Placental site trophoblastic tumors are derived from the placental site or intermediate trophoblast, a cell that has morphologic and functional features that overlap with those of trophoblasts and syncytiotrophoblasts. These uncommon diploid tumors, often XX in karyotype, typically arise a few months after pregnancy. Because intermediate trophoblasts do not produce hCG in large amounts, hCG concentrations are only slightly elevated. More typically, these tumors produce human placental lactogen. An indolent clinical course is typical, with a generally favorable outcome if the tumor is confined to the endomyometrium. Of note, however, placental site trophoblastic tumors are not as sensitive to chemotherapy as are other trophoblastic tumors, and the prognosis is poor when spread occurs beyond the uterus.
Molardiseaseisaresultofanabnormalcontributionofpaternalchromosomestotheconceptus.
Partialmolesaretriploidandhavetwosetsofpaternalchromosomes.Theytypicallyareaccompaniedbyfetaltissue.Thereisalowrateofpersistentdisease.
Completemolesarediploid,andallchromosomesarepaternal.Rarelyareembryonicorfetaltissuesassociatedwithacompletemole.
Amongcompletemoles,10%to15%areassociatedwithpersistentdiseasethatusuallytakestheformofaninvasivemole.Only2%ofcompletemolesprogresstochoriocarcinoma.
Gestationalchoriocarcinomaisahighlyinvasiveandfrequentlymetastatictumorthat,incontrastwithovarianchoriocarcinoma,isresponsivetochemotherapyandcurableinmostcases.
Placentalsitetrophoblastictumorisanindolenttumorofintermediatetrophoblastthatproduceshumanplacentallactogen.Itcanbecuredsurgicallybutonceitspreadsitdoesnotrespondwelltochemotherapy.
The development of hypertension, accompanied by proteinuria and edema in the third trimester of pregnancy, is referred to as preeclampsia. This syndrome occurs in 5% to 10% of pregnancies, particularly with first pregnancies in women older than 35 years. In those severely affected, seizures may occur, and the symptom complex is then termed eclampsia. By long-existing precedent, preeclampsia and eclampsia sometimes are referred to as toxemia of pregnancy. No blood-borne toxin has been identified, and this historically sanctified term is a misnomer. Recognition and early treatment of preeclampsia have now made eclampsia, particularly fatal eclampsia, rare.
While exact triggering events initiating these syndromes are unknown, a common feature underlying all cases is insufficient maternal blood flow to the placenta secondary to inadequate remodeling of the spiral arteries of the uteroplacental vascular bed. In normal pregnancy, the musculoelastic walls of the spiral arteries are invaded by trophoblasts, permitting them to dilate into wide vascular sinusoids. In preeclampsia and eclampsia, this vascular remodeling is impaired, the musculoelastic walls are retained, and the channels remain narrow. Decreased uteroplacental blood flow appears to result in placental hypoxia, placental dysfunction, and the altered release of circulating factors that regulate angiogenesis. Specifically, increases in the anti-angiogenic factors soluble Flt1 (sFlt1) and soluble endoglin (sEng) and reductions in proangiogenic factors, such as VEGF, have been noted. These disturbances are hypothesized to result in endothelial cell dysfunction, vascular hyperreactivity, and end-organ microangiopathy. Although the exact basis of preeclampsia remains to be further defined, several serious consequences have been associated with this condition:
Placental infarction, stemming from chronic hypoperfusion