drugs did not show any effect while CNS penetrant calcium channel blockers had some protective effects. It is plausible that blocking calcium influx into oxidatively stressed cells may provide some degree of protection. On the other hand, the association observed may be indirect indicators of some other condition that is protective. In the study, not much information was provided about details of comorbidities and how comorbidities were different between cases and controls. This study is suggestive but far from definitive in using calcium channel blockers in the clinic. As usual, more rigorous study is needed.
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