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Decreased Circulating Level of Soluble Glycoprotein-130 in Recurrent Miscarriage Patients 68 evidences indicate that antiphospholipid antibodies which are a family of autoantibodies including lupus anticoagulant and anticardiolipin, induce thrombosis and pregnancy complications including recurrent stillbirth, recurrent miscarriage, pre-eclampsia and intra-uterine growth retardation (Chamley, 1997). The results of previous studies indicate that human aCL IgG that are beta2-GPI independent can induce placental necrosis and fetal loss in BALB/c mice (Ikematsu, et al., 1998). Recent evidence shows that anti-AV and anti-beta2-GPI antibodies should be regarded as independent risk markers (Zammiti, et al., 2006). Recently, it is reported that the presence of IgG anti-laminin-1 antibodies in the blood is significantly associated with recurrent first-trimester miscarriages and subsequent negative pregnancy outcomes. Thus, anti-laminin-1 antibodies may be important in the development of autoimmune-mediated reproductive failures (Inagaki, Kondo, Lopez, Shoenfeld, & Matsuura, 2005). Some results have been shown that women with recurrent spontaneous abortion of unknown etiology are differed in some parameters of immune response such as higher incidence of antinuclear antibodies in comparison with nonpregnant normal multigravidas (Malinowski, et al., 1997). There are some reports about the presence of ANA+ serum in abortion cases (Kano, Shimizu, & Kanda; Ticconi, et al.). Based on a previous study, the frequency of positive tests for ANA was significantly higher in Kuwaiti patients with unexplained recurrent spontaneous abortions (13.6%) than in controls (1.2%). No difference was found between first and second trimester aborters in the frequency of ANA positive tests. However, secondary aborters had significantly higher frequency of ANA (Bahar, Alkarmi, Kamel, & Sljivic, 1993). In other study on the prevalence of ANA in healthy women with first trimester recurrent spontaneous abortion, it was reported that only 13.2% of them had low levels of antinuclear antibodies, none of which were specific. Thus the reported prevalence of ANA in these group was low (Eroglu & Scopelitis, 1994). But another study reported a high prevalence of ANA in the patients with habitual abortion (30%) as compared with the control group (6.6%) (Garcia-De La Torre, Hernandez-Vazquez, Angulo-Vazquez, & Romero-Ornelas, 1984). One recent study in 2010 reported that ANA could be of some value in identifying women with recurrent pregnancy loss (RPL) with potential, although still not fully defined, immune abnormalities. It was reported that antinuclear antibodies at titers >/= 1:80 were detected in 50% women with RPL and in 16% control women. Elevated ANA titers (>/=1:180) were detected only in RPL women, whereas all control women had ANA titers no greater than 1:80. No differences in ANA positivity could be detected according to the type (primary or secondary) or number (>2 versus >/=3) of losses (Ticconi, et al.). According to a study about the outcome of pregnancy in ANA positive women, the perinatal mortality rate in the ANA-positive group was 18.6%, while there were no perinatal deaths in the ANA-negative control group. But ANA titer did not also correlate with the outcome of the pregnancy (Kiuttu, Hartikainen, Makitalo, & Ruuska, 1994). In other study results demonstrated a high prevalence of low-titer ANApositive serum in patients with both explained (34.3%) and unexplained (51.5%) pregnancy losses in compare with healthy pregnant (6.8%) and nonpregnant women (5.6%) (Malinowski, et al., 1994). A review of pregnancy outcome by another study indicated that maternal antinuclear antibodies are not, in general, associated with abnormalities of the pregnancy or of the offspring (Rosenberg, Bingham, & Fong, 1986). In a more recent study on the Argentine women, there was also no significant difference between the prevalence of ANA in fertile controls and patients with recurrent pregnancy loss with ANA (Bustos, et al., 2006). In other report it was demonstrate that women with recurrent spontaneous abortions showed significantly higher incidence of antibodies to phospholipids than normal multigravida controls. In contrast, the incidence of antibodies to polynucleotides and histones was not different between these two groups (Kwak, Gilman-Sachs, Beaman, & Beer, 1992). All these mentioned evidences could help us to confirm the higher level of autoreactivity in our miscarriage patients. There are some evidences which help to confirm our results regarding to higher score and prevalence of depression in miscarriage patients. For example it is reported that abortion may be a risk factor for subsequent depression in the period of 8 years after the pregnancy event (Cougle, Reardon, & Coleman, 2003). A number of studies have discussed about the relationship between abortion and depression (Rees & Sabia, 2007). For example in one report, the depression score for recurrent
69 Kambiz Bagheri, Padideh Ebadi, Hossein Berenjeian Tabrizi and Aboozar Dehghan miscaririag women and non-miscarriage group was 27.6+/-8.8 and 19.4+/-7.1 respectively (Andalib, Rezaie, Oreizy, Shafiei, & Baluchi, 2006). Our study about the depression status of miscarriage patients lead to some interesting results. We found that beside the higher average of depression score in these women, more depressed patients had higher level of anti-dsDNA and RF but lower level of sgp130. Also surprising that, more depressed patients, averagely more smoke hookah but had not more abortion number. Taken together these results showed that the lower post-abortion level of sgp130 or higher level of some autoimmune markers may become simply a consequence of higher depression which in turn may be related to unpleasant abortive occurrence or some habits like hookah consumption. Indeed high level of several autoantibodies like ANA or anti-dsDNA as well as CRP or RF in some miscarriage cases may be an outcome of depression which resulting from recurrent miscarriage as one of the most horrible event of women's life. There are several reports about the association of psychological disorders and autoimmune processes. For example it is reported that Immune dysregulation is common in depressive patients and also depressive symptoms have been found at a high prevalence in autoimmune disease. Recent studies have found that autoantibodies play an important role in the pathogenesis of depression both in animal models and human. It is suggested that depression can be regarded as autoimmune disease caused by various autoantibodies (Chen, Jiang, Ouyang, & Chen, 2009). For example it is believed that postpartum depression may have an autoimmune etiology (Gleicher, 2007). Major depression may be also accompanied by systemic immune activation or an inflammatory response with higher autoantibody (antinuclear, antiphospholipid) titers (Maes, 1995). Some groups had also reported higher titers of autoantibodies in depressed subjects than in normal controls. Meanwhile those observations pointed towards a higher expression of antiphospholipid antibodies during depression but a much lower incidence of positive patients than in classical autoimmune disorders, such as SLE (Maes, et al., 1993). It is also reported that in the patients with major depression, the frequency of some elevated autoantibodies like ANA are significantly higher than in the control group. In addition, in the schizophrenic patients significantly more often showed increased levels of ANA. These results point towards the existence of an unspecific autoimmune disposition or reaction in at least a subgroup of patients with major depression and schizophrenia (Laske, et al., 2008). Our results about the lower post-abortion level of sgp130 as a probable consequence of their higher depression are along with the previous evidences. For example, it is showed that elevated circulating pro-inflammatory cytokines are associated with symptoms of depression, and disorders involving chronic inflammation are often co-morbid with major depression (Dhabhar, et al., 2009). Some evidence also indicates that an immune response with an increased production of proinflammatory cytokines often accompanies major depression. Indeed, depression and IL-6 are positively associated in clinical and community samples (Howren, et al., 2009). Some other evidences suggest that there is an activation of the immuneinflammatory response system in depression. For example it is reported that serum IL-6 are significantly higher in subjects with major depression than in normal controls (Maes, et al., 1997; Song, et al., 1998). It was hypothesized that the elevated IL-6 levels during the acute state of depression or schizophrenia may reflect an unspecific stress response (Frommberger, et al., 1997). Although, other study showed that IL-6 and the sIL-6R are decreased in cerebrospinal fluid of geriatric patients with major depression. In this study, the level of sgp130 had no statistically significant difference between patients and controls (Stubner, et al., 1999). Other new study indicates an association between increased levels of IL-6 with depressive symptomatology in elderly individuals (Dimopoulos, Piperi, Psarra, Lea, & Kalofoutis, 2008). New evidences suggest that higher plasma IL-6 activity is associated with the refractoriness of depression (Yoshimura, et al., 2009). Recently, It has been also revealed that depression in cancer is associated with increased plasma IL-6 concentrations (Jehn, et al.). Moreover, a direct correlation between BDI (symptoms of depression) and IL-6 levels has been found in other patients such as those on maintenance haemodialysis (Hung, et al.).
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