RESUMO
PURPOSE: Multiparametric magnetic resonance imaging (mpMRI) is a well-established imaging method for localizing primary prostate cancer (PCa) and for guiding targeted prostate biopsies. [18F]DCFPyL positron emission tomography combined with MRI (PSMA-PET/MRI) might be of additional value to localize primary PCa. The aim of this study was to assess the diagnostic performance of [18F]DCFPyL-PET/MRI vs. mpMRI in tumour localization based on histopathology after robot-assisted radical-prostatectomy (RARP), also assessing biopsy advice for potential image-guided prostate biopsies. METHODS: Thirty prospectively included patients with intermediate to high-risk PCa underwent [18F]DCFPyL-PET/MRI and mpMRI prior to RARP. Two nuclear medicine physicians and two radiologists assessed tumour localization on [18F]DCFPyL-PET/MRI and on mpMRI respectively, and gave a prostate biopsy advice (2 segments) using a 14-segment model of the prostate. The uro-pathologist evaluated the RARP specimen for clinically significant PCa (csPCa) using the same model. csPCa was defined as any PCa with Grade Group (GG) ≥ 2. The biopsy advice based on imaging was correlated with the final histology in the RARP specimen for a total-agreement analysis. An additional near-agreement correlation was performed to approximate clinical reality. RESULTS: Overall, 142 of 420 (33.8%) segments contained csPCa after pathologic examination. The segments recommended for targeted biopsy contained the highest GG PCa segment in 27/30 patients (90.0%) both for [18F]DCFPyL-PET/MRI and mpMRI. Areas under the receiver operating characteristics curves (AUC), sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) for the total-agreement detection of csPCa per segment using [18F]DCFPyL-PET/MRI were 0.70, 50.0%, 89.9%, 71.7%, and 77.9%, respectively. These results were 0.75, 54.2%, 94.2%, 82.8%, and 80.1%, respectively, for mpMRI only. CONCLUSION: Both [18F]DCFPyL-PET/MRI and mpMRI were only partly able to detect csPCa on a per-segment basis. An accurate detection (90.0%) of the highest GG lesion at patient-level was observed when comparing both [18F]DCFPyL-PET/MRI and mpMRI biopsy advice with the histopathology in the RARP specimen. So, despite the finding that [18F]DCFPyL-PET/MRI adequately detects csPCa, it does not outperform mpMRI.
Assuntos
Imageamento por Ressonância Magnética Multiparamétrica , Neoplasias da Próstata , Humanos , Biópsia Guiada por Imagem , Imageamento por Ressonância Magnética/métodos , Masculino , Tomografia por Emissão de Pósitrons , Próstata/patologia , Prostatectomia , Neoplasias da Próstata/diagnóstico por imagem , Neoplasias da Próstata/cirurgia , Tomografia Computadorizada por Raios XRESUMO
BACKGROUND: Fever is a well-known side effect of misoprostol, but clinically difficult to distinguish from an intra uterine infection. The aim of this study was to determine the incidence of fever in terminations of pregnancy (TOP) using misoprostol and to evaluate fever as indication of intra uterine infection. METHODS: A retrospective cohort study was performed. Consecutive second trimester TOP with misoprostol between January 2008 and October 2012 were selected. We included 403 cases and determined the incidence of fever. To examine intra uterine infection as plausible cause of fever, pathological examination reports of placentas were reviewed for signs of infections. RESULTS: The incidence of fever was 42%. Logistic regression showed a dose dependent association between dosage misoprostol and degree of fever (OR 1.86; 95% CI: 1.3-2.7). There was no association between fever and epidural analgesia. Fever has a sensitivity of 55% and a specificity of 58% as a marker of intra uterine infection. The positive predictive value of fever for an intra uterine infection is 4% and the negative predictive value is 98%. CONCLUSION: Administration of misoprostol for the indication TOP is strongly associated with fever during labor. Fever is a poor predictor of intra uterine infection in the context of TOP.
Assuntos
Abortivos não Esteroides/efeitos adversos , Aborto Induzido/efeitos adversos , Febre/etiologia , Misoprostol/efeitos adversos , Infecção Puerperal/diagnóstico , Doenças Uterinas/diagnóstico , Abortivos não Esteroides/administração & dosagem , Aborto Induzido/métodos , Adulto , Feminino , Febre/induzido quimicamente , Febre/epidemiologia , Humanos , Incidência , Modelos Logísticos , Misoprostol/administração & dosagem , Países Baixos/epidemiologia , Valor Preditivo dos Testes , Gravidez , Segundo Trimestre da Gravidez , Infecção Puerperal/epidemiologia , Estudos Retrospectivos , Sensibilidade e Especificidade , Doenças Uterinas/epidemiologiaRESUMO
Women with a history of spontaneous preterm birth (SPTB) have a mildly elevated cardiovascular risk (CVR) later in life and women with a history of preeclampsia have a highly elevated CVR. In placentas of women with preeclampsia pathological signs of maternal vascular malperfusion (MVM) are often seen. These signs of MVM are also seen in a substantial part of the placentas of women with SPTB. We therefore hypothesize that in women with a history of SPTB, the subgroup with placental MVM has an elevated CVR. This study is a secondary analysis of a cohort study including women 9-16 years after a SPTB. Women with pregnancy complications known to be associated with CVR were excluded. The primary outcome was hypertension defined as blood pressure ≥ 130/80 mmHg and/or treatment with antihypertensive medication. Secondary outcomes were mean blood pressure, anthropometrics, blood measurements including cholesterol and HbA1c, and creatinine in urine. Placental histology was available in 210 (60.0%) women. MVM was found in 91 (43.3%) of the placentas, most often diagnosed by the presence of accelerated villous maturation. Hypertension was diagnosed in 44 (48.4%) women with MVM and in 42 (35.3%) women without MVM (aOR 1.76, 95% CI 0.98 - 3.16). Women with a SPTB and placental MVM showed significantly higher mean diastolic blood pressure, mean arterial pressure and HbA1c approximately 13 years after delivery, compared to women with a SPTB without placental MVM. We therefore conclude that placental malperfusion in women with a SPTB might differentiate in CVR later in life.
Assuntos
Doenças Cardiovasculares , Hipertensão , Pré-Eclâmpsia , Nascimento Prematuro , Gravidez , Feminino , Recém-Nascido , Humanos , Masculino , Placenta/patologia , Nascimento Prematuro/patologia , Pré-Eclâmpsia/patologia , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/complicações , Doenças Cardiovasculares/patologia , Estudos de Coortes , Hemoglobinas Glicadas , Estudos Retrospectivos , Fatores de Risco , Fatores de Risco de Doenças CardíacasRESUMO
BACKGROUND: Massive perivillous fibrin deposition (MPFD) is associated with adverse pregnancy outcomes and is mainly caused by maternal factors with limited involvement of fetal or genetic causes. We present one consanguineous couple with six fetuses developing Fetal Akinesia Deformation Sequence (FADS) and MPFD, with a possible underlying genetic cause. This prompted a literature review on prevalence of FADS and MPFD. METHODS: Fetal ultrasound examination, motor assessment, genetic testing, postmortem examination, and placenta histology are presented (2009-2019). Literature was reviewed for the association between congenital anomalies and MPFD. RESULTS: All six fetuses developed normally during the first trimester. Thereafter, growth restriction, persistent flexed position, abnormal motility, and contractures in 4/6, consistent with FADS occurred. All placentas showed histologically confirmed MPFD. Genetic analyses in the five available cases showed homozygosity for two variants of unknown significance in two genes, VARS1 (OMIM*192150) and ABCF1 (OMIM*603429). Both parents are heterozygous for these variants. From 63/1999 manuscripts, 403 fetal outcomes were mobilized. In 14/403 fetuses, congenital abnormalities in association with MPFD were seen of which two fetuses with contractures/FADS facial anomalies. CONCLUSION: The low prevalence of fetal contractures/FADS facial anomalies in association with MPFD in the literature review supports the possible fetal or genetic contribution causing FADS and MPFD in our family. This study with literature review supports the finding that fetal, fetoplacental, and/or genetic components may play a role in causing a part of MPFDs.