Database : MEDLINE
Search on : pancytopenia [Words]
References found : 9855 [refine]
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[PMID]: 29506574
[Au] Autor:Dalugama C; Gawarammana IB
[Ad] Address:Department of Medicine, University of Peradeniya, Peradeniya, Sri Lanka. chamaradalugama@yahoo.com.
[Ti] Title:Fever with pancytopenia: unusual presentation of extrapulmonary tuberculosis: a case report.
[So] Source:J Med Case Rep;12(1):58, 2018 Mar 06.
[Is] ISSN:1752-1947
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Tuberculosis is a major health problem in the developing world. Diagnosis of extrapulmonary tuberculosis is delayed because the presentation is nonspecific. Extrapulmonary tuberculosis can present with various hematological manifestations, including pancytopenia. Pancytopenia could be due to hypersplenism, maturation arrest, hemophagocytic lymphohistiocytosis, or infiltration of the bone marrow by caseating or noncaseating granulomas causing reversible or irreversible fibrosis. CASE PRESENTATION: We report a case of a 56-year-old Sri Lankan Sinhalese man who presented with pyrexia of known origin with significant loss of weight and loss of appetite. He had mild pallor with mild hepatosplenomegaly. He had high inflammatory markers with pancytopenia in a peripheral blood smear. His chest radiograph was unremarkable, and he had a negative Mantoux test result. A diagnosis of disseminated tuberculosis was made on the basis of caseating tuberculous granulomas in the bone marrow. CONCLUSIONS: Disseminated tuberculosis remains a diagnostic challenge because the presentation is vague and nonspecific. In case of pyrexia of unknown origin with peripheral cytopenia, the possibility of disseminated tuberculosis should be considered, particularly in endemic areas. Simultaneous culture and histopathological examination of the bone marrow is important in such instances, because results of common tests such as chest radiography or Mantoux tests can be negative.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1186/s13256-018-1596-0

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[PMID]: 29522883
[Au] Autor:Teti A; Teitelbaum SL
[Ad] Address:Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. Electronic address: annamaria.teti@univaq.it.
[Ti] Title:Congenital disorders of bone and blood.
[So] Source:Bone;, 2018 Mar 06.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Bone and marrow are the two facets of the same organ, in which bone and hematopoietic cells coexist and interact. Marrow and skeletal tissue influence each-other and a variety of genetic disorders directly targets both of them, which may result in combined hematopoietic failure and skeletal malformations. Other conditions primarily affect one organ with secondary influences on the other. For instance, various forms of congenital anemias reduce bone mass and induce osteoporosis, while osteoclast failure in osteopetrosis prevents marrow development reducing medullary cavities and causing anemia and pancytopenia. Understanding the pathophysiology of these conditions may facilitate diagnosis and management, although many disorders are presently incurable. This article describes several congenital bone diseases and their relationship to hematopoietic tissue.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  3 / 9855 MEDLINE  
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[PMID]: 29519931
[Au] Autor:Li W; Sharma M
[Ad] Address:Children's Mercy Hospital.
[Ti] Title:Unusual cause of infant pancytopenia: granulomatous bone marrow lesion with disseminated histoplasmosis.
[So] Source:Blood;131(10):1154, 2018 Mar 08.
[Is] ISSN:1528-0020
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1182/blood-2017-12-820084

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[PMID]: 29519625
[Au] Autor:Fakhfakh N; Abdelmlak R; Aissa S; Kallel A; Boudawara Y; Bel Hadj S; Ben Romdhane N; Touiri Ben Aissa H; Kallel K
[Ad] Address:Laboratory of Parasitology-Mycology, Rabta Hospital, Jabbari street, 1007 Tunis, Tunisia; Infectious diseases ward, Rabta Hospital, Tunis, Tunisia.
[Ti] Title:Disseminated histoplasmosis diagnosed in the bone marrow of an HIV-infected patient: First case imported in Tunisia.
[So] Source:J Mycol Med;, 2018 Mar 05.
[Is] ISSN:1773-0449
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Histoplasmosis is a fungal infection caused by a dimorphic fungus, Histoplasma capsulatum. We report a first case of disseminated histoplasmosis in a 34-year-old woman, infected with human immunodeficiency virus (HIV), originating from Ivory Coast and living in Tunisia for 4 years. She was complaining from fever, chronic diarrhoea and pancytopenia. The Histoplasma capsulatum var. capsulatum was identified by direct microscopic examination of the bone marrow. She was treated by Amphotericin B, relayed by itraconazole. Even though a regression of symptoms and normalization of blood cell count (BCC), the patient died in a respiratory distress related to CMV hypoxemic pneumonia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  5 / 9855 MEDLINE  
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[PMID]: 29455176
[Au] Autor:Mori H; Ebisawa K; Nishimura M; Kanazawa K
[Ad] Address:Department of General Internal Medicine, Kobe University Hospital, Kobe, Hyogo, Japan.
[Ti] Title:Late diagnosis: a case of rapidly progressive extranodal NK/T cell lymphoma, nasal type.
[So] Source:BMJ Case Rep;2018, 2018 Feb 17.
[Is] ISSN:1757-790X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Extranodal natural killer (NK)/T cell lymphoma, nasal type is a condition that has poor prognosis. Accurate diagnosis of lymphoma is made by pathological findings. We report a case of extranodal NK/T cell lymphoma, nasal type affecting the lung and liver and which was difficult to diagnose because of negative biopsy results from multiple sites. A 39-year-old man who had dry cough and fever for 1 month was referred to our hospital. He had pancytopenia and elevated serum levels of lactate dehydrogenase and soluble interleukin-2 receptor. Hepatosplenomegaly and multiple lung nodules were found on imaging study. Specimens of bronchoscopic lung, percutaneous liver, bone marrow and random skin biopsies were all negative. Open lung biopsy was not definitive. Unfortunately, disease progression was rapid and fatal before results of pleural fluid cytology and a second liver biopsy showed extranodal NK/T cell lymphoma, nasal type. This report focused on diagnostic planning for rapidly progressive extranodal NK/T-cell lymphoma, nasal type.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process

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[PMID]: 29515069
[Au] Autor:Watanuki S; Kikuchi T; Toyama T; Abe R; Nakayama H; Karigane D; Shimizu T; Kikuchi J; Matsumoto K; Yasuoka H; Kataoka M; Okamoto S; Mori T
[Ad] Address:Division of Hematology, Department of Medicine, Keio University School of Medicine.
[Ti] Title:[Mixed connective tissue disease with pulmonary hypertension developing in a chronic myeloid leukemia patient on dasatinib treatment].
[So] Source:Rinsho Ketsueki;59(2):174-177, 2018.
[Is] ISSN:0485-1439
[Cp] Country of publication:Japan
[La] Language:jpn
[Ab] Abstract:A 37-year-old woman was diagnosed with chronic phase chronic myeloid leukemia. Nilotinib treatment was initiated; however, it had to be discontinued due to an allergic reaction one month later, and dasatinib treatment was provided. Although favorable response was obtained, she started complaining of shortness of breath 7 months after initiating dasatinib treatment. Chest X-ray and echocardiography indicated pulmonary congestion and hypertension. Further, she was diagnosed with mixed connective tissue disease (MCTD) based on Raynaud phenomenon, swollen fingers, sclerodactyly, pancytopenia, hypocomplementemia, and positive anti-U1-RNP antibody. Consequently, dasatinib treatment was discontinued, and she was administered prednisolone (1 mg/kg/day), which was effective and successfully tapered with concomitant administration of cyclophosphamide. This is the first case of MCTD that developed during dasatinib treatment. However, because the present case was a young woman, the development of MCTD could probably be attributed to autoimmune diatheses or it may be a coincidence. However, the possibility of patients receiving dasatinib treatment developing autoimmune diseases needs to be assessed.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.11406/rinketsu.59.174

  7 / 9855 MEDLINE  
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[PMID]: 29178470
[Au] Autor:Brisse E; Imbrechts M; Mitera T; Vandenhaute J; Berghmans N; Boon L; Wouters C; Snoeck R; Andrei G; Matthys P
[Ad] Address:Laboratory of Immunobiology, Rega Institute, KU Leuven, Leuven, Belgium.
[Ti] Title:Lymphocyte-independent pathways underlie the pathogenesis of murine cytomegalovirus-associated secondary haemophagocytic lymphohistiocytosis.
[So] Source:Clin Exp Immunol;192(1):104-119, 2018 Apr.
[Is] ISSN:1365-2249
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Haemophagocytic lymphohistiocytosis (HLH) constitutes a spectrum of immunological disorders characterized by uncontrolled immune activationand key symptoms such as fever, splenomegaly, pancytopenia, haemophagocytosis, hyperferritinaemia and hepatitis. In genetic or primary HLH, hyperactivated CD8 T cells are the main drivers of pathology. However, in acquired secondary HLH, the role of lymphocytes remains vague. In the present study the involvement of lymphocytes in the pathogenesis of a cytomegalovirus-induced model of secondary HLH was explored. We have previously reported CD8 T cells to be redundant in this model, and therefore focused on CD4 helper and regulatory T cells. CD4 T cells were activated markedly and skewed towards a proinflammatory T helper type 1 transcription profile in mice displaying a severe and complete HLH phenotype. Counter to expectations, regulatory T cells were not reduced in numbers and were, in fact, more activated. Therapeutic strategies targeting CD25 hyperactivated T cells were ineffective to alleviate disease, indicating that T cell hyperactivation is not a pathogenic factor in cytomegalovirus-induced murine HLH. Moreover, even though T cells were essential in controlling viral proliferation, CD4 T cells, in addition to CD8 T cells, were dispensable in the development of the HLH-like syndrome. In fact, no T or B cells were required for induction and propagation of HLH disease, as evidenced by the occurrence of cytomegalovirus-associated HLH in severe combined immunodeficient (SCID) mice. These data suggest that lymphocyte-independent mechanisms can underlie virus-associated secondary HLH, accentuating a clear distinction with primary HLH.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1111/cei.13084

  8 / 9855 MEDLINE  
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[PMID]: 29374141
[Au] Autor:Melguizo-Sanchis D; Xu Y; Taheem D; Yu M; Tilgner K; Barta T; Gassner K; Anyfantis G; Wan T; Elango R; Alharthi S; El-Harouni AA; Przyborski S; Adam S; Saretzki G; Samarasinghe S; Armstrong L; Lako M
[Ad] Address:Institute of Genetic Medicine, Newcastle University, Newcastle, UK.
[Ti] Title:iPSC modeling of severe aplastic anemia reveals impaired differentiation and telomere shortening in blood progenitors.
[So] Source:Cell Death Dis;9(2):128, 2018 Jan 26.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Aplastic Anemia (AA) is a bone marrow failure (BMF) disorder, resulting in bone marrow hypocellularity and peripheral pancytopenia. Severe aplastic anemia (SAA) is a subset of AA defined by a more severe phenotype. Although the immunological nature of SAA pathogenesis is widely accepted, there is an increasing recognition of the role of dysfunctional hematopoietic stem cells in the disease phenotype. While pediatric SAA can be attributable to genetic causes, evidence is evolving on previously unrecognized genetic etiologies in a proportion of adults with SAA. Thus, there is an urgent need to better understand the pathophysiology of SAA, which will help to inform the course of disease progression and treatment options. We have derived induced pluripotent stem cell (iPSC) from three unaffected controls and three SAA patients and have shown that this in vitro model mimics two key features of the disease: (1) the failure to maintain telomere length during the reprogramming process and hematopoietic differentiation resulting in SAA-iPSC and iPSC-derived-hematopoietic progenitors with shorter telomeres than controls; (2) the impaired ability of SAA-iPSC-derived hematopoietic progenitors to give rise to erythroid and myeloid cells. While apoptosis and DNA damage response to replicative stress is similar between the control and SAA-iPSC-derived-hematopoietic progenitors, the latter show impaired proliferation which was not restored by eltrombopag, a drug which has been shown to restore hematopoiesis in SAA patients. Together, our data highlight the utility of patient specific iPSC in providing a disease model for SAA and predicting patient responses to various treatment modalities.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-017-0141-1

  9 / 9855 MEDLINE  
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[PMID]: 29506772
[Au] Autor:Kural C; Ozer MI; Ezgu MC; Mehtiyev R; Yasar S; Kutlay AM; Daneyemez MK; Onguru O; Erdogan E; Izci Y
[Ad] Address:University of Health Sciences, Gulhane Training and Research Hospital, Department of Neurosurgery, Ankara, Turkey.
[Ti] Title:Intracavitary amphotericin B in the treatment of intracranial aspergillosis.
[So] Source:J Clin Neurosci;, 2018 Mar 02.
[Is] ISSN:1532-2653
[Cp] Country of publication:Scotland
[La] Language:eng
[Ab] Abstract:Intracranial aspergillosis is a rare infectious disease of the central nervous system with high mortality rates. Our aim is to present 3 cases of intracranial aspergillosis who were surgically treated with intracavitary amphotericin B administration. First case was a 21-year-old male patient. Allogeneic stem cell transplantation treatment was performed because of aplastic anemia and vocal cord paralysis developed 10 days after treatment. Multiple aspergillosis abscesses were observed in the cranial magnetic resonance imaging (MRI). Cerebral lesions were excised and 0.3 cc of amphotericin B was applied locally. Second case was a 18-year-old male patient treated for acute lymphocytic leukemia. MRI was performed on the development of consciousness change during treatment and right frontal abscess was detected. The abscess was excised and amphotericin B was applied locally. Third case was a 45-year-old woman with mastectomy. She had chemotherapy after surgery and had blood stem cell transplantation because of pancytopenia. Two months after treatments, MRI was performed on the development of ataxia and a cerebellar abscess was detected. The abscess was surgically excised and local amphotericin B was applied. The first case deceased 2 weeks after surgery and the second case died 2.5 years later due to multi-organ failure. The third case is stil alive and neurologically stable after 14 years of surgical treatment. In intracranial aspergillosis, intracavitary amphotericin B therapy may be used as an adjunct after the surgical excision of abscess. This procedure may contributes to the regression of abscess or prevention of the recurrence. But comparative clinical studies are needed for more accurate conclusions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher

  10 / 9855 MEDLINE  
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[PMID]: 29496554
[Au] Autor:Kjeldsen E; Veigaard C; Aggerholm A; Hasle H
[Ad] Address:HemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Tage-Hansens Gade 2, Ent. 4A, DK-8000 Aarhus C, Denmark. Electronic address: Eigil.Kjeldsen@clin.au.dk.
[Ti] Title:Congenital hypoplastic bone marrow failure associated with a de novo partial deletion of the MECOM gene at 3q26.2.
[So] Source:Gene;, 2018 Feb 26.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Congenital hypoplastic bone marrow failure is a rare condition in neonates. The genetics and mechanisms behind are largely obscure. Here we characterize a neonate presenting with congenital thrombocytopenia and anemia. During the first 2-4 weeks after birth the neonate developed severe neutropenia while the lymphoid lineages were unaffected. The neonate was without dysmorphic signs. A de novo mono-allelic constitutional microdeletion of 175.1 kb at 3q26.2 affecting exon 2 of MECOM, involving MDS1 but not EVI1, was identified as the only copy number alteration by oligo-based array-CGH analysis. Expression analysis showed profoundly reduced expression of multiple MECOM transcripts in the bone marrow cells. Whole exome sequencing detected no pathogenic mutations in genes known to be associated with inherited bone marrow failure syndromes. The patient was successfully treated with hematopoietic stem cell transplantation at 5 months of age. Interstitial deletions encompassing the 3q26.2 region are very rare. A literature search revealed two previous cases with microdeletions involving this region, and the cases were associated with congenital thrombocytopenia and anemia, but unaffected lymphopoiesis. Together these data indicate that MECOM may be important for normal myeloid hematopoiesis in humans but dispensable for lymphoid differentiation. We suggest that partial deletion in MECOM may be a primary event associated with congenital pancytopenia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher


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