The Keio Journal of Medicine
Online ISSN : 1880-1293
Print ISSN : 0022-9717
ISSN-L : 0022-9717
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Volume 64, Issue 3
Displaying 1-4 of 4 articles from this issue
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REVIEWS
  • Thrombosis in Lymphoma Patients and in Myeloma Patients
    Kenji Yokoyama
    Article type: Review
    2015 Volume 64 Issue 3 Pages 37-43
    Published: 2015
    Released on J-STAGE: September 25, 2015
    Advance online publication: July 25, 2015
    DOIhttps://doi.org/10.2302/kjm.2014-0017-RE
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    The risk of venous thromboembolism (VTE) in patients with cancer is several-fold higher than that in individuals without cancer. Recent studies demonstrated a high incidence of VTE in patients with hematologic malignancies as well as in patients with solid cancers. The reported incidence of VTE in lymphoma is variable, ranging from less than 5% to 59.5%. The incidence of VTE is higher in non-Hodgkin lymphoma than it is in Hodgkin lymphoma. The incidence of VTE also varies according to the disease grade, the disease stage, the performance status of the patient, and the site of disease. Most VTE cases occur at the diagnosis of cancer or early in the course of cancer treatment. An elevated incidence of VTE is also reported in cases of myeloma. VTE occurs in approximately 5% of myeloma patients treated with conventional chemotherapy, and treatment of myeloma patients with immunomodulatory drugs (IMid)-based therapy increases the risk of VTE. Prophylactic aspirin or anticoagulant is used in myeloma patients treated with IMid-based therapy. Several reports have indicated that the incidence of VTE is relatively low in Asian patients treated with IMid-based therapy, and concomitant use of bortezomib reduces the risk of VTE. The incidence of arterial thrombosis is also increased in patients with myeloma and monoclonal gammopathy of undetermined significance. Further studies are needed to develop a predictive model for identifying patients with lymphoma and myeloma who are at high risk for developing thrombosis.
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  • Mechanism Underlying Post-menopausal Osteoporosis: HIF1α is Required for Osteoclast Activation by Estrogen Deficiency
    Takeshi Miyamoto
    Article type: Review
    2015 Volume 64 Issue 3 Pages 44-47
    Published: 2015
    Released on J-STAGE: September 25, 2015
    Advance online publication: August 08, 2015
    DOIhttps://doi.org/10.2302/kjm.2015-0003-RE
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    The aging of the population worldwide has sharply increased the number of post-menopausal osteoporosis patients. Bone fragility caused by osteoporosis often results in fractures; therefore, controlling osteoporosis is crucial to prevent such injuries. To date, various drugs to treat osteoporosis have been developed and launched; however, the molecular mechanisms underlying post-menopausal osteoporosis have not been fully elucidated, and additional factors that could be targeted to treat patients remain to be characterized. Recently, hypoxia inducible factor 1 alpha (HIF1α) was identified as essential for osteoclast activation, an activity that promotes bone loss following menopausal estrogen deficiency. Although osteoclasts, which are located in hypoxic regions of the bone surface, express HIF1α mRNA, in pre-menopausal conditions the presence of estrogen decreases HIF1α protein levels in these cells. In menopausal conditions, however, estrogen deficiency allows HIF1α protein to accumulate in osteoclasts, leading to osteoclast activation and bone loss. Osteoclast-specific conditional HIF1α inactivation protects mice from estrogen deficiency-induced osteoclast activation and bone loss, as does systemic administration of a HIF1α inhibitor. Therefore, HIF1α represents a potential therapeutic target to prevent osteoclast activation and bone loss in post-menopausal patients.
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LETTER TO THE EDITOR
ABSTRACT
  • Pulmonary Macrophage Transplantation Therapy ofHereditary Pulmonary Alveolar Proteinosis
    Takuji Suzuki
    Article type: Abstravt
    2015 Volume 64 Issue 3 Pages 51
    Published: 2015
    Released on J-STAGE: September 25, 2015
    DOIhttps://doi.org/10.2302/kjm.64-002-ABST
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    Hereditary pulmonary alveolar proteinosis (hPAP) is characterized by pulmonary surfactant accumulation and respiratory failure due to defective GM-CSF receptor signaling caused by recessive genetic mutations in genes encoding the GM-CSF receptor (CSF2RA or CSF2RB), which impairs multiple alveolar macrophage (AM) functions including pulmonary surfactant clearance. An identical disease occurs in Csf2rb-/- (KO) mice. Whole lung lavage under general anesthesia is the only available therapy and is required in some patients every several months. Bone marrow transplantation corrected PAP in a murine hPAP model (KO mice) but was not successful in one child with hPAP who succumbed to lung infection before engraftment. We have recently developed a novel cell therapy, pulmonary macrophage transplantation (PMT). Murine WT bone marrow cells or KO cells transduced with a Csf2rb-expressing lentivirus were expanded/differentiated into macrophages, and administered into the lungs of KO mice without myeloablation. One PMT of WT macrophages resulted in a gradual increase in numbers of GM-CSF-Rb+ AMs that paralleled a synchronous decline in bronchoalveolar lavage (BAL) hPAP disease severity. One year after PMT, lung pathology and PAP biomarkers in BAL and AMs were markedly improved. PMT of WT or gene-corrected KO cells were equally efficacious. Importantly, the phenotype of macrophages before transplantation had changed to that of WT AMs and not KO AMs when evaluated one year after transplantation. PMT therapy of hPAP was highly efficacious, without adverse effects, and markedly improved survival. Results showed that GM-CSF and lung-specific factor(s) regulate AM phenotype, function and population size.(Presented at the 1905th Meeting, July 7, 2015)
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