Pregnancy Complications

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An increasing compilation of data supports the correlation that pregnancy complications and poor outcomes are associated with an excess of certain immune-markers. Many of the immune markers identified are proinflammatory cytokines, including IL-1P, IL-6, and TNF-a. Although there currently are no data to support the effect of pregnancy-associated sleep disturbances on pregnancy complications or poor pregnancy outcomes via increased proinflammatory cytokine production, the previously discussed data suggest a possible mediating role of sleep in the occurrence of these situations.

In an attempt to reduce their frequency, various pregnancy complications or poor outcomes and their potential causes (particularly increased proinflammatory cytokine levels) have been evaluated by researchers. Increased levels of proinflammatory cytokines, such as IL-2, IL-6, TNFa, and IFN-y, have been observed in spontaneous abortions (Clark et al. 1996), recurrent miscarriages (MacLean, Wilson, Jenkins, Miller, and Walker 2002; Raghupathy 2001), and preeclampsia (Afshari et al. 2005; Dekker and Sibai 1999), while anti-inflammatory cytokines, including IL-3, -4, and -10, have been noted to assist in the promotion, establishment, and completion of successful fetal growth (Clark et al. 1996; Dekker et al. 1999; Gaunt and Ramin 2001; Gennaro and Fehder 1996; Hanson 2000; Piccinni et al. 2000; Raghupathy 2001; Sacks, Studena, Sargent, and Redman 1998; Saito, Sakai, Sasaki, Tanebe, Tsuda, and Michimata 1999). It has been suggested that a predominance of proinflammatory cytokines at various points throughout pregnancy is incompatible with successful pregnancy (Raghupathy 2001).

About 15 to 20% of all pregnancies result in miscarriage, and the more pregnancy losses a woman experiences, the greater the risk of losing each subsequent conception (Coulam 2000). As noted previously, a healthy pregnancy is associated with alterations in the immune system, which may resemble a suppression of cellmediated immunity. Although there is incongruity in which mechanisms are involved in the success or failure of pregnancy, information continues to be ascertained regarding the role of cytokines in this process. Studies increasingly are focusing on how immunological problems can result in recurrent spontaneous abortion or miscarriage. From an alloimmune perspective, there are two possibilities that could result in RSA: either the mother's immune system does not recognize the pregnancy or the mother develops an abnormal immunologic response to the pregnancy (Coulam 2000). A few hypotheses have been suggested and tested in order to provide some evidence as to why miscarriages occur. One idea is that elevated levels of proinflammatory cytokines may impair the trophoblast from implanting, resulting in miscarriage (Hill, Polgar, and Anderson 1995; Hill et al. 1995). However, other data suggest TNF-a may be a protector of the feto-placental unit when it is exposed to teratogenic stress (Torchinsky et al. 2003). These contradictory hypotheses suggest a more complex interaction and influence of cytokines on pregnancy: when and how the shift occurs toward an anti-inflammatory cytokine profile may be most important. Since there appears to be a role for inflammation in implantation, pregnancy is not a Th2 phenomenon. Several "windows" for certain cytokines to be up-regulated or down-regulated, accompanied by precise timing and "tuning," seem essential (Chaouat et al. 2002). No study examining the causes of miscarriage has considered sleep disturbances as a possible contributor to the improperly timed increases in proinflammatory cytokines.

The occurrence of preeclampsia in women during the latter half of gestation has been identified as a pressing medical concern. The disease process includes hypertension, altered hematology, placental insufficiency, and edema (Edwards et al. 2000; Roberts 2004). It is the leading cause of preterm birth and intrauterine growth retardation and occurs in approximately 4 to 5% of all pregnancies (Dekker et al. 1999; Roberts 2004). Like RSA, preeclampsia is believed to be a result of an inappropriate activation of the maternal inflammatory response, including activation of granulocytes and increased release of TNF-a and IL-6, although the precise etiology is unclear (Dekker et al. 1999; Sacks et al. 1998). The importance of detecting preeclampsia early and halting its destructive path has been elucidated and is underscored by the numerous studies trying to understand the immunological variations associated with this disease.

Several studies have considered changes in "sleep" and preeclampsia. Two studies have considered differences in sleep quality and sleep architecture in preeclampsia. Evaluating sleep quality from subjective questionnaires and body movements in bed, Ekholm, Polo, Rauhala, and Ekblad (1992) suggested that sleep may be impaired in women with preeclampsia due to increased body movements during sleep. Examining sleep architecture, Edwards et al. (2000) showed significant increases in SWS in a group of preeclamptic women compared to healthy pregnant women. The authors propose that a "release of cytokines" may provide an explanation for the architecture differences; however, additional work is suggested (Edwards et al. 2000). Most studies, nonetheless, have assessed sleep-disordered breathing during pregnancy (Blyton, Sullivan, and Edwards 2004; Izci et al. 2005; Yinon et al. 2006) due to the strong association of increased hypertension and hypoxia that occurs in preeclampsia (Blyton et al. 2004). These relationships are subsequently associated with poor fetal outcomes. Presently, there are no studies examining the sleep-cytokine relationship in the occurrence of preeclampsia.

Another outcome that has been considered to be potentially immune-regulated is that of preterm birth. Experts have begun to view preterm birth as the final result of many possible causes, including intrauterine infections, hormonal disturbances, fetal injury, uterine ischemia, and uterine overdistention (Dudley 1999). Several immune parameters are thought to be involved in preterm birth. Evidence exists that inflammatory cytokines, such as IL-1P, TNF-a, IL-6, IL-8, and IL-4, are involved in infection-associated preterm labor (Dudley 1999). It is mostly in animal models where a clearer demonstration has been made that inflammatory cytokines can mediate early pregnancy loss; however, it appears that cytokines are only part of a cascade of events and it is an abnormally regulated maternal immune response, not an infection, that predisposes toward early pregnancy loss (Dudley 1999). Only one study assessed sleep disturbances at 22 to 26 weeks of gestation; the relationship between preterm labor and their findings were not significant (Stinson and Lee 2003). Similar to the other pregnancy complications discussed, no investigator has considered the sleep-immune relationship in the occurrence of preterm labor.

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