Antibiotic Therapy Increases the Risk of Preterm Birth in Preterm Labor without Intra‐Amniotic Microbes, but may Prolong the Gestation Period in Preterm Labor with Microbes, Evaluated by Rapid and High‐Sensitive <scp>PCR</scp> System

Yoneda, Satoshi; Shiozaki, Arihiro; Yoneda, Noriko; Ito, Mika; Saito, Tomoko; Fukuda, Kaori; Ueno, Takahiro; Niimi, Hideki; Kitajima, Isao; Kigawa, Mika; Saito, Shigeru

doi:10.1111/aji.12484

Cited by 38 publications

(36 citation statements)

References 56 publications

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“…(383–410)] that infection is a common precursor to PTB in the absence of PE. The failure of antibiotics to help can be ascribed to their difficulty of penetrating to the trophoblasts and placental regions.…”

Section: Direct Evidence For a Role Of Infectious Agents In Pementioning

confidence: 99%

A Dormant Microbial Component in the Development of Preeclampsia

Kell

Kenny

2016

Front. Med.

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Preeclampsia (PE) is a complex, multisystem disorder that remains a leading cause of morbidity and mortality in pregnancy. Four main classes of dysregulation accompany PE and are widely considered to contribute to its severity. These are abnormal trophoblast invasion of the placenta, anti-angiogenic responses, oxidative stress, and inflammation. What is lacking, however, is an explanation of how these themselves are caused. We here develop the unifying idea, and the considerable evidence for it, that the originating cause of PE (and of the four classes of dysregulation) is, in fact, microbial infection, that most such microbes are dormant and hence resist detection by conventional (replication-dependent) microbiology, and that by occasional resuscitation and growth it is they that are responsible for all the observable sequelae, including the continuing, chronic inflammation. In particular, bacterial products such as lipopolysaccharide (LPS), also known as endotoxin, are well known as highly inflammagenic and stimulate an innate (and possibly trained) immune response that exacerbates the inflammation further. The known need of microbes for free iron can explain the iron dysregulation that accompanies PE. We describe the main routes of infection (gut, oral, and urinary tract infection) and the regularly observed presence of microbes in placental and other tissues in PE. Every known proteomic biomarker of “preeclampsia” that we assessed has, in fact, also been shown to be raised in response to infection. An infectious component to PE fulfills the Bradford Hill criteria for ascribing a disease to an environmental cause and suggests a number of treatments, some of which have, in fact, been shown to be successful. PE was classically referred to as endotoxemia or toxemia of pregnancy, and it is ironic that it seems that LPS and other microbial endotoxins really are involved. Overall, the recognition of an infectious component in the etiology of PE mirrors that for ulcers and other diseases that were previously considered to lack one.

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Section: Direct Evidence For a Role Of Infectious Agents In Pementioning

confidence: 99%

A Dormant Microbial Component in the Development of Preeclampsia

Kell

Kenny

2016

Front. Med.

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“…27 (ii) This study was the first report to evaluate the efficacy of 17OHP-C for PTL according to the severity of intra-amniotic inflammation/infection. (i) The study subjects were all administered antibiotics in microbe-positive cases.…”

Section: Strengthsandweaknessesofthisstudymentioning

confidence: 99%

“…We also excluded cases where there was no evaluation of intra-amniotic microbes using a sensitive and rapid PCR system, 26 and those that had not been administered antibiotics based on the clinical severity of PTL. 27 To evaluate the effect of 17OHP-C, PTL patients who delivered within 7 days of admission were also excluded. Finally, 107 patients were enrolled in this study ( Figure 1).…”

Section: Studypopulationmentioning

confidence: 99%

“…The incidence of intra-amniotic inflammation was more frequent the lower the gestational age in PTL patients. 27 In this study, we investigated the effect of 17OHP-C in patients who received antibiotic administration based on the clinical severity of PTL (intra-amniotic microbe-positive or intra-amniotic microbe-negative case) according to the severity of intra-amniotic inflammation. However, intraamniotic infection also induces PTB, and progesterone has no antimicrobial effects.…”

Section: Introductionmentioning

confidence: 99%

“…26 Recently, we reported that antibiotics in cases positive for intra-amniotic microbes could prolong the gestational period, and conversely, administration of antibiotics to microbe-negative cases rather shortened the gestational period. 27 In this study, we investigated the effect of 17OHP-C in patients who received antibiotic administration based on the clinical severity of PTL (intra-amniotic microbe-positive or intra-amniotic microbe-negative case) according to the severity of intra-amniotic inflammation.…”

Section: Introductionmentioning

confidence: 99%

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