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Objective:To observe and compare the clinical characteristics between post-chronic pancreatitis diabetes mellitus(PPDM-C)patients and type 2 diabetes mellitus(T2DM).Methods:Data of 142 cases of CP patients confirmed in Shanghai Pudong New Area Gongli Hospital from January 2018 to December 2021 were collected, all the patients were divided into CP group without diabetes mellitus ( n=60) and PPDM-C group with diabetes mellitus ( n=82) based on whether with or without diabetes mellitus. And 82 cases T2DM without CP (T2DM group, n=82) hospitalized simultaneously were collected as control group. The age, sex, body mass index, onset characteristics, laboratory examination indicators at admission (fasting blood glucose, glycosylated hemoglobin, blood creatinine, and alanine transaminase), imaging characteristics of the pancreas (pancreatic atrophy, multiple calcifications of the pancreas, pancreatic duct stones, pancreatic duct dilation, and pancreatic duct obstruction), and treatments and efficacy of diabetes were recorded. Results:Compared with T2DM group, PPDM-C group had lower body mass index (22.2 kg/m 2vs 24.6 kg/m 2), and glycosylated hemoglobin levels (7.34% vs 9.20%) (all P values <0.001), higher alanine transaminase levels (33.00 U/L vs 18.65 U/L, P =0.021). And they had more upper abdominal pain, nausea, vomiting, weight loss and diarrhea symptoms. In addition, they had less use of combination of insulin and hypoglycemic drugs to control blood glucose. And compared with CP group, PPDM-C group had higher body mass index (22.06 kg/m 2vs 21.18 kg/m 2), higher glycosylated hemoglobin levels (7.34% vs 5.70%), higher fasting blood-glucose levels (7.91 mmol/l vs 5.31 mmol/l), higher alanine transaminase levels (33.00 U/L vs 26.50U/L), and their differences were statistically significant (all P values <0.05). And they had higher incidence of pancreatic atrophy, multiple calcifications in the pancreatic duct and pancreatic duct obstruction (all P values <0.05). Conclusions:PPDM-C patients are more likely to experience digestive system symptoms such as abdominal pain than T2DM patients, while their pancreatic malfunction is more likely to occur compared to CP patients. More attentions to PPDM-C associated clinical manifestations, biochemical and imaging changes could identify patients at potential risk for early diagnosis and treatment earlier.
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Objective:To explore auxiliary therapeutic effect of exercise intervention on hypertension and/or diabetes mellitus (DM) .Methods :A total of 456 patients with hypertension and/or DM from community were selected and randomly equally divided into intervention group (n=228 ,wore exercise amount monitor ,and lifestyle disease inte‐grated control software was used to monitor exercise ,and unique person provided quantitative exercise guidance for them for three months and they were followed up for eight times ) and control group (n=228 ,did routine activity as usual) .Body weight ,BMI ,waist circumference (WC) ,blood pressure ,blood sugar ,blood lipid etc .and exercise a‐mount were measured and compared between two groups before and after intervention .Results:Compared with be‐fore intervention ,there were no significant changes in all above indexes in control group after intervention , P>0.05 all;there were significant reductions in body weight ,BMI ,WC ,blood pressure ,blood sugar ,blood lipid etc . in intervention group after intervention ( P< 0.01 all) .After intervention ,compared with control group , there were significant reductions in body weight [ (68.28 ± 8.43) kg vs . (65.93 ± 10.43) kg] ,blood pressure [ (124.32 ± 13.70 /77.81 ± 8.22) mmHg vs . (120.94 ± 8.35 /74.58 ± 5.76) mmHg] ,HbA1c [ (7.12 ± 1.53) mmol/L vs . (6.73 ± 1.04) mmol/L] ,LDL‐C [ (2.72 ± 0.40) mmol/L vs . (2.46 ± 0.67) mmol/L] ,and significant rose in total exercise amount [ (537.85 ± 338.63) kcal vs .(637.15 ± 447.65) kcal] ,effective exercise amount [ (229.46 ± 239.04) kcal vs . (323.56 ± 257.84) kcal] in intervention group ,P<0.01 all .Conclusion:Exercise can improve ex‐ercise capacity ,reduce blood pressure ,blood sugar ,blood lipid levels ,is help to disease control and quality of life improvement in patients with hypertension and/or diabetes mellitus .
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Objectives To analyze the role and mechanisms of mast cells in the inflammation and fibrosis of 2 ,4, 6-trinitrobenzene sulfonic acid (TNBS)-induced rat pancreatic fibrosis. Methods Rats were received the aseptic instillation of TNBS in ethanol via bilo-pancreatic duct, and then injected with nedocromil sodium, a mast cell stabilizer, and compound 18/80, a mast cell activator, or saline. Rats were sacrificed respectively on 3, 7, 14, 21 or 28 days. Pancreatic inflammation and fibrosis were assessed by gross and histopathological evaluation. Pancreatic fibrosis were observed by Van Gieson. Pancreatic mast cells distribution, number and their state of activation (toluidine blue) were evaluated. The activation of pancreatic stellate cells (PSCs) were assessed by the expression of a-smooth muscle actin (?-SMA) through immunohistochemistry. The expression of angiotensin Ⅱ AT1 and AT2 receptors and transforming growth factor (TGF) ? 1 raRNA, which were the factors of fibrogenesis, were also assessed. Results Typical pancreatic fibrosis changes occurred in the model of rats received TNBS at 4th week by morphological evaluation. The positive expression of ?-SMA and TGF?1 in the pancreatic tissues were detected at day 3, especially at 4th week. The expression of angiotensin Ⅱ AT1 and AT2 receptors mRNA increased gradually in all the three groups, also especially at 4th week. Compared to the control group, there were more higher expression of ?-SMA, TGF?1, angiotensin Ⅱ AT1 and AT2 receptor in the compound 48/80 group, while there were lower expression of these proteins in the nedocromil group. Conclusions Mast cells are involved in TNBS-induced pancreatic inflammation and fibrosis in rats. After being activated, mast cells will promote the activation and proliferation of PSCs and upregulate the expression of angiotensin Ⅱ AT1 receptor and AT2 receptor, and then lead to pancreatic fibrosis gradually.