Use of antimalarial drugs is associated with a lower risk of preeclampsia in lupus pregnancy: A prospective cohort study.

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.

Clinical, histological and molecular characteristics of Mexican patients with Fabry disease and significant renal involvement.

BACKGROUND AND AIMS: Fabry's disease (FD) is an X-linked lysosomal disorder caused by a deficiency of the enzyme α-galactosidase A that produces accumulation of glycosphingolipids with clinical abnormalities of skin, eye, kidney, heart, brain, and peripheral nervous system. We undertook this study to describe the molecular characteristics of the first four Mexican patients with diagnosis of FD with significant renal involvement, correlating these molecular characteristics with clinical, pathological and biochemical findings. METHODS: Genomic DNA from Mexican nonrelated patients with presumptive diagnosis of FD was sequenced by polymerase chain reaction (PCR). DNA sequences were compared against sequences in world data bank gene for alpha-galactosidase A (α-GLA, ENSG00000102393) using the BLAST database. RESULTS: Three patients were confirmed as having FD by displaying mutations in the α-GLA gene. The mutations found are a substitution (p.L243 F) in patient 1, and a substitution (p.A156 V) in patient 3. These two mutations had been previously reported. The new mutation was in patient 2 who displayed a deletion (c.260delA) changing the open reading frame from codon 86 and a stop codon at the 105th residue of the protein, (instead of 429 AA). The fourth patient had lack of mutations in any of the seven exons of α-GLA or 25 base-pair flanking regions; had mild manifestations with kidney histopathological diagnosis of FD that gave us a final diagnosis of atypical phenotype of FD. CONCLUSIONS: Although the sample is small, it gives a first idea of the molecular and clinical heterogeneity of FD in a Mexican population.