Hemolytic Urobilinogen

In jaundice secondary to hemolysis, the increased production of bilirubin leads to increased production of urobilinogen, which appears in the urine in large amounts. Bilirubin is not usually found in the urine in hemolytic jaundice (because unconjugated bihmbin does not pass into the urine), so that the combination of increased urobilinogen and absence of bihmbin is suggestive of hemolytic jaundice. Increased blood destruction from any cause brings about an increase in urine urobilinogen. 

Alterations in the metabolism of heme. A. Hemolytic jaundice. B. Neonatal jaundice. [Note The enterohepatic circulation of urobilinogen is omitted for simplicity.] BG = bilirubin glucuronide B = bilirubin U = urobilinogen S = stercobilin. 

As there is a lot of urine urobilinogen, the liver must be conjugating the bilirubin, and it is moved into the intestinal tract where urobilinogen is formed. An increase in serum indirect (unconjugated) bilirubin indicates hemolytic disease. 

Lack of urobilinogen in the urine and feces indicates biliary obstruction stools are whitish ( clay-colored ) owing to the absence of bile pigment. Urinary and fecal urobilinogen excretion increases in hemolytic anemia. 

According to Siedel S/t-l) about one-tenth of the urobilinogen and stercobilinogen in the lower intestinal tract may be reabsorbed into the blood stream and re-excreted throu the bile. Only a small amount, 0.5-2 mg per day escapes into the urine where autoxidation to urobilin and stercobilin occurs. Gray S44) believes that reabsorption of these compounds is not a prominent process in man. The finding of urobilin in urine and plasma under abnormal conditions (e.g., in hemolytic jaundice, or partial obstruction of bile secretion) is conadered to be due either to the liver having the capacity to reduce bilirubin fiu ther (S40) or to reabsorption of urobilinogen and a limited ability of the liver to secrete it into the bile (34 ). 

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