[Clinical study of maternal and infant outcomes in patients with lupus nephritis complicated with pregnancy].

Objective: To investigate the outcomes and associated factors for adverse pregnancy outcomes (APO) in pregnant patients with lupus nephritis (LN). Methods: The clinical data of 139 LN pregnant patients from from 2009 to 2017 in the First Affiliated Hospital of Sun Yat-sen University were analyzed retrospectively. Results: Totally, 105 LN were diagnosed before pregnancy and 34 were newly diagnosed during pregnancy. One or more APO occurred in 71.2% of patients with LN and 40 (28.8%) were without any APO. Thirty-six (25.9%) of pregnancies resulted in fetal loss. A total of 54 pregnancies were preterm birth with 20 at gestational age <34 weeks, 13 were intrauterine growth retardation (IUGR), 3 were fetal distress, and 8 were neonatal lupus, pregnancy induced hypertension occurred in 18 cases, of which, 2 cases were gestational hypertension and 16 were preeclampsia. There was no eclampsia occurred.In multivariate analysis, predictors of APO included active lupus during pregnancy (OR=8.9, 95%CI: 3.7-21.7, P<0.001), rash (OR=7.3, 95%CI: 2.2-24.5, P=0.001), cylindruria (OR=5.3, 95%CI: 1.6-17.0, P=0.005) and antiphospholipid syndrome (OR=11.4, 95%CI: 1.5-88.3, P=0.02) were risk factors for pregnancy loss. Variables that were independently predictive of preterm birth included anticardiolipin antibody positive (OR=8.8, 95%CI: 1.5-51.5, P=0.02) and active lupus during pregnancy (OR=7.9, 95%CI: 2.3-24.5, P=0.001). Conclusions: Pregnancies in LN are still at high risk of APO in terms of pregnancy loss and preterm birth. Stable disease can help to reduce the risk of APO.

[Pregnancy outcome of planning pregnancies in patients with SLE].

Objectives: To investigate the pregnancy outcomes in systemic lupus erythematosus (SLE) patients with planning pregnancy.And to evaluate the value of fetal umbilical artery Doppler. Methods: A total of 130 SLE patients with planning pregnancy were prospectively recruited from January 2013 to January 2017 at the First Affiliated Hospital of Sun Yat-sen University. Results: Thirty eight (29.2%) patients had active lupus, 30 with mild activity, 5 with moderate activity and 3 with severe activity.Active disease in the first, second and third trimesters occurred in 6, 11 and 21 cases respectively.Lupus nephritis (76.3%) and hematological system involvement (39.5%) were the most common manifestation.Seven cases had pre-eclampsia during pregnancy.One or more adverse outcomes occurred in 40 patients, including 28 with premature, 12 with pregnancy loss, 9 with intrauterine growth restriction, and 8 with fetal distress.All of the pulsatility index, resistance index and S/D value of patients with adverse outcomes were higher than that of patients without adverse outcomes (P<0.05). Conclusions: In SLE patients with planning pregnancy, disease flares were infrequent, and outcomes were favorable. Fetal umbilical artery Doppler can be used as a noninvasive monitoring method for SLE patients at late pregnancy.

[Clinical features and adverse pregnancy outcomes of new onset systemic lupus erythematosus during pregnancy].

Objective: To investigate the clinical characteristics and adverse pregnancy outcomes in pregnant women with new onset systemic lupus erythematosus (SLE) during pregnancy. Methods: The clinical data of 263 pregnancies with SLE in the First Affiliated Hospital of Zhongshan University from 2001 to 2015 were collected and analyzed retrospectively. Results: Of all the 263 pregnancies, 188 were diagnosed before pregnancy and 75 were newly diagnosed during pregnancy. Among the 75 new onset SLE, 27, 31, 14 and 3 cases were diagnosed during first trimester, second trimester, third trimester and puerperium, respectively. Active lupus was noted in 81.3% of the patients with new onset SLE. The main clinical manifestations of new onset SLE were lupus nephritis (57.3%) and thrombocytopenia (38.7%). SLEPDAI scores as well as the prevalence of lupus nephritis, and thrombocytopenia in patients with new onset SLE was higher than those in the previously diagnosed ones (P<0.05). Among the 75 new onset SLE pregnancies, adverse pregnancy outcomesoccurred in 53 patients, including 34 with pregnancy loss, 15with premature, 8with intrauterine growth restriction, 5with fetal distress and5 with neonatal lupus. Compared with patients withnon-newonset SLE, patients with newonset SLEhad a higher prevalence of adverse pregnancy outcomes (56.4% vs 70.7%, P<0.05), and pregnancy loss (21.8% vs 45.3%, P<0.01) but less live birth (78.2% vs 54.7%, P<0.05). Conclusion: Most of the patients with new onset SLE occurred during the first and second trimester. The most common clinical features of new onset SLE were lupus nephritis and thrombocytopenia. Patients with new onset SLE were more prone to active lupus, lupus nephritis and thrombocytopenia, as well as more adverse pregnancy outcomes and pregnancy loss.

Mice lacking granulocyte colony-stimulating factor have chronic neutropenia, granulocyte and macrophage progenitor cell deficiency, and impaired neutrophil mobilization.

Mice lacking granulocyte colony-stimulating factor (G-CSF) were generated by targeted disruption of the G-CSF gene in embryonal stem cells. G-CSF-deficient mice (genotype G-CSF-/-) are viable, fertile, and superficially healthy, but have a chronic neutropenia. Peripheral blood neutrophil levels were 20% to 30% of wild-type mice (genotype G-CSF+/+) and mice heterozygous for the null mutation had intermediate neutrophil levels, suggesting a gene-dosage effect. In the marrow of G-CSF-/- mice, granulopoietic precursor cells were reduced by 50% and there were reduced levels of granulocyte, macrophage, and blast progenitor cells. Despite G-CSF deficiency, mature neutrophils were still present in the blood and marrow, indicating that other factors can support neutrophil production in vivo. G-CSF-/- mice had reduced numbers of neutrophils available for rapid mobilization into the circulation by a single dose of G-CSF. G-CSF administration reversed the granulopoietic defect of G-CSF-/- mice. One day of G-CSF administration to G-CSF-/- mice elevated circulating neutrophil levels to normal, and after 4 days of G-CSF administration, G-CSF+/+ and G-CSF-/- marrows were morphologically indistinguishable. G-CSF-/- mice had a markedly impaired ability to control infection with Listeria monocytogenes, with diminished neutrophil and delayed monocyte increases in the blood and reduced infection-driven granulopoiesis. Collectively, these observations indicate that G-CSF is indispensible for maintaining the normal quantitative balance of neutrophil production during "steady-state" granulopoiesis in vivo and also implicate G-CSF in "emergency" granulopoiesis during infections.

Prophylaxis or treatment of experimental brucellosis with interleukin-1.

Intravenously injected recombinant human interleukin-1 alpha (IL-1 alpha) given to mice 4 h before infection with Brucella abortus 19 depressed the growth of bacteria in the spleen and liver. However, the same dose (10(5) U) or a 10-fold higher dose was not able to decrease numbers of bacteria when given to chronically infected mice. IL-1 injected into normal mice induced a dramatic increase 2 h later in colony-stimulating activity in serum, measured by bone marrow proliferation, and in colony-stimulating factor 1, measured by radioimmunoassay. Colony-stimulating factor levels declined but remained higher than normal for at least 12 h. The early peak stimulation was not observed in chronically infected mice, but the more prolonged elevation was. As a result of IL-1 treatment, the number of colony-forming cells, especially in the spleen, was increased in normal and acutely or chronically infected mice. Myeloperoxidase staining of newly formed monocytes and polymorphonuclear cells in the spleen revealed an increase in the number of these cells in normal and acutely infected mice as a result of IL-1 treatment, but there was no increase in the already high numbers in chronically infected mice. The relationship between these observations and the basis of chronic infection are discussed.

In vivo IL-1 potentiates both specific and non-specific arms of immune response to infection.

Injection of 10(5) U interleukin-1 (IL-1) 4 hr before intravenous infection with Listeria monocytogenes hastens recovery of mice. This is accompanied not only by early stimulation of colony-forming cells in the spleen to levels higher than those in untreated, infected mice but also by accelerated activation of lymphokine-producing, specific T lymphocytes.