autoimmune thrombocytopenic purpura

Occasionally, someone might present with an infection due to suppressed immunity or funny immune phenomena like exaggerated mosquito bite reactions, but those last few are quite rare and sometimes related to a T cell problem instead.

To list them out though, some of the classic complications of CLL that a patient might present with are an immune-mediated ITP, immune thrombocytopenia, or autoimmune hemolytic anemia, possibly pure reticel aplasia, and possibly hypogammaglobulinemia, which would cause infection.

Then the signs of CLL on exam might include lymphadenopathy, which is most common.

And I mean, this can be generalized or localized to individual groups.

Therapy might include continuous BTK inhibitors, such as these are ibrutinib, acalabrutinib, or xanabrutinib, or fixed-generation venetoclax and CD20 antibodies, or fixed-generation BTK plus venetoclax combinations, which are great if you need an oral treatment in a regional setting.

Mm-hmm.

Key complications include autoimmune hemolytic anemias, or ITP, secondary to the clone, even if the actual clone itself is not particularly big, recurrent infection secondary to hypogammagobular anemia, and the dreaded Richter's transformation.

And

And the younger kid, what about the toddler? You know, the kid that's, th- that we're always worried.

These are the kids, again, we did an episode before on ITP.

We were talking about-

Mm-hmm

[laughs]

[laughs] Well, this one's only in four parts then.

But, um, going back to what you said initially, you know, I know like in ITP where we used to admit just 'cause of the convenience of being able to start treatment.

Mm-hmm.

Baseball was always a passion for him, but he was a kid that kind of played whatever sport was in that season.

I think the biggest challenge he ever had baseball wise was when he was seven or eight years old, he had ITP, which is a blood deal.

So he wouldn't clot up.

He'd get bruised.

My question is, would my spleen be the culprit behind my low platelet count? And Dr.

Roach says, low platelet counts are common, and one common reason for them is a condition called idiopathic thrombosulpinia, it's ITP, and a large spleen isn't common with ITP, even though removing the spleen is one treatment.

The red dots on your chest might be Pytacella, which are small areas where red blood cells leak through small blood vessels.

They can happen due to low platelets from any cause, but usually happen with much lower levels of platelets than you report typically.

It has been seen with platelet counts lower than 20,000 or even 10,000.

So if the splint is enlarged as new, this could be a red flag that something in your bone marrow is new and different, since people with ITP are at substantial increased risk for leukemia.

Wow.

So there was an ex-youth detention center counselor who faced a sexual assault trial in New Hampshire.

It is very effective for antibody-related diseases, for autoimmune diseases.

Very effective, graft versus host, ITP, Guillain-Barré, multiple sclerosis, very effective.

It removes the bad antibodies.

and takes down the inflammation.

And before kind of nerding out about the buckets that I'll kind of go over, you have to, like, cross-- think through all those three things.

Um, I find it helpful to, um, think of thrombocytopenia in kind of three-- a three bucket approach, that being is it an underproduction issue related to kind of bone marrow issues? Is it a peripheral destruction? And what I mean by that, is there a consumptive process such as, um, a MAHA picture, or is there a kind of destructive process, um, like in kind of ITP where you have, like, antibodies, um, targeting the, the platelets for, for destruction.

So underproduction, peripheral destruction, and then sequestration is a really important bucket to think of.

So this is in folks who have, um, portal hypertension and splenomegaly, platelets can be sequestered.

Youssef, what, what did this information do for you?

Yeah.

I, I think one thing that I'm thinking of is like, what is the mechanism of thrombocytopenia? So this is an infection, and did the infection invade the marrow, and is there underproduction because of that? Or is this an ITP triggered by an infection? 'Cause these will be like two very separate etiologies.

'Cause if I tell you invading the marrow, then you worry about TB, while if I tell you it's induced ITP, then maybe you might worry about the flu or EBV.

Okay, let’s transition from systemic infections to the autoimmune battlegrounds.

We are talking about ITP versus TTP.

This is a classic comparison that shows up on every board exam, but more importantly, it dictates fundamental surgical triage.

ITP is immune thrombocytopenic purpura.

TTP is thrombotic thrombocytopenic purpura, also known historically as Moschkowitz syndrome.

Right, the classic duo.

One of these is a surgical disease if medical therapy fails, and the other almost never sees the inside of an operating room.

That is the perfect clinical dichotomy to keep in mind.