AI Article Synopsis
- The study aimed to classify headache syndromes in patients treated with calcineurin inhibitors like cyclosporine and tacrolimus, and to see if these medications affect nitric oxide (NO) production in brain cells.
- Out of 74 patients observed after organ transplants, only 18 experienced no headaches, while most reported new or worsened headache symptoms, primarily migraines.
- The research indicated that calcineurin inhibitors led to increased production of nitric oxide in brain microvascular cells, suggesting that endothelial dysfunction linked to NO production could be contributing to these headaches.
Article Abstract
Objective: To classify the headache syndromes under treatment with calcineurin inhibitors and to investigate whether the latter influence the nitric oxide production of human brain microvascular cells (HBMEC).
Background: Single cases of cyclosporine-induced headaches have been reported. Since calcineurin inhibitors are known to influence the renal metabolism of NO, a key molecule in tension-type headache and migraine, we were interested whether calcineurin inhibitors might change NO metabolism in HBMEC as well.
Design And Methods: Headache symptoms of 74 patients receiving cyclosporine and/or tacrolimus for organ transplantation were retrospectively assessed. Furthermore, the effect of cyclosporine and tacrolimus on nitric oxide production in human brain microvascular endothelial cells was investigated after incubation.
Results: Only 18 of the 74 patients reported no headache 1-36 months after liver, lung, or bone-marrow transplantation, 28 reported a new headache, and 17 an increase in the frequency or intensity of a pre-existing headache. The headache was generally classified as migraine without aura (IHS 1.1) or migraine-like headache (IHS 1.6). Furthermore, we found significantly increased NO production after co-incubation of calcineurin inhibitors with human brain microvascular endothelial cells.
Conclusion: The pathophysiological mechanism of these headaches may be connected with an endothelial dysfunction in terms of increased production of NO.
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| http://dx.doi.org/10.1111/j.1526-4610.2005.05046.x | DOI Listing |
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