Effusive-constrictive pericarditis is an uncommon pericardial syndrome that may be missed in some patients who present with tamponade. Although evolution to persistent constriction is frequent, idiopathic cases may resolve spontaneously. In our opinion, extensive epicardiectomy is the procedure of choice in patients requiring surgery.

Systemic administration of mu-opioids at clinical doses for analgesia typically slows respiratory rate. Mu-opioid receptors (MORs) on pre-Bötzinger Complex (pre-BötC) respiratory neurons, the putative kernel of respiratory rhythmogenesis, are potential targets. The purpose of this study was to determine the contribution of pre-BötC MORs to the bradypnea produced in vivo by intravenous administration of clinically relevant infusion rates of remifentanil (remi), a short-acting, potent mu-opioid analgesic. In decerebrate dogs, multibarrel micropipettes were used to record pre-BötC neuronal activity and to eject the opioid antagonist naloxone (NAL, 0.5 mM), the glutamate agonist D-homocysteic acid (DLH, 20 mM), or the MOR agonist [D-Ala(2), N-Me-Phe(4), gly-ol(5)]-enkephalin (DAMGO, 100 microM). Inspiratory and expiratory durations (T(I) and T(E)) and peak phrenic nerve activity (PPA) were measured from the phrenic neurogram. The pre-BötC was functionally identified by its rate altering response (typically tachypnea) to DLH microinjection. During intravenous remi-induced bradypnea (approximately 60% decrease in central breathing frequency, f(B)), bilateral injections of NAL in the pre-BötC did not change T(I), T(E), f(B), and PPA. Also, NAL picoejected onto single pre-BötC neurons depressed by intravenous remi had no effect on their discharge. In contrast, approximately 60 microg/kg of intravenous NAL rapidly reversed all remi-induced effects. In a separate group of dogs, microinjections of DAMGO in the pre-BötC increased f(B) by 44%, while subsequent intravenous remi infusion more than offset this DAMGO induced tachypnea. These results indicate that mu-opioids at plasma concentrations that cause profound analgesia produce their bradypneic effect via MORs located outside the pre-BötC region.

The objective of this study was to evaluate the risk of adverse fetal outcome in systemic lupus erythematosus (SLE) women exposed to azathioprine during pregnancy. We reviewed the medical records of SLE pregnant women followed from January 2005 to April 2013. The patients were evaluated at least once in each trimester and postpartum. Relevant fetal outcomes were extracted, such as rate of liveborns, fetal loss (spontaneous abortion and stillbirth), term delivery, preterm birth, neonatal death, low birth weight, low birth weight at term, and congenital malformations. A detailed history of drug use during pregnancy was obtained. We studied 178 pregnancies (in 172 women), 87 of them were exposed to azathioprine (AZA-group) and the remaining 91 were not exposed (NO AZA-group). Exposure to other drugs was similar in both groups. The rate of live births, spontaneous abortions mean birth weight, weeks of gestation, rate of birth weight <2500 g, and low birth weight at term did not differ between groups. No infant had major congenital abnormalities. Multivariate analysis showed that preeclampsia, premature rupture of membranes (PROM), lupus flare, and anti-DNA positive were associated with an increased risk of poor fetal outcome. Our study suggests that the use of azathioprine is safe and lacks of teratogenity in patients with SLE and pregnancy. Exposure to azathioprine during pregnancy is not associated with poor fetal outcome.

Zuperku EJ, Sanchez A, Tonkovic-Capin M, Tonkovic-Capin V, Mustapic S, Stuth EA. Opioid receptors on bulbospinal respiratory neurons are not activated during neuronal depression by clinically relevant opioid concentrations. J Neurophysiol 100: 2878 -2888, 2008. First published September 24, 2008 doi:10.1152/jn.90620.2008. Opioids depress the activity of brain stem respiratory-related neurons, but it is not resolved whether the mechanism at clinical concentrations consists of direct neuronal effects or network effects. We performed extracellular recordings of discharge activity of single respiratory neurons in the caudal ventral respiratory group of decerebrate dogs, which were premotor neurons with a likelihood of 90%. We used multibarrel glass microelectrodes, which allowed concomitant highly localized picoejection of opioid receptor agonists or antagonists onto the neuron. Picoejection of the receptor agonist [D-Ala 2 , N-Mephe 4 , gly-ol 5 ]-enkephalin (DAMGO, 1 mM) decreased the peak discharge frequency (mean Ϯ SD) of expiratory neurons to 68 Ϯ 22% (n ϭ 12), the ␦ 1 agonist D-Pen 2,5 -enkephalin (DPDPE, 1 mM) to 95 Ϯ 11% (n ϭ 15), and ␦ 2 receptor agonist [D-Ala 2 ] deltorphin-II to 86 Ϯ 17% (1 mM, n ϭ 15). The corresponding values for inspiratory neurons were: 64 Ϯ 12% (n ϭ 11), 48 Ϯ 30% (n ϭ 12), and 75 Ϯ 15% (n ϭ 11), respectively. Naloxone fully reversed these effects. Picoejection of morphine (0.01-1 mM) depressed most neurons in a concentration dependent fashion to maximally 63% (n ϭ 27). Picoejection of remifentanil (240 -480 nM) did not cause any significant depression of inspiratory (n ϭ 11) or expiratory neurons (n ϭ 9). 4. Intravenous remifentanil (0.2-0.6 g ⅐ kg Ϫ1 ⅐ min Ϫ1 ) decreased neuronal peak discharge frequency to 60 Ϯ 12% (inspiratory, n ϭ 7) and 58 Ϯ 11% (expiratory, n ϭ 11). However, local picoejection of naloxone did not reverse the neuronal depression. Our data suggest that , ␦ 1 , and ␦ 2 receptors are present on canine respiratory premotor neurons. Clinical concentrations of morphine and remifentanil caused no local depression. This lack of effect and the inability of local naloxone to reverse the neuronal depression by intravenous remifentanil suggest that clinical concentrations of opioids produce their depressive effects on mechanisms upstream from respiratory bulbospinal premotor neurons.

No abstract

Introduction: Several factors have been associated with the development of preeclampsia in women with systemic lupus erythematosus (SLE). Objective:To identify risk factors associated with preeclampsia in patients with SLE and its impact on fetal outcomes. Patients and methods:We studied a prospective cohort of pregnancies in women with SLE from January 2009 to December 2018. Demographic, clinical, serological and drug use characteristics were compared between patients who developed preeclampsia and those who did not, as well as the main neonatal outcomes. An adjusted logistic regression analysis was performed to identify factors potentially associated with preeclampsia. Results:We studied 316 pregnancies of 20 or more weeks of gestation. A total of 46 pregnancies (14.5%) were complicated by preeclampsia. A higher frequency of active disease before pregnancy (24.4% vs 11.3%, P = .01) and history of lupus nephritis (56.5% vs 30.1%, P < .001) were found in those patients who developed preeclampsia compared to those who did not. Preeclampsia was associated with a higher rate of prematurity, births of very low birth weight, stillbirth, and neonatal death. The multivariate analysis showed that the activity of the disease before (relative risk [RR] 2.7, 95% CI 1.04-7.4, P = .04) and during pregnancy (RR 3.0, 95% CI 1.0-9.1, P = .04) was associated with the development of preeclampsia. The use of antimalarial drugs during pregnancy was associated with a lower risk of preeclampsia (RR 0.21, 95% CI 0.08-0.53, P < .001). Conclusions:Our study suggests that the use of antimalarial drugs during pregnancy reduces the risk of preeclampsia in lupus pregnancies. K E Y W O R D Santimalarials, preeclampsia, pregnancy, systemic lupus erythematosus

We have reviewed the largest series of patients in Latin-America reported thus far after undergoing percutaneous aortic valvoplasty, concentrating on mid term follow-up and limitations. New prospective and multicentric studies are needed from our region.

No abstract