Causes and Mechanisms of Jaundice
The pathogenesis of jaundice is viewed in the context of internal organ immaturity, primarily the liver. In premature infants, the liver is relatively large, but its enzyme systems do not function at full capacity.
The main factor determining a prolonged and pronounced course of jaundice is the insufficient activity of the enzyme glucuronyl transferase. Normally, this enzyme is responsible for the conjugation and excretion of bilirubin, which is formed as a result of the massive breakdown of fetal hemoglobin after birth.
Morphological Features of the Liver
Histological examination of the liver of a fetus or premature infant (with hematoxylin and eosin staining) reveals a characteristic picture.
The main morphological feature is the presence of pronounced extramedullary hematopoiesis. Multiple foci of blood cell formation are visualized in the liver tissue, indicating stressed functioning of the fetal hematopoietic system.
Features of Other Organs in Immature Fetuses
Because hemolytic disease is frequently associated with prematurity or immaturity of fetal systems, it is important to note the morphofunctional characteristics of other organs:
- Brain: The tissue is soft and gelatinous; the boundary between gray and white matter is indistinct due to incomplete myelination. The presence of the subependymal germinal matrix around the ventricular system is characteristic.
- Lungs: In fetuses younger than 32 weeks, alveoli are lined with cuboidal epithelium, interalveolar septa are thick, contain abundant connective tissue, and capillaries do not have close contact with the alveolar lumen.
- Kidneys: Primitive glomeruli with multi-layered cuboidal epithelium of Bowman's capsule are present in the subcapsular zone.
- Adrenal glands: The fetal cortex predominates, consisting of large cells with foamy cytoplasm, which regresses after birth.