Thread by @MELanocyteMD

#Pathologists ♥️ eosinophils.

We love scanning for them in a skin rash, admiring them when they infiltrate a tumor, & even counting them in esophageal biopsy. 🔬

But what do you know about eosinophils in the blood? 🤔

1/

#pathbracket #hemepath #pathtweetorial @EmoryPathology

If the answer is "not much 🤷🏼‍♀️", then you're in luck, because the subject of my 2nd #pathtweetorial is:

🥁🥁🥁

🩸 Approach to Peripheral Blood Eosinophilia 🩸

Here's a brief outline of what I'll be discussing:

2/

I.

Let's get started with a case!

30 y/o M, presents with 3 months of fatigue, weakness, weight loss & abdominal pain.

Peripheral blood 🩸 & bone marrow 🦴 show the following 👇

3/

How should we approach this case? 🤔

First, we need to define 🩸 eosinophilia.

Eosinophilia is defined as a 🩸 cell count of :
➡️ >500/microL (>0.5 x 10^9/L)

The next step is to determine if the eosinophilia is:

🥇 Primary (1°)
or
🥈 Secondary (2°)

4/

II.

Most eosinophilias are 2°, which means they are:
🔸 Non-clonal
🔸 Reactive to another process

That process can be:
✳️ Neoplastic
or
✳️ Non-neoplastic

5/

As you can see, A LOT of things can cause 2°🩸 eosinophilia 😬

Here's how I (try to) remember:

💡 For non-neoplastic causes:
🔭👩‍⚕️"A GII DR" 👨‍⚕️🔭
(There's no endoscope emoji, so I used a telescope 😅)

💡 For neoplastic causes:
♥️🐢 "Happy turtles mate" 🐢♥️

6/

III.

Moving to 1° eosinophilias:
🔸 Eosinophils are neoplastic (clonal)
🔸Other cells types may be also be neoplastic (i.e. granulocytes, monocytes)

I divide these entities into two categories:
✳️ "Old school" 👴
✳️ "New school" 👶

7/

"Old school":
✏️ Well-established heme neoplasms
✏️ May have 🩸 eosinophilia

This includes:
👴 AML*
👴 CML
👴 aCML
👴 CMML

➡️ I'm not going discuss these here, but here's a previous tweet I made covering some of these entities:

https://twitter.com/MELanocyteMD/status/1357357392627982339?s=19

8/

"New school":
✨ Shiny & cool (recent additions to the WHO)
✨ Many have recurrent genetic abnormalities

This includes:
👶 Myeloid/lymphoid neoplasms w/ eosinophilia (MLN Eo)
👶 Chronic eosinophilic leukemia (CEL), NOS

9/

Here's a table comparing the key features of these entities.

Important features to consider:
✳️ Chronic vs. blast phase
✳️ Dysplasia
✳️ Marrow fibrosis
✳️ Clonality

Remember, these are rare, so be sure to rule-out:
➡️ 2° causes
➡️ "Old school" mimics

10/

IV.

If you've excluded 1° & 2° causes, all that's left is:
🤷‍♀️ Idiopathic

These entities include:
✳️ Idiopathic hypereosinophilia (HE)
✳️ Idiopathic HES
✳️ Lymphocytic variant HES

Distinguishing b/tw these is pretty simple & based on:
🔸 Organ damage
🔸 Clonal T cells

11/

V.

Now, let's return to our case.

Additional work-up showed:
👩‍⚕️ Mildly ⬆️LFTs
👩‍⚕️ Positive ANA
👩‍⚕️ Reported history of IBD (awaiting records from OSH 🙄)

And...
🧬 Flow, cytogenetic & molecular testing detected NO abnormalities

12/

📊 POLL 📊

How would you sign out this case?

13/

Answer: D
➡️ This case was signed out descriptively.

So, why can't we call this HE or HES?
🔸 Can't exclude 2° causes (possible IBD?)
🔸 No organ damage (⬆️LFTs = 🚫specific)

Basically,
✳️ Unless you have an EXCELLENT clinical hx, don't call it HE/HES

14/

VI.

In conclusion,

We have discussed:
➡️ Types of 🩸 eosinophilia
➡️ Features & ddx for each type
➡️ Sign-out considerations

Here's a summary of my approach 👇

Thanks to all the great #hemepath attendings who taught me these past 3 months!
@KyleBradleyMD @Hemepathgal

15/