scholarly journals Granulocyte colony stimulating factor-associated aortitis evaluated via multiple imaging modalities including vascular echography: a case report

Author(s):  
Mikiko Harada ◽  
Hirohiko Motoki ◽  
Takahiro Sakai ◽  
Koichiro Kuwahara

Abstract Background Granulocyte colony stimulating factor (G-CSF) preparations are used for patients with granulocytopenia, especially to prevent febrile neutropenia. Arteritis has been recognized as a side effect of G-CSF treatment; however, there are no clear diagnostic criteria or treatment guidelines because not enough cases have been reported. Present case showed one of the diagnostic and treatment selection methods via multiple imaging modality including vascular echography. Case summary A 52-year-old woman underwent chemotherapy for ovarian cancer and received G-CSF because of myelosuppression. The patient experienced high and remittent fever that persisted during treatment using antibiotics and acetaminophen. Enhanced computed tomography revealed thickening of the tissue around the aortic arch and abdominal aorta. Echography of the abdominal aorta revealed thickening of the wall and a hypoechoic region around the aorta. Gadolinium-enhanced magnetic resonance imaging and 18F-fludeoxyglucose positron emission tomography also revealed that the inflammation was localized to the lesion. A suspicion of G-CSF-associated aortitis was based on the patient’s history and the exclusion of other diseases that might have caused the aortitis. Her condition rapidly improved after starting corticosteroid treatment. Discussion The differential diagnosis in similar cases should consider immune diseases that cause large-vessel arteritis (Takayasu arteritis, giant cell arteritis, and another vasculitis), infection, drug-induced disease, and immunoglobulin G4-related disease. The use of different imaging modalities, including vascular echography, helped guide the diagnosis and follow-up. It is necessary to evaluate the patient’s general condition before the selection of treatments.

2015 ◽  
Vol 35 (3) ◽  
pp. 244-250 ◽  
Author(s):  
R Navarro-Martínez ◽  
E Chover-Sierra ◽  
O Cauli

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.


1994 ◽  
Vol 70 (5) ◽  
pp. 517-520
Author(s):  
Junichi TAJIRI ◽  
Shiro NOGUCHI ◽  
Mitsuo MORITA ◽  
Masaaki TAMARU ◽  
Nobuo MURAKAMI

1995 ◽  
Vol 40 (4) ◽  
pp. 276-277 ◽  
Author(s):  
Ritsuto Fujiwaki ◽  
Toshiyuki Hata ◽  
Kohkichi Hata ◽  
Manabu Kitao ◽  
Hiroshi Furuya ◽  
...  

2021 ◽  
Vol 1 (30) ◽  
pp. 19-23
Author(s):  
N. A. Sokolova ◽  
L. V. Pozdnyakova ◽  
I. S. Tatarinova

The majority of agranulocytosis cases are caused by drugs, including nonsteroidal anti-inflammatory drugs, antibiotics, antithyroid agents, etc. Here, we report a case of severe agranulocytosis in a 67-year-old woman following nonsteroidal anti-inflammatory therapy which was successfully managed using recombinant human granulocyte colony-stimulating factor. Although metamizole, has been in use since 1922 in the management of postoperative pain, colic pain, cancer pain and migraine, agranulocytosis as a direct side effect of metamizole therapy has been rarely reported. It is important to keep in mind this rare but potentially life-threatening adverse effect of metamizole, when initiating therapy.


2000 ◽  
Vol 192 (5) ◽  
pp. 647-658 ◽  
Author(s):  
Andreas Villunger ◽  
Lorraine A. O'Reilly ◽  
Nils Holler ◽  
Jerry Adams ◽  
Andreas Strasser

The short life span of granulocytes, which limits many inflammatory responses, is thought to be influenced by the Bcl-2 protein family, death receptors such as CD95 (Fas/APO-1), stress-activated protein kinases such as p38 mitogen-activated protein kinase (MAPK), and proinflammatory cytokines like granulocyte colony-stimulating factor (G-CSF). To clarify the roles of these various regulators in granulocyte survival, we have investigated the spontaneous apoptosis of granulocytes in culture and that induced by Fas ligand or chemotherapeutic drugs, using cells from normal, CD95-deficient lpr, or vav-bcl-2 transgenic mice. CD95-induced apoptosis, which required receptor aggregation by recombinant Fas ligand or the membrane-bound ligand, was unaffected by G-CSF treatment or Bcl-2 overexpression. Conversely, spontaneous and drug-induced apoptosis occurred normally in lpr granulocytes but were suppressed by G-CSF treatment or Bcl-2 overexpression. Although activation of p38 MAPK has been implicated in granulocyte death, their apoptosis actually was markedly accelerated by specific inhibitors of this kinase. These results suggest that G-CSF promotes granulocyte survival largely through the Bcl-2–controlled pathway, whereas CD95 regulates a distinct pathway to apoptosis that is not required for either their spontaneous or drug-induced death. Moreover, p38 MAPK signaling contributes to granulocyte survival rather than their apoptosis.


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