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We have seen a patient with late CNS involvement in Waldenstrom macroglobulinemia (MW), with previously undescribed characteristics. We believe this information can be of interest. In addition, we reviewed related medical literature in PubMed and Medline, through the Ovid platform, without time limit, using as descriptors: <span class="elsevierStyleItalic">meningeal disease or neurolymphomatosis and Waldenström; hydrocephalus and Bing-Neel syndrome.</span></p><p id="par0010" class="elsevierStylePara elsevierViewall">A 76-year-old male was admitted to our hospital in May 2013 due to disorientation and successive falls. In 2004 he had been diagnosed with MW due to asthenia, pruritus, retroperitoneal lymph nodes and splenomegaly. The patient had a serum monoclonal component (MC) Mk (7<span class="elsevierStyleHsp" style=""></span>g/l) and clonal lymphoplasmacytic infiltrate in the bone marrow (18%: [CD19, 20, 23, 38]+; CD [5, 10]−; k+) and peripheral blood (8%: 192/μl). Initially, it improved with chlorambucil-prednisone, requiring various drug combinations during 7 years (fludarabine, cyclophosphamide, rituximab [RTX], dexamethasone and bendamustine) due to its progression. In January 2012 he was in clinical remission with a serum CM of 1.9<span class="elsevierStyleHsp" style=""></span>g/l. On admission he reported successive falls, urinary incontinence, dizziness and disorientation. On examination, respiratory and haemodynamic status was normal, without lymphadenopathy or splenomegaly. He was alert, with partial disorientation, coherent speech, without neurological deficit, muscular balance normal, symmetrical reflexes, plantar flexors, clumsy gait, mental blocks, anteropulsion and some festination. Ophthalmological examination was normal. Mild anaemia (Hb:<span class="elsevierStyleHsp" style=""></span>106<span class="elsevierStyleHsp" style=""></span>g/l) and thrombocytopenia were detected, general profile, liver and kidney normal, and biclonal serum CM: Mk (1.5<span class="elsevierStyleHsp" style=""></span>g/l) and Gk (0.9<span class="elsevierStyleHsp" style=""></span>g/l) with a k/¿ 76 quotient. In the bone marrow aspirate, 1.7% of lymphocytes were detected with the initial clonality. Body CT was normal. Dilation of ventricles and slight cortical atrophy was observed in the cranial computed tomography scan and magnetic resonance imaging, with Evan index (ventricles width in frontal horns/ditto of cranial cavity) of 0.44 (normal: <0.3). Lumbar puncture was performed once normal pressure hydrocephalus was suspected, obtaining xanthochromic cerebrospinal fluid (CSF), at a pressure of 30<span class="elsevierStyleHsp" style=""></span>cm of water, without blockages, proteins of 5.3<span class="elsevierStyleHsp" style=""></span>g/l and 40<span class="elsevierStyleHsp" style=""></span>cells/L (68% lymphocytes, with initial B clonality); one biclonal component was also detected, with the quotient (CM/albumin) in CSF compared to serum of 0.83 for IgM (normal <0.06)<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> and 2.23 for IgG. With a diagnose of lymphomatosis meningeal associated to lymphoplasmacytic lymphoma, a 15-day systemic treatment with RTX and methotrexate (MTX) was initiated (3<span class="elsevierStyleHsp" style=""></span>g/m<span class="elsevierStyleSup">2</span>), and triple intrathecal (MTX, cytarabine, hydrocortisone), showing progressive clinical improvement, normalization of mental status and gait, and CSF's disappearance of cells and protein decrease. Systemic RTX and MTX had to be suspended due to intolerance. After 4 doses of triple intrathecal, treatment continued with liposomal cytarabine (another 5 doses) maintaining the clinical and lab tests improvement. But the patient suffered an influenza A H1N1 virus infection, with bilobar pneumonia and bacteraemia caused by <span class="elsevierStyleItalic">Escherichia coli</span>, ESBL producer, and died the second day after admission (January 2014).</p><p id="par0015" class="elsevierStylePara elsevierViewall">CNS involvement in MW affects 10–30%,<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> preferably by hyperviscosity, immune mechanism or bleeding diathesis, and very rarely as Bing-Neel syndrome, about which there are fewer than 50 cases reported.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> 2 manifestations have been recognized<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a>: lymphoplasmacytic infiltration (A) of brain, bone marrow or meninges, neoplastic or interstitial, more common (69%),<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> diagnosed by biopsy or demonstration of tumour cells in CSF; and monoclonal IgM deposits (B) associated with progressive demyelination.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> The median of onset is 3–4 years from diagnosis, and usually occurs with clear extraneurological involvement. Clinical features may be due to involvement of long tract, cranial nerves, spinal cord, roots, intracranial hypertension or cognitive impairment.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> Our patient falls into the Type A, with its characteristic clinical presentation suggestive of normal pressure hydrocephalus which, on the contrary, was due to intracranial hypertension as well as its late appearance with no evidence of extraneurological disease. In the literature review we conducted, we only found one case of normal pressure hydrocephalus,<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a> but none similar to ours. The treatments used in these patients have been mixed, generally with partial response,<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> sometimes with prolonged survival.<a class="elsevierStyleCrossRefs" href="#bib0095"><span class="elsevierStyleSup">9,10</span></a> The use of RTX is questionable due to its low passage of the blood brain barrier. As with all CNS lymphomas, the treatment basis should be intravenous high-dose MTX; good results can be achieved with intrathecal chemotherapy with only meningeal involvement and no blocks. In our patient, the response was quite good, although frustrated by the already mentioned infectious complication. We believe this complication of MW, atypical and of very late presentation, should be taken into account, as it occurred to a patient in apparent clinical remission, and highlight the favourable outcome of the treatment used.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Alonso Alonso JJ, Cánovas Fernández A, Fernández Martínez M, Pérez Garay R. Linfomatosis meníngea como recidiva tardía de macroglobulinemia de Waldenström. Med Clin (Barc). 2016;146:141.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:10 [ 0 => array:3 [ "identificador" => "bib0055" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Prevention of CNS relapse in diffuse large B-cell lymphoma" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "R. Kridel" 1 => "P.Y. 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Journal Information
Vol. 146. Issue 3.
Pages 141 (February 2016)
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Vol. 146. Issue 3.
Pages 141 (February 2016)
Letter to the Editor
Meningeal lymphomatosis as late relapse of Waldenstrom's macroglobulinemia
Linfomatosis meníngea como recidiva tardía de macroglobulinemia de Waldenström
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