Inhibition of Behcet's disease by calcitonin.
|
| Abstract |
Behcet's disease (BD) is a chronic, multisystem inflammatory disorder characterized by relapsing oral aphthous and genital ulcers, ocular inflammation, erythemanodosum and folliculitis-like lesions of the skin, arthritis, and central nervous system involvement. Its pathogenesis has not been fully elucidated but the etiology is accepted to be multifactorial, therefore the treatment of Behcet's disease continues to be a major therapeutic challenge. The identification of novel therapeutic agents for the treatment of these disorders is important. Calcitonin (CT), a peptide hormone secreted in response to hypercalcemia, has the dual effect of inhibiting osteoclast recruitment as well as their resorptive activity. A number of reviews have concluded that salmon calcitonin is safe and effective in the treatment of osteoporosis. Calcitonin abrogated the stimulating effect of RANKL or prednisolone; similar results were obtained with OPG. Additionally, the analgesic activity of salmon calcitonin has been shown in several controlled prospective double-blind studies to improve pain. Exogenous calcitonin is thought to cross the blood-brain barrier and to accumulate slowly in the brain, inducing analgesia once sufficient receptors are occupied. Since CT could antagonize resorptive and analgesic activity by competitively binding to CTR and has been considered as a specific antagonist, we postulate that the CT could function as a novel agent to inhibit BD. In our opinion, if the hypothesis proved to be practical, CT could be widely used in clinical settings to treat BD.
|
|---|---|
| Authors | Han Qin, Jun Cai, Hongzhi Xu, Yongqing Gong |
| Journal | Medical hypotheses (Med Hypotheses) Vol. 73 Issue 1 Pg. 24-6 (Jul 2009) ISSN: 1532-2777 [Electronic] United States |
| PMID | 19299090 (Publication Type: Journal Article) |
| Chemical References |
|
| Topics |
|
Join CureHunter, for free Research Interface BASIC access!
Realize the full power of the drug-disease research graph!