Sglt2 Inhibitors Acidosis

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Most Recent Papers With The Keyword Acidosis Sglt2 | Read By Qxmd

Retrospective review of SGLT2 inhibitor exposures reported to 13 poison centers. Scott E Schaeffer, Carol DesLauriers, Henry A Spiller, Alfred Aleguas, Salvador Baeza, Mark L Ryan BACKGROUND: SGLT2 inhibitors are a new class of oral antidiabetics prescribed in the United States since 2013. They act by inhibiting reabsorption of glucose in the proximal convoluted tubule of the kidney, allowing excess glucose to be excreted. Little has been reported regarding effects of non-therapeutic exposure to this class of medication. METHODS: Retrospective records from 13 poison centers were examined for human exposures to SGLT2 inhibitors between 1st January 2013 and 31st December 2016... Acid-base and electrolyte disorders associated with the use of antidiabetic drugs. Theodosios Filippatos, Eleftheria Tzavella, Christos Rizos, Moses Elisaf, George Liamis The use of antidiabetic drugs is expected to substantially increase since diabetes mellitus incidence rises. Currently used antidiabetic drugs have a positive safety profile, but they are associated with certain acid-base and electrolyte abnormalities. The aim of the review is to present the current data regarding the antidiabetic drugs-ass Continue reading >>

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  1. zenlittleplatypus

    Just out of curiosity - I had a beer last night and I think I was close to my carb limit, but not over. I felt fine. I hardly ever come close to 25g, so this was a rarity.
    What does getting knocked out of Ketosis feel like? Is there a key indicator where I would KNOW? I'm sure I'm fine in this instance but for curiosities sake...?

  2. sfcnmone

    I gain 3 pounds overnight and I can feel it before I get on the scale. And I also have mad cravings for donuts, or for whatever carb cheat I did. For days.

  3. n7leadfarmer

    Granted, I'm only a month in.. but this is happening to me regularly. I've only crossed 22 net carbs teice in a month (28 and 35) and the whole first week I lost 6 lbs. Then the next day I gained 2.6 (didn't drink enough water?) And it took a week for me to get back to where I was. Then I lose another 4, and then I gained 2.2 more lbs, and it's taken me another week to recover from that. Is that the normal process for keto? I haven't read anywhere that this is typical, but I can assure you that I have not cheated at all. Any thoughts?

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Fda Warns That Sglt2 Inhibitors May Lead To Ketoacidosis

FDA Warns That SGLT2 Inhibitors May Lead to Ketoacidosis Twenty cases of acidosis were reported in about 14 months The FDA is warning that the type-2 diabetes medicines canagliflozin, dapagliflozin, and empagliflozin may lead to ketoacidosis, a serious condition in which the body produces high levels of blood acids called ketones that may require hospitalization. The agency is investigating to determine whether changes are needed in the prescribing information for this class of drugs, called sodium-glucose cotransporter-2 (SGLT2) inhibitors. The FDA advised health care professionals to evaluate for the presence of acidosis, including ketoacidosis, in patients experiencing the signs or symptoms: difficulty breathing, nausea, vomiting, abdominal pain, confusion, and unusual fatigue or sleepiness. Providers should discontinue SGLT2 inhibitors if acidosis is confirmed and take appropriate measures to correct the acidosis and monitor sugar levels. SGLT2 inhibitors are FDA-approved for use with diet and exercise to lower blood sugar in adults with type-2 diabetes. They lower blood sugar by causing the kidneys to remove sugar from the body through the urine. These medicines are available Continue reading >>

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  1. Skie

    Can You Use Ketone Sticks to "Diagnose"?

    I'm not on a low carb diet as far as I know, so having these in the urine would be a possible diabetes sign, right? Is it a safe idea to get a package and see what my results are? Or is this just a silly idea? I'm still working out arrangements to go see a doctor and get tested, but in the mean time while I figure that out with my friends, I figure something like this might be useful to get an idea of where I stand in the matter... Course I wish I could borrow a meter too, but alas... Don't know anyone who'd let me...

  2. Shanghaied Guy

    I think your blood sugars have to be extremely high before ketones would show up in your urine if you have not been on ketogenic diet (very low carb) for several days.
    You can get a free meter here: https://www.onetouchgold.com/simplestart/, but you will still need to buy the strips.
    Where do you live? If you live in Shanghai, I will buy you a cup of coffee some morning and test your BG. We diabetics are always curious about the blood sugar of other people and sometimes try to cajole our family and friends into testing their morning fasting blood sugar. If you want to disclose where you live, maybe somebody here at DD can help you out with the use of a meter.
    Tell us a bit about yourself. Do you have a family history of diabetes? How old are you? Are you overweight? Have you ever had high blood glucose on a test? What symptoms do you have that lead you to suspect diabetes?
    Be well.

  3. hannahtan

    i wouldn't dx yourself with just a ketostix... if there are sugar and ketones in the urine... it is a sign of diabetes... if ketones alone... i'm not sure... that is why i will not simply just assume i'm a diabetic based on a ketostix result...
    if you can't borrow a meter... can you just go to a pharmacy and get a simple finger bg test done? if it is high... and from the ketostix result which shows ketones as positive... please go see a doc immediately... but if bg is good...i wouldn't worry a lot... but still see a doc to get a proper diagnosis

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Susan Cornell, PharmD, CDE, FAPhA, FAADE, describes the risks for ketoacidosis and serious urinary tract infection associated with use of SGLT2 inhibitors. This video was recorded at APhA's 2016 Annual Meeting and Exposition in Baltimore, Maryland.

Fda Warns Of Ketoacidosis Risk With Sglt2 Inhibitors

FDA Warns of Ketoacidosis Risk With SGLT2 Inhibitors FDA Warns of Ketoacidosis Risk With SGLT2 Inhibitors FDA Warns of Ketoacidosis Risk With SGLT2 Inhibitors Look for our upcoming reactions from practicing endocrinologists on this topic. The FDA has issued a warning that SGLT2 inhibitors, indicated for the treatment of type 2 diabetes , may lead to ketoacidosis, according to a drug safety communication from the agency. From March 2013 to June 6, 2014, 20 cases of acidosis reported to the FDA Adverse Event Reporting System (FAERS) were identified as diabetic ketoacidosis (DKA), ketoacidosis or ketosis in patients treated with sodium-glucose cotransporter-2 (SGLT2) inhibitors, including canagliflozin, canagliflozin plus metformin, dapagliflozin, dapagliflozin plus metformin extended-release, empagliflozin and empagliflozin plus linagliptin. All patients required emergency room visits or hospitalization to treat the ketoacidosis. Additionally, since June 2014, FAERS has received additional reports of DKA and ketoacidosis in patients treated with SGLT2 inhibitors. The FDA noted, however, that the FAERS cases were not typical for DKA because most of the patients had type 2 diabetes an Continue reading >>

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  1. manohman

    Why can't fat be converted into Glucose?

    So the reason cited is that beta oxidation/metabolism of fats leads to formation of acetyl coa, a 2 carbon molecule, and that because of that it cannot be converted back into glucose.
    Why exactly is that the case?
    If Glucogenic amino acids can be converted into citric acid cycle intermediates and then turn back into glucose via gluconeogensis, then why cant Fatty Acids which yield Acetyl Coa. Can't you just have Acetyl Coa enter the citric acid cycle and produce the same intermediates that the glucogenic amino acids creat?

  2. Czarcasm

    manohman said: ↑
    So the reason cited is that beta oxidation/metabolism of fats leads to formation of acetyl coa, a 2 carbon molecule, and that because of that it cannot be converted back into glucose.
    Why exactly is that the case?
    If Glucogenic amino acids can be converted into citric acid cycle intermediates and then turn back into glucose via gluconeogensis, then why cant Fatty Acids which yield Acetyl Coa. Can't you just have Acetyl Coa enter the citric acid cycle and produce the same intermediates that the glucogenic amino acids creat?
    Click to expand... Both glucose and fatty acids can be stored in the body as either glycogen for glucose (stored mainly in the liver or skeletal cells) or for FA's, as triacylglycerides (stored in adipose cells). We cannot store excess protein. It's either used to make other proteins, or flushed out of the body if in excess; that's generally the case but we try to make use of some of that energy instead of throwing it all away.
    When a person is deprived of nutrition for a period of time and glycogen stores are depleted, the body will immediately seek out alternative energy sources. Fats (stored for use) are the first priority over protein (which requires the breakdown of tissues such as muscle). We can mobilize these FA's to the liver and convert them to Acetyl-CoA to be used in the TCA cycle and generate much needed energy. On the contrary, when a person eats in excess (a fatty meal high in protein), it's more efficient to store fatty acids as TAG's over glycogen simply because glycogen is extremely hydrophilic and attracts excess water weight; fatty acids are largely stored anhydrously and so you essentially get more bang for your buck. This is evolutionary significant and why birds are able to stay light weight but fly for periods at a time, or why bears are able to hibernate for months at a time. Proteins on the other hand may be used anabolically to build up active tissues (such as when your working out those muscles), unless you live a sedentary lifestyle (less anabolism and therefore, less use of the proteins). As part of the excretion process, protein must be broken down to urea to avoid toxic ammonia and in doing so, the Liver can extract some of that usable energy for storage as glycogen.
    Also, it is worth noting that it is indeed possible to convert FA's to glucose but the pathway can be a little complex and so in terms of energy storage, is not very efficient. The process involves converting Acetyl-CoA to Acetone (transported out of mitochondria to cytosol) where it's converted to Pyruvate which can then be used in the Gluconeogenesis pathway to make Glucose and eventually stored as Glycogen. Have a look for yourself if your interested: http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1002116.g003/originalimage (and this excludes the whole glycogenesis pathway, which hasn't even begun yet).
    TLDR: it's because proteins have no ability to be stored in the body, but we can convert them to glycogen for storage during the breakdown process for excretion. Also, in terms of energy, it's a more efficient process than converting FA's to glycogen for storage.

  3. soccerman93

    This is where biochem comes in handy. Czarcasm gives a really good in depth answer, but a simpler approach is to count carbons. The first step of gluconeogenesis(formation of glucose) requires pyruvate, a 3 carbon molecule. Acetyl Co-A is a 2 carbon molecule, and most animals lack the enzymes (malate synthase and isocitrate lyase) required to convert acetyl co-A into a 3 carbon molecule suitable for the gluconeogenesis pathway. The ketogenic pathway is not efficient, as czarcasm pointed out. While acetyl co-A can indeed be used to form citric acid intermediates, these intermediates will be used in forming ATP, not glucose. Fatty acid oxidation does not yield suitable amounts of pyruvate, which is required for gluconeogenesis. This is part of why losing weight is fairly difficult for those that are overweight, we can't efficiently directly convert fat to glucose, which we need a fairly constant supply of. Sorry, that got a little long-winded

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