Causes of cholestasis in infants

The physical health of babies is one of the most important concerns of the family. Since the organs of babies are not fully developed, their digestive ability and disease resistance are not as strong as those of adults. If babies do not receive good care in daily life, they are prone to various diseases. Therefore, we recommend that parents take good care of their babies. Below we introduce the causes of infant cholestasis.

1. Physiology of bile secretion Bile contains bile acid, which can increase bile secretion and promote the excretion of conjugated bilirubin, cholesterol, phospholipids and other fat-soluble organic substances (including certain drugs) from bile. When bile acid enters the duodenum, it can emulsify fat and form water-soluble particles (micelles) with fat decomposition products so that the fat can be absorbed by the intestinal mucosa. Bile acid is produced by the metabolism of cholesterol in the blood by liver cells. After combining with glycine and taurine in the cells, it is excreted into the bile capillaries and enters the intestines. After assisting in fat absorption, most of it is absorbed into the portal vein and entero-hepatic circulation at the terminal ileum and can be reused. The reaction of liver cells converting cholesterol into bile acid is regulated by the blood bile acid concentration. When bile acid increases, this reaction can be inhibited, and when it decreases, this reaction can be promoted.

2. Pathophysiology and clinical characteristics Cholestasis may cause the following pathophysiological changes and clinical consequences.

(1) Substances normally excreted through bile are retained or refluxed into the body, increasing their blood concentration and producing corresponding clinical manifestations, such as hyperconjugated bilirubinemia causing jaundice; hypercholecidemia can cause skin itching; hypercholesterolemia can cause xanthomas in severe cases. Both serum phospholipids and lipoprotein X increase, which also hinders the excretion of certain drugs and contrast agents, such as sodium bromophthalein (BSP) and 131I rose bengal.

(2) When there is a decrease or absence of bile in the intestine and a decrease in conjugated bilirubin, the stool will be light or grayish white. A decrease in bile acid will lead to fat and fat-soluble vitamin absorption disorders, and children may develop steatorrhea, malnutrition, growth stagnation, and fat-soluble vitamin deficiency. Vitamin A deficiency can cause Bitartrate spots and keratinization of the skin and mucous membranes; D deficiency can cause rickets and tetany; E deficiency can cause neuromuscular degeneration and proximal muscle atrophy; K deficiency can cause intracranial, gastrointestinal bleeding, and prolonged prothrombin time.

(3) Hepatocellular damage and/or bile stasis caused by the primary disease can often cause focal necrosis of the liver, giant changes in hepatocellular structure, hepatosplenomegaly, and abnormal liver function such as increased levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, 5-nucleotidase, and alpha-fetoprotein, and impaired albumin and coagulation factor synthesis. The disease progresses and may develop into biliary cirrhosis, eventually causing portal hypertension and/or liver failure. However, most children can recover smoothly clinically.

In the above article, we introduced one of the things that parents are most concerned about, that is, the physical health of the baby. One of the diseases that babies may suffer from is cholestasis. The above article analyzes in detail the causes of cholestasis in babies.