scholarly journals Chronic lymphocytic leukaemia/small lymphocytic lymphoma treatment with rituximab and high‐dose methylprednisolone, revisited

2021 ◽  
Author(s):  
Ana Vagos Mata ◽  
Eduardo Espada ◽  
Daniela Alves ◽  
Blanca Polo ◽  
Maria João Costa ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukaemia ◽  
Lymphocytic Leukaemia ◽  
High Dose ◽  
Small Lymphocytic Lymphoma ◽  
Lymphoma Treatment ◽  
High Dose Methylprednisolone

High-dose methylprednisolone can induce remissions in patients with fludarabine-refractory chronic lymphocytic leukaemia

2010 ◽  
Vol 46 (12) ◽  
pp. 2145-2149 ◽  
Author(s):  
Wei Xu ◽  
Kou-Rong Miao ◽  
Ming Hong ◽  
Dan-Xia Zhu ◽  
Cheng Fang ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukaemia ◽  
Lymphocytic Leukaemia ◽  
High Dose ◽  
High Dose Methylprednisolone

High Dose Methylprednisolone and Rituximab Is an Effective Therapy in Advanced Refractory Chronic Lymphocytic Leukaemia Resistant to Fludarabine Therapy.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3125-3125
Author(s):  
Moez Dungarwalla ◽  
Pamala Kanagasabapathy ◽  
Samar Kulkarni ◽  
Steve O. Evans ◽  
Unell Riley ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukaemia ◽  
Viral Infections ◽  
Lymphocytic Leukaemia ◽  
Fungal Infections ◽  
Single Agent ◽  
Progression Free Survival ◽  
High Dose ◽  
Fish Analysis ◽  
Free Survival ◽  
High Dose Methylprednisolone

Abstract The management of refractory advanced chronic lymphocytic leukaemia (CLL) continues to pose a considerable challenge to the clinician. CLL patients who are refractory or become resistant to fludarabine containing regimens currently have a poor prognosis. High dose methylprednisolone (HDMP) has been shown to be an effective therapeutic option in patients who are resistant to fludarabine particularly those with bulky lymphadenopathy or refractory cytopenias who are unsuitable for alemtuzumab therapy. We have used HDMP in combination with the anti-CD20 monoclonal antibody, Rituximab, to treat 14 patients with advanced refractory CLL. Eight of fourteen patients were male. The median age was 62.5 years (range 30–71). Twelve patients had bulky lymphadenopathy with nodal masses greater than 5 centimetres in diameter. Nine patients had Binet stage C and the remainder were stage B. Autoimmune manifestations were present in five of the patients, and in one of them fludarabine therapy was contraindicated due to active autoimmune haemolysis. FISH analysis was performed to detect 17p, 11q and 13q deletions and showed 11q23 deletions in five patients. The overall response rate was 93% with a median progression free survival (PFS) of seven months. Two patients achieved a CR, another a nodular PR and 10 patients had a PR. Responses were seen in all 4 patients who had not responded to alemtuzumab as a single agent. Only one patient failed to respond. The median survival was 20 months. All five patients with 11q23 deletions responded, and the mean progression free survival in this subgroup was 10.5 months. These results compare extremely favourably with our own previous study (Thornton et al, 1998) that used HDMP alone in the management of advanced/refractory CLL where only 43% of patients responded and no patients achieved a CR. We have demonstrated that the combination of HDMP with rituximab is more effective than HDMP alone (p<0.01) in advanced refractory CLL. Although HDMP in combination with rituximab causes little or no myelosuppression, 6/14 patients (43%) developed opportunistic fungal or viral infections and this included fungal mould infections, fungal yeast infections and opportunistic viral infections. Three patients died of pulmonary fungal infections, although 2 of these patients had been retreated with alternative regimens. While the immunosuppressive effects of high dose steroids are well recognised, it appears that the addition of rituximab has made these patients more prone to opportunistic infections. In summary, HDMP in combination with rituximab is an effective rescue regime in purine analogue refractory CLL particularly in patients with bulky lymphadenopathy who are unsuitable for alemtuzumab, and in patients with 11q23 deletions.

Cyclin D1 overexpression in proliferation centres of small lymphocytic lymphoma/chronic lymphocytic leukaemia

2017 ◽  
Vol 70 (10) ◽  
pp. 899-902 ◽  
Author(s):  
Larissa Sena Teixeira Mendes ◽  
Natalie Peters ◽  
Ayoma D Attygalle ◽  
Andrew Wotherspoon
Keyword(s):  
Chronic Lymphocytic Leukaemia ◽  
Cyclin D1 ◽  
Lymphocytic Leukaemia ◽  
Small Lymphocytic Lymphoma

scholarly journals Outcomes of patients with simultaneous diagnosis of chronic lymphocytic leukaemia/small lymphocytic lymphoma and multiple myeloma

2018 ◽  
Vol 185 (2) ◽  
pp. 347-350 ◽  
Author(s):  
Sikander Ailawadhi ◽  
Bhagirathbhai R. Dholaria ◽  
Sharad Khurana ◽  
Taimur Sher ◽  
Victoria Alegria ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Chronic Lymphocytic Leukaemia ◽  
Lymphocytic Leukaemia ◽  
Small Lymphocytic Lymphoma

Chronic lymphocytic leukaemia

2010 ◽  
pp. 4240-4247
Author(s):  
Clive S. Zent ◽  
Aaron Polliack
Keyword(s):  
North America ◽  
Chronic Lymphocytic Leukaemia ◽  
B Lymphocyte ◽  
Lymphocytic Leukaemia ◽  
Immunoglobulin Gene ◽  
Cell Of Origin ◽  
Small Lymphocytic Lymphoma ◽  
Lymphoid Neoplasm ◽  
Surface Immunoglobulin

Chronic lymphocytic leukaemia/small lymphocytic lymphoma (CLL) is the most prevalent lymphoid neoplasm in Europe and North America. The ‘cell of origin’ is a mature B lymphocyte that has a rearranged immunoglobulin gene. CLL cells express modest amounts of surface immunoglobulin, and are characterized by defective apoptosis. The cause of CLL is unknown....

ALK-positive histiocytosis associated with chronic lymphocytic leukaemia/small lymphocytic lymphoma: a multitarget response under ibrutinib

2020 ◽  
Author(s):  
Charlotte Syrykh ◽  
Loïc Ysebaert ◽  
Sarah Péricart ◽  
Solène M. Evrard ◽  
Fabienne Meggetto ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukaemia ◽  
Lymphocytic Leukaemia ◽  
Small Lymphocytic Lymphoma ◽  
Alk Positive

scholarly journals Duvelisib: A 2018 Novel FDA-Approved Small Molecule Inhibiting Phosphoinositide 3-Kinases

2019 ◽  
Vol 12 (2) ◽  
pp. 69 ◽  
Author(s):  
Daniel A. Rodrigues ◽  
Fernanda S. Sagrillo ◽  
Carlos A. M. Fraga
Keyword(s):  
Clinical Trials ◽  
Follicular Lymphoma ◽  
Chronic Lymphocytic Leukaemia ◽  
Drug Administration ◽  
Small Molecule ◽  
Lymphocytic Leukaemia ◽  
Food And Drug Administration ◽  
Small Lymphocytic Lymphoma ◽  
Dual Inhibitor ◽  
Systemic Therapies

Duvelisib (Copiktra®) is a dual inhibitor of phosphoinositide 3-kinases (PI3Kδ and PI3Kγ). In 2018, duvelisib was first approved by the Food and Drug Administration (FDA) for the treatment of adult patients with relapsed or refractory chronic lymphocytic leukaemia (CLL)/ small lymphocytic lymphoma (SLL) after at least two prior therapies. Duvelisib has also been approved under accelerated track for relapsed or refractory follicular lymphoma (FL) after at least two prior systemic therapies. In this review, we provide a series of information about duvelisib, such as the development of clinical trials for LLC/SLL and FL and the steps used for its synthesis.

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