I got a referral from my doctor's secretary, apparently my Bilirubines level is elevated. I dunno wtf those are though, can someone enlighten me and what this means? A few months ago I supposedly had lowered white blood cells level, and now this. WTF, I felt in perfect health then and I still feel in perfect health now. This is strange...
Doctor says I have elevated Bilirubines count, gotta see a specialist. WTF are these?
- Thread starter Ultima
- Start date
It is associated with the liver.
However, that's about all I can tell you...
Hope all is well for you!
However, that's about all I can tell you...
Hope all is well for you!
Here... quick search came up with this.
Good luck!
**************************
General consideration:
Bilirubin--bile pigment--accumulate in body tissues causing greenish-yellow discoloration called jaundice (icterus).
Usually, jaundice is linked to liver diseases, and jaundice is thought to mean liver diseases.
Actually, not all jaundice is induced by liver diseases and liver diseases are not always associated with jaundice.
Bilirubin, a physiological product of RBC, is metabolized in the liver and excreted into bile ducts, therefore an appearance of jaundice at first means that there is a breakdown of balance in bilirubin metabolism thus the patient has liver problem.
Except for liver diseases, hemolytic jaundice, a blood disease, will also present with jaundice. However, the incidence of this condition is rather rare, therefore it is just enough to have a knowledge of this condition and keep it in mind when you manage a case with jaundice.
You need an experienced eye to diagnose jaundice with naked eye. Experienced physician can diagnose jaudice with minimum of 2.0 mg/dl serum bilirubin level. For people, non-professional, to notice jaudice, it needs to have at least 5~6mg/dl or more of serum bilirubin level.
Therefore, the detection of serum bilirubin level is one of the basic test for the detection of the presence and extent of liver diseases.
Urobilirubinogen:
After the excretion to the alimentary tract, the bilirubin is reduced to colorless urobilinogen by intestinal pathogens, followed by oxidation to colored urobilin which is excreted out of the body by the alimentary tract. A part of urobilinogen is reabsorbed from the alimentary tract and excreted out of the body by the way of the kidney. Therefore, the detection of urinary bilirubin and urobilinogen is of important significance in the diagnosis of liver diseases.
Metabolism of bilirubin:
Bilirubin is an end product of heme metabolism, coming mainly, 70 ~ 80 %, from hemoglobin of senescent red blood cells and the others from shunt pathway, myoglobin and respiratory enzymes with the structure of heme.
The daily amount of bilirubin originated from destruction of red blood cells is around 250 ~ 300 mg.
Bilirubin is split to heme and globin at first, then the heme is further split to iron and biliverdin, and the biliverdin converts to bilirubin finally.
The bilirubin combines tightly with albumin in the blood stream, and is seperated just before being taken into liver cells.
The bilirubin taken into liver cells combine with ligandin in the hepatocyte (cytosolic protein ligandin, Y-protein) to be transferred to smooth endoplasmic reticulum.
The bilirubin in the hepatocytes conjugate with glucuronic acid to become conjugated bilirubin, which is excreted from heptocytes to the biliary tract and intestines and finally out of the body.
The original bilirubin from hemoglobin is free unconjugated bilirubin in the blood stream and is not soluble in water. After taken into hepatocytes, it is converted to soluble conjugated form and is able to be excreted into bile ducts.
The bilirubin is divided into two types, direct reacting bilirubin and indirect reacting bilirubin, according to its mode of reaction during the test process. Although, it is not completely the same, it can be recognized as that the direct reacting bilirubin is the conjugated bilirubin and the indirect reacting bilirubin the unconjugated bilirubin.
The conjugated bilirubin is not absorbed in the bile ducts and intestinal tract, and is absorbed in the end portion of the ileum after hydrolyzed and converted to urobilinogen by the intestinal pathogens.
The urobilinogen is then oxidized to orange-color urobilin (stercobilin) and excreted in the stool out of the body. The yellowish color of stool is the color of the sterocobilin. Therefore, the clay color stool means that there is no bilirubin coming from biliary ducts owing to the obstruction of the bile ducts.
About 15 ~ 20 % of the urobilinogen is reabsorbed from the intestine into portal veins and finally 90 % of them returned to the liver and re-excreted in the bile, it is called entero-hepatic circulation of bilirubin. The remainding 10 % gets into the systemic circulation and finally exreted in the urine through kidney. Thus the urine urobilinogen increases in the case of hemolytic disease, hepatocellular disease and porto-systemic shunt.
Pathogenesis of hyperbilirubinemia
The balance of the bilirubin between production from the hemoglobin and excretion from the bile duct is kept well in normal condition.
Hyperbilirubinemia, jaundice, occutrs when the bilirubin balance between production and excretion breaks.
From mechanism of the bilirubin metabolism we can learn the possible causes of hyperbilirubinemia:
1. over production of bilirubin ----- hemolysis
2. the impairment in bilirubin uptake by the liver, conjugation in the liver, and excretion from the liver cells
3. the unconjugated and conjugated bilirubin is obstructed or leak back into the blood stream in the liver cells or from bile ducts.
Therefore, the increase in serum unconjugated bilirubin is caused by over-production of bilirubin -- hemolysis or failure of uptake of unconjugated bilirubin by the liver or impairement in the conjugation process in the liver cells
and the icrease in conjugated bilirubin is caused by impairment in the excretion process of the liver cells or failure of bilirubin excretion due to the obstruction of the bile ducts.
Method of determination
Although there are many kinds of methods for the determiantion of bilirubin, most of the methods are still according to the principle of Diazo reaction method reported by Hymans va den Bergh in 1913 with improved procedure.
The bilirubin concetration is determined by the detection of Azobilirubin produced when bilirubin reacts with diazotized sulfanic acid. By this method, the conjugated bilirubin reacts without the addition of hydrolysis promotor, alcohol, thus named direct bilirubin; and indirect bilirubin reacts only after addition of alcohol, so it is called indirect bilirubin.
Reference value
The reference value measured by autoanalyzer differs somewhat by the reaction time, temperature, and promotor of the diazotization.
Total bilirubin: 0.3 ~ 1.2 mg/dl
Direct bilirubin: 0.0 ~ 0.3 mg/dl
direct type bilirubin actually does not exist in the serum, however, a small portion of indirect reacting bilirubin may presents direct reaction, thus the result of direct bilirubin may show the maximum value of 0.3 mg/dl, but never above. It is about 20 ~ 30 % of the total bilirubin concentration.
In some liver diseases, the total bilirubin will be within 1.2 mg/dl, but when the direct bilirubin concentration is above 0.3 mg/dl, the existence of liver disease should be considered.
Starvation, pregnancy, pill intake, post-operation, hemolysis, alcohol intake, and steroid administation will show the increase in bilirubin level.
Administration of sulfa drug, phenobarbital will decrease the level of serum bilirubin concentration.
Change of the serum level in diseases
We can determine two kinds of bilirubin, direct and indirect.
Each kind of bilirubin represents the product of different stage of bilirubin meatbolism.
The change of serum level in each kind of bilirubin represents the damage of bilirubin metabolism in some specific stage.
Although different diseases may show the same pattern of change in two bilirubin, we still can differentiate the diseases by the change of combination in two bilirubin.
(A) Hyper-unconjugated-bilirubinemia
(1) Overproduction:
Normal liver can manage the amount of seven times of normal daily bilirubin production.
When the production of bilirubin is increased due to hemolysis and to the amount over the ability of normal liver to handle, the serum indirect bilirubin will increase and is called prehepatic jaundice. The other liver tests, such as GOT, GPT, Alk-P, that will reflect the damage of hepatocytes will remain to be normal and only indirect bilirubin is inceased.
(a) Hemolysis:
When there is congenital or acquired shortage of life span of red blood cells, there will be increase in indirect bilirubin due to overproduction.
In chronic hepatis or cirrhosis, there will be change in life span of red blood cells due to change in red blood cell membrane induced by the change in lipid metabolism.
Although, this degree of change will be able to be managed by the normall liver, but it will fail when the liver cells are damaged.
(b) Increase in early bilirubin:
Ineffective erythropoiesis due to blood diseases or primary shunt hyperbilirubinemia will induce increase in indirect bilirubin.
(2) Abnormality in uptake and conjugation:
Serum indirect bilirubin may increase in damage of intake by the liver cells or conjugation in the liver cells of bilirubin due to the failure of change of indirect bilirubin to conjugate bilirubin. This condition is called chronic non-hemnolytic unconjugated hyperbilirubinemia.
Such as Crigler-Najjar syndrome (congenital non-hemolytic jaundice) is caused by the deficiency congenital glucuronyl transferase. The symptoms will appear in the infant stage, and there are two types, Type I is more severe than Type II, and may induce kernicterus.
Gilbert's syndrome (constitutional hepatic dysfunction) or idiopathic unconjugated hyperbilirubinemia are also considered to be caused by the similar mechanism as Crigler-Najjar syndrome, and only different in degree. The serum bilirubin level rarely exceed 3 mg/dl.
(B) Hyper-conjugated-bilirubinemia:
The unconjugated-bilirubin conjuagte with glucuronic acid to become the conjugated-bilirubin.
Usually, when there is obstruction of bile flow, the condition is called cholestasis, including stasis of bile acids, cholesterol, alkaline-phosphatase, and electrolytes in addition to bilirubin, however, sometimes not all these components are retained.
When transportation of conjugated-bilirubin is impaired in the liver and/or during excretion process from liver cells or obstructed during passage from biliary capillary, bile ductules, intra-hepatic duct throughout to the orifice of duodenum, the condition is called as cholestatic jaundice.
As in the case of Dubin-Johnson syndrome, only bilirubin is retained and no other components as cholesterol, bile acids and alkaline-phopatase are retained. Therefore, sometimes the Dubin-Johnson syndrone is classified as a condition of bilirubin retension, and the meaning of cholestasis in this context denotes bilirubin retension.
(1) Intrahepatic cholestasis:
In liver diseases, the increase in serum bilirubin is mixed in type that means increase in both direct and indirect bilirubin.
In liver diseases, the life of red blood cells is usually shortened, thus the load of liver cells also increases owing to the increase in bilirubin production.
In hepatocyte diseases, i.e. acute and chronic liver diseases including cirrhosis, the uptake, conjugation and excretion of blirubin in the hepatocytes are impaired and induce an intra-hepatic cholestasis.
Therefore, the serum bilirubin elevation presents mixed type.
The jaundice in the other condition such as drug-induced hepatitis and jaundice in pregnancy are also an intra-hepatic cholestasis.
Usually, the elevation of serum bilirubin in the intra-hepatic cholestasis is higher than extra-hepatic cholestasis. Occasionally, it is higher than 30 mg/dl.
Someone reported that the ratio of direct and indirect may be of use in differential diagnosis of intra- and extra-hepatic jaundice, but I don't think so from my experience.
Many acute hepatitis cases may not present with jaundice, therefore they are often misdiagnosed as just a case of common cold.
In icteric hepatitis cases, the jaundice usually appear 3 ~ 5 days after the onset of prodromal symptoms of general malaise and nauseation, and reach the peak in one to two weeks, and subside within two weeks to two months.
In my 67 biopsy verified cases, the average serum bilirubin level is 11.7 mg/dl (1.4 ~ 26.4 mg/dl) for the total bilirubin and for the direct bilirubin component it is 6.4 mg/dl (0.2 ~ 15.6 mg/dl). Of them, 49 (73 %) cases are with direct bilirubin over 50 % of total bilirubin.
The elevation of serum bilirubin is less in cases of chronic persitent hepatitis than chronic active hepatitis, and usually not to be notified by naked eyes. In chronic active hepatitis and cirrhosis cases the serum bilirubin level used to fluctuate.
In chronic alcoholics, the serum bilirubin level is slightly elevated in 55 % of cases. In acute alcoholic cases, the serum bilirubin level is usually over 5 mg/dl.
Dubin-Johnson Syndrome (chronic idiopathic jaundice) and Rotor Syndrome (chronic familial jaudice) are considerd as congenital intraheptic cholestsis. The increase of serum bilirubin is mainly conjugated-bilirubin, and Rotor syndrome is considered as a variant of Dubin-Johnson syndrome. Morphologically, melanin pigments deposit in the liver cells are noted in Dubin-Johnson syndrome but not in Rotor Syndrome. They show different type of BSP retension clinically.
Primary biliary cirrhosis shows obstruction of biliary ductules and inter-lobular bile ductules.
Primary/secondary sclerosing cholangitis, primary/secondary hepatic cancer and other malignancies, and binign tumor and intrahepatic biliary stone will induce hyper-conjugated-bilirubinemia.
(2) Extrahepatic cholestasis:
Stones, benign or malignant tomor in the biliary tract, and/or biliary obstruction due to external compression such as pancreatic head tumor or swelling due to pancreatitis will induce elevation in serum conjugated-bilirubin.
Generally, the serum bilirubin elevation due to biliary tract stones used to fluctuate, and that due to malignancy used to show steady increase day by day.
Urine bilirubin
No bilirubin is present in normal urine. When urine bilirubin becomes positive, it means something wrong in the biliary tract or the liver.
Only conjugated-bilirubin will pass through renal glomeruli, and it is still unclear what factors will influence the renal clearance of bilirubin.
Serum level of bilirubin does not parallel to the amount of urinary bilirubin. The urinary bilirubin becomes positive in prodromal stage of acute hepatitis when the serum bilirubin is still within normal level, and on the contrary the urine bilirubin can not be detected at the peak stage of serum conjugated-bilirubin.
Therefore, you can detect acute hepatitis by urine bilirubin test before the jaudice appears.
Urobilinogen
As stated in the previous paragraph, only a small part of urobilinogen absorbed from the intestinal tract is excreted out of the body through the kidney, and most of the urobilirunogen return to the liver and are reexcreted to the intestinal tract.
The amount of urinary urobilinogen is affected by the amount of conjugated-bilirubin in the biliary duct and also intestinal pathogens that convert bilirubin to urobilinogen.
The amount of 24-hr urinary urobilinogen in normal person is 0 ~ 4 mg. In hemolytic diseases the urinary urobilinogen will increase because of production of a large amount of bilirubin.
Good luck!
**************************
General consideration:
Bilirubin--bile pigment--accumulate in body tissues causing greenish-yellow discoloration called jaundice (icterus).
Usually, jaundice is linked to liver diseases, and jaundice is thought to mean liver diseases.
Actually, not all jaundice is induced by liver diseases and liver diseases are not always associated with jaundice.
Bilirubin, a physiological product of RBC, is metabolized in the liver and excreted into bile ducts, therefore an appearance of jaundice at first means that there is a breakdown of balance in bilirubin metabolism thus the patient has liver problem.
Except for liver diseases, hemolytic jaundice, a blood disease, will also present with jaundice. However, the incidence of this condition is rather rare, therefore it is just enough to have a knowledge of this condition and keep it in mind when you manage a case with jaundice.
You need an experienced eye to diagnose jaundice with naked eye. Experienced physician can diagnose jaudice with minimum of 2.0 mg/dl serum bilirubin level. For people, non-professional, to notice jaudice, it needs to have at least 5~6mg/dl or more of serum bilirubin level.
Therefore, the detection of serum bilirubin level is one of the basic test for the detection of the presence and extent of liver diseases.
Urobilirubinogen:
After the excretion to the alimentary tract, the bilirubin is reduced to colorless urobilinogen by intestinal pathogens, followed by oxidation to colored urobilin which is excreted out of the body by the alimentary tract. A part of urobilinogen is reabsorbed from the alimentary tract and excreted out of the body by the way of the kidney. Therefore, the detection of urinary bilirubin and urobilinogen is of important significance in the diagnosis of liver diseases.
Metabolism of bilirubin:
Bilirubin is an end product of heme metabolism, coming mainly, 70 ~ 80 %, from hemoglobin of senescent red blood cells and the others from shunt pathway, myoglobin and respiratory enzymes with the structure of heme.
The daily amount of bilirubin originated from destruction of red blood cells is around 250 ~ 300 mg.
Bilirubin is split to heme and globin at first, then the heme is further split to iron and biliverdin, and the biliverdin converts to bilirubin finally.
The bilirubin combines tightly with albumin in the blood stream, and is seperated just before being taken into liver cells.
The bilirubin taken into liver cells combine with ligandin in the hepatocyte (cytosolic protein ligandin, Y-protein) to be transferred to smooth endoplasmic reticulum.
The bilirubin in the hepatocytes conjugate with glucuronic acid to become conjugated bilirubin, which is excreted from heptocytes to the biliary tract and intestines and finally out of the body.
The original bilirubin from hemoglobin is free unconjugated bilirubin in the blood stream and is not soluble in water. After taken into hepatocytes, it is converted to soluble conjugated form and is able to be excreted into bile ducts.
The bilirubin is divided into two types, direct reacting bilirubin and indirect reacting bilirubin, according to its mode of reaction during the test process. Although, it is not completely the same, it can be recognized as that the direct reacting bilirubin is the conjugated bilirubin and the indirect reacting bilirubin the unconjugated bilirubin.
The conjugated bilirubin is not absorbed in the bile ducts and intestinal tract, and is absorbed in the end portion of the ileum after hydrolyzed and converted to urobilinogen by the intestinal pathogens.
The urobilinogen is then oxidized to orange-color urobilin (stercobilin) and excreted in the stool out of the body. The yellowish color of stool is the color of the sterocobilin. Therefore, the clay color stool means that there is no bilirubin coming from biliary ducts owing to the obstruction of the bile ducts.
About 15 ~ 20 % of the urobilinogen is reabsorbed from the intestine into portal veins and finally 90 % of them returned to the liver and re-excreted in the bile, it is called entero-hepatic circulation of bilirubin. The remainding 10 % gets into the systemic circulation and finally exreted in the urine through kidney. Thus the urine urobilinogen increases in the case of hemolytic disease, hepatocellular disease and porto-systemic shunt.
Pathogenesis of hyperbilirubinemia
The balance of the bilirubin between production from the hemoglobin and excretion from the bile duct is kept well in normal condition.
Hyperbilirubinemia, jaundice, occutrs when the bilirubin balance between production and excretion breaks.
From mechanism of the bilirubin metabolism we can learn the possible causes of hyperbilirubinemia:
1. over production of bilirubin ----- hemolysis
2. the impairment in bilirubin uptake by the liver, conjugation in the liver, and excretion from the liver cells
3. the unconjugated and conjugated bilirubin is obstructed or leak back into the blood stream in the liver cells or from bile ducts.
Therefore, the increase in serum unconjugated bilirubin is caused by over-production of bilirubin -- hemolysis or failure of uptake of unconjugated bilirubin by the liver or impairement in the conjugation process in the liver cells
and the icrease in conjugated bilirubin is caused by impairment in the excretion process of the liver cells or failure of bilirubin excretion due to the obstruction of the bile ducts.
Method of determination
Although there are many kinds of methods for the determiantion of bilirubin, most of the methods are still according to the principle of Diazo reaction method reported by Hymans va den Bergh in 1913 with improved procedure.
The bilirubin concetration is determined by the detection of Azobilirubin produced when bilirubin reacts with diazotized sulfanic acid. By this method, the conjugated bilirubin reacts without the addition of hydrolysis promotor, alcohol, thus named direct bilirubin; and indirect bilirubin reacts only after addition of alcohol, so it is called indirect bilirubin.
Reference value
The reference value measured by autoanalyzer differs somewhat by the reaction time, temperature, and promotor of the diazotization.
Total bilirubin: 0.3 ~ 1.2 mg/dl
Direct bilirubin: 0.0 ~ 0.3 mg/dl
direct type bilirubin actually does not exist in the serum, however, a small portion of indirect reacting bilirubin may presents direct reaction, thus the result of direct bilirubin may show the maximum value of 0.3 mg/dl, but never above. It is about 20 ~ 30 % of the total bilirubin concentration.
In some liver diseases, the total bilirubin will be within 1.2 mg/dl, but when the direct bilirubin concentration is above 0.3 mg/dl, the existence of liver disease should be considered.
Starvation, pregnancy, pill intake, post-operation, hemolysis, alcohol intake, and steroid administation will show the increase in bilirubin level.
Administration of sulfa drug, phenobarbital will decrease the level of serum bilirubin concentration.
Change of the serum level in diseases
We can determine two kinds of bilirubin, direct and indirect.
Each kind of bilirubin represents the product of different stage of bilirubin meatbolism.
The change of serum level in each kind of bilirubin represents the damage of bilirubin metabolism in some specific stage.
Although different diseases may show the same pattern of change in two bilirubin, we still can differentiate the diseases by the change of combination in two bilirubin.
(A) Hyper-unconjugated-bilirubinemia
(1) Overproduction:
Normal liver can manage the amount of seven times of normal daily bilirubin production.
When the production of bilirubin is increased due to hemolysis and to the amount over the ability of normal liver to handle, the serum indirect bilirubin will increase and is called prehepatic jaundice. The other liver tests, such as GOT, GPT, Alk-P, that will reflect the damage of hepatocytes will remain to be normal and only indirect bilirubin is inceased.
(a) Hemolysis:
When there is congenital or acquired shortage of life span of red blood cells, there will be increase in indirect bilirubin due to overproduction.
In chronic hepatis or cirrhosis, there will be change in life span of red blood cells due to change in red blood cell membrane induced by the change in lipid metabolism.
Although, this degree of change will be able to be managed by the normall liver, but it will fail when the liver cells are damaged.
(b) Increase in early bilirubin:
Ineffective erythropoiesis due to blood diseases or primary shunt hyperbilirubinemia will induce increase in indirect bilirubin.
(2) Abnormality in uptake and conjugation:
Serum indirect bilirubin may increase in damage of intake by the liver cells or conjugation in the liver cells of bilirubin due to the failure of change of indirect bilirubin to conjugate bilirubin. This condition is called chronic non-hemnolytic unconjugated hyperbilirubinemia.
Such as Crigler-Najjar syndrome (congenital non-hemolytic jaundice) is caused by the deficiency congenital glucuronyl transferase. The symptoms will appear in the infant stage, and there are two types, Type I is more severe than Type II, and may induce kernicterus.
Gilbert's syndrome (constitutional hepatic dysfunction) or idiopathic unconjugated hyperbilirubinemia are also considered to be caused by the similar mechanism as Crigler-Najjar syndrome, and only different in degree. The serum bilirubin level rarely exceed 3 mg/dl.
(B) Hyper-conjugated-bilirubinemia:
The unconjugated-bilirubin conjuagte with glucuronic acid to become the conjugated-bilirubin.
Usually, when there is obstruction of bile flow, the condition is called cholestasis, including stasis of bile acids, cholesterol, alkaline-phosphatase, and electrolytes in addition to bilirubin, however, sometimes not all these components are retained.
When transportation of conjugated-bilirubin is impaired in the liver and/or during excretion process from liver cells or obstructed during passage from biliary capillary, bile ductules, intra-hepatic duct throughout to the orifice of duodenum, the condition is called as cholestatic jaundice.
As in the case of Dubin-Johnson syndrome, only bilirubin is retained and no other components as cholesterol, bile acids and alkaline-phopatase are retained. Therefore, sometimes the Dubin-Johnson syndrone is classified as a condition of bilirubin retension, and the meaning of cholestasis in this context denotes bilirubin retension.
(1) Intrahepatic cholestasis:
In liver diseases, the increase in serum bilirubin is mixed in type that means increase in both direct and indirect bilirubin.
In liver diseases, the life of red blood cells is usually shortened, thus the load of liver cells also increases owing to the increase in bilirubin production.
In hepatocyte diseases, i.e. acute and chronic liver diseases including cirrhosis, the uptake, conjugation and excretion of blirubin in the hepatocytes are impaired and induce an intra-hepatic cholestasis.
Therefore, the serum bilirubin elevation presents mixed type.
The jaundice in the other condition such as drug-induced hepatitis and jaundice in pregnancy are also an intra-hepatic cholestasis.
Usually, the elevation of serum bilirubin in the intra-hepatic cholestasis is higher than extra-hepatic cholestasis. Occasionally, it is higher than 30 mg/dl.
Someone reported that the ratio of direct and indirect may be of use in differential diagnosis of intra- and extra-hepatic jaundice, but I don't think so from my experience.
Many acute hepatitis cases may not present with jaundice, therefore they are often misdiagnosed as just a case of common cold.
In icteric hepatitis cases, the jaundice usually appear 3 ~ 5 days after the onset of prodromal symptoms of general malaise and nauseation, and reach the peak in one to two weeks, and subside within two weeks to two months.
In my 67 biopsy verified cases, the average serum bilirubin level is 11.7 mg/dl (1.4 ~ 26.4 mg/dl) for the total bilirubin and for the direct bilirubin component it is 6.4 mg/dl (0.2 ~ 15.6 mg/dl). Of them, 49 (73 %) cases are with direct bilirubin over 50 % of total bilirubin.
The elevation of serum bilirubin is less in cases of chronic persitent hepatitis than chronic active hepatitis, and usually not to be notified by naked eyes. In chronic active hepatitis and cirrhosis cases the serum bilirubin level used to fluctuate.
In chronic alcoholics, the serum bilirubin level is slightly elevated in 55 % of cases. In acute alcoholic cases, the serum bilirubin level is usually over 5 mg/dl.
Dubin-Johnson Syndrome (chronic idiopathic jaundice) and Rotor Syndrome (chronic familial jaudice) are considerd as congenital intraheptic cholestsis. The increase of serum bilirubin is mainly conjugated-bilirubin, and Rotor syndrome is considered as a variant of Dubin-Johnson syndrome. Morphologically, melanin pigments deposit in the liver cells are noted in Dubin-Johnson syndrome but not in Rotor Syndrome. They show different type of BSP retension clinically.
Primary biliary cirrhosis shows obstruction of biliary ductules and inter-lobular bile ductules.
Primary/secondary sclerosing cholangitis, primary/secondary hepatic cancer and other malignancies, and binign tumor and intrahepatic biliary stone will induce hyper-conjugated-bilirubinemia.
(2) Extrahepatic cholestasis:
Stones, benign or malignant tomor in the biliary tract, and/or biliary obstruction due to external compression such as pancreatic head tumor or swelling due to pancreatitis will induce elevation in serum conjugated-bilirubin.
Generally, the serum bilirubin elevation due to biliary tract stones used to fluctuate, and that due to malignancy used to show steady increase day by day.
Urine bilirubin
No bilirubin is present in normal urine. When urine bilirubin becomes positive, it means something wrong in the biliary tract or the liver.
Only conjugated-bilirubin will pass through renal glomeruli, and it is still unclear what factors will influence the renal clearance of bilirubin.
Serum level of bilirubin does not parallel to the amount of urinary bilirubin. The urinary bilirubin becomes positive in prodromal stage of acute hepatitis when the serum bilirubin is still within normal level, and on the contrary the urine bilirubin can not be detected at the peak stage of serum conjugated-bilirubin.
Therefore, you can detect acute hepatitis by urine bilirubin test before the jaudice appears.
Urobilinogen
As stated in the previous paragraph, only a small part of urobilinogen absorbed from the intestinal tract is excreted out of the body through the kidney, and most of the urobilirunogen return to the liver and are reexcreted to the intestinal tract.
The amount of urinary urobilinogen is affected by the amount of conjugated-bilirubin in the biliary duct and also intestinal pathogens that convert bilirubin to urobilinogen.
The amount of 24-hr urinary urobilinogen in normal person is 0 ~ 4 mg. In hemolytic diseases the urinary urobilinogen will increase because of production of a large amount of bilirubin.
<< I got a referral from my doctor's secretary, apparently my Bilirubines level is elevated. I dunno wtf those are though, can someone enlighten me and what this means? A few months ago I supposedly had lowered white blood cells level, and now this. WTF, I felt in perfect health then and I still feel in perfect health now. This is strange... >>
Umm..perhaps you should ask your doctor what it means.
wnied
Diamond Member
- Oct 10, 1999
- 4,206
- 0
- 76
I had elevated bilirubines in my blood when I went on a yearly physical, at the time I had been mildly ill with what I thought was the flu for about 3 weeks. Come to find out I had "Vegetation" around my Aortic valve, and needed it replaced. Whatever your elevated bilirubines mean...its not good. So get it checked out as your doctor has suggested, and follow his instructions.
Good Luck.
wnied
Good Luck.
wnied
Bilirubin:
Bilirubin is a major breakdown product of hemoglobin. Hemoglobin is derived from red cells that have outlived their natural life and subsequently have been removed by the spleen. During splenic degradation of red blood cells, hemoglobin (the part of the red blood cell that carries oxygen to the tissues) is separated out from iron and cell membrane components. Hemoglobin is transferred to the liver where it undergoes further metabolism in a process called conjugation. Conjugation allows hemoglobin to become more water-soluble. The water solubility of bilirubin allows the bilirubin to be excreted into bile. Bile then is used to digest food.
As the liver becomes irritated, the total bilirubin may rise. It is then important to understand the difference between total bilirubin, which has undergone conjugation (that is hepatic cell metabolism), and at portion of bilirubin which has not been metabolized. These two components are called total bilirubin and direct bilirubin. The direct bilirubin fraction is that portion of bilirubin that has undergone metabolism by the liver. When this fraction is elevated, the cause of elevated bilirubin (hyperbilirubinemia) is usually outside the liver. These types of causes are typically gallstones. This type of abnormality is usually treated with surgery (such as a gallbladder removal or choleycystectomy).
If the direct bilirubin is low, while the total bilirubin is high, this reflects liver cell damage or bile duct damage within the liver itself
Bilirubin is a major breakdown product of hemoglobin. Hemoglobin is derived from red cells that have outlived their natural life and subsequently have been removed by the spleen. During splenic degradation of red blood cells, hemoglobin (the part of the red blood cell that carries oxygen to the tissues) is separated out from iron and cell membrane components. Hemoglobin is transferred to the liver where it undergoes further metabolism in a process called conjugation. Conjugation allows hemoglobin to become more water-soluble. The water solubility of bilirubin allows the bilirubin to be excreted into bile. Bile then is used to digest food.
As the liver becomes irritated, the total bilirubin may rise. It is then important to understand the difference between total bilirubin, which has undergone conjugation (that is hepatic cell metabolism), and at portion of bilirubin which has not been metabolized. These two components are called total bilirubin and direct bilirubin. The direct bilirubin fraction is that portion of bilirubin that has undergone metabolism by the liver. When this fraction is elevated, the cause of elevated bilirubin (hyperbilirubinemia) is usually outside the liver. These types of causes are typically gallstones. This type of abnormality is usually treated with surgery (such as a gallbladder removal or choleycystectomy).
If the direct bilirubin is low, while the total bilirubin is high, this reflects liver cell damage or bile duct damage within the liver itself
lots of reasaons you could have an elevated bilirubin level
some reasons benign (nothing to worry about)
some reasons not so benign
have a gastroenterlogist or hepatologist check it out and help you understand what is going on, what what if anything needs to be done.
some reasons benign (nothing to worry about)
some reasons not so benign
have a gastroenterlogist or hepatologist check it out and help you understand what is going on, what what if anything needs to be done.
lots of reasaons you could have an elevated bilirubin level
some reasons benign (nothing to worry about)
some reasons not so benign
have a gastroenterlogist or hepatologist check it out and help you understand what is going on, what what if anything needs to be done.
Finally, someone without cut and past syndrome. Isolated elevated bilis are rare sentinel events . . . ie usually if there's something seriously wrong you have other signs (jaundice) or symptoms (nausea/vomiting) of dz. Never leave the doctor's office with questions . . . granted they hate answering; particularly if they don't know; but it's your health.
some reasons benign (nothing to worry about)
some reasons not so benign
have a gastroenterlogist or hepatologist check it out and help you understand what is going on, what what if anything needs to be done.
Finally, someone without cut and past syndrome. Isolated elevated bilis are rare sentinel events . . . ie usually if there's something seriously wrong you have other signs (jaundice) or symptoms (nausea/vomiting) of dz. Never leave the doctor's office with questions . . . granted they hate answering; particularly if they don't know; but it's your health.
Kev, go get it checked out right now. Live sh*t doesn't sound very good. Maybe those times you got hangovers were a little excessive. 
Anyway, doesn't sound good, so do go get it checked out ASAP. As far as I know, I'm still in perfect health - but then again I haven't seen a doctor in a loooooong time... something keeps coming up and I don't end up having an appointment. heh, maybe I should try and get one.
Good luck...
Anyway, doesn't sound good, so do go get it checked out ASAP. As far as I know, I'm still in perfect health - but then again I haven't seen a doctor in a loooooong time... something keeps coming up and I don't end up having an appointment. heh, maybe I should try and get one.
Good luck...
<< Umm..perhaps you should ask your doctor what it means. >>
ROFL Yeah, it never ceases to amaze me how people are continually asking for medical advice on ATOT.
911paramedic
Diamond Member
- Jan 7, 2002
- 9,448
- 1
- 76
There are too many reasons as to why you have elevated levels and only a doctor can tell you why. These explanations are definitions only so don't read too much into them until your doctor gives you a diagnosis.
<<
<< Umm..perhaps you should ask your doctor what it means. >>
ROFL Yeah, it never ceases to amaze me how people are continually asking for medical advice on ATOT.
>>Geez... like I said in my post, my doctor forwarded me to a specialist. Thru his secretary. In other words, he woudln't know. I'm sure the secretary didn't know either
I have a while to wait till I see that specialist, so I had to ask, and there's enough old geezers on here to know something about medicine and health
skip everything else and just read heartsurgeon's post . . .
Medical priority
1) treatable, serious condition sepsis
2) treatable, less serious condition gallstones
3) untreatable, serious condition Primary Sclerosing Cholangitis
4) untreatable, less serious condition Gilbert Syndrome Dubin-Johnson
3-5% of the US population has Gilbert syndrome . . . one significant clinical finding . . . mild excess bili (unconjugated). The only reason we care is it is often misdiagnosed as chronic hepatitis. Most commonly detected serendipitously in young adults during evaluation for unrelated issues.
Medical priority
1) treatable, serious condition sepsis
2) treatable, less serious condition gallstones
3) untreatable, serious condition Primary Sclerosing Cholangitis
4) untreatable, less serious condition Gilbert Syndrome Dubin-Johnson
3-5% of the US population has Gilbert syndrome . . . one significant clinical finding . . . mild excess bili (unconjugated). The only reason we care is it is often misdiagnosed as chronic hepatitis. Most commonly detected serendipitously in young adults during evaluation for unrelated issues.
Gilbert's syndrome.. yeah, that's what the specialist thinks I have. He says its essentially harmless and is an enzyme defect, and I don't have anything to worry about but I'm gonna take another blood test to be sure.
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