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Objective:To investigate the relationship between pancreatic fibrotic marker transforming growth factor-β(TGF-β) and platelet derived growth factor-BB(PDGF-BB) and serum glycated hemoglobin (HbA1c) levels in patients with type 3c diabetes mellitus secondary to chronic pancreatitis(CP-T3cDM).Methods:The clinical data of 39 patients with CP-T3cDM admitted to the Department of Gastroenterology of the First Affiliated Hospital of Naval Medical University between February 2018 and August 2020 were collected, and the patients' age, gender, body mass index, duration of chronic pancreatitis and diabetes mellitus, smoking history, alcohol consumption history, serum HbA1c level at admission, degree of pancreatic atrophy, morphology of the main pancreatic duct, and treatment of diabetes mellitus were recorded. Serum TGF-β and PDGF-BB were detected by ELISA. Patients were divided into high and low level group according to the median TGF-β and PDGF-BB levels, respectively. Clinical characteristics of patients were compared between the TGF-β and PDGF-BB high and low level group. The correlation between TGF-β, PDGF-BB and HbA1c was analyzed by Spearman's correlation analysis.Results:A total of 39 CP-T3cDM patients were included; 35 were male and 4 were female. The age of first onset of chronic pancreatitis was (42±14) years old, and the duration of diabetes mellitus was 24(4, 36) months. The serum HbA1c level was (7.8±1.6)%, and the serum TGF-β and PDGF-BB levels were 20.5(10.5, 43.1) and 647.5(276.9, 1349.2)pg/ml, respectively. The serum HbA1c levels of patients in the high-level group of serum TGF-β and PDGF-BB were significantly higher than those in the corresponding low-level group [8.6%(7.4%, 9.9%) vs 6.7%(6.2%, 7.8%) and 8.6%(7.4%, 9.6%) vs 6.7%(6.1%, 7.8%), respectively] , and the difference was statistically different (both P value <0.01), while none of other indicators showed statistically significant differences between both groups. The correlation analysis showed that the levels of TGF-β and PDGF-BB were significantly positively correlated with HbA1c level ( r=0.45, 0.53, both P value <0.01). Conclusions:Increased pancreatic fibrosis in patients with CP-T3cDM was an important factor contributing to elevated blood glucose level. Patients with higher serum pancreatic fibrotic factors exhibited a significant increase in HbA1c level.
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Objective To study the clinical type and features of cerebral watershed infarction (CWI)in eldedy patients and its relationship with plasma lysophosphatidic acid(LPA).Method Analyzed the clinical data of 106 cases of CWI patients(CWI group)confirmed by cranial MRI,and compared plasma LPA levels in patients with different types of CWI,non-CWI patients(non-CWI group,36 cases)and healthy controls(control group,32 cases).Results In CWI group,anterior-cortex type 22 cases,LPA(4.93±0.72)μmol/L,posterior-cortex type 17 cases,LPA(4.75±0.81)μmoi/L,subcortical type 47 cases,LPA (5.46±1.03)μmol/L,mixed type 20 cages,LPA(6.02±1.12)μmol/L.In non-CWIgroup,LPA(5.37±1.24)μmol/L.In control group,LPA(2.92 ±0.36)μmol/L.The levels of LPA significandy increased in various types of CWI(P<0.05 or<0.01).of which mixed type and subcortical type were the highest,and the level of LPA in mixed type WaS higher than that in anterior-cortex type and posterior-cortex type(P<0.05).The level of LPA in non-CWI group was higher than that in control group,but there wss no significant difference compared with various types of CWI.Conclusions Subcortical type is the primal type in elderly CWI patients,the main cause of which is the atherosclerotic plaque formation and lumen stenosis.Platelet activation and its microemboli play an important role in the pathophysiology.LPA levels are significantly higher in various types of CWI,of which mixed type is the highest.LPA can be used as an important molecular marker to guide the sub-type treatment of CWI in elderly patients.
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Objective To observe the effects of different antithrombotic interventions on the changes of plasma lysophosphatidic acid (LPA) level in patients with nonvalvular atrial fibrillation (NVAF) and to provide the basis for clinical antithrombotic therapy. Methods A total of 235 patients with NVAF who did not receive antithrombotic therapy diagnosed by clinical and auxiliary examinations were randomly allocated to receive aspirin (100 mg/d) plus dipyridamole (100 mg/d) (n =76), aspirin (100 mg/d) plus fixed-dose warfarin (1.25 mg/d) (n =79), and dose-adjusted warfarin (international normalized ratio (INR) range of 1.5 to 2. 1) (n =80). They gore redivided into <60, 60-75, and ≥76 year-old groups according to their age. The plasma LPA levels were measured and compared before treatment and 2 and 6 weeks after treatment. Results 1he plasma LPA levels were decreased more significantly in the aspirin plus fixed-dose group than those in the aspirin plus dipyridamole and dose-adjusted warfarin groups (all P < 0.01). Two and 6 weeks after treatment with aspirin plus dipyridamole in the < 60 year-old group, the plasma LPA levels were significantly lower than those before treatment (all P<0. 01). Two and6 weeks after treatment with aspirin plus fixed-dose warfarin in the < 60 year-old group, the plasma LPA levels were significantly lower than those before treatment (all P <0. 01). Two and 6 weeks after treatment with aspirin plus fixed-dose warfarin in the 60-75 year-old group, the plasma LPA levels were significantly lover than those before treatment (all P <0.01). Two and 6 weeks after the treatment with dose-adjusted warfarin (INR 1.5-2. 1) in patients in each age group, the plasma LPA levels were significantly lower than those before treatment. Conclusions 1he different antithromhotic therapeutic modalities have different effects on platelet activation in patients with NVAF in different age groups. The patients in the < 60 year-old group can receive aspirin plus dipyridamole, the patients in the < 75 year-old group can receive aspirin plus fix-dose warfarin, and the patients > 75 year-old, dose-adjusted warfarin (INR 1. 5-2. 1) should he recommend.
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Objective To investigate the changes of plasma lysephosphatidic acid (LPA) or acidic phospholipids (AP) levels in patients with nonvalvular atrial fibrillation(NVAF) or NVAF associated with silent brain infarction (SBI) and to provide biochemistry evidence to antithrombotic therapy. Methods Plasma LPA/AP levels was examined in blood freshly sampled in 235 cases of NVAF who were not receiving any antithrombotic therapy, 116 cases SBI who were not with NVAF and 120 cases healthy volunteers as control enrolled in the LPA and stroke prevention study. Plasma LPA was assayed by measuring its inorganic phosphorus after separation by chromatograph. Meanwhile, the platelet activation in NVAF or (and) SBI were observed. Results SBI was found in 31.5% of the participants with NVAF, and in 37.6% of the elderly NVAF subjects (age60 years old). LPA/AP levels were significantly increased in NVAF with SBI group((3.78±0.61) μmol/L) compared with controls ((2.66±0.49) μmol/L, 95% CI 3.47-4.21,P = 0.000), NVAF without SBI group ((3.29±0.57) μmol/L, 95 % CI 3.01-3.76, P = 0.008), SBI without NVAF group((3.17±0.54) μmol/L, P=0.004). The platelet activation was significantly higherin NVAF with SBI group, the odds ratio (95% CI) was 21.39(10.17 to 45.02),than those in NVAF without SBI group (P<0.01). Conclusion The plasma LPA/AP levels were significantly elevated in NVAF or NVAF with SBI, NVAF contributes to the risk of SBI. Platelet activation may play an important role in the pathogenesis of thromboembolism in NVAF and the measurement of LPA reflects activation of platelets in vivo and may be a useful marker for the diagnosis of thrombosis or prothrombotic states.Consideration of the role of antiplatelet therapy should be given when choosing antithrombotic therapy to NVAF-associated ischemic stroke.
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To observe whether plasma levels of lysophosphatidic acid (LPA) can be decreased in patients with cerebrovascular diseases after the treatment with aspirin. Methods:A total of 1,400 patients were recruited. Among them,803 patients were diagnosed as probable ischemic stroke,and 343 patients were diagnosed as ischemic stroke. Thirty-four health volunteers were used as control subjects. The levels of LPA were measured by chromatography with the combination of inorganic phosphorus quantitative method. Results: The levels of LPA in the ischemic cerebrovascular group (3.11 ± 1.55 μmol/L) were significantly higher than those in the control group (1.77 ± 1.04 μmol/L) (P < 0.001). Taking aspirin (80 mg,qd) for one month significantly decreased the levels of LPA. After stopping aspirin for one month,the level of LPA re-elevated (3.90 ± 1.09 μmol/L),was higher than that during administration of aspirin (1.93 ±0.85 μmol/L(P <0.001). Conclusions: There are close correlations between the increased levels of LPA and the platelet activation. Aspirin decreases the level of plasma LPA;this may be one of the mechanisms of aspirin in prevention against ischemic stroke.