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SGLT2 inhibitors: updated advice on the risk of diabetic ketoacidosis
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<blockquote data-quote="Oldvatr" data-source="post: 1732487" data-attributes="member: 196898"><p>DKA is an Acute condition requiring immediate arttention, so it must be finger prick test or CGM type of device. A venous blood test can be assayed in a specialist lab within a few hours, but in a doctors surgery or hospital ER there is probably no immediate access to a YSI plasma analyser or a gas chromatograph facility, and bloods will have to be sent away to a lab for analysis. That route is more accurate than a fingerprick test meter, but accuracy will not help someone in DKA.</p><p></p><p>It is true that there will be delays in the circulatory system that may give false results for a spot check of rising or falling bgl, which is why hospitals will repeat on a few occasions since it takes about one minute for a cycle of the blood to complete and settle down. So in the setting of an ER admission then they should not use just one result to make a diagnosis.</p><p></p><p>You say that the glucose will already be in the cells doing its stuff. This is fine, and is what normally happens. DKA occurs when the glucose is<span style="font-size: 15px"> <u><em><strong><span style="color: #ff4d4d">not</span> </strong></em></u></span>able to get into the cells at all, and remains in the blood stream and bgl rises alarmingly. Something linked to SGLT-2 is stopping the glucose from being used normally. What is different about this version of DKA is that bgl levels do not rise into the high ranges, but remain at what would usually be regarded as a 'safe' i.e. non emergency level.</p><p></p><p>I would also point out that the kidney filtering out of glucose is not an immediate effect, and there is a delay. Bgl does not drop like a stone falling off cliff, but happens over hours. So I would be surprised if SGLT-2 DKA was happening because of a delay problem, unless it is the Stage 1 Insulin Response being suppressed following a meal. However,this means DKA by medication would self correct when the body used up the med, and ER would not be needed. However, this may need further study to evaluate.</p><p></p><p>I will just add that I have never myself experienced a DKA event, but I have had readings that my meter was unable to display except for (HI or KETONE) warnings. so DKA is not the cause of high bgl, but high bgl is a sign of possible DKA. Since I am not Insulin Dependant then it is clear that my body was still producing some of its own insulin, so I recovered naurally without intervention. In fact I felt great when my bgl was above 32 mmol/l and had no indication that I was in danger until I started self monitoring again and saw my meter readings. I was running on high octane glucose and fumes.</p><p></p><p>Edit to add: found this discussion doc on the problem. It too suggests that SGLT2 meds can decrease kidney filtering out of ketone products.</p><p><a href="https://academic.oup.com/jcem/article/100/8/2849/2836082" target="_blank">https://academic.oup.com/jcem/article/100/8/2849/2836082</a></p><p></p><p>Apparently a recent Japanese study demonstrated that SGLT2 med increased Glucagon, which in turn promoted extra lipidolysis thus leading to higher ketone levels being present, regardless of diet. </p><p></p><p>But a LC diet will add its own ketone bodies to the mix, thus amplifying the effect. Low insulin levels also makes things worse. So any Insulin users on LC need to be aware that reducing insulin bolus due to low carb may increase the risk when used in conjunction with these meds. Thus this effect has been identified as being a Class problem caused by this med type. </p><p></p><p>It is already established that this med type is not licenced for use with T1D in the USA, but in UK it is not restricted in this aspect (the restriction was lifted in May 2017) and it is also now being promoted for protecting the kidneys in T1D by NICE. Make of that what you will.......</p></blockquote><p></p>
[QUOTE="Oldvatr, post: 1732487, member: 196898"] DKA is an Acute condition requiring immediate arttention, so it must be finger prick test or CGM type of device. A venous blood test can be assayed in a specialist lab within a few hours, but in a doctors surgery or hospital ER there is probably no immediate access to a YSI plasma analyser or a gas chromatograph facility, and bloods will have to be sent away to a lab for analysis. That route is more accurate than a fingerprick test meter, but accuracy will not help someone in DKA. It is true that there will be delays in the circulatory system that may give false results for a spot check of rising or falling bgl, which is why hospitals will repeat on a few occasions since it takes about one minute for a cycle of the blood to complete and settle down. So in the setting of an ER admission then they should not use just one result to make a diagnosis. You say that the glucose will already be in the cells doing its stuff. This is fine, and is what normally happens. DKA occurs when the glucose is[SIZE=4] [U][I][B][COLOR=#ff4d4d]not[/COLOR] [/B][/I][/U][/SIZE]able to get into the cells at all, and remains in the blood stream and bgl rises alarmingly. Something linked to SGLT-2 is stopping the glucose from being used normally. What is different about this version of DKA is that bgl levels do not rise into the high ranges, but remain at what would usually be regarded as a 'safe' i.e. non emergency level. I would also point out that the kidney filtering out of glucose is not an immediate effect, and there is a delay. Bgl does not drop like a stone falling off cliff, but happens over hours. So I would be surprised if SGLT-2 DKA was happening because of a delay problem, unless it is the Stage 1 Insulin Response being suppressed following a meal. However,this means DKA by medication would self correct when the body used up the med, and ER would not be needed. However, this may need further study to evaluate. I will just add that I have never myself experienced a DKA event, but I have had readings that my meter was unable to display except for (HI or KETONE) warnings. so DKA is not the cause of high bgl, but high bgl is a sign of possible DKA. Since I am not Insulin Dependant then it is clear that my body was still producing some of its own insulin, so I recovered naurally without intervention. In fact I felt great when my bgl was above 32 mmol/l and had no indication that I was in danger until I started self monitoring again and saw my meter readings. I was running on high octane glucose and fumes. Edit to add: found this discussion doc on the problem. It too suggests that SGLT2 meds can decrease kidney filtering out of ketone products. [URL]https://academic.oup.com/jcem/article/100/8/2849/2836082[/URL] Apparently a recent Japanese study demonstrated that SGLT2 med increased Glucagon, which in turn promoted extra lipidolysis thus leading to higher ketone levels being present, regardless of diet. But a LC diet will add its own ketone bodies to the mix, thus amplifying the effect. Low insulin levels also makes things worse. So any Insulin users on LC need to be aware that reducing insulin bolus due to low carb may increase the risk when used in conjunction with these meds. Thus this effect has been identified as being a Class problem caused by this med type. It is already established that this med type is not licenced for use with T1D in the USA, but in UK it is not restricted in this aspect (the restriction was lifted in May 2017) and it is also now being promoted for protecting the kidneys in T1D by NICE. Make of that what you will....... [/QUOTE]
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