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We present the case of a 76 year old female patient admitted in the Department of Cardiology for physical asthenia, profuse sweating and dyspnea with orthopnea for about one month. Clinical and paraclinical assessments performed at admission confirmed the diagnosis of cardiac tamponade. Surgical intervention was performed and 400 mL of clear effusion were drained. Post-operative evolution was marked by recurrence of symptoms, requiring after 3 weeks a new drainage of 600 mL of clear effusion, and biopsy of the pericardium was performed. Pathological exam described serous pericarditis with chronic inflammatory infiltrate, xanthogranulomatous reaction intricated in the pericardium and mesothelial hyperplasia. The patient was subsequently transferred to the Department of Internal Medicine for further investigations. Physical examination showed a patient with altered general status, pallor, vesicular murmur absent in both bases, presenting cutaneous hyperpigmentation at the level of the right hemi-abdomen and hip with posterior extension, and a peripheral indurated erythematous plaque. The patient presented nodular masses of 3 cm in the right latero-cervical and bilateral axillary regions, non-adherent to the superficial structures, as well as adenopathic blocks in both inguinal regions. CT scan of the thorax and abdomen showed moderate bilateral pleuresia, minimal pericardial effusion (15 mm) and multiple adenopathies on both sides of the diaphragm. Skin biopsy was performed, as well as bone marrow aspirate and excision of a right axillary lymph node. Pathological exams and immunohistochemistry tests confirmed the diagnosis of Plasma Cells Castleman disease.

Background: Aplastic anemia (AA) is a rare and serious disease characterized by pancytopenia and hypoplastic bone marrow in the absence of infiltrates/fibrosis. It occurs more frequently in childhood and young adulthood (10-30 years) and with older age (>60 years), with equal distribution among men and women. As hypoplastic myelodysplastic syndromes (hMDS) are also associated with cytopenia and hypocellular marrow,they may be difficult to differentiate from AA. The presence of dysplastic features (others than erythroid) and/or blast cells >5% is essential to distinguish hMDS from AA. Cytogenetic tests may reveal clonal evolution in hMDS. As the two disorders differ greatly in means of management and prognosis, the correct diagnostic is very important.

Hereditary spherocytosis is an inherited hemolytic anemia due to red cell membrane defects, characterised by chronic hemolysis with different severity degrees, splenomegaly and microspherocytosis on the peripheral blood film.

The purpose of this work is to present the results of allogeneic stem cell transplantation as therapy for patients diagnosed with acquired aplastic anemia in the Department of Bone Marrow Transplantation of Fundeni Clinical Institute and to elaborate an algorithm of treatment in aplastic anemia starting with the observations obtained from our clinical practice and following the European treatment guidelines in this group of patients.

Kikuchi–Fujimoto disease (KFD) or histiocytic necrotizing lymphadenitis is a rare disease that is frequently underdiagnosed due to clinical features that are similar to those of non-Hodgkin lymphomas, systemic lupus erythematosus (SLE), or infectious reactive lymphadenopathy. An excisional biopsy is required. We report a young Caucasian female diagnosed with KFD with skin lesions, complicating with SLE. The clinical course, laboratory, and CT findings are described, as are histopathologic features, for a better recognition of this rare disorder in clinical practice.

Introduction. The tyrosine kinase inhibitor imatinib mesylate (IM) specifically inhibits the kinase activity of ABL, platelet-derived growth factor receptor beta (PDGFR[]), and c-KIT tyrosine kinases and has impressive clinical efficacy in chronic myeloid leukemia (CML)[1]. IM prevented also the development of atherosclerotic lesions and diabetes-induced inflammatory cytokine overexpression [2,3]. Case report. A 36 years old male patient with a history of acute myocardial infarction and double coronarian by-pass eight years ago was admitted for the first time on December 2005 complaining of wheigt loss, intermittent discomfort in upper left abdomenum, polydipsia.and polyuria. By the examination of the peripheral blood and of the bone marrow the diagnosis of chronic phase CML-Ph(+) has been established. Simultaneously, type II diabetes mellitus and dyslipidemia (Table 1) were discovered. After a short course of Hydrea, associated with diet and oral antidiabetic therapy, IM 400 mg/d has been started on April 2006. The hematologic remission and a concomitant reduction of the serum levels of cholesterol, and of low-density lipoproteins (LDL) has been obtained (Table 1). Table 1. The dynamics of the peripheral blood counts and lipidic profile during IM therapy Parameters April May June Jully Hemoglobin (g/dl) 9,6 11,1 12 12 Leukocyte count (×109/l) 5.2 4.6 7.5 7.8 Platelet count (×109/l) 168 287 210 215 Serum total cholesterol (mg/dl) 310 189 157 152 Serum LD lipoproteins (mg/dl) 219 128 85 87 Serum HD lipoproteins(mg/dL) 49 53 52 50 Comments and conclusions. The effects observed in this reported case and in other similar patients [4] indicates that the treatment with IM induces a favourable control not only on cell growth and replication but also on the homeostasis of lipoproteins and glucose. A possible mechanism of action could be the inhibition by IM of PDGFR-dependent phosphorylation of the LDL-receptor related protein. IM appears to be a novel therapeutic option to retard the development of atherosclerosis, specifically in the context of diabetes and the treatment of choice for patients suffering of CML and dyslipidemia. Further prolonged observation of this and other similar patients is necessary for more pertinent data.

Introduction. The tyrosine kinase inhibitor imatinib mesylate (IM) specifically inhibits the kinase activity of ABL, platelet-derived growth factor receptor beta (PDGFR[]), and c-KIT tyrosine kinases and has impressive clinical efficacy in chronic myeloid leukemia (CML)[1]. IM prevented also the development of atherosclerotic lesions and diabetes-induced inflammatory cytokine overexpression [2,3].