Affiliations: Heart-Lung and Lung Transplant Program
VA Palo Alto Health Care System
Palo Alto, CA,
†The University of Texas Health Science Center at San Antonio
San Antonio, TX
Correspondence to: Lianne G. Singer, MD, Heart-Lung and Lung Transplant Program, Stanford University Medical Center, 300 Pasteur Dr, Room H3143, Stanford, CA 94305-5236; e-mail: email@example.com
To the Editor:
We read with interest the article by Levine et al (November
1999)1describing the experience of one lung transplant
center with posttransplant lymphoproliferative disorder (PTLD). The
authors are fortunate to have diagnosed PTLD in only 1.8% of their
transplant recipients to date. They state that their observed
cumulative incidence of PTLD of 20% in Epstein-Barr virus (EBV)
seroconverters was lower than the incidence of 42% reported in a
similar previous study by Aris et al.2 They speculate that
the low observed incidence of PTLD may be due to a more dose-intensive
protocol of acyclovir prophylaxis.
We calculated 95% confidence intervals for the observed incidence of
PTLD in EBV seroconverters for each of these two studies. We also
compared risk ratios for the association between PTLD and pretransplant
EBV seronegativity in the two studies (Table 1
). We included subjects with pretransplant and posttransplant EBV
serology available who survived for > 1 month. Cumulative incidence
proportions were compared using Fisher’s Exact Test, while risk ratios
were compared using the Mantel-Haenszel test for homogeneity (Stata
version 6.0; Stata Corporation; College Station, TX).
Because of the wide confidence intervals for PTLD incidence in EBV
seroconverters, one cannot conclude that the prevalence estimates are
different across the two studies. In fact, the upper limits of the 95%
confidence intervals are identical. More strikingly, the relative risks
of PTLD by EBV serostatus are nearly identical when the two studies are
compared. These results suggest that the low observed incidence of PTLD
in the authors’ center is due entirely to the low prevalence of EBV
seronegativity in their recipient population and cannot be attributed
to any difference in patient management.
p = 0.6.
p = 0.7.
The further statistical analysis of the posttransplant
lymphoproliferative disorder (PTLD) data from our center is
appreciated. We agree with the comments made by Dr. Singer and
colleagues. Indeed, the low incidence of PTLD at our center may be due
to the low prevalence of Epstein-Barr virus (EBV) seronegativity in our
As for our comparison between the PTLD incidences in EBV seroconverters
in the study by Aris et al1and our study (November
1999),2 I am sure that Dr. Singer and colleagues are aware
that due to the small sample sizes in both studies, the power to detect
differences between incidences is extremely low. In fact, a Fisher’s
Exact Test with α = 0.05 (two sided) will have only 7% power to
detect the difference between a proportion of 20% and 42% when the
sample sizes are 5 and 12, respectively. Therefore, our statement
contrasting the two studies was intended to be purely observational.
We would also like to comment that we have remained “fortunate”
with our low overall incidence of PTLD. Recent analysis of our lung
transplant patients (who have survived > 1 month following
transplantation) reveals a total of six EBV-seronegative converters
with, to date, only the single case of PTLD as previously reported in
this group (1 of 6; 16.7%). We also have an additional 19 seropositive
transplant recipients without additional cases of PTLD other than the
one previously reported (1 of 123; 0.8%). Thus, our overall PTLD
incidence is 2 of 129 (1.6%), with a follow-up of > 4,800
patient-months. For now, at our center, we will continue using the
currently successful, prolonged antiviral prophylactic regimen
described in the article.
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