**12.1 Infective factors' mechanisms of action**

Toxic metabolic bio-products, endotoxins, exotoxins, or cytokines may have a direct effect on the uterus and the fetoplacental unit chronic endometrial infection following after lineal infection (M. hominis, Chlamydia, Ureaplasma urealyticum, and HSV) may affect the fetus implantation. Fetal infections are possible to cause fetal death or severe malformations incompatible with fetal livability (rubella, parvovirus B19, CMV, HSV, and syphilis). Placental infection probably causes placental deficiency with consequent fetal death. Amnionitis in the first trimester may have a similar effect on chorioamnionitis in the third trimester (causing premature labor). Various microorganisms with such effect, as L. monocytogenes, are suspected [69–74].

#### **12.2 Correlation between the various supposed mechanisms of automatic abortions and specific infectious factors**

Mechanisms:


Microorganisms: rubella, parvovirus B19, CMV, HSV, syphilis, Chlamydia, Mycoplasma, Ureaplasma, and various Gram-positive or Gram-negative bacteria (*L. monocytogenes*).

None of the above-mentioned infectious agents are usually confirmed to lead to RPL. Each high fever infection may lead to pregnancy loss. Viruses such as rubella and cytomegalovirus infection (CMV) go through the placenta and affect the embryo, as well as lead to malaria, chlamydia, mycoplasma, and trypanosomiasis [69–74].

Quite a few studies have confirmed that infections are to blame when it comes to miscarriages, especially during the second trimester of pregnancy; however, their role in the first trimester miscarriages remains unspecified.

#### **12.3 Recurrent miscarriages of unknown etiology**

New techniques in molecular biology and genetics could recognize the importance of "locality" for mutations. Detection of new mutations in immunological and other molecules is involved in the pathophysiology of abortions. It is of great importance to immediately start appropriate antibiotic therapy based on a test of cure culture, when cervical and vaginal infections are identified and to extend the treatment for both parents [75, 76].

#### **12.4 Thrombophilia**

Pregnancy is a condition that predisposes to hypercoagulation. The pregnant woman is in a state of increased tendency for coagulation (hypercoagulable state). The action of the fibrinolytic system decreases during pregnancy,

**71**

*Abortions in First Trimester Pregnancy, Management, Treatment*

particularly in the placenta, mainly due to an increase in inhibitors of the plas-

• Decrease in levels of physiologically existing anticoagulant factors (**naturally** 

• "Modified" maternal response to hemostasis ('**disordered' maternal hemo-**

Pregnancy is a state of hypercoagulation (hypercoagulable state). This hypercoagulable state do not necessarily causes thrombosis and the miscarriage is not due to thrombosis.and a lot of patients with miscarriages. This predisposition for thrombosis may lead to malfunction in the fetoplacental unit. A disorder in the balance between activators and inhibitors of plasminogen can lead to defective placentation [77–84]. The infiltration of trophoblast in arcuate arteries is essential for implantation, placentation, and consequently a regular continuation of pregnancy. Defective penetration is a common pathological finding in placenta preparations by women with excretion and also preeclampsia or intrauterine fetal growth delay

Placenta abnormalities include excessive implantation and placenta accreta. Increasing thrombophilic factors and five more frequent thrombophilic polymorphisms: a) V Leiden factor; b) MHTHFRC 677T; c) MTHFRA1298C; d) Factor VA1299H; and e) factor II G20210A are predisposition to venous thromboembolism (VTE). None of the five thrombophilic mutations, alone or in combination, was

**V Leiden:** women with RPLs and V Leiden mutation: there is no discrimination

**Treatment**: prophylactic administration of heparin without the confirmation of RCT is prescribed for known mutations of the factor V Leiden and also for the cases

5,10-methylentetrahydrofolate reductase catalyzes the conversion of 5,10-meth-

5-methyltetrahydrofolic acid takes part in the methylation of homocysteine in

The reduced activity of MTHFR and hyperhomocysteinemia is clinically mani-

Substitution of a cytosine molecule by a thymine molecule at position 677

**Treatment:** administration of 0.5–2 mg of folic acid leads to homocysteine

test for those who will have recurrent miscarriages from those that have a term

**C677T MTHFR polymorphism**: previous studies have shown conflicting results between the MTHFR C677T genotype and the recurrent miscarriages.

found to significantly increase the risk of miscarriages [77–84].

that there is indication of placental thrombosis [77–84].

ylentetrahydrofolic acid to 5-methyltetrahydrofolic acid.

increases the incidence of homocysteine and thrombophilia.

fested when lack of folic acid coexists [77–84].

**Pregnancy and coagulation mechanisms include the following:**

• Increase of coagulation precursors **(procoagulant factors)**

*DOI: http://dx.doi.org/10.5772/intechopen.86194*

**occurring anticoagulants**)

• Reduction of fibrinogenolysis

**static response)** [77–84]

**Correlation not quite clear!**

**12.5 Thrombophilic factors**

[77–84].

pregnancy.

methionine.

normal levels [77–84].

minogen activator [77–84].

particularly in the placenta, mainly due to an increase in inhibitors of the plasminogen activator [77–84].

#### **Pregnancy and coagulation mechanisms include the following:**


*Induced Abortion and Spontaneous Early Pregnancy Loss - Focus on Management*

Toxic metabolic bio-products, endotoxins, exotoxins, or cytokines may have a direct effect on the uterus and the fetoplacental unit chronic endometrial infection following after lineal infection (M. hominis, Chlamydia, Ureaplasma urealyticum, and HSV) may affect the fetus implantation. Fetal infections are possible to cause fetal death or severe malformations incompatible with fetal livability (rubella, parvovirus B19, CMV, HSV, and syphilis). Placental infection probably causes placental deficiency with consequent fetal death. Amnionitis in the first trimester may have a similar effect on chorioamnionitis in the third trimester (causing premature labor). Various microorganisms with such effect, as L. monocytogenes, are suspected

**12.2 Correlation between the various supposed mechanisms of automatic** 

Microorganisms: rubella, parvovirus B19, CMV, HSV, syphilis, Chlamydia, Mycoplasma, Ureaplasma, and various Gram-positive or Gram-negative bacteria

None of the above-mentioned infectious agents are usually confirmed to lead to RPL. Each high fever infection may lead to pregnancy loss. Viruses such as rubella and cytomegalovirus infection (CMV) go through the placenta and affect the embryo, as well as lead to malaria, chlamydia, mycoplasma, and trypanosomiasis

Quite a few studies have confirmed that infections are to blame when it comes to miscarriages, especially during the second trimester of pregnancy; however, their

New techniques in molecular biology and genetics could recognize the importance of "locality" for mutations. Detection of new mutations in immunological and other molecules is involved in the pathophysiology of abortions. It is of great importance to immediately start appropriate antibiotic therapy based on a test of cure culture, when cervical and vaginal infections are identified and to extend the

Pregnancy is a condition that predisposes to hypercoagulation. The pregnant

woman is in a state of increased tendency for coagulation (hypercoagulable state). The action of the fibrinolytic system decreases during pregnancy,

role in the first trimester miscarriages remains unspecified.

**12.3 Recurrent miscarriages of unknown etiology**

treatment for both parents [75, 76].

**12.4 Thrombophilia**

**12.1 Infective factors' mechanisms of action**

**abortions and specific infectious factors**

[69–74].

Mechanisms:

4.Amnionitis

(*L. monocytogenes*).

[69–74].

1.Embryotoxicity

2.Placental deficiency

3.Endometritis/endocervicitis

**70**

• "Modified" maternal response to hemostasis ('**disordered' maternal hemostatic response)** [77–84]

## **Correlation not quite clear!**

Pregnancy is a state of hypercoagulation (hypercoagulable state). This hypercoagulable state do not necessarily causes thrombosis and the miscarriage is not due to thrombosis.and a lot of patients with miscarriages. This predisposition for thrombosis may lead to malfunction in the fetoplacental unit. A disorder in the balance between activators and inhibitors of plasminogen can lead to defective placentation [77–84]. The infiltration of trophoblast in arcuate arteries is essential for implantation, placentation, and consequently a regular continuation of pregnancy. Defective penetration is a common pathological finding in placenta preparations by women with excretion and also preeclampsia or intrauterine fetal growth delay [77–84].

Placenta abnormalities include excessive implantation and placenta accreta.

Increasing thrombophilic factors and five more frequent thrombophilic polymorphisms: a) V Leiden factor; b) MHTHFRC 677T; c) MTHFRA1298C; d) Factor VA1299H; and e) factor II G20210A are predisposition to venous thromboembolism (VTE). None of the five thrombophilic mutations, alone or in combination, was found to significantly increase the risk of miscarriages [77–84].

### **12.5 Thrombophilic factors**

**V Leiden:** women with RPLs and V Leiden mutation: there is no discrimination test for those who will have recurrent miscarriages from those that have a term pregnancy.

**Treatment**: prophylactic administration of heparin without the confirmation of RCT is prescribed for known mutations of the factor V Leiden and also for the cases that there is indication of placental thrombosis [77–84].

**C677T MTHFR polymorphism**: previous studies have shown conflicting results between the MTHFR C677T genotype and the recurrent miscarriages.

5,10-methylentetrahydrofolate reductase catalyzes the conversion of 5,10-methylentetrahydrofolic acid to 5-methyltetrahydrofolic acid.

5-methyltetrahydrofolic acid takes part in the methylation of homocysteine in methionine.

Substitution of a cytosine molecule by a thymine molecule at position 677 increases the incidence of homocysteine and thrombophilia.

The reduced activity of MTHFR and hyperhomocysteinemia is clinically manifested when lack of folic acid coexists [77–84].

**Treatment:** administration of 0.5–2 mg of folic acid leads to homocysteine normal levels [77–84].
