Postnatal depression screening in a paediatric primary care setting in Italy.

BACKGROUND: Postnatal depression is a non-psychotic depressive disorder that begins within 4 weeks of childbirth and occurs in 13% of mothers and 10% of fathers. A prospective study with the aim to evaluate the prevalence of postnatal depression by screening parents with the Edinburgh Postnatal Depression Scale (EPDS) in the Italian paediatric primary care setting was performed. METHODS: Mothers and fathers of infants born between 1 February and 31 July 2012, living in Italy's Milan-1 local health unit area, represented the target population of this pilot study. Parents attending well-child visits at any of the family paediatricians' offices between 60 to 90 days postpartum were asked to participate in the screening and to fill out the EPDS questionnaire. A cut-off score of 12 was used to identify parents with postnatal depression symptoms. Maternal and paternal socio-demographic variables and information concerning pregnancy and delivery were also collected. To investigate the association between screening positivity (dependent variable) and socio-demographic variables and factors related to pregnancy and delivery, a Pearson's χ2 test was used. Moreover, a stepwise multivariate logistic regression was carried out to evaluate the risk factors that most influence the probability of suffering from postnatal depression. RESULTS: In all, 126 out of 2706 (4.7%, 95% CI 3.9-5.5%) mothers and 24 out of 1420 (1.7%, 95% CI 1.0-2.4%) fathers were found to be positive for depressive symptoms. Women with mood disorders and anxiety during pregnancy were at increased risk of postpartum depression (OR 22.9, 95% CI 12.1-43.4). Only 11 mothers (8.7%) positive to EPDS screening attended a psychiatric service, and for 8 of them the diagnosis of postnatal depression was confirmed. CONCLUSIONS: The prevalence of postnatal depression was lower than previously reported. Routine screening resulted ineffective, since few mothers found positive for depression symptoms decided to attend psychiatric services.

Required role of apoptotic myogenic precursors and toll-like receptor stimulation for the establishment of autoimmune myositis in experimental murine models.

OBJECTIVE: Muscle regeneration is a hallmark of the idiopathic inflammatory myopathies (IIMs), a group of autoimmune disorders that are characterized by leukocyte infiltration and dysfunction of the skeletal muscle. Despite detailed studies describing the clinical and histopathologic features of IIMs, the immunopathogenesis of these disorders remains undefined. The aim of this study was to investigate the immunopathologic processes of autoimmune myositis in experimental murine models. METHODS: Expression of the autoantigen histidyl-transfer RNA synthetase (HisRS) was analyzed in mice with acutely injured or dystrophic muscles, in inflammatory leukocytes, and in purified satellite cells. Anti-HisRS antibodies and myositis induction were assessed in mice after muscle injury and immunization with apoptotic satellite cells or C2C12 myoblasts, in the presence or absence of the Toll-like receptor 7 (TLR-7) agonist R848. RESULTS: Muscle necrosis, leukocyte infiltration, and myofiber regeneration induced by toxic agents (cardiotoxin or glycerol) or promoted by genetic disruption of the α-sarcoglycan/dystrophin complex in mice were uniformly associated with up-regulated expression of HisRS. Although regenerating myofibers and purified satellite cells are known to show increased expression of HisRS in these settings, anti-HisRS antibodies were not detectable. However, intramuscular immunization with ultraviolet B-irradiated, HisRS-expressing apoptotic myoblasts in the presence of R848 triggered the production of anti-HisRS IgG antibodies as well as persistent lymphocyte infiltration and prolonged/delayed muscle regeneration. Conversely, intramuscular administration of R848 alone or in combination with living or postapoptotic/necrotic myoblasts failed to generate this myositis phenotype. CONCLUSION: In the presence of TLR/adjuvant signals and underlying muscle injury, apoptotic myogenic precursors expressing high levels of autoantigen can provoke autoantibody formation and lymphocytic infiltration of muscle tissue, effectively replicating the features of IIM.