scholarly journals Acute Leukemia Clinical Presentation

Leukemia ◽  
10.5772/53531 ◽  
2013 ◽  
Author(s):  
Gamal Abdul
Keyword(s):  
Acute Leukemia ◽  
Clinical Presentation

scholarly journals Mixed Phenotype Acute Leukemia with 3 lineages differentiation & the challenge in the establishing of the diagnosis: a case report

2020 ◽  
Vol 8 (4) ◽  
pp. 71-73
Author(s):  
Mariam Al Ghazal ◽  
Rehab Bu Khamseen
Keyword(s):  
Acute Leukemia ◽  
Clinical Presentation ◽  
Flow Cytometric Analysis ◽  
The Other ◽  
Antigenic Determinants ◽  
Rare Form ◽  
Lineage Differentiation ◽  
Flow Cytometric ◽  
Mixed Phenotype Acute Leukemia ◽  
Mixed Phenotype

Mixed phenotype acute leukemia (MPAL) is a rare form of acute leukemia comprising 2% to 3% of all acute leukemia diagnoses. The diagnosis of MPAL is based on flow cytometric analysis of the immunophenotype, which demonstrates expression of differentiation-related antigens belonging to multiple lineages commonly, one lineage is myeloid and the other is B and/or T lymphoid. Whether lineage differentiation determines clinical presentation and outcomes is unclear. Here we report a case of 37 years old man who presented with leukocytosis & found to have MPAL (mixed phenotype acute leukemia) with possible differentiation to 3 lineages as evident by flowcytometry cases with trilineage antigenic determinants are very rare.

scholarly journals A clinical presentation of drug-induced cardiotoxicity event in an oncohematology patient: A case report

2020 ◽  
Author(s):  
Ainur Bilmakhanbetova ◽  
Meruyert Beisenbay ◽  
Daulet Marat ◽  
Gulnur Zhakhina
Keyword(s):  
Case Report ◽  
Acute Leukemia ◽  
Inpatient Treatment ◽  
Clinical Case ◽  
Clinical Presentation ◽  
Underlying Disease ◽  
Clinical Death ◽  
Qtc Prolongation ◽  
Drug Induced ◽  
Selection Of

This case report deals with a clinical case of a patient who underwent inpatient treatment of the underlying disease acute leukemia. In the selection of treatment for complications, medications of various groups were prescribed. This therapy led to the clinical death of the patient, caused by drug-induced QT/QTc prolongation.

Gut Aspergillus Infections in Leukemia and Stem Cell Transplant Patients: A Rare and Unrecognized Disease.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2220-2220
Author(s):  
Eyad Kazan ◽  
J. Maertens ◽  
Raoul Herbrecht ◽  
Maja Weisser ◽  
Bertrand Gachot ◽  
...  
Keyword(s):  
Stem Cell ◽  
Retrospective Study ◽  
Small Bowel ◽  
Acute Leukemia ◽  
Stem Cell Transplant ◽  
Clinical Presentation ◽  
Bowel Perforation ◽  
Response To Treatment ◽  
Cell Transplant ◽  
Gut Colonization

Abstract Abstract 2220 Poster Board II-197 Introduction: Invasive aspergillosis is a life-threatening infection in immunocompromised patients, mainly in acute leukemia and stem cell transplant (SCT) patients. Aspergillosis mainly involves the lower respiratory tract and sinuses. Other sites of infection are rarely observed, except in the setting of aspergillus dissemination. Gut aspergillosis has been exceptionally reported in the literature, sometimes diagnosed only at autopsy. The goal of this retrospective study was to report on cases of gut aspergillosis in hematology patients, clinical presentation, risk factors, and outcome. Methods: This is a multicenter retrospective study in French, Swiss and Belgium hematology centers. We collected data from patients with hematologic disease and proven gut aspergillosis. Patients with only liver or spleen lesions were excluded. As the EORTC-MSG criteria do not propose a diagnosis of probable gut aspergillosis on the basis of gut imaging and indirect microbiological data, we only collected patients with biopsy, autopsy, or tissue-culture proven gut aspergillosis. The data were collected from the medical charts through a specific questionnaire. Segal et al. criteria were used to assess the response to treatment at 12 weeks after the diagnosis (CID 2008;47:674). Patients: 20 patients from 9 centers were included. The underlying disease was acute leukemia in 12, acceleration of CML in 2, lymphoma in 2, myeloma in 3, and myelodysplasia in 1. Nine patients had received an allogeneic SCT, The mean age was 48 years. Eleven out of 20 (55%) were neutropenic at time of gut aspergillosis. Results: Four patients had upper gut localization of aspergillosis (oesophagus: 2; stomach: 2), 11 had lower localizations (small bowel, colon, rectum) and 5 patients had concomitant upper and lower localizations. On the basis of imaging, aspiration, biopsy or autopsy, 12 patients had disseminated aspergillosis, and 8 had localized gut infection. Diagnosis was made by autopsy in 5 patients, endoscopic biopsy in 6, and biopsy through laparoscopy in 9 patients. All gut biopsies showed filaments evocative of aspergillus sp. Additionally, among 12 of them who were cultured, 9 grew A fumigatus, 1 grew A flavus and 2 were negative in culture. Clinical presentation was poorly specific. In lower gut lesions, we noted febrile diarrhea in 10 patients, abdominal pain in 16, gut hemorrhage in 7, intestinal occlusion in 5, and perforation in 1. These symptoms mostly led to endoscopy when lesions were accessible. However, only surgery or laparoscopy could get small-bowel lesions, mostly in emergency. In upper gut lesions, dysphagia and odynophagia usually led to endoscopy and the diagnosis was easier than for lower gut lesions. For 19 patients where the data was available, 15 had a positive galactomannan (GM) test (> 0.5 ng/mL). Among them, all the patients who got a negative GM test under treatment survived at 12 weeks except one. Five of the 11 operated patients survived, one died during surgery, from septic shock with small bowel perforation. All patients diagnosed before death received antifilamentous drugs, mostly voriconazole. At 12 weeks after the diagnosis, excluding the 5 patients diagnosed at autopsy, 8/15 (53%) were alive, with 6 in complete response, 1 in partial response, and 1 not evaluable. It is noteworthy that 4 patients were either from Africa or Pacific Ocean islands, one had an African diet, and one had lived in Tahiti two years before diagnosis. We hypothesize that a food enriched in spices may favor aspergillus gut colonization and increase the risk of developing aspergillosis during immunodepression. Conclusion: The diagnosis of gut aspergillosis is a difficult one in the absence of surgery, due to the poor specificity of the symptoms and the absence of characteristic imaging. The mortality is high. Patients with a positive GM unexplained by respiratory lesions should be suspected of gut aspergillosis each time there is gut symptoms. Hematologists have to be aware of this complication whose frequency is likely underestimated. In most cases, it seems logical to associate medical and surgical therapy. However, the optimal therapy is so far not determined. Disclosures: Herbrecht: Pfizer: Research Funding, Speakers Bureau; Gilead: Consultancy, Speakers Bureau; MSD: Consultancy, Speakers Bureau; Schering-Plough/Essex: Consultancy, Speakers Bureau.

Myelomalacia as clinical presentation of acute leukemia

1989 ◽  
Vol 91 (1) ◽  
pp. 95-97 ◽  
Author(s):  
Agustin Avilés ◽  
Guillermo Gómez ◽  
M. Eugenia Rubio
Keyword(s):  
Acute Leukemia ◽  
Clinical Presentation

scholarly journals S100B Is a Useful Marker for the Diagnosis of Haemophagocytic Lymphohistiocytosis

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 3711-3711
Author(s):  
Rosemarie Tremblay-Lemay ◽  
Lourdes Calvente ◽  
Monali Gupta ◽  
Anne Tierens ◽  
David Barth ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Leukemia ◽  
Sensitivity And Specificity ◽  
Research Funding ◽  
Clinical Presentation ◽  
Morphological Evidence ◽  
Histopathological Diagnosis ◽  
Haemophagocytic Lymphohistiocytosis ◽  
Cell Counts ◽  
Rosai Dorfman Disease

Abstract Haemophagocytic lymphohistiocytosis (HLH) is a life-threatening systemic inflammatory clinical syndrome that can be primary/familial or secondary to a variety of underlying conditions. The 2004 diagnostic criteria for HLH require 5 out of 8 of the following clinical and pathological variables to be present: fever, splenomegaly, cytopenia in at least 2 lineages, hypertriglyceridemia/hypofibrinogenemia, haemophagocytosis on pathology examination, low/absent NK cell activity, ferritin greater than 500µg/L or soluble IL-2 receptor (sCD25) greater than 2400 U/mL. At least 5 of these criteria must be met, as each one lacks specificity. With regard to the pathology detection of haemophagocytosis, the sensitivity and specificity reported in the literature were 83% and 60% respectively. Indeed, a degree of haemophagocytosis can be seen outside the context of HLH. Furthermore, some of the diagnostic features of HLH may not be useful when applied to single cases because they may be intrinsic to the underlying condition. Therefore, we wondered whether the histopathological diagnosis might be improved. We investigated whether testing for S100B expression in macrophages might render the detection of haemophagocytosis more specific and sensitive. S100B is a marker of macrophage activation, and can routinely be detected by immunohistochemistry. S100B has pro-inflammatory properties and has been shown to affect macrophage function. It is typically expressed in macrophages of Rosai-Dorfman disease apart of having also a tissue-specific expression pattern, marking melanocytes as well as Langerhans cells and other subsets of dendritic cells. A natural language search of the pathology database at our institution identified 32 patients with bone marrow samples reporting haemophagocytosis as evaluated on bone marrow smear preparations, between January 2002 and July 2015. Cases that did not have available paraffin-embedded bone marrow trephine biopsy and clinical data were excluded. The bone marrow samples of three patients without haemophagocytosis and without any clinical features of HLH were used as controls: a new diagnosis of acute leukemia, a follow-up of acute leukemia post-transplant and a known lymphoma patient with unexplained pancytopenia. Clinical parameters relevant to the diagnosis of HLH were evaluated. Cases were clinically categorized as diagnostic for HLH (≥5 criteria), clinically likely (<5 criteria, but clinical presentation consistent) or clinically non suspicious (<5 criteria and clinical presentation not consistent with HLH). Stains for S100B and CD68 were performed. The percentage of S100B positive cells of all bone marrow cells as well as the percentage of CD68 positive macrophages was calculated from 500-cell counts using a 40x objective lens. The median patient age was 57 years (range 18-80). Underlying clinical diagnoses are reported in Table 1. Expression of S100B ranged from 0-76.4%. Cases without morphological evidence of haemophagocytosis had less than 1% S100B-positive cells. Cases with presence of haemophagocytic cells showed various levels of S100B-positive cells. Of interest, >10% S100B-positive cells (of all cells) was 100% specific for cases meeting ≥4 HLH criteria, 91% specific for cases clinically likely HLH or confirmed HLH. The sensitivity was 60% for cases meeting ≥4 HLH criteria, 52% for cases being likely HLH or confirmed HLH. Percentage of CD68-positive cells or S100B/CD68 ratio did not add relevant information. The high specificity of S100B expression by immunohistochemistry indicates it may be an additional diagnostic feature of HLH. Of note, the test is available in routine immunohistochemistry laboratories. Since not all cases of HLH show increased numbers of S100B-expressing macrophages, the test does not obviate the need for the 2004 criteria. Serological immunoassays for S100B have been developed for use in the context of brain disease/injuries and malignant melanoma. Based on our data, we intend to further investigate the sensitivity and specificity of S100B as a serological marker of HLH. Disclosures Kuruvilla: BMS: Consultancy, Honoraria; Gilead: Consultancy, Honoraria; Abbvie: Consultancy; Amgen: Honoraria; Seattle Genetics: Consultancy, Honoraria; Leukemia and Lymphoma Society Canada: Research Funding; Merck: Consultancy, Honoraria; Karyopharm: Honoraria; Celgene: Honoraria; Janssen: Consultancy, Honoraria, Research Funding; Roche: Consultancy, Honoraria, Research Funding; Princess Margaret Cancer Foundation: Research Funding; Lundbeck: Honoraria.

Clinical Presentation, Treatment Response and Survival in Adult Acute Biphenotypic Leukemia: Single Centre Experience.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4330-4330 ◽  
Author(s):  
Amal S. Abdulwahab ◽  
Mahmoud D. AlJurf ◽  
Nasser M. Elkum ◽  
Fahad I. Almohareb ◽  
Tarek M. Owaidah
Keyword(s):  
Acute Leukemia ◽  
Clinical Presentation ◽  
Poor Response ◽  
Antigen Expression ◽  
Salvage Chemotherapy ◽  
Complex Karyotype ◽  
Single Centre Experience ◽  
Hybrid Drugs ◽  
Wbc Count ◽  
Work Done

Abstract Background: Acute leukemia is classified as lymphoid or myeloid depends on antigen expression. Knowledge about acute biphenotopic leukemia (BAL) is limited; both in terms of clinical and biological presentation and also in regard to treatment outcome. Hereby we are completing the work done by our group which looked at the laboratory features of BAL by reviewing the clinical presentation and response to different chemotherapy protocols used at our institute for treatment of patients with BAL to estimate over all survival. Methods: Out of 478 adult patients with acute leukemia, we analyzed 15(3.1%) cases classified as BAL according to EGIL score system. Clinical data were collected retrospectively and analyzed. Five different chemotherapy protocols had been used. Six(40%) patients had received VCEPM (Vincristine 1.4mg/m2 x 4 doses, Cyclophosphamide 600mg/ m2 , Etoposide 100mg m2 daily for 5 doses, Prednisone 60mg/m2 for28 days). Four (27%)cases had received 1423 KFSH protocol (Cyclophosphamide 1200mg/m 2 x 1 dose, Daunorubicin 45mg/m2 for 3 doses, Vincristine 1.4mg/m2 once every week x 4 doses, Prednisone 60mg/m2 for 21 days, L-Asparaginase 6000 iu/m 2 every 3 days x 6 doses). Standard ICE protocol was used for induction in 3 cases and in 2 patients modified St Jude protocol (Vincristine 1.5mg/m 2 once every week x 4 doses, Daunomycin 25mg/m2 once every week x 2 doses, Prednisone 40mg/m 2 daily for 25 dose, L-Asparaginase 10000u/m 2 every 3 days for 6 doses, Etoposide 300mg/m 2 every 4 days x 3 doses and Cytarapin 300mg/m 2 every 4 days x 3 doses). Results: We had 11 males and 4 females with mean WBC count on presentation of 74.7 x 109/L.Chromosomal karyotype was done for all except one, 4(29%) were normal and 8(53%) had complex karyotype Of all patients with BAL leukemia, 4(27%), 8(53%) and 10(67%) had hepatomegaly,splenomegaly and lymphadenopathy respectively. Initial evaluation done on D14 post chemotherapy revealed evidence of residual leukemia (> 5% blasts) in 1 out of 6 patients treated with VCEPM and 7 out of the other 9 patients received different other protocols. Out of the eight patients with residual leukemia, 4 had received salvage chemotherapy with FA (Fludarabine 30mg/ m2, Cytarabine2mg/ m2 x 5doses) and 2 had received MEC (Mitoxantrone 6mg/ m2 , Etopside 80mg/ m2, Cytarabine1mg/ m 2 x 6 doses) and one received modified St Jude while one underwent for SCT. ALL except one had achieved CR. Total of 10(66%) underwent SCT in CR. Although there were 9 (60%) died during the follow up, the OS at two years was (50%). Conclusion: Adult BAL is an aggressive disease that is associated with complex karyotype with poor response to single lineage treatment. The use of hybrid drugs (VCEPM like) that are effective for lymphoid and myeloid leukemia improve the respond. Figure Figure

Jansky-Bielschowsky syndrome, a lysosomal disease: First diagnosed cash in Oman

1992 ◽  
Vol 50 (1) ◽  
pp. 632-633
Author(s):  
Line Buhl ◽  
David Muirhead
Keyword(s):  
Mental Retardation ◽  
Clinical Picture ◽  
Neurological Disorder ◽  
Clinical Presentation ◽  
Neuronal Ceroid Lipofuscinosis ◽  
Infantile Form ◽  
Lysosomal Disease ◽  
Juvenile Form ◽  
Progressive Encephalopathy ◽  
Lysosomal Diseases

There are four lysosomal diseases of which the neuronal ceroid lipofuscinosis is the rarest. The clinical presentation and their characteric abnormal ultrastructure subdivide them into four types. These are known as the Infantile form (Santavuori-Haltia), Late infantile form (Jansky-Bielschowsky), Juvenile form (Batten-Spielmeyer-Voght) and the Adult form (Kuph's).An 8 year old Omani girl presented wth myclonic jerks since the age of 4 years, with progressive encephalopathy, mental retardation, ataxia and loss of vision. An ophthalmoscopy was performed followed by rectal suction biopsies (fig. 1). A previous sibling had died of an undiagnosed neurological disorder with a similar clinical picture.

An Overview of Dementias

2012 ◽  
Vol 21 (3) ◽  
pp. 75-84
Author(s):  
Venkata Vijaya K. Dalai ◽  
Jason E. Childress ◽  
Paul E Schulz
Keyword(s):  
Clinical Presentation ◽  
Treatment Options ◽  
Current Treatment ◽  
Great Variability ◽  
Health Concern ◽  
Public Health Concern ◽  
Life Threatening ◽  
The Common ◽  
Neurodegenerative Dementias ◽  
Made In

Dementia is a major public health concern that afflicts an estimated 24.3 million people worldwide. Great strides are being made in order to better diagnose, prevent, and treat these disorders. Dementia is associated with multiple complications, some of which can be life-threatening, such as dysphagia. There is great variability between dementias in terms of when dysphagia and other swallowing disorders occur. In order to prepare the reader for the other articles in this publication discussing swallowing issues in depth, the authors of this article will provide a brief overview of the prevalence, risk factors, pathogenesis, clinical presentation, diagnosis, current treatment options, and implications for eating for the common forms of neurodegenerative dementias.

Sign in / Sign up

Export Citation Format

Share Document