Pentoxifylline attenuates HPV-16 associated necrosis in placental trophoblasts.

PURPOSE: Human papillomaviruses (HPV) have been associated with placental inflammation resulting in high-risk preterm birth. The premise for this study was that treatment with anti-inflammatory pentoxifylline would inhibit HPV-mediated placental cell death. The objectives were: (1) to study the effects of HPV-16 exposure on trophoblast cells and (2) to evaluate pentoxifylline in preventing the damaging effects of HPV-16. METHODS: Mouse embryos (1-cell) were cultured (G1plus medium, 72 h, 37 °C, 5 % CO2 in air), divided into four groups at blastocyst-stage and incubated to implantation stage. Implanted trophoblasts were exposed to either HPV-16 (group 1), concomitant HPV-16 and 3 mM pentoxifylline (group 2), 3 mM pentoxifylline only (group 3) or control medium (group 4) and further incubated for 24 h. HPV-16 were from SiHa cell lysates. Trophoblast structural integrity was assessed by morphometric analysis while apoptosis and necrosis were detected using dual-stain fluorescence assay. RESULTS: Trophoblast outgrowth was reduced by 90% (P < 0.05) in HPV-16 presence (629 ± 265 µ(2), mean + SEM) when compared with controls (6,456 ± 795 µ(2)). Pentoxifylline attenuated the effects of HPV-16 (4,308 ± 362 µ(2)). Nuclear size of HPV-16 infected trophoblasts was smallest among the groups (P < 0.005). HPV-16 decreased cell viability and increased necrosis but not apoptosis. Pentoxifylline prevented HPV-16 associated necrosis in trophoblasts. CONCLUSIONS: HPV-16 decreased nuclear size and trophoblast outgrowth but these effects were attenuated by the phosphodiesterase inhibitor, pentoxifylline. The action of HPV-16 on trophoblasts was increased cell necrosis suggesting that HPV-16 pathogenesis involved either cAMP inhibition and/or activated TNF pathways.

A concise method of calculating fetal weight percentile.

OBJECTIVE: Assessment of fetal growth used in clinical decision making for managing pregnancies is based on percentiles relative to normal values for gestational age. Most clinicians utilize visual interpolation of look-up tables or graphs, which is neither accurate nor convenient. Calculation of growth percentile by numerical integration formulas requires digital computers with advanced computational capabilities and/or the storage of large data tables. STUDY DESIGN: Using established ultrasound measurement formulas and published fetal weight/gestational age tables, mean weights and standard deviations for gestational ages from 10 to 44 weeks were determined. From this Z-scores were calculated for the gestational ages. Z-scores plotted against 1st through 50th percentiles resulted in a curve. A polynomial equation was derived to fit the curve resulting in an expression for converting the Z-score to percentile: Percentile = 0.0994 * Z score2 - 0.44 * Z score + 0.5026. RESULTS: Comparing calculated values from this equation against standard percentiles from a Z-score to percentile table, all calculated values varied from the table value by < 1 percentile for Z-scores ranging from 0 to 2.33. Values > 2.33 are assigned to the 99th percentile. The equation performed to the goal of calculating percentile to an accuracy of < or = 1 percentile. CONCLUSION: A method whereby the estimated fetal weight can be used to calculate a percentile using two simple equations and only standard math functions allows implementation on a standard personal digital assistant device commonly available for clinical use. This implementation gives the needed accuracy, ease of interpretation, and portability, making it a useful tool in clinical practice.

Recurrence of microangiopathic hemolytic anemia after apparent recovery from the HELLP syndrome. A case report.

BACKGROUND: The syndrome of hemolytic anemia, elevated liver enzymes and low platelets (HELLP) can accompany preeclampsia and eclampsia. Delivery of the infant usually results in improvement in the mother's condition, with the recovery time dependent on the severity of the disease. We report a case of eclampsia with the HELLP syndrome in which microangiopathic hemolytic anemia (MAHA) and thrombocytopenia recurred after apparent recovery. CASE: A 28-year-old woman, gravida 4, para 0, therapeutic abortion 3, presented with signs and symptoms of severe preeclampsia and became eclamptic. The patient's condition improved as expected following cesarean delivery. However, the hemolytic anemia recurred and was successfully treated with a course of fresh frozen plasma (FFP). CONCLUSION: Hemolytic anemia in women with eclampsia and the HELLP syndrome occurs secondary to microvascular endothelial damage. In this case resolution of the HELLP syndrome and eclampsia occurred, as expected, in two to three days; however, MAHA and low platelets recurred on day 4. Treatment of MAHA with FFP was successful.