Initially, the patient suffered from a mild peripheral neuropathy. minimal or no lymphadenopathy. Elevated lymphocyte counts (often 100109/L) are common, with prolymphocytes exceeding 55% of circulating lymphoid cells. Disease Trazodone HCl evolution is more aggressive than chronic lymphocytic leukaemia.1 We reported a case of a 62-year-old man treated for BPLL who subsequently developed an asymmetric sensorimotor neurological disorder (mononeuritis multiplex, MNM). Case presentation A 62-year-old man was first seen in June 2004 for splenic infarction, splenomegaly and hyperlymphocytosis with a total lymphocyte count of 181109/L, composed of 90% B-cell prolymphocytes. Haemoglobin level and platelet count were, respectively, 122?g/L and 167109/L. BPLL was diagnosed through the examination of morphology, immunophenotype (CD5+, CD19+, CD20+, CD38+, CD79b+, CD22+, high-intensity lambda light chain immunoglobulin, CD10?, CD23?, cyclin D1?) and karyotyping (t(8;14) by conventional cytogenetic analysis and fluorescence in situ hybridisation. The patient was initially treated with fludarabine (6 regimens), then with R-FND (6 regimens of rituximabCfludarabineCmitoxantroneCdexamethasone) for his first Rabbit Polyclonal to EGFR (phospho-Ser1026) cytological and karyotypic relapse (October 2008). He was in complete remission twice between 2004 and 2008, and between 2009 and 2010. In July 2010, he relapsed only with left cervical adenopathy showing the same initial (in 2004 and 2008) karyotipic features. The patient received R-VACP (2 regimens of vincristineCdoxorubicineCcyclophosphamideCprednisone), then R-ESAP (3 regimens of etoposideCcisplatineCcytarabineCprednisone) due to a partial response to R-VACP. Examination of the patient showed no clinical lymph nodes but 18F-fluoro-2-deoxy-d-glucose (FDG) positron emission tomography- CT revealed persistent non-fixing nodes in IIA area. Complete response was considered and the treatment was consolidated by left cervical lymphatic irradiation. It was planned to irradiate right cervical lymph nodes (II A, II B, III, IV and V areas), 2?Gy, five times per week, during 4?weeks. After a total radiation dose of 20?Gy, in January 2011, the patient was diagnosed with neuralgia of the left upper limb and C8-D1 sensory and motor disorders. Unstable walking was reported because of cerebellar ataxia. Investigations Electromyography (EMG) of his four extremities showed MNM with reduced motor and sensory potential amplitudes and evidence of acute and chronic denervation within the boundary of organ involvement. Cerebrospinal fluid (CSF) analysis was normal, without onconeural antibodies (antibodies against Hu, Yo, Ri, CV2, Ma, VGKC testing in blood and CSF). No sign of infiltration or compression was seen on imaging (cervicothoracic CT, medullar MRI. Neuromuscular biopsy from anterolateral compartment of left leg did not show any evidence of vasculitis, amyloidosis or lymphoma infiltration. Differential diagnosis Differential diagnosis included neoplastic infiltration or compression, paraneoplastic neurological syndrome, toxic Trazodone HCl processes of chemotherapy or radiotherapy, autoimmune (cryoglobulinemia, amyloid) Trazodone HCl or infectious (Lyme neuroborreliosis) mechanisms. Treatment During the following month, his symptoms progressively deteriorated until he had complete lower limbs and left upper limb paralysis, amyotrophy and ataxia. Neuralgia was reported to be severe despite administration of morphine and antidepressant agents. High-dose intravenous methylprednisolone pulse therapy and polyvalent immunoglobulins stopped the development from the neuropathy eventually. Final result and follow-up EMG of his four extremities was repeated 1?month later on (Feb 2011) and revealed complete neuropathy from the still left brachial plexus and both common fibular and tibial nerves. Fibrillation potentials, denervation lack and potentials of voluntary electric motor activity suggested acute diffuse axonal damage. MRI demonstrated an intrusive mass, relating to the brachial plexus towards the lung apex, with infiltration from the still left neurovascular plexus (amount 1). A neuromuscular biopsy and PET-CT weren’t reiterated with time to confirm medical diagnosis of supplementary neurolymphomatosis (NL). RituximabCcytarabineCmethotrexate was selected for their great neural (bloodCbrain and bloodCnerve hurdle) penetration; Trazodone HCl one routine was presented with but without tumour response. Bilateral higher extremities paralysis and tumoural mass infiltration from the airways had been reported. The individual passed away 2.5 months (March 2011) following the onset of neurological symptoms. No autopsy was performed. Open up in another window Amount?1 Plexus brachial MRI, T2: hyperintensity of still left cervical and axillary regions (93?cm). Debate The individual had a former background of B haematological.
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