Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematologic tumor that typically occurs in older adults. Patients with BPDCN usually present with solitary or multiple skin lesions. Localized or disseminated lymphadenopathy at presentation is common. A case report illustrating histopathologically proven BPDCN initially misdiagnosed as breast infiltrating ductal carcinoma in a 39-year-old woman is presented. In this case, the patient presented with a breast mass without an obvious skin lesion initially. The morphology of the tumor cells mimicked high grade breast carcinoma cells. Without complete immunohistochemical study, this case was initially misdiagnosed as infiltrating ductal carcinoma. Reviewing the previous literature about BPDCN, no case with a breast mass and an absence of characteristic skin lesions initially has been reported. The purpose for which we are discussing this case is to reduce misdiagnosis when the initial symptom is unusual.

A Case Report Blastic Plasmacytoid Dendritic Cell Neoplasm Is Misdiagnosed as Breast Infiltrating Ductal Carcinoma

Prognosis of vasculitis associated myelodysplasia.

Systemic vasculitis involving the lung is a rare manifestation of myelodysplastic syndrome (MDS), and secondary vasculitis is considered to have poor prognosis. A 44-year-old man presented with fever and dyspnea of 1 month duration. A chest radiograph revealed bilateral multiple wedge shaped consolidations. In addition, the results of a percutaneous needle biopsy for non-resolving pneumonia were compatible with pulmonary vasculitis. Bone marrow biopsy was performed due to the persistence of unexplained anemia and the patient was diagnosed with MDS. We reported a case of secondary vasculitis presenting as non-resolving pneumonia, later diagnosed as paraneoplastic syndrome of undiagnosed MDS. The cytopenia and vasculitis improved after a short course of glucocorticoid treatment, and there was no recurrence despite the progression of underlying MDS.

/pdf/pulmonary-leukocytoclastic-vasculitis-as-an-initial-1jd509gykd.pdf

Pulmonary Leukocytoclastic Vasculitis as an Initial Presentation of Myelodysplastic Syndrome.

We have read with interest the report by Laporte et n/(l9YO) in which they describe the effect of folinic acid on the expansion of the peripheral blood stem cell (PBSC) pool during haematopoietic recovery after chemotherapy. We have collected PBSC from 34 adult patients with acute leukaemia following consolidation chemotherapy. However, it was possible to obtain > 1 x loi of granulocyte/macrophage progenitor cells (CFU-GM) per kg of body weight in only 1 3 / 34 ( 38.20/,) cases during a single course of leukaepheresis consisting of four collections. For the remaining 2 1 patients, in whom the dose of CFU-GM collected was not sufficient for valid haemopoietic reconstitution, another course of leukapheresis was required to obtain sufficient CFLJGM. In patients with acute lymphoblastic leukaemia (ALL). malignant lymphoma, and solid tumours. we have employed granulocyte colony-stimulating factor (G-CSF) and > 1 x 10' CFU-CM/kg were collected in 10/14 (71.4%) cases tested during a single course of leukapheresis. Thus, the use of GCSF is a promising strategy for patients with low yields of CFU-GM. However, in patients with acute myelogenous leukaemia (AMI,) the use of G-CSF is restricted. since AML blasts have receptors for G-CSF and may be stimulated by GCSF. The report by Laporte rt ( I / ( 1 Y90) suggested the use of folinic acid for the expansion of the PBSC pool and we evaluated the effect of folinic acid on two patients with AML. Each patient underwent two courses of leukapheresis: the first leukapheresis was performed without folinic acid and the second one with folinic acid during haemopoietic recovery from intensive chemotherapy for the consolidation of complete remission. The chemotherapy regimens used were the same for the two courses of consolidation chemotherapy. Folinic acid ( 5 0 mg/d) was intravenously administered on day 1 5 from initiation of consolidation chemotherapy and continued through the leukapheresis. The numbers of CFUGM collected at the first leukapheresis were 5.6 x lO'/kg and 5.6 x I04/kg in the two patients, respectively. At the second course of leukapheresis with folinic acid, the yields of CFU-CM were 2.1 x 104/kg and 2 .4 x I04/kg, respectively. The numbers of erythroid progenitor cells (BFU-E) at the first course of leukapheresis were 1 5.0 x 1 O+/kg and 18.4 x 1 04/ kg, respectively, while the numbers a t the second leukapheresis with folinic acid were 5.0 x lO'/kg and 6.3 x 10'/kg, respectively. These data indicate that folinic acid did not result in an increase of CFU-GM and BFU-E. though the yields of CFU-GM have been reported to diminish following successive courses of chemotherapy (Reiffers et a/. 1987) . Therefore the effect of folinic acid should be evaluated in patients who achieved complete remission. In the report by Laporte et a/ (1 990) the first course of leukapheresis was performed during a recovery phase from remission induction chemotherapy while the second one was done during a recovery from consolidation chemotherapy. Since chemotherapy-induced myelosuppression is more profound after remission induction than after consolidation, it is difficult to compare the yields of PBSC under these different situations.

Folinic acid did not expand the peripheral blood stem cell pool during recovery from consolidation chemotherapy

[Refractory anaemia with an excess of myeloblasts and cutaneous vasculitis (author's transl)].

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[Refractory anaemia with an excess of myeloblasts and cutaneous vasculitis (author's transl)].