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Message: <blockquote data-quote="Oldvatr" data-source="post: 2598533" data-attributes="member: 196898">OK think I understand the DKA aspect.  Most of the info on SGLT2 meds harps on about excretion of glucose in the wee as the primary modus operandi of this class of drugs.  However, what is known but not said is that the med increases glucagon, which in turn lowers insulin production, and induces ketosis by lipolysis.  So anyone with insulin deficiency may find their insulin dropping and their ketones rising (like my 8 mmol.l) and this can lead to DKA since the glucose in the blood is not being used or stored since the body is turning into a fat burner instead.  The med itself overrides the body mechanisms and hence the ketosis will remain as long as the med is in control.  As the med passes its half life, the body will normalise and store glucose away as normal so the bgl levels drop again and the ketones also drop.  So that T1D patient probably did have a full DKA but by the time they got her into A&E and sorted it out her bloods were returning to her residual state  where she probably had enough self propelled insulin to recover to the levels they measured.There is another case of euDKA on this drug.  Again it was someone who needed continued post release insulin therapy after the event since they too were found to be insulin deficientSo it does seem that when I felt a bit off and measured my ketones at 4mmol/l then my 8mmol/l then I was on my way to la la land but the drug dissipated in time thus giving a miracle recovery from this miracle drug.  I now have no doubts about stopping it.  Il ne passeront pas!</blockquote>

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