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Objective:To evaluate the value of endogenous digitalis-like factor (EDLF) dynamic changes in predicting myocardial injury and prognosis in patients with sepsis.Methods:A total of 160 sepsis patients admitted to the emergency department of Beijing Friendship Hospital Affiliated to Capital Medical University from July 2017 to January 2019 were selected and divided into the myocardial injury(MI) group ( n=75) and the non-myocardial injury (NMI) group ( n=85) according to whether there was myocardial injury. The plasma EDLF concentration was tested on the 1 st, 3 rd and 7 th day after admission. The predictive factors of MI and 90-days outcome were evaluated by logistics regression analysis. Cox proportional hazards regression model was used to estimate the prognostic value of EDLF concentration on the 90 days after admission for sepsis. Results:Septic patients with MI had increased levels of myocardial enzymes, decreased left ventricular fractional shortening index (FS) and interventricular septum (IVS) amplitude and abnormal wall motion, when compared to NMI patients (all P<0.05). EDLF concentration on the 7 th day in the MI group was significantly lower than in the NMI group ( P=0.019). Logistic regression showed that EDLF 7 th was an independent protective factor for MI and 90-day mortality in sepsis respectively ( OR=0.964, 95% CI: 0.934-0.994, P=0.021; OR=0.931, 95% CI: 0.871-0.995, P=0.036). Cox proportional hazards regression analysis suggested that EDLF 7 th concentration <26.7 pmol/L was an independent predictor of 90-day mortality in patients with sepsis ( HR=4.601, 95% CI: 1.030-20.563, P=0.046). Conclusions:EDLF 7 th may serve as a protective factor for sepsis-induced MI and adverse outcome. The exogenous supplement of cardiotonic drugs at one week after MI may be a potential treatment to improve the survival rate of septic patients.
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Patient one was a 19-year-old woman of periodic fever with urticaria during the first week of life.And there were typicalfacies,oligoarthritis and central nervous system involvement.She also exhibited a persistent elevation of acute phase reactants.The diagnosis of chronic infantile neurological cutaneous and articular syndrome was made.Short-term dosing of tumor necrosis factor-α receptor antagonist was administrated and was substituted by glucocorticoid and methotrexate.Another two males had an earlyonset of increased acute phase reactants during inflammation attacks.One of them had recurrent fever with urticaria-like rash,arthralgia and headache.Muckle-Wells syndrome was diagnosed on basis of NLRP3 gene mutation (c.92A ＞ T).And another had recurrent urticaria-like rash with conjunctivitis,oligoarthritis,hepatosplenomegaly and increased serum IgD.The clinical diagnosis was mevalonate-kinase deficiency.Autoinflammatory diseases should be suspected by physicians and diagnosed with a combination of phenotype and genotype.Biological agents,especially interleukin-1 antagonist,have broad prospects in the therapy of autoinflammatory diseases.
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Objective To investigate the effects of β1-adrenergic receptor autoantibodies (β1-AA) on the proliferation of different subtypes of T lymphocytes in patients with heart failure .Methods β1-AA-positive IgG antibodies isolated from patients with heart failure were purified by using affinity chromatog -raphy.CD3 +CD4 +T and CD3 +CD8 +T lymphocytes were sorted by flow cytometry analysis .The prolifera-tion of different subtypes of T lymphocytes was tested by using CCK-8 kit.Tests for lactate dehydrogenase ( LDH) level and cell apoptosis were performed to evaluate T lymphocytes damage .Results The prolifera-tion of activated lymphocytes was inhibited by β1-AA isolated from the serum of patients with heart failure in a concentration dependent manner , but it could be blocked by β1 receptor blocker .The damage of lympho-cytes induced by β1-AA was increased.Moreover, β1-AA promoted the necrosis and apoptosis of CD 3 +CD4 +T and CD3 +CD8 +T lymphocytes and thus inhibited the proliferation of them .Conclusion β1-AA isolated from the serum of patients with heart failure inhibited the proliferation of CD 3 +CD4 +T and CD3 +CD8 +T lymphocytes through increasing the necrosis and apoptosis of them .This study suggests that β1-AA might induce immune disorders in addition to causing pathological changes in heart tissues .