Jaundice is a clinical sign that is characterized by the yellowish color of the skin, mucous membranes and eyes. It arises when there is too much of a substance called bilirubin. Jaundice is a typical symptom of liver and biliary disease, with hepatitis, cirrhosis and biliary tract obstruction being its main causes.
Before talking about jaundice itself, it is important to spend a few lines explaining what bilirubin is and in what situations it can accumulate in the blood.
Before talking about jaundice itself, it is important to spend a few lines explaining what bilirubin is and in what situations it can accumulate in the blood.
Our red blood cells have an average life of 120 days. When they become old, they are taken to the spleen to be destroyed. One of the products released in this destruction process is bilirubin, a yellow-green pigment.
Every day millions of erythrocytes are destroyed and a large amount of bilirubin is released. The great organ responsible for metabolizing the substances of our organism is the liver; that is where all the bilirubin produced is sent.
The only way to carry any substance through the body is through the bloodstream. The bilirubin produced in the spleen does not dissolve in the water. Thus, to be carried by the blood she needs to bind to a protein called albumin.
This insoluble bilirubin produced in the spleen is called indirect bilirubin (or unconjugated bilirubin). Their normal blood concentration ranges from 0.1 to 0.7 mg/dL.
When it reaches the liver, indirect bilirubin is metabolized and converted into a water-soluble substance, now called direct bilirubin (or conjugated bilirubin). Direct bilirubin is eliminated through the bile ducts to the gastrointestinal tract, where it will be eliminated in the stool.
When it reaches the intestines bilirubin is again metabolized, now by the intestinal bacteria, becoming a brown pigment responsible for the color characteristic of our feces.
A small part of the bilirubin produced in the liver passes into the bloodstream. The normal concentration of direct bilirubin in the blood ranges from 0.1 to 0.4 mg/dL. This direct bilirubin diluted in the blood is filtered through the kidneys and eliminated in the urine. Some yellowing of the urine is due to the presence of small amounts of bilirubin in it.
Therefore, normal blood bilirubin levels in adults are as follows:
Total bilirubin: 0.2 to 1.1 mg/dL
Indirect bilirubin: 0.1 and 0.7 mg/dL
Direct bilirubin: 0.1 to 0.4 mg/dL
Note: These values may vary slightly depending on the laboratory and the method used for measurement.
Jaundice arises when, for some reason, there is an accumulation of direct and/or indirect bilirubin in the blood. When bilirubin concentrations exceed 1.5-2.0 mg/dL, this excess pigment exudes to the skin, mucous membranes, and to the membrane that covers the sclera (whites of the eyes), leading to the characteristic yellowish appearance of jaundice.
Jaundice arises, basically, when there is excessive production of bilirubin and/or when there is a deficient elimination of bilirubin.
Jaundice due to indirect bilirubin increase
Indirect bilirubin can accumulate when there is a large destruction of the red blood cells - in addition to what is considered normal - by throwing into the bloodstream an amount of bilirubin greater than the liver's ability to excrete it.
This destruction is called hemolysis and can occur for several reasons:
Use of drugs (ribavirin, benzocaine, dapsone, phenazopyridine, paraquat, arsenic gas, lead, etc.)
Infections, such as malaria and leptospirosis
Defects in the own red blood cell, such as hereditary spherocytosis, nocturnal paroxysmal hemoglobinuria, sickle cell anemia, thalassemia, etc.
Autoimmune diseases
The accumulation of indirect bilirubin may also occur due to the inability of the liver to conjugate it to direct bilirubin. Gilbert syndrome and Crigler-Najjar syndrome are two genetic diseases that can cause jaundice due to deficiency of the liver enzyme responsible for bilirubin conjugation.
Jaundice by direct bilirubin increase
Jaundice by direct bilirubin occurs when the liver manages to conjugate bilirubin, but for some reason can not excrete it toward the intestines. Among the main causes we can mention:
In addition to yellowing of the skin and eyes, jaundice usually affects the mucous membranes. The tongue lock is another point where you can notice the yellowish pigment of bilirubin.
The deposition of the pigment on the skin, besides being responsible for the yellowish color, also causes an intense itching. Often, the patient complains more of the itching than of the own color change of the skin.
When jaundice is of direct origin, ie due to water-soluble bilirubin, we can have 2 other typical findings:
Coluria: When there is too much direct bilirubin in the blood, there is consequently too much bilirubin being filtered through the kidneys. The result is a dark urine (Coke type) or a strong orange, caused by too much pigment in it.
Because indirect bilirubin is not soluble in water, it is not filtered through the kidneys. Therefore, coluria is a typical sign of jaundice by direct bilirubin.
Fecal acolia: when there is an impediment in the excretion of conjugated bilirubin into the intestines, the patient may present with very clear stools, sometimes almost white, due to the absence of pigment in the intestine.
Jaundice is not a disease, but a sign of disease. Therefore, in the vast majority of cases, your treatment first passes through the treatment of the disease that is causing the jaundice. If it is a hepatitis, it is hepatitis; if it is an obstruction of the bile ducts, it is the obstruction; if it is a reaction to a medicine, the medicine is discontinued.
One of the few situations that the treatment directly targets the reduction of jaundice is in the case of neonatal jaundice, since excess bilirubin may be toxic to the infant's brain.
There is no specific remedy that can be taken to lower hyperbilirubinemia in all cases. Each situation should be treated individually.