Gastric cancer with bone marrow invasion presenting as severe thrombocytopenia

2015 ◽  
Vol 25 (1) ◽  
pp. 229-230 ◽  
Author(s):  
Mladen Mimica ◽  
Monika Tomić ◽  
Emil Babić ◽  
Maja Karin ◽  
Milenko Bevanda ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Bone Marrow ◽  
Severe Thrombocytopenia

scholarly journals A case of disseminated carcinomatosis of the bone marrow from gastric cancer developing rapidly after a gastrectomy

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Shunsuke Sato ◽  
Yuji Ishibashi ◽  
Koichiro Kawasaki ◽  
Ryoto Yamazaki ◽  
Fumihiko Hatao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Bone Marrow ◽  
Poor Prognosis ◽  
Laboratory Tests ◽  
Distal Gastrectomy ◽  
Postoperative Bleeding ◽  
Laboratory Data ◽  
Severe Thrombocytopenia ◽  
Case Presentation ◽  
Lower Back

Abstract Background Disseminated carcinomatosis of the bone marrow (DCBM) is often associated with disseminated intravascular coagulation (DIC) and a poor prognosis. Moreover, the timing of the diagnosis varies. We presented herein the first report of a case of DCBM from gastric cancer that developed rapidly after a gastrectomy. Case presentation A 42-year-old male patient was referred to us for gastric cancer. Preoperative laboratory tests were normal. Abdominal computed tomography (CT) revealed no obvious bone metastasis, and he underwent a laparoscopic distal gastrectomy. On postoperative day (POD) 1, laboratory data indicated severe thrombocytopenia. Postoperative bleeding requiring reoperation was found. Afterwards, he complained of lower back pain. His ALP and LDH gradually became elevated. On POD 8, DIC was diagnosed. CT and bone scintigraphy showed multiple, widespread bone metastases. Based on these findings, DCBM from gastric cancer was diagnosed. Systemic chemotherapy was started on POD 12. The DIC subsided during the first course, and he was discharged on POD 21. The patient died of tumor progression 7 months later. Conclusion When thrombocytopenia is observed immediately after a gastrectomy for gastric cancer, the possibility of DCBM should be considered.

scholarly journals Drug-induced thrombocytopenia associated with trastuzumab in a patient with HER2-positive recurrent gastric cancer

2021 ◽  
Author(s):  
Yuko Takano ◽  
Satoshi Furune ◽  
Yuki Miyai ◽  
Sachi Morita ◽  
Megumi Inoue ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Monoclonal Antibody ◽  
Bone Marrow ◽  
Elevated Level ◽  
Oral Prednisolone ◽  
Severe Thrombocytopenia ◽  
Her2 Positive ◽  
Drug Induced ◽  
Recurrent Gastric Cancer ◽  
Positive Recurrent

AbstractHere, we report a 57-year-old female patient with HER2-positive recurrent gastric cancer who experienced drug-induced thrombocytopenia associated with trastuzumab, a humanized anti-HER2 monoclonal antibody. Shortly after the initiation of S-1, oxaliplatin, and trastuzumab chemotherapy, the patient experienced severe thrombocytopenia and did not respond to platelet transfusions. Based on the findings of increased numbers of polynuclear megakaryocytes in the bone marrow and an elevated level of platelet-associated IgG (PA-IgG), the patient was diagnosed with drug-induced thrombocytopenia (DITP). The platelet count recovered rapidly with oral prednisolone (1 mg/kg). Since we initially suspected oxaliplatin as the causal agent, S-1 was restarted as a monotherapy, followed by trastuzumab after a 3-week interval, without oxaliplatin. On the second day after the addition of trastuzumab, severe thrombocytopenia occurred again, which suggests that trastuzumab was responsible for the DITP. The patient no longer experienced severe thrombocytopenia during the subsequent S-1 and oxaliplatin chemotherapy, which supports this hypothesis.

scholarly journals Lymph node metastasis-derived gastric cancer cells educate bone marrow-derived mesenchymal stem cells via YAP signaling activation by exosomal Wnt5a

Oncogene ◽  
2021 ◽  
Vol 40 (12) ◽  
pp. 2296-2308
Author(s):  
Mei Wang ◽  
Xinxin Zhao ◽  
Rong Qiu ◽  
Zheng Gong ◽  
Feng Huang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Metastatic Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Node Metastasis ◽  
Signaling Activation

AbstractLymph node metastasis (LNM), a common metastatic gastric-cancer (GC) route, is closely related to poor prognosis in GC patients. Bone marrow-derived mesenchymal stem cells (BM-MSCs) preferentially engraft at metastatic lesions. Whether BM-MSCs are specifically reprogrammed by LNM-derived GC cells (LNM-GCs) and incorporated into metastatic LN microenvironment to prompt GC malignant progression remains unknown. Herein, we found that LNM-GCs specifically educated BM-MSCs via secretory exosomes. Exosomal Wnt5a was identified as key protein mediating LNM-GCs education of BM-MSCs, which was verified by analysis of serum exosomes collected from GC patients with LNM. Wnt5a-enriched exosomes induced YAP dephosphorylation in BM-MSCs, whereas Wnt5a-deficient exosomes exerted the opposite effect. Inhibition of YAP signaling by verteporfin blocked LNM-GC exosome- and serum exosome-mediated reprogramming in BM-MSCs. Analysis of MSC-like cells obtained from metastatic LN tissues of GC patients (GLN-MSCs) confirmed that BM-MSCs incorporated into metastatic LN microenvironment, and that YAP activation participated in maintaining their tumor-promoting phenotype and function. Collectively, our results show that LNM-GCs specifically educated BM-MSCs via exosomal Wnt5a-elicited activation of YAP signaling. This study provides new insights into the mechanisms of LNM in GC and BM-MSC reprogramming, and will provide potential therapeutic targets and detection indicators for GC patients with LNM.

Immature platelet values indicate impaired megakaryopoietic activity in neonatal early-onset thrombocytopenia

2010 ◽  
Vol 103 (05) ◽  
pp. 1016-1021 ◽  
Author(s):  
Hannes Hammer ◽  
Christoph Bührer ◽  
Christof Dame ◽  
Malte Cremer ◽  
Andreas Weimann
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
Intensive Care ◽  
Early Onset ◽  
Absolute Number ◽  
Severe Thrombocytopenia ◽  
Platelet Counts ◽  
Immature Platelet Fraction ◽  
Neonatal Thrombocytopenia ◽  
Immature Platelets

SummaryNewly released platelets, referred to as immature platelets, can be reliably quantified based on their RNA content by flow cytometry in an automated blood analyser. The absolute number of immature platelets (IPF#) and the immature platelet fraction (IPF%) reflect megakaryopoietic activity. We aimed to analyse the implication of these parameters in analysing the pathomechanism of early-onset neonatal thrombocytopenia. Platelet counts and IPF were determined at day 1 to 3 (d1 to d3) in 857 neonates admitted to intensive care. In thrombocytopenic patients (platelet counts<150 x 109/l, n=129), IPF# was significantly lower (8.5 ± 2.7 x 109/l), than in non-thrombocytopenic neonates (9.5 ± 3.6 x 109/l, n=682, p<0.05). IPF% was significantly higher in thrombocytopenic (9.3 ± 7.9%) vs. non-thrombocytopenic neonates (4.1 ± 1.8%, p<0.001). While neonates with early-onset infection (n=134) had lower platelet counts (199 ± 75 x 109/l) compared to controls (230 ± 68 x 109/l, n=574, p<0.01), there were no differences in IPF# or IPF%. Likewise, “small for gestational age” infants (SGA, n=149) had lower platelet counts at d1 (199 ± 75 x 109/l, p<0.001) than controls, but no differences in IPF. A trend towards lower IPF# was detected if SGA infants with platelet counts <100 x 109/l (5.4 ± 3.9 x 109/l, n=11) and thrombocytopenic neonates with infection (9.9 ± 7.3 x 109/l, n=10, p=0.11) were compared. The evaluation of IPF# indicates that thrombocytopenia in neonates is likely due to a combination of increased platelet consumption and inadequate megakaryopoietic response by the neonatal bone marrow. Furthermore, SGA neonates with moderate and severe thrombocytopenia might have a pronounced suppression of megakaryopoiesis compared to neonates with infection.

Hematologic Toxicity of High-Dose Iodine-131–Metaiodobenzylguanidine Therapy for Advanced Neuroblastoma

2004 ◽  
Vol 22 (12) ◽  
pp. 2452-2460 ◽  
Author(s):  
Steven G. DuBois ◽  
Julia Messina ◽  
John M. Maris ◽  
John Huberty ◽  
David V. Glidden ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Radiation Dose ◽  
Red Cells ◽  
Whole Body ◽  
High Dose ◽  
Hematologic Toxicity ◽  
Severe Thrombocytopenia ◽  
Hematopoietic Stem ◽  
Iodine 131 ◽  
Mibg Therapy

Purpose Iodine-131–metaiodobenzylguanidine (131I-MIBG) has been shown to be active against refractory neuroblastoma. The primary toxicity of 131I-MIBG is myelosuppression, which might necessitate autologous hematopoietic stem-cell transplantation (AHSCT). The goal of this study was to determine risk factors for myelosuppression and the need for AHSCT after 131I-MIBG treatment. Patients and Methods Fifty-three patients with refractory or relapsed neuroblastoma were treated with 18 mCi/kg 131I-MIBG on a phase I/II protocol. The median whole-body radiation dose was 2.92 Gy. Results Almost all patients required at least one platelet (96%) or red cell (91%) transfusion and most patients (79%) developed neutropenia (< 0.5 × 103/μL). Patients reached platelet nadir earlier than neutrophil nadir (P < .0001). Earlier platelet nadir correlated with bone marrow tumor, more extensive bone involvement, higher whole-body radiation dose, and longer time from diagnosis to 131I-MIBG therapy (P ≤ .04). In patients who did not require AHSCT, bone marrow disease predicted longer periods of neutropenia and platelet transfusion dependence (P ≤ .03). Nineteen patients (36%) received AHSCT for prolonged myelosuppression. Of patients who received AHSCT, 100% recovered neutrophils, 73% recovered red cells, and 60% recovered platelets. Failure to recover red cells or platelets correlated with higher whole-body radiation dose (P ≤ .04). Conclusion These results demonstrate the substantial hematotoxicity associated with high-dose 131I-MIBG therapy, with severe thrombocytopenia an early and nearly universal finding. Bone marrow tumor at time of treatment was the most useful predictor of hematotoxicity, whereas whole-body radiation dose was the most useful predictor of failure to recover platelets after AHSCT.

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