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thedasd82
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thedasd82
@drdasdo
Indonesian - . Into: #run, #exercise, #music, & #sing. Fan of Carrie Underwood, Michael Buble, Josh Groban. #swing #jazz #painting
ÜT: 0.152122,117.474042 Katılım Temmuz 2009
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🧵 New 2026 NICE Update on Initial Drug Therapy in Type 2 Diabetes Detailed Thread
1️⃣ Big Shift in Philosophy
This is no longer just about lowering HbA1c.
The new guidance prioritises:
• Cardiovascular protection
• Renal protection
• Individualised treatment
• Early combination therapy
Glucose control is important but outcomes matter more.
2️⃣ First-Line Therapy (No Major Comorbidities)
For most adults:
✅ Modified-release metformin
PLUS
✅ An SGLT-2 inhibitor
If metformin cannot be used → start SGLT-2 inhibitor alone.
➡️ This is a major shift from traditional “metformin first, add later.”
3️⃣ Why SGLT-2 So Early?
Because evidence now strongly supports:
• Reduction in heart failure hospitalization
• Slowing CKD progression
• Cardiovascular mortality benefit
• Weight reduction
• Low hypoglycaemia risk
This class is now foundational therapy.
4️⃣ If the Patient Has Heart Failure
Start immediately:
✅ Metformin
✅ SGLT-2 inhibitor
If metformin contraindicated → SGLT-2 alone.
HF benefit drives this decision independent of HbA1c.
5️⃣ If Atherosclerotic CVD Is Present
Initial therapy can include:
✅ Metformin
✅ SGLT-2 inhibitor
✅ Subcutaneous semaglutide (GLP-1 RA)
If Yes 👉🏻 GLP-1 RA can now be started upfront in ASCVD.
This reflects strong CV outcome trial data.
6️⃣ Early-Onset Type 2 Diabetes
(Younger patients, aggressive phenotype)
Start:
✅ Metformin
✅ SGLT-2 inhibitor
Consider adding:
• GLP-1 receptor agonist
• Tirzepatide
This group often needs earlier intensification.
7️⃣ Obesity + Type 2 Diabetes
Initial therapy:
✅ Metformin
✅ SGLT-2 inhibitor
Weight-neutral or weight-reducing strategies are preferred.
Avoid agents that promote weight gain unless necessary.
8️⃣ Chronic Kidney Disease (CKD)
Treatment depends on eGFR:
🔹 eGFR >30 → Metformin + SGLT-2
🔹 eGFR 20–30 → Dapagliflozin or Empagliflozin + DPP-4 inhibitor
🔹 eGFR <20 → Consider DPP-4 inhibitor
If DPP-4 not suitable → consider pioglitazone or insulin.
Renal protection is central in this update.
9️⃣ Frailty
Be cautious.
Offer:
✅ Metformin
Consider SGLT-2 only if risk of:
• Hypotension
• Dehydration
• Falls
If risk is high → DPP-4 inhibitor may be safer.
Individualisation is critical here.
🔟 What’s Clearly De-emphasised?
Sulfonylureas are no longer early go-to drugs.
Reasons:
• Hypoglycaemia risk
• Weight gain
• No cardiovascular benefit
They are now secondary options.
1️⃣1️⃣ Key Takeaway
The 2026 update moves us from:
“Glucose-centric diabetes care”
➡️ to
“Cardio-renal-metabolic protection from day one.”
Early combination therapy is now the norm, not the exception.
1️⃣2️⃣ Practical Clinical Message
When starting treatment in Type 2 Diabetes, now ask:
• Does this patient have HF?
• ASCVD?
• CKD?
• Obesity?
• Frailty?
The comorbidity determines the drug choice not just HbA1c.
nice.org.uk/guidance/ng28/…
#MedTwitter #MedX

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Great to be back in sunny Amsterdam for the #ESC2023 meeting with my vienna umbrella 😜 can't wait to see everyone


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New Study Demonstrates How Inflammation🔥pulls LDL into the Artery Wall - 🧵 for the lay-reader (upon request)
LDL particles play a role in the pathway of atherosclerosis. To do this, they must enter the artery wall by passing through the endothelium, a thin membrane that lines the walls of blood vessels
But how? Do LDL particles just passively flow through the endothelium like grains of rice thrown at a chicken-wire fence?
Well, the diameter of an LDL is on the order of 20-30 nm, whereas the gaps between endothelial cells is ~3-6nm... so, instead, LDL must be transported, actively, into the artery wall. Inflammation plays a role here.
This new study shows that inflammatory transcriptional regulators and cytokines (signaling molecules) increase the expression of proteins involved in the formation of pockets of membrane,"caveole," that 'suck up' LDL particles.
Specifically, the inflammatory cytokines include TNFalpha and IL-1Beta, which activate NLRP3 inflammasome, which causes increased expression of proteins that compose caveole and contribute to LDL transcytosis (active transport through the endothelium)
Earlier studies also showed the elevated glucose promotes this transcytosis process
In summary, inflammation and elevated glucose are 2 factors that cause LDL to be taken into artery walls and promote atherosclerosis.
Questions that remain (for me) are:
- what is the relative impact of high LDL alone is the ABSENCE of chronic pathological inflammation and/or elevated glucose?
- what therapeutic approaches could prevent cardiovascular disease by targeting these pathways (by extension, what cardioprotective role might ketosis play via beta hydroxybutyrate, which inhibits NLRP3)?
- what are other pathways involved in transcytosis (including the undiscovered and understudied), and might there be a more bidirectional and dynamic process, in the context of a healthy metabolism, than we previously thought?
pubmed.ncbi.nlm.nih.gov/37100720/
pubmed.ncbi.nlm.nih.gov/36935311/

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If you like this thread, please retweet the first tweet 😀
twitter.com/ATRightMovies/…
All The Right Movies@ATRightMovies
There's a tradition of film directors and studios congratulating each other for beating their box office records. A THREAD In 1977, when STAR WARS beat Jaws to become the highest-grossing movie ever, Steven Spielberg took out the below ad for George Lucas in @Variety 1/11
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@DoctorTro Would support low-carb diet as a cardiologist who treat a lot of patients with metabolic syndrome. Unfortunately, almost all refuse to comply.
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