The SOLID Platelet Study

Platelet transfusion can be a life-saving procedure in preventing or treating serious
bleeding in patients who have low and/or dysfunctional platelets. Treatment of blood cancer
and other blood diseases, as well as bone marrow transplantation, is not possible without
platelet transfusion support. Unfortunately, 15- 25% of chronically transfused patients
platelet counts will stop responding to these transfusions, putting them at risk for serious
bleeding complications. The development of HLA antibodies is responsible for 4- 8% of this
platelet transfusion refractoriness. The presence of HLA antibodies is a clinical
complication that is generally managed by the selection of products that are negative for the
antigens for which the patient has antibodies. Often, for patients with chronic and ongoing
need, this selection is facilitated by targeted recruitment of donors with known HLA types
(i.e., types that lack antigens cognate to the patient s known antibodies and are thus
predicted to be compatible). However, for very broadly HLA- alloimmunized patients,
compatible products may be exceedingly scarce or completely unavailable, precluding the
ability to consistently provide products the patient will likely increment from. This
research protocol is designed to evaluate the efficacy of a 4-HOUR continuous infusion of
single donor, apheresis platelets in overcoming both alloimmune-mediated and
non-alloimmune-mediated platelet refractoriness. We hypothesize that when we transfuse
patients over a long duration, who have platelet refractoriness, the platelet counts will
increase to higher numbers for an extended period of time in the peri-transfusion period when
compared to shorter transfusion intervals.

- INCLUSION CRITERIA:

- Ability to comprehend the investigational nature of the study and provide informed
consent

- Thrombocytopenia

- Causes of thrombocytopenia may be due to:

1. Congenital causes

2. Bone marrow

3. Hematologic malignancies

4. Treatment related

- Thrombocytopenia is generally defined as one of the following:

1. <10K/uL without bleeding

2. <20K/uL for "complicated prophylaxis" in patient s determined to be at
increased risk of bleeding or other complications

3. <50K/uL with evidence of active bleeding, such as intracranial hemorrhage,
GI bleeding, pulmonary hemorrhage, uncontrolled epistaxis, hematuria.

The treating provider may change the platelet transfusion threshold based on
the clinical circumstance, patient population, and/or concurrent primary
protocol considerations - similar to the PLADO study.

- Diagnosed with PTR, characterized by the following:

- Lack of adequate post-transfusion platelet count increment, defined by, CCI
<5000/ul at 10-60 min after each of at least 2 consecutive platelet transfusions

- Presence of anti-HLA class 1 type A and/or type B antibody, in the setting of
PTR, as defined above, constitutes the HLA alloimmune-mediated subtype of PTR.
Presence of one or more HPA antibodies in the setting of PTR, as defined
above,constitutes the HPA alloimmune-mediated subtype of PTR. Failure to detect
HLA or HPA antibodies will be categorized as non-alloimmune-mediated PTR. .

EXCLUSION CRITERIA:

- Less than 18-years-old

- Lack of ability to obtain informed consent

- Pregnant female

- Presence of ITP/autoimmune thrombocytopenia

- Immune platelet refractoriness responsive to treatment with IVIg or eculizumab, or
other immunosuppressive therapy within the 3 preceding months. This is based on the
wide variation in the duration therapeutic antibodies, with the upper limit frequently
cited as 3 months.