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Tony Breu Profile picture
@tony_breu
Sep 17, 2020 • 5 tweets • 3 min read • Read on X
1/4
 Why does amphotericin B lead to rigors and fever?

I learned about his side effect by the moniker "shake and bake" (thank you First Aid).

Let's have a brief look at this commonly tested side-effect.
2/
 Amphotericin B was introduced in the 1950s.

It was clear early on that fevers and chills were common side effects.

More contemporary data show lower - though still relevant - rates of both side effects.

pubmed.ncbi.nlm.nih.gov/13749466/ - 1960
pubmed.ncbi.nlm.nih.gov/10072411/ - 1999
3/
 When thinking back to the mechanism of fever, recall that PGE₂ is a key mediator.

Amphotericin B leads to an increase in PGE₂. This is likely the mechanism of chills and fever.

As this study shows, amphotericin B acts in a similar way to LPS!

pubmed.ncbi.nlm.nih.gov/3309074/
4/4
 Given these effects, amphotericin has been examined as an "immunostimulant" in combination with antineoplastic chemotherapy.

I am unaware of its use in any current regimen.

pubmed.ncbi.nlm.nih.gov/7362372/
This is my first follow-up to a tweetorial on fevers, chills, and rigors.

Next up: meperidine (Demerol)

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More from @tony_breu

Tony Breu Profile picture
Apr 9
1/12 - Mystery #1

You are seeing a patient recently diagnosed with heart failure and started on GDMT. You notice that their hemoglobin (HGB) has increased (12 → 13 g/dL) in the intervening weeks.

🤔Which medication is the likely cause of this increase in HGB?
2/12 - An Answer

Empagliflozin

💡All SGLT2 inhibitors have been associated with an increase in hematocrit/hemoglobin soon after initiation.

The average increase is 2.3% in hematocrit and 0.6 g/dL in hemoglobin.

ncbi.nlm.nih.gov/pmc/articles/P…Image
3/12 - An Initial Explanation (I)

The effect of SGLT2 inhibitors on HCT/HGB has been noted since the very first randomized control trial of dapagliflozin, published in 2010.

Initially, investigators assumed this was related to the diuretic effect of these drugs (i.e., a reduction in plasma volume led to an increase in HCT/HGB).

pubmed.ncbi.nlm.nih.gov/20609968/Image
Read 12 tweets
Tony Breu Profile picture
Feb 22
1/10
🤔Why is pulmonary embolism (PE) relatively rare in those with Factor V Leiden?

This Factor V Leiden Paradox was pointed out to me by @DrSamelsonJones after I posted about a similar difference with Behçet Syndrome.

Let's have a look.
2/
 In 1993, Dahlback, Carlsson, and Svensson first described a heritable resistance to activated protein C.

A year later the same group found this to be the most common form of hereditary hypercoagulability.


ncbi.nlm.nih.gov/pmc/articles/P…
pubmed.ncbi.nlm.nih.gov/8302317/Image
Image
3/
 The mutation in the Factor V gene conferring resistance to activated protein C was detailed the following year by a group in Leiden, The Netherlands.

Thus the name for the condition: Factor V Leiden.

pubmed.ncbi.nlm.nih.gov/8164741/Image
Read 10 tweets
Tony Breu Profile picture
Feb 18
1/8
 🤔Why is pulmonary embolism (PE) so rare in Behçet Syndrome?

The condition is associated with a 14-fold increased risk of deep vein thrombosis (DVT) but almost none of these result in PE.

What is it about the thrombus in Behçet that makes it so unable to embolize?
2/
 Numerous case series have reported a markedly increased risk of deep vein thrombosis with Behçet Syndrome.

One reported the following rates of venous thrombosis:
➣ Behçet Syndrome: 18/73 (25%)
➣ Controls: 4/146 (3%)

pubmed.ncbi.nlm.nih.gov/11426022/Image
3/
 Another study of 882 patients with vascular Behçet Syndrome reported the following rates of deep vein thrombosis (DVT) and pulmonary embolism (PE):

➣ DVT: 592/882 (67%)
➣ PE: 0%!

pubmed.ncbi.nlm.nih.gov/24907156/Image
Read 9 tweets
Tony Breu Profile picture
Dec 12, 2023
1/7
 🤔What is the hemodynamic response to a chronic hemoglobin of 1.5 g/dL.

A fascinating 1963 study published in @CircAHA provides some interesting answers. Let's have a look at Patient One.

ahajournals.org/doi/pdf/10.116…
Image
@CircAHA 2/
Patient One had chronic anemia with a hemoglobin 1.5 g/dL. You'll see that before receiving blood they had the following cardiac parameter:

• HR 100 (elevated)
• Cardiac index 8.9 (elevated)
• Stroke index 89 (elevated) Image
@CircAHA 3/
After transfusion to a hemoglobin of 10 g/dL, the following changes were noted:

• HR 100 (elevated but unchanged)
• Cardiac index 3.4 (decreased and now normal)
• Stroke index 34 (decreased and now normal)
Image
Image
Read 7 tweets
Tony Breu Profile picture
Dec 10, 2023
1/17
🤔Why don't we transfuse to a normal hemoglobin?

In many cases, we aim to restore values to the normal range. Potassium and other electrolytes. Even white blood cells.

But not hemoglobin.

In most situations, we accept >7g/dL, far less than normal. Why are we so tolerant? Image
2/
 The principal rationale for red blood cell transfusion is to increase the O₂-carrying capacity and therefore O₂ delivery to tissues.

As hemoglobin is lowered O₂ delivery decreases, assuming all else remains unchanged.

So giving blood makes sense.
3/
 Historically we did not transfuse to normal because we did not transfuse. The risks far outstripped the benefits.

There were also technical constraints and storage limitations. This meant that transfusions were reserved for acute conditions.

onlinelibrary.wiley.com/doi/pdfdirect/…
Image
Read 17 tweets
Tony Breu Profile picture
Oct 12, 2023
1/7 - The Mystery

A 57-year-old presents with the following labs:

WBC 2.7 / HGB 2.2 / PLT 111
Bili 3.2 (direct 0.4)
LDH 4360
Haptoglobin <10
INR 1.6 / PTT 35
Reticulocyte count 3.4
Smear with schistocytes

🤔What is the most likely diagnosis?
2/7 - The Answer

💡This patient was diagnosed with profound B12 deficiency secondary to pernicious anemia (PA)!
3/7 - The Clue

One of the clues in this case is the markedly elevated LDH.

Multiple studies from the 1960s demonstrated that PA is the condition associated with the highest serum LDH levels.

pubmed.ncbi.nlm.nih.gov/5805997/
Image
Read 8 tweets

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