Annals of Oncology Advance Access originally published online on May 26, 2006
Annals of Oncology 2006 17(11):1720-1721; doi:10.1093/annonc/mdl113
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© 2006 European Society for Medical Oncology
letters to the editor |
Rituximab-related urticarial reaction in a patient treated for primary cutaneous B-cell lymphoma
Division of Medical Oncology, Ospedale Civile, Vittorio Veneto, Treviso, Italy
*(E-mail: domenico.errante{at}ulss7.it)
A 37-year-old man was referred to our institution by a dermatologist in November 2005 with a diagnosis of non-Hodgkin's lymphoma. Two punch biopsies had showed an infiltrate of CD20 positive cells grouped in follicles accompanied by a network of CD21 positive dendritic cells consistent with follicular B-cell lymphoma. Follicular cells were Bcl-6 positive, CD10 and Bcl-2 negative. The patient had noticed in the previous 8 years the onset of confluent erythematous skin patches involving the dorsal and right infra-axillar regions. He was initially treated with a variety of topical ointments, including corticosteroids, with partial improvement. The rash had worsened 2 months before the dermatologist's evaluation.
The patient had no fever, weight loss or night sweats. Chest X-ray, abdominal ultrasound, CT scan of the thorax and abdomen, positron emission tomography and bone marrow biopsy did not reveal additional disease manifestation. Therefore, the patient was diagnosed a primary cutaneous B-cell lymphoma (CBCL). This lymphoma type belongs to a rare and heterogeneous group of B-lymphoproliferative diseases characterised by restriction to the skin, a high incidence of recurrence after various treatment modalities (including surgical excision, radiotherapy, interferon, psoralen plus UVA, or chemotherapy) and a variable but mostly favourable prognosis [1].
Our patient was treated with eight intravenous (i.v.) administrations of weekly rituximab at a dose of 375 mg/m2 body surface. As a premedication, i.v. chlorpheniramine and oral paracetamol were used before each rituximab infusion.
At first administration, rituximab infusion was initiated at a rate of 50 mg/h. After 1 h, the patient developed an urticarial reaction at the site of the tumour patches and excision scars (Figure 1). This reaction was accompanied only by a very light and transient itch in the same sites. Urticarial skin lesions disappeared spontaneously after withdrawing rituximab infusion temporarily for 1 h. No medical intervention with topical or systemic drugs was necessary. Rituximab administration was thereafter uneventfully completed. A complete clinical remission was obtained after eight courses of rituximab. Histological assessment of response showed no tumour-specific infiltration.
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A similar case was previously described by Heinzerling et al. as part of a series of 10 patients with CBCLs treated with rituximab [2]. Rituximab is a human/murine monoclonal antibody targeted against the CD20 antigen on the surface of B lymphocytes. Adverse events associated with treatment are mainly mild infusion-related reactions such as fever, nausea and headache. First-dose side-effects can be severe, notably in patients with a high number of circulating tumour cells that can lead to the characteristic syndrome secondary to cytokine release [3]. It is known that complement plays a pivotal role in the pathogenesis of side-effects of rituximab treatment and that the infusion of rituximab induces rapid complement activation, preceding the release of TNF-
, IL-6 and IL-8 [4]. Occasional skin eruptions and erythema have been reported, with severe mucocutaneous toxicity such as Stevens–Johnson syndrome in one case [5]. Moreover, the underlying disease (autoimmune diseases or chronic lymphocytic leukaemia and follicular non-Hodgkin's lymphoma) may also play a role in the development of delayed or cutaneous reactions [6]. We believe that the urticarial reaction observed in our patient could probably be explained as an epiphenomenon of the killing of the B-cells bearing the CD20 antigen in the sites of the disease, with a local cytokine release, rather than the occurrence of a hypersensitivity reaction. In fact, other significant post-infusion syndromes, including Stevens–Johnson syndrome, serum sickness and vasculitis, typically occur some days after exposure [6]. Because patients, prior to the treatment with rituximab, usually receive antihistamine therapy, the true frequency of these side-effects may be underestimated.
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1. Willemze R, Jaffe ES, Burg G, et al. (2005) WHO-EORTC classification for cutaneous lymphomas. Blood 105:3768–3785.
2. Heinzerling LM, Urbanek M, Funk JO, et al. (2000) Reduction of tumor burden and stabilization of disease by systemic therapy with anti-CD20 antibody (rituximab) in patients with primary cutaneous B-cell lymphoma. Cancer 89:1835–1844.[CrossRef][Web of Science][Medline]
3. Winkler U, Jensen M, Manzke O, et al. (1999) Cytokine-release syndrome in patients with B-cell chronic limphocytic leukemia and high lymphocyte counts after treatment with an anti-CD20 monoclonal antibody (rituximab, IDEC-C2B8). Blood 94:2217–2224.
4. van der Kolk LE, Grillo-Lopez LE, Baars JW, et al. (2001) Complement activation plays a key role in the side-effects of rituximab treatment. Br J Haematol 115:807–811.[CrossRef][Web of Science][Medline]
5. Lowndes S, Darby A, Meal G, Lister A. (2002) Stevens–Johnson syndrome after treatment with rituximab. Ann Oncol 13:1948–1950.
6. Hellerstedt B and Ahmed A. (2003) Delayed-type hypersensitivity reaction or serum sickness after rituximub treatment. Ann Oncol 14:1792.
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