Sir,
Calcium biometabolism is usually an aberrant in abnormal parathyroid neoplasm. How
blood calcium level is controlled in such cases is very interesting. The calcium-sensing
receptor (CASR) plays an important role in this regard, and its polymorphism is widely
studied.[1] The interrelationship between parathyroid malignancy, blood calcium, and underlying
CASR polymorphism is very interesting. Whether different CASR polymorphisms have an
effect on the drug treatment of the neoplasm is an important question that needs to
be addressed.
An important parathyroid neoplasm with aberration of blood calcium is type 1 multiple
endocrine neoplasia (MEN1). MEN1 on is usually related to primary hyperparathyroidism
and has a high postsurgery recurrence rate.[2] In a recent study, Filopanti et al. reported the response to cinacalcet and its relationship with the CASR gene variant
Arg990Gly.[3] Filopanti et al. mentioned no significant effect of such a polymorphism.[3] Here, the authors perform reappraisal on the effect of CASR Arg990Gly based on the
quantum medicine assessment on molecular change in the polymorphism using the same
technique as presented in previous publications.[4]
[5]
[6] It can be seen that Arg990Gly has a lower protein molecular weight than naïve type
(the magnitude of decrease molecular mass per molecule is equal to 56.9%). The lower
molecular mass means lower final bioaction product. This implies that MEN1 with CASR
Arg990Gly should have a lower blood calcium level. If MEN1 with CASR Arg990Gly is
responsive to the same dose of cinacalcet, it is likely to result in a less minimizing
of blood calcium level. Of interest, this finding is concordant with the report by
Filopanti et al.[3]
