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1.
J Perinat Med ; 50(6): 753-762, 2022 Jul 26.
Artigo em Inglês | MEDLINE | ID: mdl-34587673

RESUMO

OBJECTIVES: Placental examination in a case of stillbirth can provide insight into causative/associated factors with fetal demise. The aim of this study was to compare placental and umbilical cord pathologies in singleton stillbirth and livebirth placentas, and to find prevalence of various associated maternal and fetal clinical factors. METHODS: This case-control study was conducted at a tertiary-care center in India over a period of 20 months. About 250 women who delivered stillborn fetus ≥28 weeks' gestation and 250 maternal-age-matched controls were recruited. Sociodemographic and clinical details were noted and placental gross and microscopic examination was done. Placental findings were compared between stillbirth and livebirth (overall), preterm stillbirth and preterm livebirth as well as term stillbirth and term livebirth in six categories - placenta gross, cord gross, membranes gross, maternal vascular malperfusion, fetal vascular malperfusion and inflammatory response. Prevalence of 11 maternal and fetal factors were studied in all categories of placental findings in both livebirth and stillbirth. RESULTS: Placental findings in all six categories were significantly associated with stillbirths (p<0.05). The placental findings associated with stillbirth with highest odds included placental hypoplasia (OR 9.77, 95% CI 5.46-17.46), necrotizing chorioamnionitis (OR 9.30, 95% CI 1.17-73.96) and avascular villi (OR 8.45, 95% CI 3.53-20.25). More than half of the women with stillbirths had medical disorders (n=130, 52.0%) and the most prevalent was hypertensive disorder (n=45, 18.0%). CONCLUSIONS: Changes in placenta are associated with development of stillbirth. Therefore, antenatal investigations to identify placental dysfunction should be investigated to determine whether these reduce stillbirth. Also, placental examination in a case of stillbirth can detect/diagnose many maternal/fetal conditions and thereby can help in preventing future stillbirths.


Assuntos
Doenças Placentárias , Natimorto , Estudos de Casos e Controles , Feminino , Morte Fetal , Humanos , Recém-Nascido , Placenta/patologia , Doenças Placentárias/diagnóstico , Doenças Placentárias/epidemiologia , Doenças Placentárias/patologia , Gravidez , Natimorto/epidemiologia
5.
Int Immunopharmacol ; 135: 112269, 2024 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-38781610

RESUMO

Idiopathic pulmonary fibrosis (IPF) presents a challenging progression characterized by lung tissue scarring and abnormal extracellular matrix deposition. This review examines the influence of immune responses, emphasizing their complex role in initiating and perpetuating fibrosis. It highlights how metabolic pathways modulate immune cell function during IPF. Immune cell modulation holds promise in managing pulmonary fibrosis (PF). Inhibiting neutrophil recruitment and monitoring mast cell levels offer insights into PF progression. Low-dose IL-2 therapy and regulation of fibroblast recruitment present potential therapeutic avenues, while the role of innate lymphoid cells (ILC2s) in allergic lung inflammation sheds light on disease mechanisms. The review focuses on metabolic reprogramming's role in shaping immune cell function during IPF progression. While some immune cells use glycolysis for pro-inflammatory responses, others favor fatty acid oxidation for regulatory functions. Targeting specialized pro-resolving lipid mediators (SPMs) presents significant potential for managing fibrotic disorders. Additionally, it highlights the pivotal role of amino acid metabolism in synthesizing serine and glycine as crucial regulators of collagen production and exploring the interconnectedness of lipid metabolism, mitochondrial dysfunction, and adipokines in driving fibrotic processes. Moreover, the review discusses the impact of metabolic disorders such as obesity and diabetes on lung fibrosis. Advocating for a holistic approach, it emphasizes the importance of considering this interplay between immune cell function and metabolic pathways in developing effective and personalized treatments for IPF.


Assuntos
Fibrose Pulmonar Idiopática , Humanos , Fibrose Pulmonar Idiopática/imunologia , Fibrose Pulmonar Idiopática/metabolismo , Animais , Pulmão/imunologia , Pulmão/patologia , Pulmão/metabolismo , Imunidade Inata , Metabolismo dos Lipídeos
6.
Cureus ; 12(4): e7502, 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-32373406

RESUMO

Lethal congenital malformations (LCMs) are fatal birth defects that are an important cause of fetal/neonatal death. There is a lack of informative data about these malformations in India, a country that shares the maximum burden of neonatal mortality due to congenital birth defects. Therefore, we conducted a retrospective analysis to know the prevalence of LCMs in late pregnancy, to find out associated factor/variables and to evaluate fetal/neonatal outcome of such anomalies; at a tertiary-care referral centre in North India. All deliveries with LCMs after 24 weeks of gestation were included in the study. Data about antepartum history (maternal age, parity, education, socioeconomic status, consanguineous marriage, folic acid intake, any chronic medical disorder, availability of anomaly scan, unplanned pregnancy); intrapartum events (gestational age at delivery, mode of delivery); postpartum events (weight of the baby, gender of the baby); newborn evaluation; and details of hospital stay were recorded from medical record sheet over the duration of one year. We found that anencephaly, severe meningomyelocele, multicystic dysplastic kidneys and non-immune hydrops with major cardiac defects were more prevalent among all LCMs. On the evaluation of the various studied variables, maximum babies with LCMs were born to mothers who were between 20 and 35 years of age, those who were illiterate, belonged to middle/lower socio-economic class, multigravida, and those who had no detailed anomaly scan. We feel that there is an urgent need to formulate a universally accepted definition of LCMs, to identify preventable risk factors and to formulate management strategy for both mother and liveborn baby with LCMs, in order to minimize the hidden burden of these defects in stillbirth/ perinatal/ neonatal mortality statistics.

7.
Cureus ; 11(2): e4048, 2019 Feb 11.
Artigo em Inglês | MEDLINE | ID: mdl-31016076

RESUMO

Dubin-Johnson syndrome is an autosomal recessive condition characterized by recurrent episodes of jaundice and conjugated hyperbilirubinemia. It exacerbates during pregnancy and needs to be differentiated from other causes of jaundice. A 30-year-old patient presented to us with jaundice in her fourth pregnancy. She had intermittent episodes of jaundice earlier, with exacerbation in each pregnancy during the second trimester. The diagnosis of Dubin-Johnson syndrome was made on detailed evaluation along with histopathological confirmation on liver biopsy tissue. The patient was managed conservatively and had a good perinatal outcome.

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