Hyperbilirubinemia syndrome

Capecitabine is used for the treatment of colorectal and breast cancers. It is contraindicated in patients with known hypersensitivity to capecitabine or any of its components or to 5-fluorouracil and in patients with known dihydropyrimidine dehydrogenase (DPD) deficiency. The use of capecitabine is restricted in patients with severe renal impairment. The drag can induce diarrhea, sometimes severe. Other side effects include anemia, hand-foot syndrome, hyperbilirubinemia, nausea, stomatitis, pyrexia, edema, constipation, dyspnea, neutropenia, back pain, and headache. Cardiotoxicity has been observed with capecitabine. A clinically important drag interaction between capecitabine and warfarin has been demonstrated. Care should be exercised when the drag is co-administered with CYP2X9 substrates. 

Wada M, Toh S, Taniguchi K, Nakamura T, Uchiumi T, Kohno K et al. Mutations in the canalicular multispecific organic anion transporter (cMOAT) gene, a novel ABC transporter, in patients with hyperbilirubinemia I I/Dubin-Johnson syndrome. Hum Mol Genet 1998 7(2) 203-207. 

Jaundice. A syndrome characterized by hyperbilirubinemia (excessive concentrations of bilirubin in the blood) and deposition of bile pigment in the skin, mucous membranes, and sclera with resulting yellow appearance of the patient Karyotype. The chromosome characteristics of an individual or of a cell line, usually presented as a systematized array of metaphase chromosomes from a photomicrograph of a single cell nucleus arranged in pairs in descending order of size and according to the position of centromere. 

Some patients receiving indinavir exhibit nephrolithiasis/urolithiasis including flank pain that may be accompanied by hematuria. The frequency of nephrolithiasis is dependent on the period of treatment with indinavir. Other side effects associated with indinavir include insulin resistance, hyperglycemia, asymptomatic hyperbilirubinemia, HIV lipodystrophy syndrome and skin abnormalities. Indinavir should not be coadministered with drugs that affect the cytochrome P-450 system (CYP3A4). Antacids are not recommended within 2 h of its administration, specifically didano-sine containing an antacid buffer. 

Rotger M, Taffe P, Bleiber G, et al. Gilbert syndrome and the development of antiretroviral therapy-associated hyperbilirubinemia. J Infect Dis 2005 192(8) 1381-1386. 

Finally, there are hereditary causes of non-conjugated, nonhemolytic hyperbilirubinemias. These are Crigler-Najjar types 1 and 2 and Gilbert s syndrome (discussed in the section on Genetic Diseases of Bilirubin Metabolism). 

Miyaoka T, Yasukawa R, Mizuno S, Sukegawa T, Inagaki T, et al. 2005. Proton magnetic resonance spectroscopy (lh-mrs) of hippocampus, basal ganglia, and vermis of cerebellum in schizophrenia associated with idiopathic unconjugated hyperbilirubinemia (gilbert s syndrome). J Psychiatr Res 39 29-34. 

Since mutism with olanzapine has been reported in cases of overdose, and detoxification of bilirubin by conjugation with glucuronic acid, the pathway olanzapine uses, is altered in Gilbert s syndrome, which affects 10% of the population, the authors claimed that we should keep in mind idiopathic unconjugated hyperbilirubinemia when prescribing olanzapine. 

Defective excretion of conjugated bilirubin into the bile. This occurs in the Ehibin-Johnson and Rotor syndromes. The resultant hyperbilirubinemia is mainly of the conjugated type as is the hyperbilirubinemia of extiahepatic obstruction of the biliaiy ducts (as by tumor or gallstones). 

Kemeny N, Seiter K, Martin D, Urmacher C, Niedzwiecki D, Kurtz RC, Costa P, Murray M. A new syndrome ascites, hyperbilirubinemia, and... 

Indinavir has been compared with abacavir in a randomized equivalence trial in 562 patients who were also taking lamivudine and zidovudine (10). The only significant difference in adverse effects was that there was hyperbilirubinemia in 8% of those taking indinavir and 2% of those taking abacavir. It has been postulated that indinavir-induced hyperbilirubinemia is due to inhibition of bilirubin UDP glucuronyl transferase activity, since it is more common in individuals with Gilbert s syndrome (11). 

Palmar-plantar erythrodysesthesia (hand-foot syndrome) diarrhea stomatitis dermatitis bone marrow depression hyperbilirubinemia ocular irritation and corneal deposits... 

Gilbert syndrome is a benign condition manifested by mild unconjugated hyperbilirubinemia. This abnormality, affecting 3% to 5% of the population, is clinically important, because it is often misdiagnosed as chronic hepatitis. The serum concentration of bihrubin fluctuates between 1.5 and 3mg/dL (26 and 51 Limol/L) and tends to increase with... 

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