17 alpha hydroxyprogesterone/inflammation

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In an in-vitro model using human fetal membranes, 17-α hydroxyprogesterone caproate is not an optimal progestogen for inhibition of fetal membrane weakening.

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The progestogen 17-α hydroxyprogesterone caproate (17-OHPC) is 1 of only 2 agents recommended for clinical use in the prevention of spontaneous preterm delivery, and studies of its efficacy have been conflicting. We have developed an in-vitro model to study the fetal membrane weakening process that

17-α Hydroxyprogesterone Caproate for the Prevention of Recurrent Preterm Birth: One Size May Not Fit All.

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Spontaneous preterm birth is a syndrome with many causes and thus unresponsive to a single intervention. It logically follows that patients with a prior spontaneous preterm birth are a heterogeneous group unlikely to respond equally to a single preventive intervention such as 17-α

Successful treatment of severe intra-amniotic inflammation and cervical insufficiency with continuous transabdominal amnioinfusion and cerclage: A case report

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Severe intra-amniotic inflammation, even with a negative bacterial culture, can lead to premature labor. We report a 43-year-old multiparous woman with severe intra-amniotic inflammation and cervical insufficiency at 23 weeks and 5 days of gestation. Continuous transabdominal amnioinfusion was

17OHP-C in patients with spontaneous preterm labor and intact membranes: is there an effect according to the presence of intra-amniotic inflammation?

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OBJECTIVE It is not known whether 17-alpha-hydroxyprogesterone caproate (17OHP-C) is effective for preventing preterm delivery with an episode of preterm labor (PTL) with or without intra-amniotic inflammation/infection. METHODS This was a retrospective cohort study. One hundred and seven PTL

Efficacy of midtrimester short cervix interventions is conditional on intraamniotic inflammation.

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BACKGROUND Midtrimester ultrasound is a valuable method for identifying asymptomatic women at risk for spontaneous preterm delivery (PTD). However, response to various treatments (cerclage, progestogen) has been variable in the clinical setting. It remains unclear how other biomarkers may be used to

In an in-vitro model using human fetal membranes, α-lipoic acid inhibits inflammation induced fetal membrane weakening.

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BACKGROUND We established an in-vitro model for the study of human fetal membrane (FM) weakening leading to pPROM. In this model, granulocyte-macrophage colony-stimulating factor (GM-CSF) is a critical intermediate for both tumor necrosis factor-α (TNF; modeling infection/inflammation) and thrombin

17-alpha hydroxyprogesterone caproate for preterm birth prevention: Where have we been, how did we get here, and where are we going?

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Prematurity is a major public health problem in the United States and worldwide. Women with a history of a previous preterm birth are at high risk for recurrence. Progesterone is a key hormone involved in pregnancy maintenance. In general, progesterone is thought to maintain pregnancy through

The use of progestational agents for preterm birth: lessons from a mouse model.

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OBJECTIVE On the basis of the recent Maternal Fetal Medicine Unit Networks clinical trial, the American College of Obstetricians and Gynecologists supports the administration of 17-alpha hydroxyprogesterone caproate to high-risk patients. Because inflammation/infection is believed to be a

Ovarian hydroxyeicosatetraenoic acids compared with prostanoids and steroids during ovulation in rats.

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Hydroxyeicosatetraenoic acid methyl esters (HETEs) are lipoxygenase products of arachidonic acid that are generated along with prostaglandins (PGs) during acute inflammatory reactions. Whereas it is well known that ovarian PG levels increase during the ovulatory process, little is known about

Human decidual cell Toll-like receptor signaling in response to endotoxin: the effect of progestins.

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OBJECTIVE The purpose of this study was to determine whether progesterone, 17-alpha-hydroxyprogesterone, and 17-alpha hydroxyprogesterone caproate modulate the Toll-like receptor (TLR) pathway in the response of decidua to lipopolysaccharide. METHODS Cultured human decidual cells were incubated

17-hydroxyprogesterone caproate significantly improves clinical characteristics of preeclampsia in the reduced uterine perfusion pressure rat model.

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Preeclampsia is characterized by increased uterine artery resistance index, chronic immune activation, and decreased circulating nitric oxide levels. 17-α-Hydroxyprogesterone caproate (17-OHPC) is a synthetic metabolite of progesterone used for the prevention of recurrent preterm birth. We

[Purification and some properties of 3 alpha-hydroxysteroid dehydrogenase from pig adrenal cytosol].

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A 3 alpha-reducing activity of 5 alpha-dihydrotestosterone (5 alpha-DHT) was found in pig adrenal cytosol. The enzyme (3 alpha-hydroxysteroid dehydrogenase: 3 alpha-HSD) has been purified to homogeneity from pig adrenal cytosol by ammonium sulfate precipitation followed by DEAE-cellulose, 2',

Progesterone blunts vascular endothelial cell secretion of endothelin-1 in response to placental ischemia.

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OBJECTIVE Preeclampsia (PE) is associated with hypertension and elevated endothelin (ET-1), an indicator of endothelial cell activation and dysfunction. Reduction of uteroplacental perfusion (RUPP) in the pregnant rat model of PE is characterized by elevated mean arterial pressure, inflammatory

Gonadal and adrenal sex steroids in ankylosing spondylitis.

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A role for sex steroids in the pathogenesis of AS is suggested by the male predominance, the peak age of onset in young adults, the increased number of first manifestations and flares after pregnancy, and the fact that sex steroids may modulate immune functions. There is a theoretic possibility that

Progesterone supplementation attenuates hypertension and the autoantibody to the angiotensin II type I receptor in response to elevated interleukin-6 during pregnancy.

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OBJECTIVE Preeclampsia is a multisystem disorder recognized as hypertension with proteinuria developing >20 weeks' gestation. Preeclampsia is associated with chronic immune activation characterized by increased T and B lymphocytes, cytokines, and antibodies activating the angiotensin II type I

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