Vitamin B6 deficiency and OCPs

[Northerncardinal]

How do OCPs lead to vitamin B6 deficiency? Came across this in First Aid 2016.

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[Reperfused]

Good point. I would like to know the answer to this too.

I do know that Isoniazid is a competitive antagonist of pyridoxal kinase (required for the synthesis of GABA from pyridoxine), that's how it manifests as Vit B6 deficiency.

Don't know exactly how OCPs do that? Something similar perhaps. Anyone please?

 

[Kazaki]

I do know that Isoniazid is a competitive antagonist of pyridoxal kinase (required for the synthesis of GABA from pyridoxine), that's how it manifests as Vit B6 deficiency.

This causes a functional vit b6 deficiency because the vitamin is there, but it can't get activated. The second mechanism is by INH metabolites directly binding pyridoxine.

As for OCPs, it's a bit more complex.
Vit b6 is required to convert homocysteine to cystathione. OCPs increase the levels of homoccysteine, which needs more b6 to be converted into cystathione, causing a deficiency in b6.
I pretty much connected random bits of info to come up with this, but it does make sense. However medscape did say that a deficiency in b6 can cause a rise in homocysteine, the opposite should be true since you consume more b6 to get rid of excess homocysteine.
Feel free to correct me.

 

[IMG217]

According to Katzung *** Isoniazid promotes excretion of pyridoxine, and this toxicity is....***
CMMRS also says *** INH increases the urinary excretion and depletion of pyridoxine (vitamin B6), which is needed for proper nerve function. INH will thus lead to decreased B6 levels..***

But yeah, there are other mechanisms, like the ones mentioned by Reperfused and Kazaki; INH inhibits pyridoxal kinase and binds/inactivates PLP (the active form of vit B6).
So INH
1- increases vit B6 urinary excretion 2- blocks its conversion to the active form (inhibits pyridoxal kinase) 3- inactivates PLP (the active form)

I just can't get the OCP-induced vit B6 deficiency out of my head, nothing conclusive on Google. The vitamin is "depleted", but there's nothing about any Homocysteine-related mechanism. It's just used up in some vit B6-dependent reaction...

 

[Kazaki]

It's just used up in some vit B6-dependent reaction...

Which is homocysteine to cystathione...