Reference weights for placentas delivered before the 28th week of gestation.

CONTEXT: Very few studies have measured the weight of large numbers of placentas delivered before the 28th post-menstrual week. METHODS: We measured the weight of 930 singleton placentas delivered before the 28th post-menstrual week, and examined the distributions of weights in selected groups (week of gestation, reason for preterm birth, birth weight Z-score categories, placenta histology). We excluded 90 singleton placentas based on growth restriction as indicated by birth weight Z-score, resulting in a normative sample of 840 placentas. Weights for unfused twin placentas are also presented. RESULTS: Standard weights derived from our data set differ from those previously published, partly due to a larger sample size. Placenta weight varied with birth weight. Placentas from pregnancies ending due to preeclampsia, fetal indications or those showing evidence of poor perfusion on histology were among the smallest and their weights correlated with the smallest birth weights for gestational age. CONCLUSIONS: Placenta weights appear to be influenced by multiple maternal and fetal processes. We present a standard weight table for singleton placentas among live infants born between 23 and 27 completed weeks.

Fetal obstructive uropathy in trisomy syndromes.

Fetal obstructive uropathy has seldom been described in trisomy syndromes, and its relationship to these syndromes remains unclear. Five trisomic male fetuses, four with trisomy 18 and one with trisomy 21, were identified out of 110 fetuses evaluated for fetal obstructive uropathy. We performed detailed examination on the urinary tracts of four of these fetuses, three with trisomy 18 and one with trisomy 21, following termination in the second trimester. All four had a markedly distended urinary bladder (megacystis), abdominal wall distension, and a small, poorly developed urethra thoughout its full length. All four also had poor development of the prostate with virtual absence of glandular development, as compared to age-matched controls. Posterior urethral valves were not identified in any case. Three of the fetuses (two with trisomy 18 and one with trisomy 21) had unilateral or bilateral hydroureters, and resulting renal tubulocystic or glomerulocystic change. Review of this database reveals an unexpectedly high frequency of trisomies, particularly trisomy 18, suggesting that the relationship may not be coincidental. Abnormal prostate development may be causally related to fetal obstructive uropathies and may be an under-recognized trait in trisomy syndromes. Karyotypic analysis of all fetuses with obstructive uropathy is important since in utero surgical intervention may be contraindicated in cases of fetal aneuploidy.

Immature teratomas of the genital tract in older women.

We report the clinicopathologic features of three women, 40 years of age or older, with malignant genital tract immature teratomas. All had FIGO stage III, grade II or grade III tumors. One tumor arose from the fallopian tube, the second from the ovary, and the third involved the cortical surfaces of both ovaries with minimal parenchymal involvement. The tumors weighed 1700, 5660, and 330 g and had histologic features similar to those generally seen in younger women. Two of the women died within 1 year of diagnosis. Interval growth of tumor after treatment with chemotherapy was documented in the third patient; she was reexplored and all of the excised tumor was composed of mature tissues. These cases affirm that, although rare, malignant germ cell tumors can occur in older peri- or postmenopausal women.

Ovarian smooth muscle metaplasia: an uncommon and possibly underrecognized entity.

Smooth muscle differentiation in the ovary is rare, and its histopathologic spectrum, including ovarian smooth muscle metaplasia (SMM), has not been well described. The clinicopathologic findings in 48 ovaries with SMM from 40 women are reported. The average age of women with ovarian SMM was 55.6 years (range, 34 to 86 years). Foci of SMM were semiquantitatively characterized as 1+ in 46% (1 to 3 foci), 2+ in 37% (4 to 6 foci), and 3+ in 17% (> 6 foci). SMM was bilateral in 8 (23%) of the 35 patients who had bilateral oophorectomies. SMM was intimately associated with another ovarian process in 28 (58%) cases, including ovarian cysts (11), endometriosis (3), granulosa cell tumors (3), extensive stromal luteinization (1), ovarian fibroma (1), adhesions (1), and folliculogenesis (8). Ovaries with 2+ to 3+ SMM were associated with another ovarian lesion significantly more often than those with 1+ SMM (p < 0.01). Most women with ovarian SMM (86%) also had uterine leiomyomas. Significant endometrial pathology was present in 13 (37%) of 35 simultaneously removed uteri. In conclusion, SMM occurs most often in perimenopausal or postmenopausal women, most of whom also have uterine leiomyomas. Ovarian SMM is usually confined to a few microscopic fields, is bilateral in < 25% of patients, and is often associated with other ovarian lesions.

Ovarian leiomyomas: clinicopathologic features in fifteen cases.

Ovarian leiomyomas are uncommon and have not been systematically studied. The clinical and histopathologic features of 15 ovarian leiomyomas were evaluated, including their clinical presentation, size, cellularity, mitotic index, presence of degeneration, and hyalinization. The mean age of women with ovarian leiomyomas was 45.8 years. The presenting sign was an adnexal mass in 7 (47%), uterine leiomyomas in 4 (26%), contralateral adnexal mass in 2 (13%), and other signs in 2 (13%) women. Thirteen leiomyomas had mitotic indices < 1/10 high-power-fields (HPFs), including one cellular leiomyoma, and 2 had mitotic indices between 1 and 2/10 HPFs. The cellular leiomyoma and those with a mitotic index of > or = 1/10 HPFs had an average size of 3.4 cm. Two leiomyomas exhibited central degeneration, and hyaline change was present in 5 leiomyomas, 4 of which were at least 4 cm in size. The majority of ovarian leiomyomas (78%) were associated with uterine leiomyomas; hyperplastic endometrial polyps were present in 2 cases. Follow-up (mean, 9.6 months) was available in 8 cases, and all had no evidence of recurrence. In conclusion, ovarian leiomyomas exhibit a spectrum of features that are similar to uterine leiomyomas. Although the prognosis is presumed to be good, the short follow-up period of this series precluded definitive evaluation of their natural history.

Maternal scleroderma: placental findings and perinatal outcome.

Pregnancy after the onset of scleroderma is uncommon; therefore, placental findings and perinatal outcome have rarely been correlated. The histopathologic features of placentas from 13 pregnancies in eight women with scleroderma were recorded and correlated with the clinical features of the mother and fetus. Adverse perinatal outcome included intrauterine fetal demise in five, and previable or preterm delivery in four. A decidual vasculopathy was seen in 5 of the 13 placentas, four of which were associated with intrauterine fetal demise. Decidual blood vessels in the scleroderma patients were evaluated immunohistochemically for platelet-derived growth factor (PDGF), transforming growth factor beta1 (TGF-beta1), T-helper and T-suppressor lymphocytes, macrophages, immunoglobulin (Ig) M, and IgG, and compared with those from hypertensive and uncomplicated third-trimester pregnancies. The atherotic blood vessels in scleroderma were characterized by mural macrophages and IgM and IgG deposition and were similar to those seen in placentas from hypertensive pregnancies. CD8-positive T cells predominated in normal and hypertensive decidua compared with scleroderma, in which CD4-positive T cells were more frequent. No difference in PDGF or TGF-beta1 staining was found between scleroderma and control groups. In conclusion, decidual vasculopathy is common in scleroderma, is similar to that seen in hypertension, and is associated with poor perinatal outcome. A trend toward a reversed ratio of decidual CD4 to CD8-positive T cells is seen in scleroderma compared with hypertension and uncomplicated pregnancies. PDGF and TGF-beta1 do not appear to be involved in the pathogenesis of decidual vasculopathy in scleroderma.

Intraplacental choriocarcinoma associated with viable pregnancy: pathologic features and implications for the mother and infant.

Choriocarcinoma arising in the placenta, or intraplacental choriocarcinoma, has seldom been reported, particularly in the absence of maternal metastases. Reluctance to diagnose choriocarcinoma in the presence of chorionic villi can delay diagnosis; however, timely diagnosis of choriocarcinoma is prognostically important, both for the mother and infant. We report the clinicopathologic findings in five mothers and infants in whom choriocarcinoma was identified in the placenta. None of the mothers had a history of gestational trophoblastic disease in previous pregnancies. Three placentas were similar with a single small lesion grossly suggesting a small infarct; microscopically these consisted of infarcted areas surrounded by choriocarcinoma. These three mothers were unusual in that none had metastatic choriocarcinoma; two were treated with chemotherapy and remained disease-free; the third was lost to follow-up shortly following delivery. The remaining two mothers had known pulmonary metastases at time of delivery. One of these latter two placentas contained a large marginal lesion microscopically identified as choriocarcinoma. The fifth placenta had rare microscopic foci of choriocarcinoma, and sheets of necrotic choriocarcinoma were identified in "blood clot" submitted with the placenta. In four of the five cases the choriocarcinoma appeared to be arising from otherwise normal chorionic villi, and in no case was there invasion of the villous stroma. All of the infants survived, and none had evidence of choriocarcinoma. These cases support the concept that choriocarcinoma associated with otherwise normal pregnancy arises in the placenta and may be more common than reported.

Placental involvement in congenital hepatoblastoma.

We describe extensive placental involvement by hepatoblastoma in a 2600 g, 33-week estimated gestational age (EGA) hydropic female fetus with the hepatoblastoma otherwise limited to the liver. The placenta weighed 1190 g and histopathologic examination revealed diffuse tumor emboli in chorionic villous vessels. The placental tumor exhibited a cytologic appearance similar to the primary tumor and showed strong alpha-fetoprotein staining. Although unusual, other congenital tumors, including neuroblastoma and leukemia, have also been described metastatic to the placenta. This case emphasizes the important role of careful histopathologic examination of the placenta which, combined with immunohistochemistry and clinicopathologic correlation, may establish a diagnosis and possibly obviate the need for invasive neonatal diagnostic procedures.

Neuropathologic findings in a case of OFDS type VI (Váradi syndrome).

Oral-facial-digital syndrome type VI (OFDS VI) or Váradi syndrome is a rare autosomal-recessive disorder distinguished from other oral-facial-digital syndromes by metacarpal abnormalities with central polydactyly and by cerebellar abnormalities. Histopathologic characterization of the cerebellar abnormalities has not been described previously. We describe the neuropathologic findings in a stillborn, 21-week estimated gestational age (EGA) male fetus diagnosed antenatally with signs of OFDS VI. Autopsy findings included: facial abnormalities, postaxial central polydactyly of the right hand, bilateral bifid toes, and absence of cerebellar vermis with hypoplasia of the hemispheric cortex. Microscopic analysis of the cerebellum demonstrated absence of the subpial granular cell layer and disruption or dysgenesis of the glial architecture. These histopathologic findings suggest that a primary neuronal or glial cell defect, rather than an associated Dandy-Walker malformation, may account for the cerebellar abnormalities in this form of oral-facial-digital syndrome.

Extratubal secondary trophoblastic implants: clinicopathologic correlation and review of the literature.

Extratubal secondary trophoblastic implants (ESTI) are a rare complication of conservative laparoscopic procedures for tubal ectopic pregnancies. These implants present with persistent beta-hCG titers postoperatively and are probably the result of disruption of the ectopic pregnancy at salpingostomy or morcellation of the fallopian tube at salpingectomy. We describe the case of a 32-year-old woman who underwent a laparoscopic salpingectomy for a tubal ectopic pregnancy that was complicated postoperatively by peritoneal ESTI including extensive omental implants. Intraoperatively the lesions appeared as 0.3 cm red-black nodules and, microscopically, consisted of degenerating chorionic villi associated with implantation changes in the surrounding tissue. To the pathologist unaware of the clinical entity of ESTI, these lesions may present a diagnostic challenge.

Massive chronic intervillositis associated with recurrent abortions.

Massive chronic intervillositis (MCI) is an unusual placental lesion associated with poor fetal growth and adverse pregnancy outcome; it has not previously been associated with spontaneous abortion or recurrent pregnancy loss. This article reports a patient who had 10 spontaneous abortions with repetitious massive chronic intervillositis documented in four of five gestations spanning all three trimesters. Characteristic placental histology induced massive infiltration of the maternal intervillous space by chronic inflammatory cells and fibrin, without associated chronic villitis; the cellular infiltrate was composed predominantly of LCA and CD68 immunoreactive cells with scattered CD45RO positivity, consistent with a monocyte/macrophage population with occasional T lymphocytes. Elevated maternal serum alpha-fetoprotein was documented in two pregnancies. These findings support the concept that this unusual placental lesion may have an immunologic basis, and suggest that MCI may be a histopathologically recognizable cause of recurrent spontaneous abortion.

Esterase activity, exclusion of propidium iodide, and proliferation in tumor cells exposed to anticancer agents: phenomena relevant to chemosensitivity determinations.

Cellular esterase activity and the ability to exclude propidium iodide were examined after exposing tumor cells to anticancer agents. In general, esterase activity and the ability to exclude propidium iodide continued when cells proliferated and disappeared when proliferation was inhibited. However, with a number of preparations, drug exposure inhibited proliferation while esterase activity and propidium iodide exclusion persisted. These indications of persisting cell function or viability after drug exposure may be relevant to a potential for tumor cell recovery. When the viability of established cell lines progressively declined on days 4 and 7 following drug exposure, recovery did not occur. When proliferative recoveries occurred, viabilities remained elevated. Estimates of in vitro sensitivity by proliferation-related criteria were contrasted by persistent high viability estimates in 22% of the determinations performed with primary tumor cell preparations. The potential for recovery may explain the disappointing ability of proliferative chemosensitivity assays to predict clinical sensitivity.