[Observations on pe-eclampsia-eclampsia and the advances in the evolution of some laboratory tests]. / Algunos conceptos sobre preeclampsia-eclampsia y los avances en su evalución por algunas pruebas de laboratorio.

The preeclampsia-eclampsia syndrome is a vasospastic disorder and probably has a placental origin. Once the hypertensive syndrome is established the uteroplacental blood flow is reduced as well as the intervillous blood flow. Since 18-24 weeks of gestation and before the symptoms of preeclampsia become overt, changes in placental flow velocity can be detected with Doppler technics. The placental theories for the etiology of preeclampsia are focused on the hypoxic effect in the trophoblastic tissue of second trimester. The placental ischemic changes are evident and seen in the uteroplacental bed. They are interrelated with the stages of trophoblastic invasion of the spiral arteries during the 14 and 20 weeks. When the trophoblastic invasion is over, the spiral arteries become a high resistance system. The defect observed in preeclampsia is the lack of invasion of the trophoblast to the maternal arteries. The diminished placental perfusion probably creates endothelial damage. This damage has several effects: decreased prostaglandin production, activated coagulation cascade, stimulated fibrin aggregation, and increased vascular permeability. The ideal laboratory test for preeclampsia shall predict the onset of this entity. Recent findings seem promising. The fibronectin concentration increases 2-3 wks. prior to the clinical manifestation of preeclampsia. Severe hypertension shows an abnormal decrease in fibronectin levels. Hypocalciuria has been described as an early predictor in the development of preeclampsia. Other agents undergoing extensive evaluation as predictors are: uric acid, b-thromboglobin, prolactin and atrial natriuretic peptide. Recently high levels of b-HCG (human corionic gonadotrophin) have been linked to a lack of trophoblastic invasion during the second trimester, therefore this is a potential marker for those patients that will eventually develop preeclampsia.

[Uterine arteriovenous malformations, Review of the literature]. / Malformaciones arteriovenosas del útero. Revisión de la literatura.

Uterine arteriovenous malformation (AVMs) are fairly rare. Seventy four cases have been reported in the medical literature. The clinical presentation of this entity is quite diverse. The approach to uterine AVM requires clinical alertness and to make the diagnosis a high index of suspicion is required. Prompt treatment is often essential. This article reviews the entire literature on uterine AVM emphasizing the various clinica presentations and treatment modalities available for the gynecologist.

Markedly elevated cytokines in pleural effusion during the ovarian hyperstimulation syndrome: transudate or ascites?

OBJECTIVE: To study levels of proinflammatory cytokines in pleural fluid during the severe ovarian hyperstimulation syndrome (OHSS). DESIGN: Case report. SETTING: Tertiary academic medical center. PATIENT(S): A 35-year-old female with a 6-year history of unexplained infertility on menotropin therapy and 28 healthy normal controls. INTERVENTION(S): Thoracentesis for severe pleural effusion and venipunctures. MAIN OUTCOME MEASURE(S): Interleukin-1 beta (IL-beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) levels were measured by ELISA and compared between pleural effusion and serum from normal controls. RESULT(S): Pleural effusion IL-1 beta and IL-6 levels were higher than serum. Interleukin-6 levels were elevated particularly in pleural effusion (1,961.89 pg/mL) compared with serum (3.9 +/- 0.41 pg/mL). CONCLUSION(S): Our results confirm the high cytokine levels observed in OHSS. Cytokines have been implicated in capillary permeability, extravasation of fluid, oliguria, and shock. We have postulated that these mediators are released from the corpora lutea into the peritoneum and systemic circulation. Alternatively, the presence of high cytokine levels in pleural fluid maybe the result of diaphragmatic defects, which allow for the migration of ascites into the pleural space.

Uterine arteriovenous malformation in a patient with recurrent pregnancy loss and a bicornuate uterus. A case report.

BACKGROUND: Arteriovenous malformations (AVM) of the uterus are a rare but potential cause of recurrent pregnancy loss. Only four cases of uterine AVM have resulted in a live birth after conservative management. There is no previous report in which a combination of a müllerian anomaly and an AVM existed concomitantly. CASE: A 33-year-old woman with a history of recurrent pregnancy loss was found to have a coexistent uterine AVM and a bicornuate uterus. The patient underwent arterial embolization and Strassman metroplasty and subsequently had a term pregnancy with a live birth. CONCLUSION: Management of uterine AVM should be individualized, taking into account the patient's desire for future fertility and the stability of her health at presentation.

[Placenta accreta during the first trimester of pregnancy. A case report]. / Placenta increta en el primer trimestre de embarazo. Presentación de un caso.

Placenta accreta is defined as the abnormal adherence of the placenta, totally or in part, to the underlying uterine surface. It is uncommon to find this abnormality of the attachment of the placenta in the first half or pregnancy. Only 10 cases have been reported. We present a case of placenta accreta in the first trimester in a patient with three previous curettages as a risk factor, diagnosed during curettage for a fourth missed abortion that required total abdominal hysterectomy. This case follows the pattern of those previously reported.