![]() Prostaglandin E2 is contraindicated in patients with a known hypersensitivity to prostaglandins. In all of these cases, removal of the product resulted in a return to normal, though one case did require treatment with tocolytics. There were also associated fetal heart rate changes, with and without distress. Additionally, they also have an increased chance of fetal distress without uterine hyperstimulation (over 2%) versus placebo (1%). However, studies have shown that they have links to a higher chance of uterine hyperstimulation with and without fetal distress (greater than 2%) versus placebo (under1%). The insert and gel have a less than one percent incidence of gastrointestinal symptoms. Anti-emetics and anti-diarrheal medications may be necessary before and during the drug administration to counteract these side effects. Other adverse effects include temperature elevation in half of the patients, headache in one-tenth, and shivering and chills in one-tenth. The suppository correlates with the most severe side effects, with two-thirds of patients experiencing vomiting, two-fifths experiencing diarrhea, and one-third experiencing nausea. The most common side effects of prostaglandin E2 concern its impact on gastrointestinal smooth muscle. Importantly, though in vitro experiments have demonstrated that prostaglandin E2 can inhibit T-cell production, in vivo studies have not yet shown similar results. It can promote the activation of inflammatory Th17 cells but suppress IL-2 and IL-12 production in other T cell subsets. These diverse functions appear to depend on the cell type and expression patterns of various receptors. The role of prostaglandin E2 in inflammation is complex it has demonstrated pro-inflammatory activity in specific settings and plays an anti-inflammatory role in others. The efficacy of prostaglandin E2 during pregnancy may link to the expression of these receptors. Prostaglandin E2 also promotes cervical dilation, effacement, and softening, similar to the natural progression of pregnancy, possibly due to increased collagenase secretion. As some of the known receptors for prostaglandin E2 antagonize each other, researchers have hypothesized that the expression of these receptors determines the specific effects. For example, EP receptors in the myometrium act via cell membrane calcium channels and intracellular cyclic 3’5’-adenosine monophosphate (cAMP). It binds to G protein-coupled receptors (GPCRs) EP1-4 that lead to a variety of downstream events depending on the EP subtype and cell-type-specific expression patterns. While the exact mechanism of action is unknown, prostaglandin E2 causes contractions in the myometrium via direct stimulation.
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