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• W2355116985 abstract "Targeting the B-cell receptor signalling pathway by inhibiting Bruton tyrosine kinase (BTK) produces significant clinical benefit to patients with non-Hodgkin lymphoma (NHL) and chronic lymphocytic leukaemia (CLL). We describe the case of a patient with CLL presenting with destructive lytic bone lesions that responded to treatment with the BTK-inhibitor ibrutinib and led to successful remineralization of cortical bone. A 66-year-old woman presented with a pathological fracture of the right femoral neck, lymphadenopathy and widespread lytic bone disease. Histopathology of the femoral neck revealed a population of small lymphocytes, positive for CD5, CD20, CD23, and negative for CD10, cyclin D1 and BCL6 (proliferation index 3%). A peripheral blood sample demonstrated a normal lymphocyte count (3·3 × 109/l) confirming a diagnosis of small lymphocytic lymphoma (SLL). After a total hip replacement, complete remission was achieved with fludarabine, cyclophosphamide and rituximab. Three years later, the patient developed severe left hip pain and diffuse lymphadenopathy. Magnetic resonance imaging (MRI) revealed bony infiltration throughout the spine and complete replacement of the left ischium by a soft-tissue mass (Fig 1), a biopsy of which confirmed disease relapse. Palliative radiotherapy (20 Gy in 5 fractions) was administered to the left hemi-pelvis and mobilization was restricted to touch-weight-bearing due to a high risk of fracture. Treatment was commenced with ibrutinib monotherapy (420 mg q.d.) with monthly denosumab (120 mg s.c.) to help aid remineralization. Computerized tomography after 3 months demonstrated a good partial response with no measurable adenopathy and evidence of sclerosis in the skeletal lesions, consistent with remineralization. Serial imaging, including MRI, demonstrated significant improvement in the skeletal lesions, especially the ischium (Fig 1). After 6 months, partial-weight-bearing was permitted and after 9 months the patient was able to walk with a stick. Twelve months after the initiation of ibrutinib, the patient is independently mobile and in a partial remission with lymphocytosis. Lytic skeletal lesions associated with B-cell malignancies other than myeloma and including CLL/SLL have been previously described (Rossi et al, 1987, 1990; Van de Casteele et al, 1994; Jajeh, 2012). BTK has been demonstrated to be important in the processes of osteoclastogenesis and osteoclast maturation (Lee et al, 2008). Furthermore, ibrutinib has been demonstrated to suppress bone resorption by inhibiting osteoclast differentiation and function, and can ameliorate the bone loss seen in an osteoporosis mouse model (Shinohara et al, 2008, 2014). However, bone remineralization and normal marrow regeneration following treatment with ibrutinib is a relatively little known occurrence and may signify an additional therapeutic advantage to BTK inhibition in patients with skeletal lesions from B-cell neoplasia. SR has received honoraria from Janssen-Cilag Ltd. and Pharmacyclics Inc. and research funding from Janssen-Cilag Ltd. DT, RR and LM have no conflicts of interest to declare. DT and LM wrote the manuscript. SR and RR contributed specialist knowledge and reviewed the manuscript. RR provided the images." @default.
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• W2355116985 date "2016-05-12" @default.
• W2355116985 modified "2023-10-05" @default.
• W2355116985 title "Remineralization of lytic bone disease in a patient with small lymphocytic lymphoma using ibrutinib" @default.
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• W2355116985 doi "https://doi.org/10.1111/bjh.14118" @default.
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