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bleeding, and more specifically amongst class A and Bcirrhotic patients.7 Unfortunately, issues of generalisabilityin the aforementioned trial prevent definitive conclusionsabout the impact of transfusion policy on the outcomesof patients with nonvariceal bleeding; importantly, addi-tional information will soon be available from a clusterrandomized trial in the United Kingdom.8
In the interim, based on all currently available evi-dence, clinicians should continue to follow consensusrecommendations for patients with nonvariceal bleeding.We would also like to correct Dr Lin regarding his com-ments about current recommendations. The 2010 Inter-national Consensus Group in fact suggested a restrictivetransfusion practice, with blood transfusions adminis-tered to patients with a haemoglobin level of 7 g/dL orless, pending further data.8 Furthermore, threshold hae-moglobin levels of 6–10 g/dL may warrant transfusion inpatients with underlying cardiac disease.9
ACKNOWLEDGEMENTThe authors’ declarations of personal and financial inter-ests are unchanged from those in the original article.2
REFERENCES
1. Lin H-J. Letter: is blood transfusion really a risk factor forrebleeding in nonvariceal gastrointestinal bleeding? AlimentPharmacol Ther 2013; 37: 838–9.
2. Restellini S, Kherad O, Jairath V, Martel M, Barkun AN. Redblood cell transfusion is associated with increased rebleeding inpatients with nonvariceal upper gastrointestinal bleeding. AlimentPharmacol Ther 2013; 37: 316–22.
3. Barkun A, Sabbah S, Enns R, et al. The Canadian Registry onNonvariceal Upper Gastrointestinal Bleeding and Endoscopy(RUGBE): endoscopic hemostasis and proton pump inhibition areassociated with improved outcomes in a real-life setting. Am JGastroenterol 2004; 99: 1238–46.
4. Stanley AJ, Dalton HR, Blatchford O, et al. Multicentrecomparison of the Glasgow Blatchford and Rockall Scores in theprediction of clinical end-points after upper gastrointestinalhaemorrhage. Aliment Pharmacol Ther 2011; 34: 470–5.
5. Romagnuolo J, Barkun AN, Enns R, Armstrong D, Gregor J.Simple clinical predictors may obviate urgent endoscopy inselected patients with nonvariceal upper gastrointestinal tractbleeding. Arch Intern Med 2007; 167: 265–70.
6. Hearnshaw SA, Logan RF, Palmer KR, Card TR, Travis SP,Murphy MF. Outcomes following early red blood cell transfusionin acute upper gastrointestinal bleeding. Aliment Pharmacol Ther2010; 32: 215–24.
7. Villanueva C, Colomo A, Bosch A, et al. Transfusion strategiesfor acute upper gastrointestinal bleeding. N Engl J Med 2013; 368:11–21.
8. Available at: http://www.nhsbt.nhs.uk/trigger/. Accessed January2013.
9. Barkun AN, Bardou M, Kuipers EJ, et al. International consensusrecommendations on the management of patients withnonvariceal upper gastrointestinal bleeding. Ann Intern Med2010; 152: 101–13.
Letter: infliximab therapy in inflammatorybowel disease patients after livertransplantationA. Indriolo*, S. Fagiuoli†, L. Pasulo†, G. Fiorino‡,S. Danese* & P. Ravelli*
*Gastroenterology and Digestive Unit, Ospedali Riuniti di Bergamo,Bergamo, Italy.†Gastroenterology and Hepatology of Transplantation Unit, OspedaliRiuniti di Bergamo, Bergamo, Italy.‡IBD Center, Gastroenterology Unit, Humanitas Clinic Institute,Rozzano, Italy.E-mail: [email protected]
doi:10.1111/apt.12256
SIRS, We read with great interest the studies by Sandhuet al.1 and Mohabbat et al.,2 which evaluated antitumournecrosis factor-alpha (TNFa) therapy for patients withrefractory inflammatory bowel disease (IBD) post ortho-
topic liver transplant (OLT). To date, there have been only18 patients treated with anti-TNF for relapsing IBD fol-lowing OLT; this number includes patients with UC, CD,indeterminate colitis and pouchitis.1–5 Such data are oftennot homogeneous in terms of administered therapy andoutcomes.
We have evaluated the efficacy and safety of inflix-imab therapy in a homogeneous series of patients withrefractory UC following OLT for advanced-stage primarysclerosing cholangitis (PSC). Four patients (all malepatients; median age 39 years, range 22–54 years) withUC (n = 3) or pouchitis (n = 1) who underwent OLTwere identified (Table 1). The median duration of inflix-imab therapy was 18 months (range: 3–30).
Three patients (75%) experienced sustained improve-ment of IBD. A significant decrease in Mayo score wasobserved after infliximab therapy, from a mean score of9.0 (range: 7–10) to a mean score of 1.0 (range: 0–3)(P < 0.0001) (Figure 1). At week 54, complete mucosal
840 Aliment Pharmacol Ther 2013; 37: 835-843
ª 2013 Blackwell Publishing Ltd
Letters to the Editors
Alimentary Pharmacology and Therapeutics
Table1|Caseserialsof
patie
ntstreatedwith
inflixim
abtherap
yforUCan
dpo
uchitis
followingorthotop
icliver
tran
splantation
Case
Age
(years)
Gen
der
Indicatio
n
forOLT
Age
atPS
C
Age
at
OLT
Anti
rejection
therap
y
Age
atUC
Durationof
IFX
therap
y
(mon
ths)
Pre-an
ti-
IFXMSS
Post-anti-
IFX
MSS
Pre-
anti-
IFX
PDAI
Post-
anti-
IFX
PDAI
Pre-an
ti-
IFX
MCES
I
Post-anti-
IFX
MCSI
Adverse
even
ts
after
IFX
Hep
atic
rejection
130
Male
PSC
1224
Tacrolim
us
1mg+
1.5mg/day;
Azathiprine
75mg/day;
Pred
nisone
5mg/day
530
100
––
30
Molluscum
contagiosum
No
248
Male
PSC
2342
Tacrolim
us
3.5mg+
3.5mg/day
2128
93
––
22
Non
eNo
322
Male
PSC
1516,2
1Ciclosporine
250mg+
200mg/
day
123
71
––
2Wait
endo
scop
y
Non
e
454
Male
PSC
42
45
Tacrolim
us
1mg+
1.5mg/day;
Sirolim
us
3mg/day
3212
––
1412
––
Non
eNo
Tot.
Med
ian
age,
rang
e
(years)
Gen
der
PSC
Med
ian
age,
rang
e
(years)
Med
ian
age,
rang
e
(years)
Med
ian
age,
rang
e
(years)
Med
ian
age,
rang
e
(mon
ths)
Med
ian
Pre-anti-
IFX MSS
,range
Med
ian
Post-anti-
IFX MSS
,
rang
e
Pre-
anti-
IFX PDAI
Post-
anti-
IFX PDAI
Med
ian
Pre-anti
IFX
MCES
I,
rang
e
Med
ian
Post-anti-
IFX
MCSI,
rang
e
Num
ber,
percen
tage
Num
ber,
percen
tage
439
(22–
54)
4/4
Male
4/4
19(12–
42)
33(24–
45)
16.5
(5–
32)
18(3–3
0)
9(7–10)
1.0*(0
–3)
1412†
2(2–3
)1(0
–2)
1/4(25%
)0/4
(0%)
*Sign
ificativ
emed
ianMMSscorede
creasedafterinflixim
abtherapyitwas
observed
,from
9(range:7
–10)to
1.0(range:0
–3)(P
<0.0001).
†Nosign
ificant
differen
cein
PDAIafterinflixim
abtherapyitwas
observed
,from
14to
12(P
=NS).
Aliment Pharmacol Ther 2013; 37: 835-843 841
ª 2013 Blackwell Publishing Ltd
Letters to the Editors
healing (defined as absence of lesions) was observed inone of three patients (33%). In the one patient withrefractory pouchitis, a nonstatistically significant decreasein pouch disease activity index was observed (from 14 to12). Subsequently, this patient presented with worseningof endoscopic lesions after interruption of infliximabtherapy, and he underwent ileostomy.
Steroid treatment was successfully withdrawn duringinfliximab therapy in all patients. Adverse eventsincluded only one infection by Molluscum contagiosum,which resolved without sequelae. No malignancies wereobserved in any patient following infliximab therapy. Nocases of hepatic rejection were documented. One patient(25%) presented with a recurrence of PSC 2 years beforeinfliximab therapy (3 years after OLT) and he underwenta second OLT 5 years after the first.
Our results are consistent with the studies of Sandhuand Mohabbat and are in line with data on IBD patientswho have not previously undergone liver transplantation.We assessed a homogenous series of refractory UC
patients, who were treated with the same anti-TNFa agent.In previous studies, some patients were treated with inflix-imab3–5 others with adalimumab5 and others patients withadalimumab for secondary loss of response to infliximab.4
Mucosal healing has been previously evaluated in onlythree studies.1, 3–5 Moreover, in contrast to previousreports, we objectively assessed clinical response, utilisinga clinical score for UC and pouchitis, and assessed muco-sal healing using an endoscopic score.
In conclusion, our small study supports previous dataon the efficacy and safety of infliximab therapy in patientswith refractory UC after OLT, and adds new data on ahomogenous population with UC and previous OLT, alltreated by infliximab. Although no cases of hepatic graftdysfunction or rejection were observed, larger studies areneed to evaluate the safety profile of biological therapycombined with anti rejection treatment in patients withrefractory IBD following liver transplantation.
ACKNOWLEDGEMENTDeclaration of personal and funding interests: None.
REFERENCES
1. Sandhu A, Alameel T, Dale CH, Levstik M, Chande N. The safetyand efficacy of antitumor necrosis factor-alpha therapy forinflammatory bowel disease in patients post liver transplantation:a case series. Aliment Pharmacol Ther 2012; 36: 159–65.
2. Mohabbat AB, Sandborn WJ, Loftus EV Jr, Wiesner RH, BruiningDH. Anti-tumor necrosis factor treatment of inflammatory boweldisease in liver transplant recipients. Aliment Pharmacol Ther 2012;36: 569–74.
3. Lal S, Steinhart AH. Infliximab for ulcerative colitis following livertransplatation. Eur J Gastroenterol Hepatol 2007; 19: 277–80.
4. El-Nachef N, Terdiman J, Mahdevan U. Anti-tumor necrosisfactor therapy for inflammatory bowel disease in the setting ofimmunosuppression for solid organ transplantation. Am JGastroenterol 2010; 105: 1210–1.
5. Indriolo A, Fagiuoli S, Pasulo L, et al. Infliximab in patients withulcerative colitis and primary sclerosing cholangitis before andafter liver transplantation. JCC 2012; 6(Suppl. 1): S117.
Letter: Coca-Cola can dissolve gastricphytobezoarsK. Uchida
Department of Anesthesiology, St. Marianna University School ofMedicine, Kawasaki, Japan.E-mail: [email protected]
doi:10.1111/apt.12263
SIRS, I read with interest the systematic review by Ladaset al. regarding Coca-Cola therapy for phytobezoars.1
For lack of an alternative, their outcome was based ondata from case reports and retrospective studies. In gen-eral, the selection bias included in their outcome is largerthan the bias that would have been produced using datafrom double-blinded, randomised, placebo-controlledstudies.
0
1
2
3
4
5
6
7
8
9
10
Pre-anti IFX MSS, Median, range (7–10)
Post-anti IFX MSS,Median, range (0–3)
MS
S s
core
*P < 0.0001
Figure 1 | MSS score before and after IFX therapy.Significant decrease in median Mayo score system(MMS) after infliximab therapy was observed from 9.0(range 7–10) to 1.0 (range 0–3) (P < 0.0001)*.
842 Aliment Pharmacol Ther 2013; 37: 835-843
ª 2013 Blackwell Publishing Ltd
Letters to the Editors