BACKGROUND: Neonatal alloimmune thrombocytopenia (NAIT) is caused when maternal alloantibodies react with paternally inherited antigens present on the fetal PLTs, a reaction mainly due to antibodies against human PLT antigens. Cases in which NAIT has been caused by HLA antibodies are relatively rare. In this study, three cases of NAIT associated with HLA antibodies that occurred in a 1‐year period are reported. STUDY DESIGN AND METHODS: The presence of HLA antibodies in these three NAIT case studies was elucidated by examining reactions of the neonatal and maternal sera with lymphocytes, PLTs, and beads from an HLA antibody screening test (FlowPRA, One Lambda Inc.). Absorption and elution tests with paternal cells were also conducted. In addition, the influence of titer and specificity of HLA antibodies on NAIT was analyzed in light of 24 other documented cases in Japan. RESULTS: In the three case studies presented herein, antibodies against human PLT antigens were found in neither the maternal nor neonatal sera, while specific HLA antibodies were identified in both sera. Absorption of maternal serum with paternal PLTs eliminated the reactivity against paternal PLTs and lymphocytes. CONCLUSION: Transplacental passage of maternal HLA antibodies was observed in the three neonates cited in the present study.
Normal P wave signal-averaged electrocardiogram (SAE) values were determined in 120 healthy Japanese adults (56 men, 64 women), aged 44.5±10.2 years (mean±SD). The P wave trigger method was used with a Fukuda FDX6500 recorder. We used bipolar Frank leads (X,Y,Z), and recordings were made with forward and backward digital Butterworth filters [40 Hz (18 dB / oct) -300 Hz (12 dB / oct)]. The recordings were taken for the following five parameters: forward and backward filtered P wave duration [fPd (F); fPd (B)]; bidirectionally corrected fPd [fPd (C)]; and 20 ms of the terminal portions of voltage at forward and backward filtering (RMS20). Overall, fPd (F) was 117.8-136.4 ms, fPd (B) 116.4-134.4 ms, fPd (C) 97.4-115.2 ms, RMS20 (F) 1.6-3.6 μV, and RMS20 (B) was 2.2-5.4 μV. Between the sexes, there were significant differences in fPd (F) (p<0.001) and fPd (B) (p<0.01) and in RMS20 (F) (p<0.05) and RMS20 (B) (p<0.05). Weak positive correlations were observed between fPd (F) and body surface area, fPd (F) and age, fPd (B) and body surface area, fPd (B) and age, fPd (C) and body surface area, and fPd (C) and age. There was no evident correlation, however, between either forward or backward RMS20 and body surface area or between forward or backward RMS20 and age. Differences in the normal P wave values between the sexes and age groups were evaluated in this study.
To evaluate the dose-response effects of granulocyte-colony stimulating factor (G-CSF) on atherosclerosis, we examined how G-CSF treatment at different concentrations affects atherosclerotic plaque formation in the aorta of cholesterol-fed rabbits.Japanese White rabbits (n=8 each) fed on a 1.5% cholesterol diet were subcutaneously injected with G-CSF at 50 (GL), 100 (GM), or 300 microg/kg/day (GH) for five days, or with 3 cycles of G-CSF at 100 microg/kg/day at 3-week intervals (GM3), or human serum albumin (Control). The extent and composition of atherosclerosis was evaluated 14 weeks after cholesterol feeding.Although G-CSF treatment did not affect plasma lipid levels, the percentage of aortic surface involvement in the GM3 group was significantly decreased (p<0.05) compared with the Control group. Histological analysis revealed that the intima media ratio was also diminished in GM and GM3 groups. The extent of intimal smooth muscle cell accumulation was higher in GL and GM3 groups than in the Control group. TIMP-2 mRNA expression in the aortic tissue was increased by G-CSF treatment.Our results suggest that appropriate doses of G-CSF reduced atherosclerotic plaque formation and increased plaque stability in cholesterol-fed rabbits.
Malignancies that include hepatocellular carcinoma often occurred in patients with chronic liver disease. The aim of this retrospective match control study was to assess the cumulative development incidence and predictive factors for total malignancies in elderly Japanese patients with non-alcoholic hepatic diseases (NAFLD) or hepatitis C virus (HCV). A total of 1600 NAFLD patients with age of ≥60 years were enrolled, and 1600 HCV patients with age of ≥60 years were selected as control by matching 1:1 with NAFLD group for age, sex, and follow-up period. The primary goal is the first development of malignancies. Evaluation was performed by the use of the Wilcoxon rank sum test, the Kaplan-Meier method, and Cox proportional hazard model. The mean observation period is 8.2 years in both NAFLD and HCV group, respectively. The number of patients with the development of malignancies was 167 in the NAFLD group and 395 in the HCV group. The 10th development rate of malignancies was 13.9% in the NAFLD group and 28.2% in the HCV group (risk ratio 2.27; P < 0.001). The incident rates of hepatocellular carcinoma in all the malignancies were 6.0% (10/167) in the NAFLD group and 67.6% (267/395) in the HCV group (P < 0.001). The malignancies in the NAFLD group were observed in the following order: gastric cancer 34 cases (20.4%) > colon cancer 31 cases (18.6%) > prostate cancer 21 cases (12.6%). The incident rates of hepatocellular carcinoma in all the malignancies were approximately 6% in the NAFLD group and two-thirds in the HCV group.
