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ID: 575 Thrombotic microangiopathy Do we care why? M. Alves, R. Pimentel, A. Pinheiro, A. Lages, F. Friões, G. Rocha, P. Dias, V. Braz, J. Almeida Internal Medicine, Centro Hospitalar São João, Porto, Portugal Thrombotic microangiopathy (TM) denes a pathology char- acterised by microangiopathic haemolytic anaemia and thrombocy- topenia, which may assume different expressions in several organs. Among the possible causes are malignancy and chemotherapeutic agents (CA) like gemcitabine. We present the case of a 65 year-old male patient, a former smoker, with a known epidermoid lung carcinoma diagnosed in December 2011. He was submitted to treatment with carboplatin plus gemcitabine until March 2012, and tumor regression was achieved. A lobectomy and excision of the involved lymph nodes were performed in April 2012. In November 2012 he presented with anaemia (haemoglobin 6.1 g/dL), severe thrombocytopenia, hyper- bilirubinemia and elevated lactate dehydrogenase (N 1000 U/L). Nu- merous schistocytes were present on peripheral smear. Coombs test was negative. There was no evidence of renal failure or neurologic abnormalities. We assumed the diagnosis of TM, and started plasma exchange and high-dose corticosteroids. The performed exams showed a new small liver nodule and a lytic lesion in the iliac bone suggestive of tumor relapse. There was no response to the therapeutic, so plasma exchange was intensied to twice daily. Anyway the patient died of haemorragic complications. Malignancy and CA are rare causes of TM. In both cases, it's a highly fatal disease, and the treatment with plasma exchange is controversial in these patients. This case illustrates how challenging it can be to distinguish, in the clinical practice, a TM associated to malignancy from that caused by antitumor agents used to control those same diseases. doi:10.1016/j.ejim.2013.08.443 ID: 579 Severe hypercalcemia due to large B-cell non-Hodgkin lymphoma J. Trindade Nave, L. Santos Pinheiro, M. Lucas, R.M.M. Victorino Internal Medicine 2, Hospital Santa Maria, Lisboa, Portugal Introduction: Neoplasias can be complicated by hypercalcemia due to bone metastasis or humoral mechanisms (ectopic production of parathyroid hormone (PTH), PTH related peptide or 1,25-(OH)2 Vitamin D). In lymphomas it occurs in 15% of patients during the course of the disease and rarely at presentation. In B-cell lymphoma hypercalcemia is less frequent (78%) when compared to other types of lymphoma. We present a case of severe hypercalcemia associated with large B-cell lymphoma. Case report: 79 year old woman with stage 4 chronic kidney disease and bilateral breast cancer submitted to surgery and radiother- apy without recurrence, admitted for severe asymptomatic hypercalce- mia (15.2 mg/dL) with no response to therapy with bisphosphonates and limited response to furosemide and intra-venous hydration. The patient responded only transiently to systemic corticosteroids. Clinical observation showed palpable lymph nodes on the inguinal and sub- mandibular chains. Laboratorial evaluation revealed normocytic anae- mia (8.5 g/dL) and kidney function within the known range. The PTH was low (5.1 ng/dL) with non-detectable PTH related peptide, insuf- cient levels of 25(OH)Vitamin-D (17.2 mg/dL), monoclonal serum IgM(K) in immunoxation and normal bone marrow biopsy/ myelogram. There were no identiable lesions in the bone scintigraphy, whereas the computerized tomography showed multiple mediastinal, retroperitoneal and iliac adenopathies. The submandibular adenopathy biopsy established the diagnosis of diffuse large B-cell lymphoma. Therapy with rituximab + CHOP was instituted and calcium levels normalized with no need for additional calcium lowering therapy. Discussion: In the presented case, we admit that severe hypercalcemia was caused by the production of 1,25(OH)Vitamin D by lymphoma related cells. Hypercalcemia constitutes an atypical nding in the context of lymphoma and is considered an independent factor of poor prognosis. Studies in this area are scarce, but suggest that the median survival after the identication of hypercalcemia is about 9 months. doi:10.1016/j.ejim.2013.08.444 ID: 605 Transient hypereosinophilia in a patient with immune thrombocytopenic purpura and positive antinuclear antibodies C. Marinho, J. Nave, L. Pinheiro, M. Lucas, R. Victorino Medicine 2, Hospital Santa Maria, Lisbon, Portugal Introduction: Immune thrombocytopenic purpura (ITP) is an acquired disorder leading to immune-mediated destruction of platelets and possibly inhibition of platelet release from the bone marrow. We describe a case of ITP with unusual manifestations. Clinical case: Male, 74 years old, previously healthy, without atopy, admitted with severe thrombocytopenia (platelet count: 3 × 10^9/L) associated with pruritic purpuric lesions on the back, abdomen and lower limbs for two weeks without bleeding events. Laboratory ndings: Peripheral blood eosino- philia (15%), normal serum protein electrophoresis, slight increase of IgA and K and L chains and bone marrow aspirate with 10% eosinophil and 0.7% of megakaryocytes. The viral serologies were negative. The anti- DNAds antibodies and the antinuclear antibodies (ANA) (1/160) were positive. Other causes of thrombocytopenia were excluded, including pharmacological and toxic. ITP was diagnosed and pharmacological therapy with IV immunoglobulin (400 mg/kg/dia-5 days) and prednis- olone (1 mg/kg) was instituted, with good response (platelet count: 126 × 10^9/L at day 5 and 263 × 10^9/L at day 12). There was a complete resolution of eosinophilia. Discussion: In the present case the immuno- logical study revealed positivity for ANA and antiDNAds. This auto- antibody prole is present in 740% of ITP cases, but is not considered per se an indicator of systemic autoimmune disease (SAD). Indeed, in three studies none of the patients with ANA-positive developed SAD and another showed an incidence of SAD of 28.2% over 3 years. This laboratory ndings may be associated with poor initial response to steroid treatment (which did not happen in this case), lower probability of complete remission, greater risk of progression to chronicity and appears to be associated with a less durable remission after splenectomy. In this case, although the patient had positive ANA and Anti-DNAds there was a good response to steroid therapy, with no evidence of disease relapse after a 12 week follow-up. The association of ITP and transient isolated hypereosinophilia without organ involvement is rare and is documented in the literature only in individual cases. doi:10.1016/j.ejim.2013.08.445 ID: 609 Paraplegia associated with dorsal plasmocytoma and light chain multiple myeloma C. Marinho, J. Nave, L. Pinheiro, M. Lucas, R. Victorino Medicine 2, Hospital Santa Maria, Lisbon, Portugal Abstracts e172

Transient hypereosinophilia in a patient with immune thrombocytopenic purpura and positive antinuclear antibodies

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Page 1: Transient hypereosinophilia in a patient with immune thrombocytopenic purpura and positive antinuclear antibodies

ID: 575Thrombotic microangiopathy — Do we care why?M. Alves, R. Pimentel, A. Pinheiro, A. Lages, F. Friões, G. Rocha, P. Dias,V. Braz, J. Almeida

Internal Medicine, Centro Hospitalar São João, Porto, Portugal

Thrombotic microangiopathy (TM) defines a pathology char-acterised by microangiopathic haemolytic anaemia and thrombocy-topenia, which may assume different expressions in several organs.Among the possible causes are malignancy and chemotherapeuticagents (CA) like gemcitabine.We present the case of a 65 year-oldmalepatient, a former smoker, with a known epidermoid lung carcinomadiagnosed in December 2011. He was submitted to treatment withcarboplatin plus gemcitabine until March 2012, and tumor regressionwas achieved. A lobectomy and excision of the involved lymph nodeswere performed in April 2012. In November 2012 he presented withanaemia (haemoglobin 6.1 g/dL), severe thrombocytopenia, hyper-bilirubinemia and elevated lactate dehydrogenase (N1000 U/L). Nu-merous schistocytes were present on peripheral smear. Coombs testwas negative. There was no evidence of renal failure or neurologicabnormalities. We assumed the diagnosis of TM, and started plasmaexchange and high-dose corticosteroids. The performed exams showeda new small liver nodule and a lytic lesion in the iliac bone suggestiveof tumor relapse. There was no response to the therapeutic, so plasmaexchange was intensified to twice daily. Anyway the patient died ofhaemorragic complications. Malignancy and CA are rare causes of TM.In both cases, it's a highly fatal disease, and the treatment with plasmaexchange is controversial in these patients. This case illustrates howchallenging it can be to distinguish, in the clinical practice, a TMassociated to malignancy from that caused by antitumor agents used tocontrol those same diseases.

doi:10.1016/j.ejim.2013.08.443

ID: 579Severe hypercalcemia due to large B-cell non-Hodgkin lymphomaJ. Trindade Nave, L. Santos Pinheiro, M. Lucas, R.M.M. Victorino

Internal Medicine 2, Hospital Santa Maria, Lisboa, Portugal

Introduction: Neoplasias can be complicated by hypercalcemia dueto bone metastasis or humoral mechanisms (ectopic production ofparathyroid hormone (PTH), PTH related peptide or 1,25-(OH)2VitaminD). In lymphomas it occurs in 15% of patients during the course of thedisease and rarely at presentation. In B-cell lymphoma hypercalcemia isless frequent (7–8%) when compared to other types of lymphoma. Wepresent a case of severe hypercalcemia associated with large B-celllymphoma. Case report: 79 year oldwomanwith stage 4 chronic kidneydisease and bilateral breast cancer submitted to surgery and radiother-apy without recurrence, admitted for severe asymptomatic hypercalce-mia (15.2 mg/dL) with no response to therapy with bisphosphonatesand limited response to furosemide and intra-venous hydration. Thepatient responded only transiently to systemic corticosteroids. Clinicalobservation showed palpable lymph nodes on the inguinal and sub-mandibular chains. Laboratorial evaluation revealed normocytic anae-mia (8.5 g/dL) and kidney function within the known range. The PTHwas low (5.1 ng/dL) with non-detectable PTH related peptide, insuffi-cient levels of 25(OH)Vitamin-D (17.2 mg/dL), monoclonal serumIgM(K) in immunofixation and normal bone marrow biopsy/myelogram. There were no identifiable lesions in the bone scintigraphy,whereas the computerized tomography showed multiple mediastinal,

retroperitoneal and iliac adenopathies. The submandibular adenopathybiopsy established the diagnosis of diffuse large B-cell lymphoma.Therapy with rituximab + CHOP was instituted and calcium levelsnormalized with no need for additional calcium lowering therapy.Discussion: In the presented case, we admit that severe hypercalcemiawas caused by the production of 1,25(OH)Vitamin D by lymphomarelated cells. Hypercalcemia constitutes an atypical finding in thecontext of lymphoma and is considered an independent factor of poorprognosis. Studies in this area are scarce, but suggest that the mediansurvival after the identification of hypercalcemia is about 9 months.

doi:10.1016/j.ejim.2013.08.444

ID: 605Transient hypereosinophilia in a patient with immunethrombocytopenic purpura and positive antinuclear antibodiesC. Marinho, J. Nave, L. Pinheiro, M. Lucas, R. Victorino

Medicine 2, Hospital Santa Maria, Lisbon, Portugal

Introduction: Immune thrombocytopenic purpura (ITP) is anacquired disorder leading to immune-mediated destruction of plateletsand possibly inhibition of platelet release from the bone marrow. Wedescribe a case of ITP with unusual manifestations. Clinical case: Male,74 years old, previously healthy, without atopy, admitted with severethrombocytopenia (platelet count: 3 × 10^9/L) associated with pruriticpurpuric lesions on the back, abdomen and lower limbs for two weekswithout bleeding events. Laboratory findings: Peripheral blood eosino-philia (15%), normal serum protein electrophoresis, slight increase of IgAand K and L chains and bone marrow aspirate with 10% eosinophil and0.7% of megakaryocytes. The viral serologies were negative. The anti-DNAds antibodies and the antinuclear antibodies (ANA) (1/160) werepositive. Other causes of thrombocytopenia were excluded, includingpharmacological and toxic. ITP was diagnosed and pharmacologicaltherapy with IV immunoglobulin (400mg/kg/dia-5 days) and prednis-olone (1 mg/kg) was instituted, with good response (platelet count:126 × 10^9/L at day 5 and 263 × 10^9/L at day 12). Therewas a completeresolution of eosinophilia. Discussion: In the present case the immuno-logical study revealed positivity for ANA and antiDNAds. This auto-antibody profile is present in 7–40% of ITP cases, but is not considered perse an indicator of systemic autoimmune disease (SAD). Indeed, in threestudies none of the patients with ANA-positive developed SAD andanother showed an incidence of SAD of 28.2% over 3 years. Thislaboratory findings may be associated with poor initial response tosteroid treatment (which did not happen in this case), lower probabilityof complete remission, greater risk of progression to chronicity andappears to be associatedwith a less durable remission after splenectomy.In this case, although the patient had positive ANA and Anti-DNAds therewas a good response to steroid therapy, with no evidence of diseaserelapse after a 12 week follow-up. The association of ITP and transientisolated hypereosinophilia without organ involvement is rare and isdocumented in the literature only in individual cases.

doi:10.1016/j.ejim.2013.08.445

ID: 609Paraplegia associated with dorsal plasmocytoma and light chainmultiple myelomaC. Marinho, J. Nave, L. Pinheiro, M. Lucas, R. Victorino

Medicine 2, Hospital Santa Maria, Lisbon, Portugal

Abstractse172