scholarly journals Pure White Cell Aplasia and Necrotizing Myositis

2016 ◽  
Vol 2016 ◽  
pp. 1-5
Author(s):  
Peter Geon Kim ◽  
Joome Suh ◽  
Max W. Adelman ◽  
Kwadwo Oduro ◽  
Erik Williams ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Liver Injury ◽  
White Cell ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Drug Induced ◽  
Hematologic Disorder ◽  
Necrotizing Myositis ◽  
Stimulating Factor ◽  
Pure White

Pure white cell aplasia (PWCA) is a rare hematologic disorder characterized by the absence of neutrophil lineages in the bone marrow with intact megakaryopoiesis and erythropoiesis. PWCA has been associated with autoimmune, drug-induced, and viral exposures. Here, we report a case of a 74-year-old female who presented with severe proximal weakness without pain and was found to have PWCA with nonspecific inflammatory necrotizing myositis and acute liver injury on biopsies. These findings were associated with a recent course of azithromycin and her daily use of a statin. Myositis improved on prednisone but PWCA persisted. With intravenous immunoglobulin and granulocyte-colony stimulating factor therapies, her symptoms and neutrophil counts improved and were sustained for months.

scholarly journals Pure White Cell Aplasia an exceptional condition in the inmunological conundrum of thymomas: Responses to inmunosupresion and Literature Review.

2021 ◽  
Author(s):  
Roberto Céspedes López ◽  
Elena Amutio ◽  
Xabier Martín Martitegui ◽  
Amaia Balerdi Malcorra ◽  
Lucia Insunza Oleaga ◽  
...  
Keyword(s):  
Literature Review ◽  
White Cell ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Good Syndrome ◽  
Stimulating Factor ◽  
Factor G ◽  
Pure White

Thymomas are tumours frequently associated with autoinmune manifestations or immunodeficiencies like Good syndrome. In rare cases, pure white cells aplasia (PWCA) has been described in association with thymomas. PWCA is characterized by agranulocytosis of autoinmune background primary refractory to granulocyte colony-stimulating factor (G-CSF). It is necessary to use inmunosupressor drugs.

Treatment of Clozapine- and Molindone-Induced Agranulocytosis with Granulocyte Colony-Stimulating Factor

1993 ◽  
Vol 27 (10) ◽  
pp. 1190-1192 ◽  
Author(s):  
Charles B. Geibig ◽  
Louis W. Marks
Keyword(s):  
Bone Marrow ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Short Term ◽  
Drug Induced ◽  
Clozapine Therapy ◽  
Case Summary ◽  
Wbc Count ◽  
Stimulating Factor

OBJECTIVE: To report a case of clozapine- and molindone-induced agranulocytosis and to discuss treatment using filgrastim, a granulocyte colony-stimulating factor. CASE SUMMARY: A 64-year-old woman who had been on long-term clozapine therapy for schizophrenia was hospitalized with presumed drug-induced agranulocytosis. She had also been on short-term molindone therapy. A bone marrow biopsy and the initial white blood cell (WBC) count were consistent with drug-induced agranulocytosis. Following seven days of treatment with subcutaneous filgrastim 300 μg/d, her absolute neutrophil count was above 500 × 106/L. DISCUSSION: Reports in the literature discussing antipsychotic drug-induced agranulocytosis are reviewed. A relationship between treatment with filgrastim and WBC response is postulated. CONCLUSIONS: Filgrastim may be useful in ameliorating the effects of clozapine- and molindone-induced agranulocytosis.

scholarly journals Investigating the Possibility of Intervertebral Disc Regeneration Induced by Granulocyte Colony Stimulating Factor-Stimulated Stem Cells in Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Wen-Ching Tzaan ◽  
Hsien-Chih Chen
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Intervertebral Disc ◽  
Bone Marrow Stem Cells ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Hematopoietic Stem ◽  
Disc Regeneration ◽  
Intervertebral Disc Regeneration ◽  
Stimulating Factor

Intervertebral disc (IVD) degeneration is a multifactorial process that is influenced by contributions from genetic predisposition, the aging phenomenon, lifestyle conditions, biomechanical loading and activities, and other health factors (such as diabetes). Attempts to decelerate disc degeneration using various techniques have been reported. However, to date, there has been no proven technique effective for broad clinical application. Granulocyte colony-stimulating factor (GCSF) is a growth factor cytokine that has been shown to enhance the availability of circulating hematopoietic stem cells to the brain and heart as well as their capacity for mobilization of mesenchymal bone marrow stem cells. GCSF also exerts significant increases in circulating neutrophils as well as potent anti-inflammatory effects. In our study, we hypothesize that GCSF can induce bone marrow stem cells differentiation and mobilization to regenerate the degenerated IVD. We found that GCSF had no contribution in disc regeneration or maintenance; however, there were cell proliferation within end plates. The effects of GCSF treatment on end plates might deserve further investigation.

Non-chemotherapy drug-induced agranulocytosis in a tertiary hospital

2015 ◽  
Vol 35 (3) ◽  
pp. 244-250 ◽  
Author(s):  
R Navarro-Martínez ◽  
E Chover-Sierra ◽  
O Cauli
Keyword(s):  
Adverse Drug Reaction ◽  
Drug Reaction ◽  
Tertiary Hospital ◽  
Negative Association ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Drug Induced ◽  
Common Drug ◽  
Low Incidence ◽  
Stimulating Factor

Drug-induced agranulocytosis is a rare haematological disorder considered as severe adverse drug reaction. Due to its low incidence, the number of studies are low and the variability of clinical features and presentation in hospitalized patients is rarely described. Awe performed an observational, transversal and retrospective study in the haematology and toxicology unit in a tertiary hospital located in Spain (Valencia) (1996–2010) in order to assess its incidence, the drugs involved, the management and outcomes of drug-induced agranulocytosis. Twenty-one cases of agranulocytosis were retrieved. All of them presented severe and symptomatic agranulocytosis (fever and infection). The most common drug associated with drug-induced agranulocytosis was metamizole administration but other drugs belonging to different pharmacological classes as well (carbimazol, sulfasalazine, bisoprolol, itraconazole, amitryptiline, ketorolac and claritomicine+cefuroxime). No differences between sex and age were found in relationship with the manifestations or course of agranulocytosis. In contrast, a significantly negative association was found between age of patients and the percentage of increase in neutrophil count. Administration of human granulocyte colony-stimulating factor did not significantly enhance the recovery of the process or the restoration of leucocytes count, suggesting a limited utility in this type of agranulocytosis.

scholarly journals CXCR4 is a key regulator of neutrophil release from the bone marrow under basal and stress granulopoiesis conditions

Blood ◽  
2009 ◽  
Vol 113 (19) ◽  
pp. 4711-4719 ◽  
Author(s):  
Kyle J. Eash ◽  
Jacquelyn M. Means ◽  
Douglas W. White ◽  
Daniel C. Link
Keyword(s):  
Bone Marrow ◽  
Listeria Monocytogenes ◽  
Host Tissue ◽  
Microbial Pathogens ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Cxcr4 Signaling ◽  
Listeria Monocytogenes Infection ◽  
A Cell ◽  
Stimulating Factor

Abstract The number of neutrophils in the blood is tightly regulated to ensure adequate protection against microbial pathogens while minimizing damage to host tissue. Neutrophil homeostasis in the blood is achieved through a balance of neutrophil production, release from the bone marrow, and clearance from the circulation. Accumulating evidence suggests that signaling by CXCL12, through its major receptor CXCR4, plays a key role in maintaining neutrophil homeostasis. Herein, we generated mice with a myeloid lineage–restricted deletion of CXCR4 to define the mechanisms by which CXCR4 signals regulate this process. We show that CXCR4 negatively regulates neutrophil release from the bone marrow in a cell-autonomous fashion. However, CXCR4 is dispensable for neutrophil clearance from the circulation. Neutrophil mobilization responses to granulocyte colony-stimulating factor (G-CSF), CXCL2, or Listeria monocytogenes infection are absent or impaired, suggesting that disruption of CXCR4 signaling may be a common step mediating neutrophil release. Collectively, these data suggest that CXCR4 signaling maintains neutrophil homeostasis in the blood under both basal and stress granulopoiesis conditions primarily by regulating neutrophil release from the bone marrow.

scholarly journals A comparison of hematopoiesis in normal and splenectomized mice treated with granulocyte colony-stimulating factor

Blood ◽  
1990 ◽  
Vol 75 (3) ◽  
pp. 563-569 ◽  
Author(s):  
G Molineux ◽  
Z Pojda ◽  
TM Dexter
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Extramedullary Hematopoiesis ◽  
High Dose ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Response Data ◽  
Hematopoietic Precursor ◽  
Stimulating Factor

Abstract Recombinant human granulocyte colony-stimulating factor (rhG-CSF) induces leukocytosis in vivo in both intact and splenectomized mice. Full dose response data showed a plateau in this effect at doses over 500 micrograms rhG-CSF/kg body weight/d in intact mice. The effect is magnified in splenectomized mice, where leukocyte numbers reach 100 x 10(6) mL after 4 days' treatment at 250 micrograms/kg/d. Further hematopoietic precursor populations are also affected in both marrow and the spleen; in general, marrow parameters were depressed, while splenic populations were enlarged. In splenectomized mice, both blood- borne stem cells were enhanced, and foci of extramedullary hematopoiesis were enlarged in addition to the effects seen in intact mice. In the marrow of splenectomized and intact mice treated with a high dose of G-CSF, erythroid suppression in the marrow was confirmed with radioactive iron. Our studies confirm and extend previous work on the mode of action of G-CSF, and indicate that side effects of high dose G-CSF therapy might include erythroid suppression in the bone marrow.

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