BJH: Therapeutic plasma exchange for severely refractory autoimmune HIT with thrombosis

Heparin-induced thrombocytopenia (HIT) is a highly promoting thrombus formation diseases, for the platelet factor 4 (PF4) - New pathogenic epitopes heparin complex of immune induced immunoglobulin (an Ig) G
.

In some HIT patients with thrombosis (HITT), HIT antibodies cause platelet activation by cross-linking PF4 molecules with non-heparin polyanions or even in the absence of polyanions at all

Although thrombotic immunity is still the main treatment method for HITT by discontinuing heparin and starting alternative anticoagulation therapy, they will not change the underlying pathological process and may not be suitable for refractory HITT

The BJH Journal reported a case of HITT that was associated with the progression of venous thromboembolism due to flushing from exposure to unfractionated heparin (UFH), despite treatment with therapeutic fondaparinux and direct thrombin inhibitors
.

This case is also notable due to the failure of IVIg and dexamethasone and the successful treatment of TPE

The BJH Journal reported a case of HITT that was associated with the progression of venous thromboembolism due to flushing from exposure to unfractionated heparin (UFH), despite treatment with therapeutic fondaparinux and direct thrombin inhibitors

Stem Cell Diabetes

Unfractionated heparin flushing solution is used to maintain apheresis catheters
.

Twelve days after heparin exposure, the patient developed pain at the apheresis catheter and the platelet count was 12 × 10 ⁹/l (Figure1 )

⁹ 1 Blood vessels

Figure 1: The clinical course of a thrombotic patient with continuous platelet count and partial thromboplastin time
.

PTT, partial thromboplastin time; DVT, deep vein thrombosis; PE, pulmonary embolism; IVIG, intravenous immunoglobulin

Figure 1: The clinical course of a thrombotic patient with continuous platelet count and partial thromboplastin time

Since HIT was not immediately suspected, the patient first received a 12- hour therapeutic intravenous injection of uh on admission
.

However, anticoagulant therapy quickly transitioned to Fondaparinux on the first day of the hospital

12 Tension diagnosis

Although the partial platelet activity time value of argatroban treatment is 50-80 s, plasma exchange treatment is started for severe and refractory HIT caused by persistent thrombocytopenia
.

The patient received 4 treatments every other day, and the platelet count increased from 38 to × 10 ⁹ /l after the first TPE

50-80 ^{9 9}

After normalizing the platelet count, in view of the presence of gangrene, the patient underwent a left metatarsal amputation
.

After taking argatroban for 25 consecutive days, she switched to taking 20 mg rivaroxaban daily

The case emphasizes the rapid treatment effect of TPE in refractory HITT, and emphasizes the need to explore the potential role of TPE as an early intervention for severe HITT
.
For patients with refractory HITT, IVIg and TPE should be considered to destroy platelet activation, and platelet activation can continue to be effective after heparin is stopped
.
Although TPE is mainly used before emergency cardiac surgery in patients with acute or subacute HIT, TPE may also play an important role in the treatment of refractory HITT, although further research is needed to fully clarify this role
.
The current case also reminds the use of Fondaparinux in HITT patients
.

The case emphasizes the rapid treatment effect of TPE in refractory HITT, and emphasizes the need to explore the potential role of TPE as an early intervention for severe HITT
.
For patients with refractory HITT, IVIg and TPE should be considered to destroy platelet activation, and platelet activation can continue to be effective after heparin is stopped
.
The case emphasizes the rapid treatment effect of TPE in refractory HITT, and emphasizes the need to explore the potential role of TPE as an early intervention for severe HITT
.
For patients with refractory HITT, IVIg and TPE should be considered to destroy platelet activation, and platelet activation can continue to be effective after heparin is stopped
.

Original source:

Bavli, N.
, Christensen, B.
, Sarode, R.
, Hofmann, S.
and Ibrahim, I.
(2021), Therapeutic plasma exchange in severe refractory autoimmune heparin-induced thrombocytopenia with thrombosis.
Br J Haematol.
https:// doi.
org/10.
1111/bjh.
17917

Bavli, N.
, Christensen, B.
, Sarode, R.
, Hofmann, S.
and Ibrahim, I.
(2021), Therapeutic plasma exchange in severe refractory autoimmune heparin-induced thrombocytopenia with thrombosis.
Br J Haematol.
  https:// doi.
org/10.
1111/bjh.
17917 leave a message here