TY  - JOUR
A1  - Chen, You-Peng
A1  - Li, Jian
A1  - Wang, Zi-Neng
A1  - Reichetzeder, Christoph
A1  - Xu, Hao
A1  - Gong, Jian
A1  - Chen, Guang-Ji
A1  - Pfab, Thiemo
A1  - Xiao, Xiao-Min
A1  - Hocher, Berthold
T1  - Renin angiotensin aldosterone system and glycemia in pregnancy
JF  - Clinical laboratory : the peer reviewed journal for clinical laboratories and laboratories related to blood transfusion
N2  - Background: The renin-angiotensin-aldosterone system (RAAS) is involved in the pathogenesis of insulin resistance and type 2 diabetes in the general population. The RAAS is activated during pregnancy. However, it is unknown whether the RAAS contributes to glycemia in pregnant women.
 Methods: Plasma renin activity (PRA) and plasma aldosterone levels were quantified at delivery in 689 Chinese mothers. An oral glucose tolerance test in fasted women was performed in the second trimester of pregnancy. The diagnosis of gestational diabetes mellitus (GDM) and impaired glucose tolerance during pregnancy were made according to the guidelines of the Chinese Society of Obstetrics.
 Results: Plasma aldosterone was significantly higher in pregnant women with GDM as compared to those without impairment of glycemic control (normal pregnancies: 0.27 +/- 0.21 ng/mL, GDM: 0.36 +/- 0.30 ng/mL; p<0.05). Regression analyses revealed that PRA was negatively correlated with fasting blood glucose (FBG) (R-2 = 0.03, p = 0.007), whereas plasma aldosterone and aldosterone/PRA ratio were positively correlated with FBG (R-2 = 0.05, p<0.001 and R-2 = 0.03, p = 0.007, respectively). Multivariable regression analysis models considering relevant confounding factors confirmed these findings.
 Conclusions: This study demonstrated that fasting blood glucose in pregnant women is inversely correlated with the PRA, whereas plasma aldosterone showed a highly significant positive correlation with fasting blood glucose during pregnancy. Moreover, plasma aldosterone is significantly higher in pregnant women with GDM as compared to those women with normal glucose tolerance during pregnancy. Although causality cannot be proven in association studies, these data may indicate that the RAAS during pregnancy contributes to the pathogenesis of insulin resistance/new onset of diabetes during pregnancy.
KW  - Renin-angiotensin-aldosterone system
KW  - pregnancy
KW  - fasting blood glucose
KW  - glycemic control
Y1  - 2012
SN  - 1433-6510
VL  - 58
IS  - 5-6
SP  - 527
EP  - 533
PB  - Clin Lab Publ., Verl. Klinisches Labor
CY  - Heidelberg
ER  - 
TY  - JOUR
A1  - Chen, You-Peng
A1  - Lu, Yong-Ping
A1  - Li, Jian
A1  - Liu, Zhi-Wei
A1  - Chen, Wen-Jing
A1  - Liang, Xu-Jing
A1  - Chen, Xin
A1  - Wen, Wang-Rong
A1  - Xiao, Xiao-Min
A1  - Reichetzeder, Christoph
A1  - Hocher, Berthold
T1  - Fetal and maternal angiotensin (1-7) are associated with preterm birth
JF  - Journal of hypertension
N2  - Background: Recent studies show that preterm birth is associated with hypertension in later life. The renin-angiotensin system (RAS) during pregnancy influences fetal growth and development. In the current study, we investigated the impact of fetal as well as maternal angiotensin (1-7) [Ang (1-7)] and angiotensin II (Ang II) plasma concentrations on the risk of preterm birth.
 Methods: Three hundred and nine pregnant women were prospectively included into the study. The pregnant women were divided into two groups, for example, preterm birth of lower than 37 gestational weeks (n = 17) and full-term birth of 37 gestational weeks or more (n = 292). Maternal and neonatal plasma Ang (1-7) and Ang II concentrations were analyzed at birth from maternal venous blood and umbilical cord blood, respectively. Risk factors for premature birth were determined by multiple logistic regression analysis.
 Results: Fetal and maternal plasma Ang (1-7) concentrations in the preterm group were lower than those of the term group fetal Ang (1-7) preterm birth: 486.15 +/- 337.34 ng/l and fetal Ang (1-7) term birth: 833.84 +/- 698.12 ng/l and maternal Ang (1-7) preterm birth: 399.86 +/- 218.93 ng/l; maternal Ang (1-7) term birth: 710.34 +/- 598.22 ng/l. Multiple logistic regression analysis considering confounding factors revealed that preeclampsia (P < 0.001), premature rupture of membranes (P = 0.001), lower concentration of maternal Ang (1-7) (P = 0.013) and fetal plasma Ang (1-7) (P = 0.032) were independently associated with preterm birth. We could furthermore demonstrate that the maternal Ang (1-7)/Ang II ratio is independently associated with gestational hypertension or preeclampsia, factors causing preterm birth.
 Conclusions: Lower concentrations of maternal and fetal Ang (1-7) are independently associated with preterm birth - a risk factor of hypertension in later life.
KW  - angiotensin (1-7)
KW  - angiotensin II
KW  - cardiovascular disease
KW  - fetal programming
KW  - intrauterine fetal growth
KW  - pregnancy
KW  - preterm delivery
Y1  - 2014
U6  - https://doi.org/10.1097/HJH.0000000000000251
SN  - 0263-6352
SN  - 1473-5598
VL  - 32
IS  - 9
SP  - 1833
EP  - 1841
PB  - Lippincott Williams & Wilkins
CY  - Philadelphia
ER  - 
TY  - JOUR
A1  - Li, Jian
A1  - Chen, You-Peng
A1  - Wang, Zi-Neng
A1  - Liu, Tie-Bin
A1  - Chen, Dan
A1  - Dong, Yun-Peng
A1  - Hocher, Berthold
T1  - A functional fetal HSD11B2[CA]n microsatellite polymorphism is associated with maternal serum cortisol concentrations in pregnant women
JF  - Kidney & blood pressure research : official organ of the Gesellschaft für Nephrologie
N2  - Background/Aims: Cortisol plays an important role during pregnancy. It controls maternal glucose metabolism and fetal development. Cortisol metabolism is partially controlled by the 11b-HSD2. This enzyme is expressed in the kidney and human placenta. The activity of the enzyme is partially controlled by functional polymorphisms: the HSD11B2[CA]n microsatellite polymorphism. The impact of this functional gene polymorphism on cortisol metabolism and potential effects on the newborn's is unknown so far. Methods: In the current prospective birth cohort study in southern Asia, we analyzed the association of the HSD11B2[CA]n microsatellite polymorphisms in 187 mothers and their newborn's on maternal and newborn's serum cortisol concentrations. Results: Using multivariable regression analyses considering known confounding ( gestational age, newborn's gender, the labor uterine contraction states and the timing during the day of blood taking), we showed that the fetal HSD11B2[CA]n microsatellite polymorphisms in the first intron was related to maternal cortisol concentration ( R2=0.26, B=96.27, p=0.007), whereas as the newborn's cortisol concentrations were independent of fetal and maternal HSD11B2[CA] n microsatellite polymorphism. Conclusions: Our study showed for the first time that the fetal HSD11B2[CA]n microsatellite polymorphism of the HSD11B2 gene in healthy uncomplicated human pregnancy is associated with maternal cortisol concentration. This indicates that fetal genes controlling cortisol metabolism may affect maternal cortisol concentration and hence physiology in healthy pregnant women.
KW  - Pregnancy
KW  - Placenta
KW  - Cortisol vertical bar metabolism
KW  - 11 beta-hydroxysteroid dehydrogenase 2
KW  - HSD11B2[CA]n polymorphism
Y1  - 2013
U6  - https://doi.org/10.1159/000355761
SN  - 1420-4096
SN  - 1423-0143
VL  - 38
IS  - 1
SP  - 132
EP  - 141
PB  - Karger
CY  - Basel
ER  - 
TY  - JOUR
A1  - Reichetzeder, Christoph
A1  - Chen, Hong
A1  - Foeller, Michael
A1  - Slowinski, Torsten
A1  - Li, Jian
A1  - Chen, You-Peng
A1  - Lang, Florian
A1  - Hocher, Berthold
T1  - Maternal vitamin D deficiency and fetal programming - lessons learned from humans and mice
JF  - Kidney & blood pressure research : official organ of the Gesellschaft für Nephrologie
N2  - Background/Aims: Cardiovascular disease partially originates from poor environmental and nutritional conditions in early life. Lack of micronutrients like 25 hydroxy vitamin D-3 (25OHD) during pregnancy may be an important treatable causal factor. The present study explored the effect of maternal 25OHD deficiency on the offspring. Methods: We performed a prospective observational study analyzing the association of maternal 25OHD deficiency during pregnancy with birth outcomes considering confounding. To show that vitamin D deficiency may be causally involved in the observed associations, mice were set on either 25OHD sufficient or insufficient diets before and during pregnancy. Growth, glucose tolerance and mortality was analyzed in the F1 generation. Results: The clinical study showed that severe 25OHD deficiency was associated with low birth weight and low gestational age. ANCOVA models indicated that established confounding factors such as offspring sex, smoking during pregnancy and maternal BMI did not influence the impact of 25OHD on birth weight. However, there was a significant interaction between 25OHD and gestational age. Maternal 25OHD deficiency was also independently associated with low APGAR scores 5 minutes postpartum. The offspring of 25OHD deficient mice grew slower after birth, had an impaired glucose tolerance shortly after birth and an increased mortality during follow-up. Conclusions: Our study demonstrates an association between maternal 25OHD and offspring birth weight. The effect of 25OHD on birth weight seems to be mediated by vitamin D controlling gestational age. Results from an animal experiment suggest that gestational 25OHD insufficiency is causally linked to adverse pregnancy outcomes. Since birth weight and prematurity are associated with an adverse cardiovascular outcome in later life, this study emphasizes the need for novel monitoring and treatment guidelines of vitamin D deficiency during pregnancy.
KW  - Vitamin D
KW  - Birth weight
KW  - Preterm delivery
KW  - Fetal programming
KW  - Glucose tolerance
KW  - Cardiovascular diseases
Y1  - 2014
U6  - https://doi.org/10.1159/000355809
SN  - 1420-4096
SN  - 1423-0143
VL  - 39
IS  - 4
SP  - 315
EP  - 329
PB  - Karger
CY  - Basel
ER  - 
TY  - CHAP
A1  - Chen, Hong
A1  - Reichetzeder, Christoph
A1  - Föller, Michael
A1  - Slowinski, Torsten
A1  - Li, Jian
A1  - Chen, You-Peng
A1  - Lang, Florian
A1  - Hocher, Berthold
T1  - Maternal vitamin D deficiency and fetal programming
T2  - Acta physiologica : official journal of the Federation of European Physiological Societies
Y1  - 2015
SN  - 1748-1708
SN  - 1748-1716
VL  - 213
SP  - 155
EP  - 156
PB  - Wiley-Blackwell
CY  - Hoboken
ER  - 
TY  - JOUR
A1  - Chen, Jian
A1  - Stöcklein, Walter F. M.
A1  - Scheller, Frieder W.
A1  - Wollenberger, Ursula
T1  - Electrochemical determination of human hemoglobin by using ferrocene carboxylic acid modified carbon powder microelectrode
Y1  - 2003
ER  - 
TY  - JOUR
A1  - Middeldorp, Christel M.
A1  - Mahajan, Anubha
A1  - Horikoshi, Momoko
A1  - Robertson, Neil R.
A1  - Beaumont, Robin N.
A1  - Bradfield, Jonathan P.
A1  - Bustamante, Mariona
A1  - Cousminer, Diana L.
A1  - Day, Felix R.
A1  - De Silva, N. Maneka
A1  - Guxens, Monica
A1  - Mook-Kanamori, Dennis O.
A1  - St Pourcain, Beate
A1  - Warrington, Nicole M.
A1  - Adair, Linda S.
A1  - Ahlqvist, Emma
A1  - Ahluwalia, Tarunveer Singh
A1  - Almgren, Peter
A1  - Ang, Wei
A1  - Atalay, Mustafa
A1  - Auvinen, Juha
A1  - Bartels, Meike
A1  - Beckmann, Jacques S.
A1  - Bilbao, Jose Ramon
A1  - Bond, Tom
A1  - Borja, Judith B.
A1  - Cavadino, Alana
A1  - Charoen, Pimphen
A1  - Chen, Zhanghua
A1  - Coin, Lachlan
A1  - Cooper, Cyrus
A1  - Curtin, John A.
A1  - Custovic, Adnan
A1  - Das, Shikta
A1  - Davies, Gareth E.
A1  - Dedoussis, George V.
A1  - Duijts, Liesbeth
A1  - Eastwood, Peter R.
A1  - Eliasen, Anders U.
A1  - Elliott, Paul
A1  - Eriksson, Johan G.
A1  - Estivill, Xavier
A1  - Fadista, Joao
A1  - Fedko, Iryna O.
A1  - Frayling, Timothy M.
A1  - Gaillard, Romy
A1  - Gauderman, W. James
A1  - Geller, Frank
A1  - Gilliland, Frank
A1  - Gilsanz, Vincente
A1  - Granell, Raquel
A1  - Grarup, Niels
A1  - Groop, Leif
A1  - Hadley, Dexter
A1  - Hakonarson, Hakon
A1  - Hansen, Torben
A1  - Hartman, Catharina A.
A1  - Hattersley, Andrew T.
A1  - Hayes, M. Geoffrey
A1  - Hebebrand, Johannes
A1  - Heinrich, Joachim
A1  - Helgeland, Oyvind
A1  - Henders, Anjali K.
A1  - Henderson, John
A1  - Henriksen, Tine B.
A1  - Hirschhorn, Joel N.
A1  - Hivert, Marie-France
A1  - Hocher, Berthold
A1  - Holloway, John W.
A1  - Holt, Patrick
A1  - Hottenga, Jouke-Jan
A1  - Hypponen, Elina
A1  - Iniguez, Carmen
A1  - Johansson, Stefan
A1  - Jugessur, Astanand
A1  - Kahonen, Mika
A1  - Kalkwarf, Heidi J.
A1  - Kaprio, Jaakko
A1  - Karhunen, Ville
A1  - Kemp, John P.
A1  - Kerkhof, Marjan
A1  - Koppelman, Gerard H.
A1  - Korner, Antje
A1  - Kotecha, Sailesh
A1  - Kreiner-Moller, Eskil
A1  - Kulohoma, Benard
A1  - Kumar, Ashish
A1  - Kutalik, Zoltan
A1  - Lahti, Jari
A1  - Lappe, Joan M.
A1  - Larsson, Henrik
A1  - Lehtimaki, Terho
A1  - Lewin, Alexandra M.
A1  - Li, Jin
A1  - Lichtenstein, Paul
A1  - Lindgren, Cecilia M.
A1  - Lindi, Virpi
A1  - Linneberg, Allan
A1  - Liu, Xueping
A1  - Liu, Jun
A1  - Lowe, William L.
A1  - Lundstrom, Sebastian
A1  - Lyytikainen, Leo-Pekka
A1  - Ma, Ronald C. W.
A1  - Mace, Aurelien
A1  - Magi, Reedik
A1  - Magnus, Per
A1  - Mamun, Abdullah A.
A1  - Mannikko, Minna
A1  - Martin, Nicholas G.
A1  - Mbarek, Hamdi
A1  - McCarthy, Nina S.
A1  - Medland, Sarah E.
A1  - Melbye, Mads
A1  - Melen, Erik
A1  - Mohlke, Karen L.
A1  - Monnereau, Claire
A1  - Morgen, Camilla S.
A1  - Morris, Andrew P.
A1  - Murray, Jeffrey C.
A1  - Myhre, Ronny
A1  - Najman, Jackob M.
A1  - Nivard, Michel G.
A1  - Nohr, Ellen A.
A1  - Nolte, Ilja M.
A1  - Ntalla, Ioanna
A1  - Oberfield, Sharon E.
A1  - Oken, Emily
A1  - Oldehinkel, Albertine J.
A1  - Pahkala, Katja
A1  - Palviainen, Teemu
A1  - Panoutsopoulou, Kalliope
A1  - Pedersen, Oluf
A1  - Pennell, Craig E.
A1  - Pershagen, Goran
A1  - Pitkanen, Niina
A1  - Plomin, Robert
A1  - Power, Christine
A1  - Prasad, Rashmi B.
A1  - Prokopenko, Inga
A1  - Pulkkinen, Lea
A1  - Raikkonen, Katri
A1  - Raitakari, Olli T.
A1  - Reynolds, Rebecca M.
A1  - Richmond, Rebecca C.
A1  - Rivadeneira, Fernando
A1  - Rodriguez, Alina
A1  - Rose, Richard J.
A1  - Salem, Rany
A1  - Santa-Marina, Loreto
A1  - Saw, Seang-Mei
A1  - Schnurr, Theresia M.
A1  - Scott, James G.
A1  - Selzam, Saskia
A1  - Shepherd, John A.
A1  - Simpson, Angela
A1  - Skotte, Line
A1  - Sleiman, Patrick M. A.
A1  - Snieder, Harold
A1  - Sorensen, Thorkild I. A.
A1  - Standl, Marie
A1  - Steegers, Eric A. P.
A1  - Strachan, David P.
A1  - Straker, Leon
A1  - Strandberg, Timo
A1  - Taylor, Michelle
A1  - Teo, Yik-Ying
A1  - Thiering, Elisabeth
A1  - Torrent, Maties
A1  - Tyrrell, Jessica
A1  - Uitterlinden, Andre G.
A1  - van Beijsterveldt, Toos
A1  - van der Most, Peter J.
A1  - van Duijn, Cornelia M.
A1  - Viikari, Jorma
A1  - Vilor-Tejedor, Natalia
A1  - Vogelezang, Suzanne
A1  - Vonk, Judith M.
A1  - Vrijkotte, Tanja G. M.
A1  - Vuoksimaa, Eero
A1  - Wang, Carol A.
A1  - Watkins, William J.
A1  - Wichmann, H-Erich
A1  - Willemsen, Gonneke
A1  - Williams, Gail M.
A1  - Wilson, James F.
A1  - Wray, Naomi R.
A1  - Xu, Shujing
A1  - Xu, Cheng-Jian
A1  - Yaghootkar, Hanieh
A1  - Yi, Lu
A1  - Zafarmand, Mohammad Hadi
A1  - Zeggini, Eleftheria
A1  - Zemel, Babette S.
A1  - Hinney, Anke
A1  - Lakka, Timo A.
A1  - Whitehouse, Andrew J. O.
A1  - Sunyer, Jordi
A1  - Widen, Elisabeth E.
A1  - Feenstra, Bjarke
A1  - Sebert, Sylvain
A1  - Jacobsson, Bo
A1  - Njolstad, Pal R.
A1  - Stoltenberg, Camilla
A1  - Smith, George Davey
A1  - Lawlor, Debbie A.
A1  - Paternoster, Lavinia
A1  - Timpson, Nicholas J.
A1  - Ong, Ken K.
A1  - Bisgaard, Hans
A1  - Bonnelykke, Klaus
A1  - Jaddoe, Vincent W. V.
A1  - Tiemeier, Henning
A1  - Jarvelin, Marjo-Riitta
A1  - Evans, David M.
A1  - Perry, John R. B.
A1  - Grant, Struan F. A.
A1  - Boomsma, Dorret I.
A1  - Freathy, Rachel M.
A1  - McCarthy, Mark I.
A1  - Felix, Janine F.
T1  - The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia
BT  - design, results and future prospects
JF  - European journal of epidemiology
N2  - The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.
KW  - Genetics
KW  - Consortium
KW  - Childhood traits and disorders
KW  - Longitudinal
Y1  - 2019
U6  - https://doi.org/10.1007/s10654-019-00502-9
SN  - 0393-2990
SN  - 1573-7284
VL  - 34
IS  - 3
SP  - 279
EP  - 300
PB  - Springer
CY  - Dordrecht
ER  - 
TY  - JOUR
A1  - Li, Jian
A1  - Wang, Zi-Neng
A1  - Chen, You-Peng
A1  - Dong, Yun-Peng
A1  - Shuai, Han-Lin
A1  - Xiao, Xiao-Min
A1  - Reichetzeder, Christoph
A1  - Hocher, Berthold
T1  - Late gestational maternal serum cortisol is inversely associated with fetal brain growth
JF  - Neuroscience & biobehavioral reviews : official journal of the International Behavioral Neuroscience Society
N2  - To analyze the association between fetal brain growth and late gestational blood serum cortisol in normal pregnancy.Blood total cortisol was quantified at delivery in 432 Chinese mother/child pairs. Key inclusion criteria of the cohort were: no structural anomalies of the newborn, singleton pregnancy, no alcohol abuse, no drug abuse or history of smoking no hypertensive disorders and no impairment of glucose tolerance and no use of steroid medication during pregnancy. Differential ultrasound examination of the fetal body was done in early (gestational day 89.95 +/- 7.31), middle (gestational day 160.17 16.12) and late pregnancy (gestational day 268.89 +/- 12.42). Newborn's cortisol was not correlated with any of the ultrasound measurements during pregnancy nor with birth weight. Multivariable regression analysis, considering timing of the ultrasound examination, the child's sex, maternal BMI, maternal age, maternal body weight at delivery, the timing of cortisol measurement and maternal uterine contraction states, revealed that maternal serum total cortisol was significantly negative correlated with ultrasound parameters describing the fetal brain: late biparietal diameter (R-2 =0.512, p =0.009), late head circumference (R-2 = 0.498, p= 0.001), middle biparietal diameter (R-2= 0.819, p = 0.013), middle cerebellum transverse diameter R-2 = 0.76, p= 0.014) and early biparietal diameter(R-2 = 0.819, p = 0.013). The same analysis revealed that birth weight as well as ultrasound parameters such as abdominal circumference and femur length were not correlated to maternal cortisol levels.
 In conclusion, our study demonstrates that maternal cortisol secretion within physiological ranges may be inversely correlated to fetal brain growth but not to birth weight. It remains to be demonstrated whether maternal cortisol secretion negatively influencing fetal brain growth translates to adverse neurological outcomes in later life.
KW  - Brain development
KW  - Fetal programming
KW  - Cortisol Maternal cortisol
KW  - Head circumference
KW  - Biparietal diameter
Y1  - 2012
U6  - https://doi.org/10.1016/j.neubiorev.2011.12.006
SN  - 0149-7634
VL  - 36
IS  - 3
SP  - 1085
EP  - 1092
PB  - Elsevier
CY  - Oxford
ER  - 
TY  - JOUR
A1  - Liang, Xu-Jing
A1  - Huang, Si-Min
A1  - Li, Jian-Ping
A1  - Zhu, Xian-Nv
A1  - Lu, Yong-Ping
A1  - Hocher, Berthold
A1  - Chen, You-Peng
T1  - Hepatic impairment induced by scrub typhus is associated with new onset of renal dysfunction
JF  - Clinical laboratory : the peer reviewed journal for clinical laboratories and laboratories related to blood transfusion
N2  - Background: Scrub typhus is a potentially fatal infectious disease caused by Orientia tsutsugamushi. There is little attention given to hepatic impairment in the adults with scrub typhus. This study investigated the incidence and the prognostic implications of hepatic impairment in patients with scrub typhus.
 Methods: We retrospectively reviewed a total of 143 adult patients with scrub typhus who were admitted between January 1999 and December 2010 in Guangdong province, China. The patients were divided into three groups, e.g., normal, mild, and moderate to severe groups based on the elevated serum ALT and/or total bilirubin levels. Furthermore, clinical characteristics and prognosis of the patient groups were compared.
 Results: 109 patients (76.2%) had abnormal liver function. Among the patients with hepatic impairment 45 cases (31.4%), 54 cases (37.8%), and 10 cases (7.0%) had mild, moderate, and severe hepatic damage, respectively. The moderate to severe hepatic impairment group had higher levels of serum creatinine compared with that of normal hepatic function. The incidence of new onset of renal dysfunction - defined as peak serum creatinine >= 176 mu mol/L during hospital stay with no evidence of renal disease prior hospitalization - was 0% in the mild hepatic impairment group, 8.9% in the moderate hepatic impairment group, and 21.9% in the severe hepatic impairment group, (p = 0.005 for trend). Additionally, the patients with hepatic impairment (n = 109) had higher incidences of episodes of thrombocytopenia (45.9% vs. 8.82%, p < 0.001), hypoalbuminemia (50.5% vs. 11.8%, p < 0.001), new onset of renal dysfunction (16.5% vs. 0.0%, p = 0.011), and electrocardiogram abnormality (28.4% vs. 8.82%, p = 0.019) than the patients without hepatic impairment.
 Conclusions: The degree of hepatic impairment induced by scrub typhus is associated with new onset of renal dysfunction.
KW  - hepatic impairment
KW  - renal dysfunction
KW  - complication
KW  - outcome
KW  - scrub typhus
Y1  - 2014
U6  - https://doi.org/10.7754/Clin.Lab.2013.121203
SN  - 1433-6510
VL  - 60
IS  - 1
SP  - 63
EP  - 68
PB  - Clin Lab Publ., Verl. Klinisches Labor
CY  - Heidelberg
ER  - 
TY  - JOUR
A1  - Lu, Yong-Ping
A1  - Lung, Xu-Jing
A1  - Xiao, Xiao-Min
A1  - Huang, Si-Min
A1  - Liu, Zhi-Wei
A1  - Li, Jian
A1  - Hocher, Berthold
A1  - Chen, You-Peng
T1  - Telbivudine during the second and third trimester of pregnancy interrupts HBV intrauterine transmission: a systematic review and meta-analysis
JF  - Clinical laboratory : the peer reviewed journal for clinical laboratories and laboratories related to blood transfusion
N2  - Beckground: Evaluate the efficacy and safety of telbivudine during the 2nd and 3rd trimester of pregnancy in intrauterine transmission of hepatitis B virus (HBV). Based on the principle of Cochrane systematic reviews, a database was constructed from Medline, EMBASE, Cochrane Library, the US National Science Digital Library (NSDL), the China Biological Medicine Database (CBM-disc), and contact with Chinese experts in the field from November 2006 to February 2013.
 Results: Either the Mantel-Haenszel or Inverse Variance fixed-effects model or Mantel-Haenszel or Inverse Variance random-effects model was applied for all analyses indicated by odds ratio (OR) and 95% confidence interval (CI). The meta-analysis based on new onset of HBsAg seropositivity of infants at 6 - 12 months postpartum revealed that the control group had an intrauterine transmission rate of 8.25 - 42.31%. This rate was reduced to 0 - 14.29% in the telbivudine treatment group (OR 0.09, 95% CI 0.04 - 0.22, including seven trials, p < 0.001). The rates of intrauterine transmission based on new onset of HBV DNA seropositivity of infants at 6 - 12 months postpartum were 8.25 - 19.23% in the control group and 0 - 3.57% in the treatment group (OR 0.07, 95% CI 0.02 - 0.22, p < 0.001, including only five trials, since two trials had no data on HBV DNA in infants). With the exception of CK elevations, adverse effect frequencies were similar in both groups.
 Conclusions: Telbivudine is an effective and safe drug for preventing intrauterine transmission of HBV.
KW  - telbivudine
KW  - meta-analysis
KW  - intrauterine
KW  - transmission of hepatitis B virus (HBV)
KW  - clinical studies
KW  - safety efficacy
Y1  - 2014
U6  - https://doi.org/10.7754/Clin.Lab.2013.130408
SN  - 1433-6510
VL  - 60
IS  - 4
SP  - 571
EP  - 586
PB  - Clin Lab Publ., Verl. Klinisches Labor
CY  - Heidelberg
ER  -