Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the hemocoagulative and fibrinolytic dynamics of the perinatal period and also to seek the cause of SGA (small for gestational age) baby birth, the coagulation and fibrinolysis of the cord blood were examined, and moreover a comparison with the maternal blood, discussion on the difference in birth weight, and an examination of the difference due to the sex of babies were made in 68 cases with full-term, vaginal, spontaneous delivery, and the following conclusions were reached. In comparison with maternal blood, cord blood significantly showed any of the following: Prolongations of the prothrombin time, and the activated partial thromboplastin time, a decrease in fibrinogen, and a decrease in the platelet aggregation, antithrombin III, and plasminogen. In addition, high values for thromboxane B2 and 6-ketoprostaglandin F1 alpha were observed. In the SGA group, significant decreases were observed in the platelet count, antithrombin III, plasminogen, and alpha 2-plasmin inhibitor as compared with the AGA (appropriate for gestational age) and LGA (large for gestational age) baby groups. No sex difference was observed in the hemocoagulative and fibrinolytic capacities of the cord blood. These hemocoagulative and fibrinolytic capacities, particularly changes in the fibrinolytic system observed in the SGA group, seem to be attributable to chronic DIC (disseminated intravascular coagulation) and mild acidosis due to various stresses during pregnancy and at parturition, in turn due to immaturity of the liver in babies.
 ...
PMID:[Blood coagulation and fibrinolysis in cord blood with reference to birth weight]. 405 31

Unexplained intra-uterine fetal death is still a problem in diabetic pregnancies, especially in those with an LGA-infant. We hypothesized that in these pregnancies impaired placental function, in terms of abnormal placental weight and/or abnormal placental histology, may account for this phenomenon. To test this hypothesis, we assessed the relative placental weight and scored several histological abnormalities in 34 AGA- and 24 LGA-placentae of type 1 diabetic women and in 22 AGA- and 16 LGA-placentae of control women. Relative placental weight was comparable in the LGA-diabetic cases and in the control groups, but was significantly higher in the AGA-diabetic subgroup. Histological abnormalities such as the presence of nucleated fetal red blood cells, fibrinoid necrosis, villous immaturity and chorangiosis were observed more often in the diabetic placentae compared with the control placentae. These differences in histology were particularly observed when we compared both AGA-groups. LGA-control placentae showed a high incidence of histological abnormalities, almost comparable to the diabetic placentae. Only fibrinoid necrosis was significantly more common in the LGA-diabetic placentae. Three of the four cases of perinatal death/asphyxia in the diabetic group concerned an LGA-infant with a relative low placental weight. In conclusion, placentae of women with type 1 diabetes showed several abnormalities that can be associated with impaired functioning. The difference between AGA- and LGA-diabetic placentae was related to relative placental weight and our data suggest that an increase in relative weight may protect the fetus from asphyxia. Placentae from LGA-non-diabetic women showed several similarities to those of women with diabetes.
 ...
PMID:Placental pathology in women with type 1 diabetes and in a control group with normal and large-for-gestational-age infants. 1312 78