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1.
Anticancer Res ; 42(8): 4139-4143, 2022 Aug.
Article in English | MEDLINE | ID: mdl-35896231

ABSTRACT

BACKGROUND/AIM: Post-menopausal breast cancer (BC) patients who receive adjuvant aromatase inhibitor (AI) therapy may be at increased risk of bone loss, osteoporosis, and bone fracture. We aimed to evaluate the efficacy and safety of oral bisphosphonate minodronate in preventing bone loss complications. PATIENTS AND METHODS: Patients receiving AI and 80% of those with suboptimal bone mineral density (BMD) were prescribed monthly oral minodronate 50 mg every 4 weeks for 72 weeks. BMD, bone metabolism markers, incidence of bone fractures, medication compliance, and other adverse events (AE) were examined every 24 weeks following administration. RESULTS: Fifty postmenopausal BC patients with a median age of 64.0 years were enrolled. The mean value of lumbar spine BMD was higher than that of the value before the minodronate administration at each observation point. Before and after the treatment, the median serum values of Tartrate-resistant Acid Phosphatase 5b (TRACP-5b) (mU/dl) and serum type I collagen cross-linked N-telopeptide (NTX) (nmolBCE/l) were decreased from 535.7 and 18.5 to 230.1 and 11.9, respectively. No adverse grade 2 or higher event was observed throughout this study. CONCLUSION: The combined administration of minodronate and AIs was safe and effective in preventing bone loss complications in postmenopausal BC patients.


Subject(s)
Bone Density Conservation Agents , Bone Diseases, Metabolic , Breast Neoplasms , Fractures, Bone , Aromatase Inhibitors/adverse effects , Bone Density , Bone Density Conservation Agents/adverse effects , Breast Neoplasms/complications , Diphosphonates/adverse effects , Female , Fractures, Bone/etiology , Humans , Imidazoles , Middle Aged , Postmenopause
2.
Gan To Kagaku Ryoho ; 47(8): 1225-1227, 2020 Aug.
Article in Japanese | MEDLINE | ID: mdl-32829360

ABSTRACT

Clinical evidence has indicated that, after neo-adjuvant chemotherapy(NAC), sentinel node(SN)identification rates(IR) were lower and false-negative rates(FNR)were higher for patients(pts)with local advanced breast cancer(BC)than for pts with early stage BC who did not receive NAC. Our previous clinical trial indicated that the real-time indocyanin green (RT-ICG)fluorescence imaging technique could improve the diagnostic sensitivity and detection accuracy of sentinel node biopsy(SNB). Nine pts with histologically confirmed Stage ⅡA to ⅢB, T1-T3, N0-2, M0 BC were selected to receive NAC, and the standard surgeries were performed after NAC completion. The SNs were detected by using conventional procedures with the blue dye(indigo carmine)plus 99mTc radioisotope techniques combined with concurrent RT-ICG. Clinically positive nodes were diagnosed by the radiologists using axillary ultrasound, MRI, and/or CT scans. All pts provided written informed consent before surgery. The surgical SNB was guided via RT-ICG fluorescence under standard light conditions by using the HEMS imaging system as previously published. All pts underwent SNB followed by completion node dissection(CND). The IR and FNR were calculated by comparing the results of the SNB and the histopathology of the resection specimens obtained via CND. The IR and FNR for each procedure of SNB were, respectively, 35.3% and 41.7% when indigo carmine blue was used, 82.4% and 0 when ICG fluorescence was used, and 58.8% and 5% when RI was used. In contrast, the total calculation of the triple tracer showed that IR reached 100% and FNR was 0. These data suggest that IR and FNR of SNB might be improved in pts with BC treated with NAC by using the novel triple tracer technique.


Subject(s)
Breast Neoplasms , Sentinel Lymph Node Biopsy , Axilla , Breast Neoplasms/therapy , Humans , Indocyanine Green , Lymph Nodes , Neoadjuvant Therapy , Radioisotopes
3.
Muscle Nerve ; 25(3): 409-18, 2002 Mar.
Article in English | MEDLINE | ID: mdl-11870719

ABSTRACT

Experimental allergic myositis (EAM) in Lewis rats, induced with partially purified myosin, is regarded as a model of human polymyositis. To clarify the role of adhesion molecules in the pathogenesis of EAM in Lewis rats, we investigated intramysial expressions of the intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, and the serum level of soluble ICAM-1 in EAM rats. All the EAM rat muscles had scattered inflammatory foci, as well as cell infiltration and necrosis, by week 4 after the initial immunization (i.e., day 0 after the last immunization). As compared with the control muscles, ICAM-1 and VCAM-1 were strongly expressed immunohistochemically in the endothelium of vessels in the endomysium and perimysium, and to lesser extents in the inflammatory infiltrates and on the sarcolemma of nonnecrotic muscle fibers adjacent to the inflammatory infiltrates or invaded muscle fibers. ICAM-1 in the muscle extracts and sera from EAM rats increased on each test day, as compared with extracts from the normal controls. The values peaked on day 0 after the last immunization, then gradually decreased with time. ICAM-1 elevations in the muscle extracts were correlated with the percent of sections that had inflammatory lesions (P = 0.032) and the histological scores (P = 0.005) on day 0, whereas there was no significance on days 3 and 7. These findings suggest that the adhesion molecules ICAM-1 and VCAM-1 increase in the early stage of EAM, and function in the initiation of the inflammatory process of myositis.


Subject(s)
Intercellular Adhesion Molecule-1/biosynthesis , Nervous System Autoimmune Disease, Experimental/metabolism , Vascular Cell Adhesion Molecule-1/biosynthesis , Animals , Autoantibodies/blood , Blotting, Western , Female , Immunization , Immunohistochemistry , Intercellular Adhesion Molecule-1/analysis , Muscle, Skeletal/chemistry , Muscle, Skeletal/metabolism , Muscle, Skeletal/pathology , Myosins/analysis , Myosins/immunology , Nervous System Autoimmune Disease, Experimental/immunology , Nervous System Autoimmune Disease, Experimental/pathology , Rabbits , Rats , Rats, Inbred Lew , Vascular Cell Adhesion Molecule-1/analysis
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