Biography
Dr.Kshitij C.Joshi has completed his MBBS from MUHS & MD in General Medicine from VNSGU ,India.At the age of 32 ,he is final year student in course of DM in Medical Oncology ,Gujarat Cancer Research Institute,India. He has published many papers in reputed journals and presented oral papers and posters in many national conferencesrn
Abstract
The author describes paediatric case of relapsed Acute lymphoblastic leukaemia (ALL) presented as Aleukemic leukaemia cutis (ALC). A 2 year old child was admitted in tertiary oncology centre. He suffered from pre B cell ALL with absent Philadelphia chromosome. This patient received multiagent induction chemotherapy as per Berlin-Frankfurt-Munster (BFM) protocol for ALL. He achieved remission after 28 days of treatment.rnSubsequently he presented with multiple skin lesions in the form of multiple small erythematous violaceous macules, papules, plaques and nodules on face, chest and back regions. Histopathological examination of biopsy of skin revealed diffuse infiltration of tumor cells with prominent nucleoli, scant eosinophilic cytoplasm and numerous mitotic figures consistent with LC. Immunohistochemistry was positive for CD 10, CD 19, CD 22, CD 24, CD 79-a and TdT while negative for surface Immunoglobulin(sIg). At the time of presentation his peripheral blood smear and bone marrow examination was negative for malignant cells. Sanctuary sites including Central nervous system(CNS) and testicles were not involved. So patient was diagnosed as ALC.rn He was managed as per BFM relapse protocol for ALL. Skin lesions disappeared completely after 2 weeks of treatment. Unfortunately patient developed bone marrow and testicular relapse after 2 months. He was given testicular radiotherapy and systemic chemotherapy for relapsed ALL. But his marrow was showing persistent activity and he expired after 4 months.rnConclusion:rnIsolated cutaneous relapse is rare .This appears to be first reported case of paediatric B cell ALL presented as ALC,as sole sign of relapse.ALC must be considered as one of the differential diagnosis of cutaneous lesions in ALL.rn
Biography
She has completed his PhD at the age of 30 years from Catholic University in Rome and postdoctoral studies from Catholic University School of Medicine in Rome. rnShe is M.D. at Clinical Hematology and Bone Marrow Transplantation Centre, Department of Hematology, Transfusion Medicine and Biotechnology, “Spirito Santo†Civic Hospital, Pescara, Italy.rnResearch Activity and interest: -Biological and diagnostic aspects of cronic Philadelphia-negative Myeloproliferative diseases like Myelofibrosis, Essential Thrombocythemia and Polycythemia. -Familiar and ereditary thrombocytosis and erytrocytosis.rn-Study of molecular involvment of Oxigen sensing pathway in erythrocytosis.rn-Study of endothelial progenitors in thrombofilic disorders. rn-Infections in multiple myeloma and plasmacell disorders. rnShe has published more than 15 papers in reputed journals and several abstracts in international onco-hematologist conferences.rn
Abstract
Introduction Immune dysfunction is a biological and clinical feature of Multiple Myeloma (MM) patients. Defects of the immune system have been described including hypogammaglobulinemia, impaired lymphocyte function, steroid-related immunosuppression.rnMaterials and methods We describe the occurrence of visceral leishmaniasis in an overtreated MM patient.rnA 68-year old Italian man was diagnosed with IgG-k MM in stage IA. He was initially treated with lenalidomide and dexamethasone according to EMN 441 protocol (four cycles).rnFor recurrent disease a second-line therapy according to PAD regimen (four cycles) was administered, obtaining a very good partial response (VGPR). rnTandem autologous haematopoietic stem cell transplantation (HSCT) was carried out obtaining a VGPR; maintenance therapy with low dose thalidomide (100 mg) was discontinued owing to severe bradycardia. Treatment with Len-Dex regimen then was delivered because of progressive disease. rnAfter 25 cycles of treatment the patient developed pancytopenia without fever, mild hepatosplenomegaly, with increasing monoclonal paraprotein, showing a relapse of MM.rnResults The bone marrow aspirate and biopsy showed monoclonal CD 138 positive k plasma cells and several amastigotes in the cytoplasm of macrophages consistent with visceral Leishmaniasis (VL) (Figure 1 and 2). Serological workup obtained a positive antibody titer for Leishmania species. Polymerase chain reaction (PCR) performed on the bone marrow demonstrated a sequence analysis positive for Leishmania Donovani. After treatment with liposomial amphotericin B the bone marrow smear became negative. rnDiscussion VL is an extremely rare example of opportunistic infection found in MM patients treated with new drugs. Here prolonged steroid therapy, high dose chemotherapy, tandem HSCT and the disease itself could lead to a cumulative immunosuppression. Bortezomib significantly decreases the number of CD4+ and CD8+ T cells. A careful investigation of opportunistic infections in MM patients should always carried out. It would be desiderable monitoring CD4 lymphocytes in peripheral blood as in HIV-positive patients.rn