Splenectomy after angiographic embolization of the splenic artery in patients with massive splenomegaly and severe thrombocytopenia, in juvenile subacute myelomonocytic leukemia

1984 ◽  
Vol 12 (1) ◽  
pp. 28-32 ◽  
Author(s):  
Peter G. Steinherz ◽  
Philip R. Exelby ◽  
Jean Young ◽  
Robin C. Watson
Keyword(s):  
Splenic Artery ◽  
Severe Thrombocytopenia ◽  
Angiographic Embolization ◽  
Massive Splenomegaly ◽  
Myelomonocytic Leukemia

Outcome of laparoscopic splenectomy with preoperative splenic artery embolization for massive splenomegaly

2010 ◽  
Vol 24 (8) ◽  
pp. 2008-2012 ◽  
Author(s):  
Artan Reso ◽  
Mantaj Singh Brar ◽  
Neal Church ◽  
Philip Mitchell ◽  
Elijah Dixon ◽  
...  
Keyword(s):  
Laparoscopic Splenectomy ◽  
Splenic Artery ◽  
Artery Embolization ◽  
Massive Splenomegaly ◽  
Splenic Artery Embolization

scholarly journals Preoperative splenic artery embolization in klippel-Trenaunay syndrome with massive splenomegaly: A case report

2014 ◽  
Vol 4 (2) ◽  
pp. 40 ◽  
Author(s):  
Zishu Zhang ◽  
ScottR Owens ◽  
Ranjith Vellody ◽  
PaulaM Novelli ◽  
JamesJ Shields ◽  
...  
Keyword(s):  
Case Report ◽  
Splenic Artery ◽  
Artery Embolization ◽  
Massive Splenomegaly ◽  
Splenic Artery Embolization ◽  
Klippel Trenaunay Syndrome

scholarly journals Treatment of refractory splenomegaly in myeloproliferative disease by splenic artery infusion

Blood ◽  
1979 ◽  
Vol 53 (5) ◽  
pp. 1014-1017
Author(s):  
GP Canellos ◽  
SB Sutliffe ◽  
VT DeVita ◽  
TA Lister
Keyword(s):  
Cytosine Arabinoside ◽  
Splenic Artery ◽  
Symptomatic Relief ◽  
Spleen Size ◽  
Myeloproliferative Disease ◽  
Massive Splenomegaly ◽  
Chronic Granulocytic Leukemia ◽  
Previous Therapy ◽  
Blastic Phase ◽  
Granulocytic Leukemia

Five patients in the blastic phase of chronic granulocytic leukemia with massive splenomegaly were treated by intraarterial splenic artery infusion of cytosine arabinoside. All patients had massive splenomegaly associated with pain and/or hypersplenism and were refractory to previous therapy. All 5 patients demonstrated responses to treatment, with reduction in spleen size as well as symptomatic relief. Systemic toxicity was minimal in 4 of the 5 patients.

scholarly journals Combined inhibition of Bruton’s Tyrosine Kinase (BTK) and Phosphoinositide 3-kinase (PI3K) p110δ improves monocytosis and splenomegaly in a JMML Mouse Model

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Roshni Patel ◽  
Baskar Ramdas ◽  
Lisa Deng ◽  
Victoria Jideonwo-Auman ◽  
Reuben Kapur
Keyword(s):  
Mouse Model ◽  
Clinical Investigation ◽  
Myeloid Cells ◽  
Specific Inhibitor ◽  
Juvenile Myelomonocytic Leukemia ◽  
Severe Thrombocytopenia ◽  
Erk Activation ◽  
Valuable Treatment ◽  
Phosphoinositide 3 Kinase ◽  
Myelomonocytic Leukemia

Background and Hypothesis: Juvenile myelomonocytic leukemia (JMML) is an aggressive, childhood leukemic disorder for which there are no efficacious chemotherapeutics. Gain-of-function (GOF) mutations in the SHP2 phosphatase oncogene, Ptpn11, are the most common associated mutations. In hematopoietic cells, these mutations lead to increased AKT and ERK activation, which results in hyperproliferation of myeloid cells. Clinically, this manifests as monocytic leukocytosis and marked splenomegaly with the consequence of severe thrombocytopenia. Previously, this lab has shown that pharmacological inhibition of p110d, the hematopoietic-specific catalytic subunit of PI3K, moderates monocytosis and splenomegaly in a JMML mouse model with a SHP2 GOF mutation (E76K mice). Additionally, BTK has been identified as a potential therapeutic target as it cooperates with PI3K to increase activation of AKT and ERK in myeloid cells. Using a dual-hit approach of targeting both PI3K p110d and BTK may serve as a valuable treatment design for JMML.   Experimental Design or Project Methods: We have treated E76K mice with a combination of 20mg/kg ACP319, a PI3K p110d-specific inhibitor, and 20mg/kg acalabrutinib, a BTK-specific inhibitor, via oral gavage twice daily for 21 days and performed hematopoietic analysis including the degree of splenomegaly, monocytosis, and thrombocytopenia.  Results: The combination treatment scheme significantly decreased monocytosis and ameliorated thrombocytopenia compared to vehicle treated mice. Furthermore, splenomegaly was significantly reduced in the combination-treated mice compared to vehicle.   Conclusion and Potential Impact: Combination chemotherapy with PI3K p110d- and BTK-specific inhibitors profoundly corrects disease state hallmarks of JMML, and may warrant further clinical investigation of efficacy.

Partial splenic embolization in a child with Gaucher disease, massive splenomegaly and severe thrombocytopenia

2009 ◽  
Vol 39 (9) ◽  
pp. 1006-1009 ◽  
Author(s):  
Andres H. Pena ◽  
Paige Kaplan ◽  
Jaya Ganesh ◽  
Egor Clevac ◽  
Anne Marie Cahill
Keyword(s):  
Gaucher Disease ◽  
Severe Thrombocytopenia ◽  
Partial Splenic Embolization ◽  
Massive Splenomegaly ◽  
Splenic Embolization

scholarly journals Severe thrombocytopenia and clinical bleeding associated with rituximab infusion in a lymphoma patient with massive splenomegaly without leukemic invasion

Leukemia ◽  
2001 ◽  
Vol 15 (1) ◽  
pp. 186-187 ◽  
Author(s):  
C Rigamonti ◽  
C Volta ◽  
S Colombi ◽  
L Forti ◽  
F Savinelli ◽  
...  
Keyword(s):  
Severe Thrombocytopenia ◽  
Lymphoma Patient ◽  
Massive Splenomegaly
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