Feces, bilirubin

In the hver, bilirubin is made water-soluble by conjugation with two molecules of glucuronic acid and is secreted into the bile. The action of bacterial enzymes in the gut produces urobihnogen and urobihn, which are excreted in the feces and urine. 

Bilirubin digiucuronide is excreted from the liver via the bile into the intestine. Within the bowel, it is hydrolyzed, and the bilirubin is reduced to urobilinogen and stercobilinogen. These are excreted in urine as urobilin after reabsorption from the bowel, and in feces as stercobilin these pigments give urine and feces their characteristic colors. 

The normal range of serum copper in the adult is 11 to 24 Urinary copper is normally about 20 jjg/day. This level is equivalent to 0.5 to 3.0% of copper intake. Most of the copper absorbed into the body is excreted by way of the bile and lost via the feces. About 1.7 mg of copper is excreted in bile per day this amount varies with the amount absorbed from the diet. This copper occurs complexed with protein and bilirubin. Bilirubin is a catabolite of heme. The copper is excreted in the bile and lends not to be absorbed back Into the body, There is little or no enterohepatic circulation of copper. The concentration of bile copper drops markedly with a copper deficiency, contributing to the conservation of this mineral by the body. 

In the intestine, bacteria deconjugate bilirubin diglucuronide and convert the bilirubin to urobilinogens (see Fig. 44.7). Some urobilinogen is absorbed into the blood and excreted in the urine. However, most of the urobilinogen is oxidized to urobilins, such as stercobilin, and excreted in the feces. These pigments give feces their brown color. 

In adult humans, the catabolism of heme is the only known source of bilirubin IXa, 300-500 mg of the pigment being manufactured daily. It is a puzzle just why mammals should go to the trouble of reducing the water-soluble green biliverdin to insoluble yellow bilirubin. The body then has to esterify bilirubin with various sugars in order to solubilise it ready for excretion, via the bile duct, into the intestinal tract. Here, bilirubin undergoes further transformation to urobilinoids prior to its final excretion in feces. 

In goat kids orally administered 1 to 5 g/kg myrrh daily, grinding of teeth, salivation, soft feces, loss of appetite, jaundice, shortness of breath, ataxia, and recumbency were seen, and the animals died between days 5 and 16. Intestinal, hepatic, and renal toxicity were accompanied by anemia, leukopenia, increases in serum ALP activity and in concentrations of bilirubin, cholesterol, triglycerides and creatinine, and decreases in total protein and albumin. A dose of 0.25 g/kg was not toxic (Omer and Adam 1999). 

In rats administered myrrh at doses of 1000 mg/kg orally, 500 mg/kg intramuscularly, or 250 mg/kg intraperitoneally for 2 weeks, animals exhibited the following symptoms depression, soft feces, jaundice, ruffled hair, hepatone-phropathy, hemorrhagic myositis and patchy peritonitis (at the injection site), and death. These were accompanied by increases in serum ALP and ALT activities, bilirubin, and creatinine concentrations, and decreases in total protein and albumin levels, and macrocytic anemia and leukopenia. Doses of 500 mg/kg administered orally or 250 mg/kg administered intramuscularly were not lethal, and when given daily for 1 week the effects were less marked (Omer et al. 1999). 

Stercobillnogen. Formula, see stercobilin (saturated at C-10- and N-23). C33H4,N40, Mr 596.77. S. is formed in the intestines by bacterial degradation of the bile pigment bilirubin via urobilinogen and thus represents the actual final product of porphyrin degradation in warm-blooded organisms. It is excreted in urine and feces where it is easily oxidized to stercobilin. 

In conclusion, bile pigment metabolism can be divided into at least seven separate steps (1) hemoglobin breakdown in the reticuloendothelial cell (2) transfer of bilirubin from the reticuloendothelial to the hepatic cell by way of the blood (3) conversion of bilirubin to bilirubin glucuronide inside the hepatic cell (4) excretion of conjugated bile in the bile duct (5) urobilinogen formation (6) urobilinogen reabsorption and (7) re-excretion of urobilinogen in feces and urine (see Fig. 6-13). 

Pharmacokinetics Docetaxel administered intravenously over 1-2 hours has linear pharmacokinetics and the AUC increases proportionately with dose [117 ]. Plasma protein binding is 76-89% [118 ]. The half-life is 11 hours. Elimination is mainly by biliary excretion into the feces [119 ]. In patients with raised bilirubin and/or liver aminotransferases, there is a 12-27% reduction in docetaxel elimination, and dosage reductions should be considered [117 ]. In patients with raised bilirubin concentrations or aminotransferases more than 3.5 times the upper limit of the reference range, and alkaline phosphatase more than six times, no recommendations for dosage reduction can be made and docetaxel should be avoided [111 ]. 

Bilirubinoids are colored compounds occurring in vertebrates, in some invertebrates, and even in algae. They are formed by the biological oxidation of porphyrins. The most important representative is the orange-colored bilirubin (98). It occurs in the bile and in gallstones and is excreted in the feces and in urine. Bilirubin was first isolated by Staedeler (1864) and can be purified via its crystalline ammonium salt. It is oxidized to blue-green bihverdin (99) by iron(III) chloride ... 

The colorless urobilinogen and stercobilinogen autoxidize in air to brown-red urobilin and stercobilin. The brown color of the feces is for the most part due to the intense color of the fuscins since the urobilin and stercobilin pigments are excreted mainly in their reduced forms (S4IS). In the newborn during the first 3 weeks there is no reduction of bilirubin. Aureomycin and broad spectrum antibiotics sterilize the tract so that... 

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