OBJECTIVE: To analyze the therapeutic effect of proton pump inhibitor(PPI) on alleviation of hoarseness symptoms in patients with laryngopharyngeal reflux(LPR). METHOD: The LPR outpatients in ENT department of our hospital(60 cases)complained of hoarseness were enrolled in the study from August of 2013 to October of 2014. All of them were randomly divided into group A and B. The individuals in group A (30 cases) taked golden voice capsule to treat for 3 months, while the individuals in group B (30 cases) taked golden voice capsule and omeprazole to treat for 3 months. The data about reflux symptom index (RSI), reflux finding score (RFS) and voice handicap index (VHI)from the first month to the third month after treatment were recorded and compared group A with group B. RESULT: The scores of RSI and RFS in patients (60 cases) before treatment were significantly correlated with their VHI (r=0. 823, P<0. 01; r=0. 873, P<0. 01). The score changes of RSI and VHI from the first to the third month after treatment in group B were significantly higher than those in group A (P<0. 01). Meanwhile, the score changes of RFS from the third month after treatment in group B were significantly higher than those in group A (t=8. 307, P<. 01), but the differences were not significant for RFS from the first to the second month after treatment between group A and group B(t=1. 128, P>0. 05; t=0. 376, P> 0. 05). CONCLUSION PPI therapy could significantly alleviate the hoarseness symptom in LPR patients.
Hoarseness ; drug therapy ; Humans ; Laryngopharyngeal Reflux ; drug therapy ; Proton Pump Inhibitors ; therapeutic use

OBJECTIVE: To analyze the role and significance of pepsin and pepsinogen in the pathogenesis of OME in children. METHOD: Pediatric patients with otitis media aged 2-8 years who enrolled in our department of the hospital from May of 2012 to December of 2012 were set as experimental group (38 cases, 48 ears) which should be underwent tympanic membrane puncture/tube insertion. Meanwhile, pediatric patients waiting for cochlear implant without otitis media (10 ears), were set as control group. Middle ear lavage fluid and plasma samples from the two groups were collected and detected using enzyme-linked immune method for pepsin and pepsinogen. RESULT: The concentrations of pepsin and pepsinogen in the middle ear lavage fluid of OME group [(48.8 ± 415.99) ng/ml and 676.32 ± 336.71)ng/ml] were significantly higher than those in the control group [(8.20 ± 4.59)ng/ml and (77.27 ± 50.33) ng/ml] (P < 0.01). Meanwhile, the concentration of pepsinogen in the middle ear lavage of OME patients was significantly higher than that of plasma (P < 0.01). The concentration of pepsin in the middle ear lavage fluid from the dry ear subgroup was lower than those in the serum ear and mucous ear subgroups (P < 0.01), but there was no significant difference about concentrations of pepsinogen among the dry ear, serum ear and mucous ear subgroups (P > 0.05). CONCLUSION Pepsin and pepsinogen in the middle ear cavity of OME patients maybe originated from laryngopharyngeal reflux (LPR), indicating that LPR is associated with the pathogenesis of OME in children.
Child ; Child, Preschool ; Ear, Middle ; metabolism ; Enzyme-Linked Immunosorbent Assay ; Humans ; Laryngopharyngeal Reflux ; physiopathology ; Otitis Media with Effusion ; metabolism ; Pepsin A ; metabolism ; Pepsinogen A ; metabolism ; Tympanic Membrane ; surgery

Objective: To investigate the association between plasma selenium exposure and the risk of impaired glucose regulation (IGR). Methods: A case-control study was conducted to select IGR patients who were admitted to the outpatient clinic of the Department of Endocrinology to perform oral glucose tolerance test(OGTT) at the Tongji Hospital affiliated to the Tongji Medical College from September 2004 to 2016 as a case group. Participants with normal glucose tolerance recruited from an unselected group of population undergoing routine health examinations in the same hospital were selected as a control group. The control group was matched according to the age (±5 years old) and sex of the case group. The inclusion criteria for subjects recruited were as follows: age ≥30 years, body mass index (BMI) <40 kg/m², no history of a diagnosis of IGR or type 2 diabetes, and no history of receiving pharmacological treatment for hyperlipidemia or hypertension. Patients with any clinically systemic disease such as neurological or endocrine disease, acute illness, chronic inflammatory disease or infectious disease were excluded from the study. A total of 1 957 subjects, 897 in the case group and 1 060 in the control group, were included. Questionnaires were used to collect information of all subjects, and peripheral venous blood was collected after fasting and OGTT, respectively. Plasma selenium, fasting blood glucose, blood lipid (total cholesterol, triglycerides, high density lipoprotein cholesterol, and low density lipoprotein cholesterol) and 2 h OGTT plasma glucose concentration were detected, respectively. The subjects were divided into low, medium and high concentration groups according to the tertiles of plasma selenium concentration in the control group. The multivariate unconditional logistic regression analysis was performed to analyze the association between plasma selenium exposure and IGR. Results: The age (mean±SD) of the case and control group was (53.71±11.38) and (53.95±12.17) years old. The plasma selenium concentration [M (P₂₅, P₇₅)] in the case group was 92.81(77.07, 107.05) μg/L, which was significantly higher than the control group [88.73 (77.13, 100.88) μg/L] (P<0.05). The results of multivariate unconditional logistic regression analysis showed that after adjusting for age, sex, BMI, family history of diabetes and hypertension, the risk of IGR was higher in the high-concentration group and the low-concentration group compared with the middle-concentration group, the values of OR (95%CI) were 1.22 (95%CI: 0.94-1.59) and 1.81 (95%CI: 1.42-2.30), respectively. Conclusion The study suggested a U-shaped association between plasma selenium and IGR.

Objective To investigate the association between plasma selenium exposure and the risk of impaired glucose regulation (IGR). Methods A case?control study was conducted to select IGR patients who were admitted to the outpatient clinic of the Department of Endocrinology to perform oral glucose tolerance test(OGTT) at the Tongji Hospital affiliated to the Tongji Medical College from September 2004 to 2016 as a case group. Participants with normal glucose tolerance recruited from an unselected group of population undergoing routine health examinations in the same hospital were selected as a control group. The control group was matched according to the age (±5 years old) and sex of the case group. The inclusion criteria for subjects recruited were as follows: age≥30 years, body mass index (BMI)<40 kg/m2, no history of a diagnosis of IGR or type 2 diabetes, and no history of receiving pharmacological treatment for hyperlipidemia or hypertension. Patients with any clinically systemic disease such as neurological or endocrine disease, acute illness, chronic inflammatory disease or infectious disease were excluded from the study. A total of 1 957 subjects, 897 in the case group and 1 060 in the control group, were included. Questionnaires were used to collect information of all subjects, and peripheral venous blood was collected after fasting and OGTT, respectively. Plasma selenium, fasting blood glucose, blood lipid (total cholesterol, triglycerides, high density lipoprotein cholesterol, and low density lipoprotein cholesterol) and 2 h OGTT plasma glucose concentration were detected, respectively. The subjects were divided into low, medium and high concentration groups according to the tertiles of plasma selenium concentration in the control group. The multivariate unconditional logistic regression analysis was performed to analyze the association between plasma selenium exposure and IGR. Results The age (mean± SD) of the case and control group was (53.71± 11.38) and (53.95±12.17) years old. The plasma selenium concentration [M (P25, P75)] in the case group was 92.81(77.07, 107.05) μg/L, which was significantly higher than the control group [ 88.73 (77.13, 100.88) μg/L] (P<0.05). The results of multivariate unconditional logistic regression analysis showed that after adjusting for age, sex, BMI, family history of diabetes and hypertension, the risk of IGR was higher in the high?concentration group and the low?concentration group compared with the middle?concentration group, the values of OR (95%CI) were 1.22 (95%CI: 0.94-1.59) and 1.81 (95%CI: 1.42-2.30), respectively. Conclusion The study suggested a U?shaped association between plasma selenium and IGR.

Objective To investigate the association between plasma selenium exposure and the risk of impaired glucose regulation (IGR). Methods A case?control study was conducted to select IGR patients who were admitted to the outpatient clinic of the Department of Endocrinology to perform oral glucose tolerance test(OGTT) at the Tongji Hospital affiliated to the Tongji Medical College from September 2004 to 2016 as a case group. Participants with normal glucose tolerance recruited from an unselected group of population undergoing routine health examinations in the same hospital were selected as a control group. The control group was matched according to the age (±5 years old) and sex of the case group. The inclusion criteria for subjects recruited were as follows: age≥30 years, body mass index (BMI)<40 kg/m2, no history of a diagnosis of IGR or type 2 diabetes, and no history of receiving pharmacological treatment for hyperlipidemia or hypertension. Patients with any clinically systemic disease such as neurological or endocrine disease, acute illness, chronic inflammatory disease or infectious disease were excluded from the study. A total of 1 957 subjects, 897 in the case group and 1 060 in the control group, were included. Questionnaires were used to collect information of all subjects, and peripheral venous blood was collected after fasting and OGTT, respectively. Plasma selenium, fasting blood glucose, blood lipid (total cholesterol, triglycerides, high density lipoprotein cholesterol, and low density lipoprotein cholesterol) and 2 h OGTT plasma glucose concentration were detected, respectively. The subjects were divided into low, medium and high concentration groups according to the tertiles of plasma selenium concentration in the control group. The multivariate unconditional logistic regression analysis was performed to analyze the association between plasma selenium exposure and IGR. Results The age (mean± SD) of the case and control group was (53.71± 11.38) and (53.95±12.17) years old. The plasma selenium concentration [M (P25, P75)] in the case group was 92.81(77.07, 107.05) μg/L, which was significantly higher than the control group [ 88.73 (77.13, 100.88) μg/L] (P<0.05). The results of multivariate unconditional logistic regression analysis showed that after adjusting for age, sex, BMI, family history of diabetes and hypertension, the risk of IGR was higher in the high?concentration group and the low?concentration group compared with the middle?concentration group, the values of OR (95%CI) were 1.22 (95%CI: 0.94-1.59) and 1.81 (95%CI: 1.42-2.30), respectively. Conclusion The study suggested a U?shaped association between plasma selenium and IGR.

There is no unified international guidelines or consensus on seizures and epilepsy following acute stroke reperfusion therapy so far.In this review,we briefly summarize its definitions and mechanisms.Post stroke epilepsy after reperfusion treatment is defined as patients with ischemic stroke who have received intravenous thrombolysis and/or endovascular therapy,without other definitive causes or epilepsy history before stroke,have at least two epileptic seizures occurred within 7 days of stroke onset,or at least one epileptic seizures occurred within 30 days of stroke onset.The incidence rate of epilepsy after intravenous thrombolysis is about 6.4%-20.6%,and arterial thrombectomy is about 5%.The pathophysiological mechanism of post stroke epilepsy after reperfusion treatment may be related to local hyperfusion,epileptogenic properties of tPA and hemorrhagic transformation.Higher stroke severity,cortical involvement,middle cerebral artery infarction,and early post-stroke seizures may be predictive factors for post-stroke epilepsy after reperfusion therapy.Levetiracetam and lamotrigine may be effective drugs for post-stroke epilepsy after reperfusion therapy.Sustained seizures after thrombolysis may increase the risk of death.