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Blood, Vol. 91 No. 10 (May 15), 1998:
pp. 3601-3606
Safety and Cost Effectiveness of a 10 × 109/L Trigger
for Prophylactic Platelet Transfusions Compared With the Traditional 20 × 109/L Trigger: A Prospective Comparative Trial in 105 Patients With Acute Myeloid Leukemia
By
Hannes Wandt,
Markus Frank,
Gerhard Ehninger,
Christiane Schneider,
Norbert Brack,
Ali Daoud,
Irene Fackler-Schwalbe,
Jürgen Fischer,
Ringfried Gäckle,
Thomas Geer,
Peter Harms,
Birgit Löffler,
Siegfried Öhl,
Burkhard Otremba,
Monika Raab,
Petra Schönrock-Nabulsi,
Gerhard Strobel,
Rolf Winter, and
Hartmut Link
From the 5th Medical Department and
Institute of Medical Oncology and Hematology, Nürnberg, Germany;
the Department of Internal Medicine, Hematology/Oncology, Medical
School Hannover, Hannover, Germany; and the Medical Clinic I, Technical
University Dresden, Dresden, Germany.
 |
ABSTRACT |
In 105 consecutive patients with de novo acute myeloid leukemia
(French-American-British M3 excluded), we compared prospectively the
risk of bleeding complications, the number of platelet and red blood
cell transfusions administered, and the costs of transfusions using two
different prophylactic platelet transfusion protocols. Two hundred
sixteen cycles of induction or consolidation chemotherapy and 3,843 days of thrombocytopenia less than 25 × 109/L were
evaluated. At the start of the study, each of the 17 participating centers decided whether they would use a 10 × 109/L
prophylactic platelet transfusion trigger (group A/8 centers) or a 20 × 109/L trigger (group B/9 centers). Bleeding
complications (World Health Organization grade 2-4) during treatment
cycles were comparable in the two groups: 20 of 110 (18%) in group A
and 18 of 106 (17%) in group B (P = .8). Serious bleeding
events (grade 3-4) were generally not related to the patient's
platelet count but were the consequence of local lesions and plasma
coagulation factor deficiencies due to sepsis. Eighty-six percent of
the serious bleeding episodes occurred during induction chemotherapy.
No patient died of a bleeding complication. There were no significant
differences in the number of red blood cell transfusions administered
between the two groups, but there were significant differences in the number of platelet transfusions administered per treatment cycle: pooled random donor platelet concentrates averaged 15.4 versus 25.4 (P < .01) and apheresis platelets averaged 3.0 versus 4.8 (P < .05) for group A versus group B,
respectively. This resulted in the cost of platelet
therapy being one third lower in group A compared with group B without
any associated increase in bleeding risk.
| |
INTRODUCTION |
THERE IS AN INCREASING demand for
platelet transfusions, and it remains an ongoing challenge for most
blood centers to maintain an adequate platelet inventory. Platelet
transfusions doubled in the United States and in Canada from 1980 to
1987.1-3 Between 1989 and 1992, the number of platelet
concentrates decreased in the United States by 8.9%, whereas the
number of apheresis platelets administered increased by
75%.4 There is no doubt that platelet transfusions are
beneficial and that they have permitted the use of more aggressive
chemotherapy and bone marrow transplantation. However, there is still
controversy regarding when platelets should be administered to maximize
their benefit while minimizing the risk of bleeding.5-12
In the 1960s, studies demonstrated a relationship between hemorrhage
and platelet count in patients with acute leukemia.13 Since
that time, most hematologists have used a 20 × 109/L
platelet trigger for administering prophylactic platelet transfusions with a considerable interinstitutional heterogeneity in transfusion policies. A study performed in 1992 by the Transfusion Practice Committee of the American Association of Blood Banks reported the
current practice for prophylactic platelet transfusion. More than 70%
of hospitals transfused platelets primarily for prophylaxis. Eighty
percent of these hospitals set the threshold for prophylactic transfusion at 20 × 109/L or even higher.3
During the last 10 years, there has been increasing debate based on
both old and more recent data that have brought into question the
traditional platelet transfusion policy.7-11,14 Those data
indicate that there is no real threshold for bleeding complications.
Other factors affect bleeding risk, such as platelet function, rapid
platelet consumption during febrile episodes, plasma coagulation factor
deficiencies, and local factors such as vascular lesions or organ
infiltrations. With regard to the safety and practicability of a more
restrictive platelet transfusion policy, there has been only one study
in the last 10 years that has addressed this question prospectively
when we started our trial.14 In this single-center study,
leukemia patients were routinely transfused with platelets if the
morning count was <5, <10, or <20 × 109/L,
depending on different clinical situations. This transfusion policy was
demonstrated to be safe. On the basis of this study and other data
available in 1992, we started a prospective multicenter trial in the
cooperative acute myeloid leukemia (AML) study group of
the Süddeutsche Hämoblastosegruppe evaluating the safety of
a 10 × 109/L versus a 20 × 109/L morning
trigger for routine prophylactic platelet transfusions. Because half of
the centers of our group were reluctant to use this more restrictive
platelet transfusion policy, we decided to perform a prospective
nonrandomized comparative study. Each center decided to use either the
10 × 109/L or the traditional 20 ×109/L
platelet transfusion trigger. Study objectives were to document bleeding complications, the number of platelet and red blood cell (RBC)
transfusions, and the costs of transfusion support in the two groups.
| |
PATIENTS AND METHODS |
Over a 15-month period, all patients with de novo AML
(French-American-British [FAB] M3 excluded) and without uncontrolled infection admitted to the participating hospitals were enrolled in the
study. Seventeen departments of hematology in 17 different hospitals (4 university and 13 community hospitals, most with university
affiliation; 7 departments treating 10 newly diagnosed AML patients per
year and 10 departments treating >10 patients per year) participated
in the study. Small and large centers were equally distributed to both
groups (group A 3 and 5, group B 4 and 5, respectively). Eight centers
used the 10 × 109/L prophylactic platelet transfusion
trigger (group A) and 9 centers used the 20 × 109/L
trigger (group B). The chemotherapy for induction and consolidation in
the two groups was the same. Two induction chemotherapy cycles were
followed by two consolidation cycles in patients less than 60 years of
age. The induction regime consisted of daunorubicin at 60 mg/m2/d for 3 days, ara-C at 200 mg/m2 as a
3-hour infusion daily for 3 days followed by 100 mg/m2/d as
continuous infusion for 5 days, and etoposide at 150 mg/m2/d for 3 days (DAE). During the second induction
cycle, daunorubicin was reduced to two doses. Consolidation I was
composed of m-AMSA at 100 mg/m2/d and ara-C at 2 × 1 g/m2/d for 5 days. Consolidation II included mitoxantrone
at 10 mg/m2/d for 3 days combined with 6 days of ara-C at
the dose of 2 × 3 g/m2/d for patients up to the age of 50 years, and for patients between 51 and 60 years of age, ara-C in the
dose of 2 × 1 g/m2/d. Induction chemotherapy for elderly
patients (>60 years of age) consisted of daunorubicin at 45 mg/m2/d for 3 days and ara-C at 100 mg/m2/d for
7 days as continuous infusion for the first cycle followed by a second
cycle, in which daunorubicin was reduced to two doses. In patients more
than 60 years of age, consolidation therapy was not obligatory and was
administered according to clinical indication. When consolidation was
administered to older patients, it was analogous to consolidation I of
the patient group 51 to 60 years of age. Prophylactic oral antibiotics
and antimycotics, the initiation of intravenous antibiotics for fevers
greater than 38.5°C, and the use of intravenous amphotericin were
standardized for all patients. Hematopoietic growth factors were not
administered in this study. Aspirin or nonsteroidal anti-inflammatory
drugs were avoided. Paracetamol or metamizol were used as antipyretics.
All patients were hospitalized during the study. When disseminated intravascular coagulation (DIC) or hyperfibrinolysis was clinically suspected in patients with high cell counts
(>50 × 199/L) or sepsis with bleeding complication,
the following coagulation laboratory tests were performed: prothrombin
time, partial thromboplastin time, Quick's test, fibrinogen,
antithrombin III, factor XIII, and fibrin(ogen) degradation products.
DIC was treated according to each center's standard. Hyperfibrinolysis
was treated by intravenous infusion of tranexamic acid and additional
substitution of fibrinogen and factor XIII or by infusion of fresh
frozen plasma, as needed.
Daily morning blood counts were performed as long as patients were
receiving platelet transfusions or until the platelet count was
self-supporting of greater than 25 × 109/L for 2 to 3 days. Blood counts were performed on EDTA-anticoagulated blood using a
flow cytometer. The patients were examined daily for evidence of
hemorrhage. Fundoscopy was performed only in case of impairment of
vision.
Hemoglobin levels were maintained at greater than 80 g/L by packed RBC
transfusions.
During each course of chemotherapy, bleeding complications according to
World Health Organization (WHO) criteria (0, none; 1, petechial; 2, mild blood loss; 3, gross blood loss; 4, debilitating blood loss) were
recorded as well as the number of RBCs and platelet transfusions
administered. The bleeding complication scores were recorded in
parallel to the treatment of each patient by the treating physician and
controlled by a board-certified hematologist responsible for the study
at each center. Major bleeding complications (WHO grade 3 and 4) were
verified by chart review performed by the study coordinator. Platelet
transfusions were administered at the discretion of each center as
pooled random donor platelet concentrates (normally 4 to 6) or as
apheresis single-donor products. The use was determined by the standard
of each center and by the actual availability of the different platelet
products. All centers used standardized and quality controlled platelet
products according to the "Deutsche Gesellschaft für
Transfusionsmedizin und Immunhämatologie." It was recommended,
but not a study requirement, that platelets be leuko-reduced by
filtration at the bedside. Random ABO-compatible (non-HLA-typed)
platelet transfusions were administered until a major bleeding episode
and alloimmunization necessitated HLA-matched platelet transfusions.
All patients were followed from the beginning of each chemotherapy
cycle until discharge with a stable platelet count greater than 25 × 109/L, treatment failure, or death.
Platelet transfusion protocol.
In group A patients, prophylactic platelet transfusions were
administered routinely for morning platelet counts less than 10 × 109/L. Platelet transfusions were administered for morning
platelet counts of less than 15 × 109/L if patients had a
fever of greater than 38.5°C and a rapid decrease in platelet count
(>10 × 109/L), if patients had plasma coagulation
factor deficiencies due to sepsis or leukemia, or when
hyperleucocytosis (>50 × 109/L) was present at the
start of chemotherapy. In group B patients, platelets were transfused
prophylactically for morning platelet counts of less than 20 ×109/L (Table 1). The
platelet counts were maintained at greater than 20 × 109/L in both groups when biopsies (bone marrow biopsies
excluded) were performed and in case of major bleeding. Major bleeding
was defined as melena, hematemesis, macrohematuria, hemoptysis, vaginal bleeding, epistaxis for more than 1 hour with gross blood loss, retinal
hemorrhages with impairment of vision, or soft tissue bleeding
requiring blood transfusion.
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Table 1.
Protocol for Prophylactic Platelet Transfusion in
AML (FAB M 3 Excluded): No Sign of Major Bleeding or Retinal
Bleeding With Impairment of Vision
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Statistics.
Mean values were compared using the Student's t-test and
frequencies of bleeding complications between the two groups were calculated using the  2 test. The duration of
thrombocytopenia as well as the number of platelet units administered
per treatment cycle or per patient were calculated with the
nonparametric Kolmogorov-Smirnov test running on a computer-based
program (STATISTICA/w 5.0; Statsoft Inc, Tulsa, OK).
The study was approved by the Institutional Review Board of the
Cooperative AML Study Group of the Süddeutsche
Hämoblastosegruppe.
| |
RESULTS |
The study included 105 consecutive patients (mean age, 47 years; range,
17 to 73 years) with AML (FAB-M3 excluded). We evaluated 216 cycles of
myelosuppressive chemotherapy and 3,843 days of thrombocytopenia with
platelet counts less than 25 × 109/L. In group A, results
were evaluated in 58 patients during 110 cycles of chemotherapy and
2,198 thrombocytopenia days, and these data were compared with results
obtained in 47 patients in group B who received 106 chemotherapy cycles
and were thrombocytopenic for 1,645 days.
Patients' characteristics were well balanced in the two groups (Table
2). The characteristics of the treatment
cycles were also quite comparable for the two groups (Table 3)
with regard to the ratio of induction to consolidation
therapy and the ratio of the different platelet products, as well as
the use of leukocyte filters in both groups. There were statistically
significant differences in favor of group B versus group A patients for
platelet counts ( < or >100 × 109/L) at the
beginning of each chemotherapy cycle and, as a consequence, in the
median duration of thrombocytopenia (P < .05 for both). The
median platelet count at study entry was 72 × 109/L in
group A and 151 × 109/L in group B, respectively. The
median duration of thrombocytopenia was 5 days longer in group A
compared with that in group B (Table 3). This finding was independently
seen whether we looked to all patients or to patients in complete
remissions.
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Table 2.
Patient's Characteristics (n = 105), Leukemia
Subtypes, and Leukocyte Count at Diagnosis in the Two Groups
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Bleeding complications.
Bleeding complications of WHO grade 1 were regarded as clinically
insignificant and were counted together with WHO grade 0. Hemorrhages
of WHO grade 2-4 occurred in 20 of 110 (18.2%) and 18 of 106 (17.0%)
chemotherapy cycles and in 19 of 58 (32.8%) and 13 of 47 (27.7%)
patients in groups A and B, respectively. Both differences are
statistically not significant (P = .8 and P = .6,
respectively). Bleeding complications during chemotherapy cycles in
group A patients were all grade 2, whereas those in group B patients
were grade 2 in 9.4%, grade 3 in 6.6%, and grade 4 in 1%. For all
study patients, there was no clear increase in bleeding risk (WHO
grades 2-4) during induction compared with consolidation chemotherapy:
31 bleeding events during 159 induction cycles (20%) versus 7 events
during 47 consolidation cycles (15%), respectively (P = .5).
Platelet refractoriness of clinical significance related to
alloimmunization was not reported in the two groups.
WHO grade 3 and 4 hemorrhages were seen exclusively in 7 patients in
group B, despite the higher threshold for platelet transfusions. We
examined these hemorrhages in detail (Table 4). In 5 of
these 7 patients, significant morbidity related to the bleeding
complication was stated by the treating physician. Four patients
developed major bleeding complications in parallel with serious
infections and sepsis. In 1 patient, sepsis was related to pneumonia.
In a second patient, sepsis was related to a local infection of the central venous line. Both patients showed no sign of DIC or
hyperfibrinolysis. Bleeding (WHO grade 3) could be stopped in these 2 patients due to a combined therapeutic approach with antibiotics,
removal of the venous line, and transfusion of platelets. Two other
patients died. One patient developed septic shock related to a severe
pneumonia needing mechanical ventilation on an medical intensive care
unit. Gastrointestinal bleeding (grade 4) occurred after 1 day of
ventilation related to a stress ulcer of the stomach. The patient
showed signs of DIC [fibrinogen < 100 mg/dL, antithrombin
III < 50%, and positive fibrin(ogen) degradation products]. The
hemoglobin level could be maintained at greater than 80 g/L due to the
transfusion of 6 RBC packs. Despite intensive treatment with dopamine,
antibiotics, antimycotics, transfusion of fresh frozen plasma, and
antithrombin III, the patient died in persistent septic shock
with adult respiratory distress syndrome (ARDS). The
platelet count at the end was 36 × 109/L. The treating
physician stated that death was clearly not related to the bleeding
complication. The other patient who died related to septic shock also
had a progressive pneumonia with signs of DIC [fibrinogen < 200
mg/dL, antithrombin III < 60%, and positive fibrin(ogen)
degradation products] and hemorrhagic diarrhea (grade 3). The platelet
count was 50 × 109/L at that time. Despite intensive
treatment, including fresh frozen plasma, antithrombin III, and
platelet and RBC transfusions, the rectal bleeding
persisted. The patient died from causes related to
unresolved septic shock with multiorgan failure. Also, in this patient,
bleeding was not the cause of death, despite the fact that the bleeding
could not be stopped.
In 4 of these 7 patients, bleeding (WHO grade 3 and 4) occurred while
their platelet counts were greater than 20 × 109/L (36 to
58 × 109 platelets/L). Five of 7 patients had local
lesions. Five of the patients had AML FAB type M4 or M5. These subtypes
are more frequently associated with hyperleucocytosis (Table 4),
leukostasis, and organ infiltration, which may be additional risks for
bleeding, as shown in other studies.14,15 In the subgroup
of patients with grade 3 and 4 bleeding, 6 of 7 (86%) experienced this
complication during induction chemotherapy.
Platelet and RBC transfusions.
Beside the comparison of transfusions in group A and group B patients,
we performed additional comparisons between group A and a subgroup of
group B patients omitting the 7 patients with WHO grade 3 and 4 bleeding episodes. We did this additional comparison because we wanted
to see whether the differences between group A and B could still be
seen when we omitted patients with WHO grade 3 and 4 bleeding
complications, which occurred exclusively in group B.
The number of platelet transfusions administered per chemotherapy cycle
was significantly different between group A and B patients related to
both single-donor apheresis products (P < .05) as well as
to pooled random donor concentrates (P < .01). These differences were still observed even when we compared group A with the
subgroup of non-major-bleeding group B patients (Table 5). The mean number of apheresis platelets
and platelet concentrates administered in group A were 3.0 (0 to 16)
and 15.4 (0 to 152), in group B were 4.8 (0 to 33) and 25.4 (0 to 188),
and in the subgroup of group B were 4.4 (0 to 21) and 23.2 (0 to 160),
respectively. Platelet use was one third lower in group A compared with
group B patients. This difference between the two groups was still more evident when platelet transfusions administered were not calculated per
chemotherapy cycle but rather per thrombocytopenic day: apheresis platelets averaged 0.15 versus 0.31 per day and platelet concentrates averaged 0.77 versus 1.65 per day for group A versus group B, respectively. The mean number of RBC transfusions administered to group
A patients was 7.3 (0 to 22), group B patients received 8.3 (2 to 28),
and the subgroup of group B patients received 7.6 (2 to 28). RBC usage
did not differ among the groups (Table 5).
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Table 5.
Mean Number of Platelet and RBC Transfusions Per
Treatment Cycle in Group A Compared With Group B and the
Nonbleeding Subgroup of B Patients
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Cost calculation for platelet and RBC transfusions.
The calculation of costs for the platelet transfusions, RBC
transfusions, leukocyte filters, and medical personal in the two groups
is based on data for Germany (data not shown here). There was a cost
reduction for platelet transfusion per treatment cycle of about one
third for group A patients compared with group B patients. Because
costs for RBC transfusion did not differ significantly, this led to a
mean overall cost reduction of one third for transfusions. Concerning
the total costs for transfusions, one has to calculate not only the
charges for transfusions, but also the costs for medical personnel
administering transfusions to the patients.
| |
DISCUSSION |
This multicenter study shows that a platelet transfusion trigger of 10 ×109/L for routine prophylactic platelet transfusion
therapy during induction and consolidation chemotherapy for AML is safe
and not associated with a higher bleeding risk than the more generally used threshold of 20 ×109/L. The significantly longer
duration of thrombocytopenia in group A patients transfused at the
lower trigger did not result in a higher bleeding risk. The longer
duration of thrombocytopenia in group A reflects the significantly
lower platelet count at study entry for these patients. Significantly
more patients in group A started their chemotherapy with platelet
counts less than 100 × 109/L (Table 3). This imbalance is
related to the comparative, nonrandomized design of our study. This
negative factor for group A was certainly seen by chance on one side.
On the other side, it underlines the safety of the lower trigger for
prophylactic platelet transfusion observed in our study. The trend to
higher complete remission rates (P = .09) in group B compared
with group A patients in our study was clearly not related to the
different triggers for platelet transfusion, because all data available
indicate that different transfusion policies do not lead to different
remission rates despite the same chemotherapy in those
groups.7,16 Despite the fact that bleeding complications
(WHO grade 2-4) were seen at the same rate in both groups, bleeding of
WHO grades 3 and 4 was seen exclusively in group B patients who were
being transfused at the higher platelet trigger. This unexpected
observation occurred by chance, we suppose. The analysis of these
serious bleeding episodes showed clearly that they were not related to
a platelet count less than 10 × 109/L. These observations
are in line with the results reported by two other centers using a
comparably low trigger level.14,16 These bleeding episodes
were mainly associated with local lesions (in 5 of 7 patients).
Patients with M4 and M5 leukemias may be at a higher risk for bleeding
(Table 4) at the beginning of chemotherapy, because these leukemias are
more often associated with organ infiltration and high leukocyte
counts. In 2 patients, major bleeding could be recorded in parallel
with DIC caused by sepsis. In these 2 patients with persistent septic
shock, bleeding could not be stopped despite adequate intensive
therapy. These 2 patients died both related to septic shock and not as
a consequence of the bleeding complication. In the study by Gmür
et al,14 there were 3 fatal bleeding episodes in 102 patients. None of these hemorrhagic deaths was related to the use of
stringent prophylactic platelet transfusion policy. Two of the bleeding
deaths were mainly related to associated coagulation factor
deficiencies. In 1 of these 2 patients, cerebral bleeding occurred at a
platelet count of greater than 50 × 109/L in parallel
with a white blood cell count of 430 × 109/L
(M5 leukemia). The third patient died because of refractoriness to
platelet transfusions and the lack of an HLA-identical platelet donor.
Eighty-six percent of serious bleeding episodes (WHO grade 3-4) in our
study occurred during induction chemotherapy. In contrast, WHO grade 2 bleeding episodes occurred with equal frequency during induction and
consolidation chemotherapy. This result is in accord with prior studies
demonstrating that the risk of bleeding in acute leukemia is clearly
increased during induction chemotherapy when the patient is not yet in
complete remission.14,15,17
Patients with acute promyelocytic leukemia were excluded from our
study, because these patients were being treated in a separate European
protocol including all-transretinoic acid. This type of leukemia is
associated with a well-known high bleeding risk during induction
chemotherapy because of severe plasma coagulation factor deficiencies.
However, we think that our data collected during consolidation
chemotherapy show that the stringent platelet transfusion policy can be
safely used even in these patients during consolidation chemotherapy
after they have achieved a complete remission.
Our study confirms the results of the three other platelet transfusion
trials published during the last 15 years that have shown that
prophylactic platelet transfusion therapy can be safely postponed until
platelets decrease to less than 10 × 109/L.14,16,17 The single center study by
Gmür et al14 used an even more stringent transfusion
protocol with three different platelet transfusion triggers based on
the clinical condition of the patient as well as their platelet count.
The lowest trigger used in this study was a platelet count of 5 × 109/L. This policy proved to be safe in an experienced
leukemia center. Our study was performed in 17 different centers,
including large and small departments of hematology and university and
community hospitals, an approach that represents the real heterogeneity in the treatment of leukemia patients. Additional support for the
safety of the 10 × 109/L trigger in the multicenter
setting comes from an interim analysis of a randomized Italian
multicenter study.18
In a study of 92 children with acute leukemia performed 35 years ago,
the investigators stated that they could not determine a threshold
platelet level to prevent bleeding. Serious bleeding was more often
associated with a platelet count less than 5 × 109/L, but
from 5 to 100 ×109/L there was little difference in the
frequency of serious bleeding complications.13 These
clinical observations of a serious bleeding risk were gathered when
aspirin was still used in thrombocytopenic patients. A clinical study
that involved patients with aplastic anemia evaluated fecal blood loss
as an indicator of bleeding in 1978, when aspirin was no longer used in
thrombocytopenic patients. Stool blood loss did not increase
substantially until platelet counts were less than 5 ×109/L.19
The number of platelet transfusions in our study was reduced by one
third using the lower trigger, whereas the number of RBC transfusions
administered was similar in the two different trigger groups. This
result is in line with comparable studies.16,18 In our
study, the 10 × 109/L platelet trigger was increased to
15 × 109/L only in certain clinical situations
when platelet consumption was increased due to fever greater than
38°C or, when plasma coagulation factor deficiencies were present,
due to sepsis or leukemia or in case of hyperleukocytosis
(>50 × 109/L) at the start of induction chemotherapy.
The use of different platelet products (random donor and apheresis
platelets) did not influence our results, because they were equally
distributed in both groups (Table 3). The reduction in the use of
platelet transfusions shown in patients transfused at the lower
trigger, as in our study, has important economic consequences.
Calculated (according to the study results presented here) for the
expected frequency of newly diagnosed AML in adults per year in the
United States, assuming that two thirds of them will be treated by two
cycles of chemotherapy, leads to a saving of 83,200 random donor
platelet concentrates and 14,976 apheresis products.20
A more stringent platelet transfusion policy is not only safe and cost
effective, but it is also less harmful to patients. Blood transfusions
can never be made entirely safe because of the risk of transmitting
viral and bacterial diseases.21,22 However, this risk is
much greater for platelet than for RBC transfusions, because platelets
are often pooled from 4 to 8 donors.10,23
Further debate and additional clinical studies will be required to
answer the question of whether there is even a need for prophylactic
platelet transfusion therapy or whether platelet transfusions should be
administered only when active bleeding is documented. Previous studies
comparing bleeding risks in patients who received therapeutic rather
than prophylactic transfusions indicated that bleeding was corrected in
all patients. Thus, a therapeutic platelet transfusion policy is a
promising approach, but its actual efficacy is unproven because of the
small numbers of patients included in these prior
studies.7,8,24
| |
FOOTNOTES |
Submitted September 25, 1997;
accepted December 29, 1997.
Supported by Grant No. M 32/90/Li 1 of the Deutsche Krebshilfe e.V.
Address reprint requests to Hannes Wandt, MD, 5th Medical
Department and Institute of Medical Oncology and Hematology,
Flurstrasse 17, D-90340 Nürnberg, Germany.
The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" is accordance with 18 U.S.C. section 1734 solely to indicate this fact.
| |
ACKNOWLEDGMENT |
The authors thank Dr Dorle Messerer for supporting the study analysis
by her statistical expertise.
| |
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Abstract
Introduction
Abstract