Impact of palifermin on intestinal mucositis of HSCT recipients after BEAM

Herbers, A.H.E.; Velden, Walter J.F.M. van der; Haan, A.F.J. de; Donnelly, J. Peter; Blijlevens, Nicole M. A.

doi:10.1038/bmt.2013.118

Cited by 16 publications

(13 citation statements)

References 16 publications

(16 reference statements)

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“…Not surprisingly, preserving the mucosal barrier by using less mucotoxic non-myeloablative conditioning regimens and drugs, including rh-KGF and Wnt signalling agonist R-spondin-1, has been shown to ameliorate or delay acute GVHD, although thus far only in animal studies (Panoskaltsis-Mortari et al, 1998;Takashima et al, 2011). In humans, rh-KGF seemed not to be protective for GVHD, despite the reduced incidence of oral mucositis, but this is probably explained by a virtual lack of effect of the growth factor on intestinal mucositis (Langner et al, 2008;Herbers et al, 2014b).…”

Section: Clinical Consequences Of Mbimentioning

confidence: 99%

Mucosal barrier injury, fever and infection in neutropenic patients with cancer: introducing the paradigm febrile mucositis

et al. 2014

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SummaryInfection remains one of the most prominent complications after cytotoxic treatment for cancer. The connection between neutropenia and both infections and fever has long been designated as 'febrile neutropenia', but treatment with antimicrobial agents and haematopoietic growth factors has failed to significantly reduce its incidence. Moreover, emerging antimicrobial resistance is becoming a concern that necessitates the judicious use of available antimicrobial agents. In addition to neutropenia, patients who receive cytotoxic therapy experience mucosal barrier injury (MBI) or 'mucositis'. MBI creates a port-de-entr ee for resident micro-organisms to cause blood stream infections and contributes directly to the occurrence of fever by disrupting the highly regulated hostmicrobe interactions, which, even in the absence of an infection, can result in strong inflammatory reactions. Indeed, MBI has been shown to be a pivotal factor in the occurrence of inflammatory complications after cytotoxic therapy. Hence, the concept 'febrile neutropenia' alone may no longer suffice and a new concept 'febrile mucositis' should be recognized as the two are at least complementary. This review we summarizes the existing evidence for both paradigms and proposes new therapeutic approaches to tackle the perturbed host-microbe interactions arising from cytotoxic therapyinduced tissue damage in order to reduce fever in neutropenic patients with cancer.

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Section: Clinical Consequences Of Mbimentioning

confidence: 99%

Mucosal barrier injury, fever and infection in neutropenic patients with cancer: introducing the paradigm febrile mucositis

et al. 2014

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“…[6][7][8] These discrepancies may depend on the type of conditioning used. The importance of conditioning is suggested, in fact, by studies from Herbers et al who reported that palifermin administration in patients treated using a BEAM conditioning schedule leads to a reduction in the rate of some infections such as 'fever of unknown origin' (FUO), 9 while the same group did not find this effect in patients treated with high-dose melphalan (HD-PAM). 10 In a previous work we indeed found that conditioning significantly interacts with the effects of palifermin and that this agent is able to reduce the rate of severe mucositis only after conditioning based on BEAM or on BU/Thiothepa treatment but not after 'HD-PAM' conditioning.…”

Section: Introductionmentioning

confidence: 94%

“…These observations are fully in keeping with the data reported by Herberts on reduction of the FUO rate after paliferminin patients were treated by BEAM. 9 How can a prophylactic agent be more active based on type of conditioning? This could be due to differences in the toxicity of different drugs used in high-dose chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Palifermin reduces infection rate and hyperfibrinogenemia in patients treated with high-dose chemotherapy based on beam or BU-thiothepa

Milone

Leotta

Cupri

et al. 2014

Bone Marrow Transplant

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We performed a retrospective study in patients who underwent high-dose chemotherapy and auto-SCT because of haematological malignancies. Forty patients were treated with palifermin while 80 were controls selected after being matched for diagnosis and length of neutropenia. Patients treated with BEAM or BU-CY or THIO-CY (BEAM/BUS) displayed, after palifermin, a lower rate of severe oral mucositis (P = 0.03). This beneficial effect of palifermin was not evident in the stratum of patients treated with high-dose melphalan (HD-PAM). After palifermin, we observed in the whole treated population a reduced rate of 'fever of unknown origin' (FUO, P = 0.02) and of severe infections not related to Gram-positive bacteria (FUO, Gram-negative bacteremia or pneumonia) (P = 0.003). This effect of palifermin on infections not related to Gram-positive bacteria was evident only in patients receiving BEAM/BUS (P = 0.01) and not in patients treated with HD-PAM (P = 0.11). Fibrinogen peak in plasma was found to be reduced after palifermin in the whole population (P = 0.01) and in the stratum who received BEAM/BUS (P = 0.02) but not in the stratum of HD-PAM. In conclusion, antiinfectious beneficial effects of palifermin are more evident in BEAM/BUS-treated patients and toward some types of infections. Reduction of fibrinogen level after palifermin suggests that this agent reduces not only the rate of infections but also their severity.

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“…Interventions aimed at attenuating proinflammatory cytokines or stimulating anti-inflammatory cytokines may offer a way to prevent toxicities [120, 121, 127–131]. …”

Section: Mucosal Injurymentioning

confidence: 99%

Local and Systemic Pathogenesis and Consequences of Regimen-Induced Inflammatory Responses in Patients with Head and Neck Cancer Receiving Chemoradiation

Russi

Raber-Durlacher

Sonis

2014

Mediators of Inflammation

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Treatment-related toxicities are common among patients with head and neck cancer, leading to poor clinical outcomes, reduced quality of life, and increased use of healthcare resources. Over the last decade, much has been learned about the pathogenesis of cancer regimen-related toxicities. Historically, toxicities were separated into those associated with tissue injury and those with behavioural or systemic changes. However, it is now clear that tissue-specific damage such as mucositis, dermatitis, or fibrosis is no longer the sole consequence of direct clonogenic cell death, and a relationship between toxicities that results in their presentation as symptom clusters has been documented and attributed to a common underlying pathobiology. In addition, the finding that patients commonly develop toxicities representing tissue injury outside radiation fields and side effects such as fatigue or cognitive dysfunction suggests the generation of systemic as well as local mediators. As a consequence, it might be appropriate to consider toxicity syndromes, rather than the traditional approach, in which each side effect was considered as an autonomous entity. In this paper, we propose a biologically based explanation which forms the basis for the diverse constellation of toxicities seen in response to current regimens used to treat cancers of the head and neck.

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Impact of palifermin on intestinal mucositis of HSCT recipients after BEAM

Abstract: The matched-control study failed to show a clinical relevant impact of palifermin on intestinal mucositis, although there was a reduced inflammatory response and less febrile neutropenia among patients who had no bacteraemia.

Cited by 16 publications

References 16 publications

Mucosal barrier injury, fever and infection in neutropenic patients with cancer: introducing the paradigm febrile mucositis

Mucosal barrier injury, fever and infection in neutropenic patients with cancer: introducing the paradigm febrile mucositis

Palifermin reduces infection rate and hyperfibrinogenemia in patients treated with high-dose chemotherapy based on beam or BU-thiothepa

Local and Systemic Pathogenesis and Consequences of Regimen-Induced Inflammatory Responses in Patients with Head and Neck Cancer Receiving Chemoradiation

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