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17 Apr, 6 tweets, 2 min read
1/6
 Does doxycycline protect against clostridium difficile infection (CDI)?

If so, why?

These questions came up on rounds yesterday. Here are some potential answers.
2/
 One study found an adjusted hazard ratio of 0.73 for CDI with the use of doxycycline.

A separate meta-analysis supported this finding with an odds ratio of 0.62 with all tetracyclines. The forest plot is attached.

pubmed.ncbi.nlm.nih.gov/22563022/
pubmed.ncbi.nlm.nih.gov/29401273/
3/
 One potential explanation is that tetracyclines have in vitro activity against C. difficile.

This was demonstrated in a study reporting that 84% of C. difficile isolates had an MIC of ≤0.25 mg/L to tetracycline.

pubmed.ncbi.nlm.nih.gov/19732094/
4/
 Other possibilities:
🔹Because doxycycline decreases protein production it may also attenuate toxin production
🔹Doxycycline has less of an affect on the gut microbiome, a key part of the pathophysiology of CDI
5/
 Do other antibiotics have favorable profiles against CDI?

A review published in 2020 also found a protective effect for daptomycin.

As with doxy, daptomycin has activity against C. difficile and less effect on the gut microbiome.

pubmed.ncbi.nlm.nih.gov/31964789/
6/6
 I am curious if others preferentially reach for doxycycline in patients with a history of C. difficile infection.

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More from @tony_breu

Tony Breu Profile picture
2 Apr
1/13
Why doesn't hemolysis cause acute kidney injury as easily as rhabdomyolysis?

I see a lot of hemolysis and can't think of a case of AKI that resulted.

Rhabdo? I immediately worry about AKI.

If heme is the toxic molecule, shouldn't both conditions be equally nephrotoxic?
2/
 🔑Heme is contained in both hemoglobin and myoglobin and is the toxic molecule in BOTH hemolysis and rhabdomyolysis.

The mechanism of heme toxicity won't be covered in this thread. Instead, we'll stick with why rhabdo causes more AKI.

pubmed.ncbi.nlm.nih.gov/31018590/
3/
 Before moving on, it is important to note that hemolysis CAN cause AKI.

Historically, massive hemolysis from ABO mismatch was a major cause. Now the causes are more varied.

pubmed.ncbi.nlm.nih.gov/31668630/
Read 13 tweets
Tony Breu Profile picture
31 Mar
1/9
 Great question!

From what I gather, the exact explanation for the low alkaline phosphatase in Wilson's disease remains unexplained.
2/
 The first description of the association between low AP and Wilson's came in a 1986 paper by Shaver, Bhatt, and Combes.

pubmed.ncbi.nlm.nih.gov/3758940/
3/
 They describe patients with acute hemolytic anemia in the setting of Wilson's disease who are noted to have low AP.

They wonder whether the acute increase in serum copper may compete with zinc for incorporation into AP.

pubmed.ncbi.nlm.nih.gov/3758940/
Read 9 tweets
Tony Breu Profile picture
28 Mar
1/11
Why is alkaline phosphatase elevated in biliary obstruction?

This question was debated for decades. The current explanation is NOT what I had expected.

Will you be surprised too?
2/
 Let's start with a question.

What explanation have you heard for the increased alkaline phosphatase (AP) in biliary obstruction?
3/
 One potential explanation is that AP leaks into the blood when hepatocytes are injured.

The problem: AP isn't markedly elevated in conditions with marked acute liver injury. For example, AP is only mildly elevated in acute viral hepatitis.

bit.ly/39kxaom
Read 11 tweets
Tony Breu Profile picture
21 Mar
1/12
Why do we use ACE inhibitors in scleroderma renal crisis?

I learned this early in training but never understood why these drugs were so game-changing.

Let's have a look.
2/
 To start, a few key features of scleroderma renal crisis (SRC). Most patients present with:

• Abrupt onset of hypertension
• Oliguric acute kidney injury
• Normal urinalysis

Up to 50% have signs of microangiopathic hemolytic anemia.

pubmed.ncbi.nlm.nih.gov/27641135/
3/
 Decades ago, the mortality for scleroderma involving the kidney was high with SRC considered universally fatal.

Things began to change in the 1970s.

pubmed.ncbi.nlm.nih.gov/4587746/
Read 12 tweets
Tony Breu Profile picture
13 Mar
1/14
How does fever help us fight infections?

For millennia, fever has been recognized as a beneficial response to invading pathogens.

If this is so, why don't we have a resting temperature of 102°F (38.9°C)? Wouldn't that protect us even better?

Let's have a look.
2/
 Fever emerged approximately 600 million years ago and is conserved in vertebrates. This suggests its benefit.

As you'll see in the next tweet, even ectothermic (cold-blooded) vertebrates demonstrate a "febrile" response.

pubmed.ncbi.nlm.nih.gov/24692136/
3/
 In a 1975 study, ectothermic lizards were infected with A. hydrophila and placed in environments at varying temperatures.

😀75% survived at 42°C (107.6°F)
😕25% survived at 38°C (100.4°F)
🥴0% survived at 34°C (93.2°F)

🔑↑temperatures = ↑survival

pubmed.ncbi.nlm.nih.gov/1114347/
Read 18 tweets
Tony Breu Profile picture
27 Jan
1/14
Why is cerebrospinal fluid (CSF) glucose low in bacterial meningitis?

Before we review potential mechanisms, I'm interested in the explanation you've heard/used.

What do you think causes low CSF glucose (hypoglycorrhachia)?
2/
 First, let's examine the most common causes of hypoglycorrhachia.

☞ While bacterial meningitis is the single most common cause, it accounts for fewer than a quarter of cases.

We'll come back to this.

pubmed.ncbi.nlm.nih.gov/24326618/
pubmed.ncbi.nlm.nih.gov/26299186/ Image
3/
 Now to the potential mechanisms. A number of hypotheses have been offered to explain hypoglycorrhachia.

🔹Bacterial consumption of glucose
🔹WBC consumption
🔹Brain consumption
🔹Decreased entry into CSF

...and others

Let's examine these.
Read 14 tweets

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