Abstract:
:Hyperbilirubinemia has been presumed to prevent the process of atherogenesis and cancerogenesis mainly by decreasing oxidative stress. Dubin-Johnson syndrome is a rare, autosomal recessive, inherited disorder characterized by biphasic, predominantly conjugated hyperbilirubinemia with no progression to end-stage liver disease. The molecular basis in Dubin-Johnson syndrome is absence or deficiency of human canalicular multispecific organic anion transporter MRP2/cMOAT caused by homozygous or compound heterozygous mutation(s) in ABCC2 located on chromosome 10q24. Clinical onset of the syndrome is most often seen in the late teens or early adulthood. In this report, we describe a case of previously unrecognized Dubin-Johnson syndrome caused by two novel pathogenic mutations (c.2360_2366delCCCTGTC and c.3258+1G>A), coinciding with cholestatic liver disease in an 82-year-old male patient. The patient, suffering from advanced atherosclerosis with serious involvement of coronary arteries, developed colorectal cancer with nodal metastases. The subsequent findings do not support the protective role of Dubin-Johnson type hyperbilirubinemia.
journal_name
World J Gastroenteroljournal_title
World journal of gastroenterologyauthors
Sticova E,Elleder M,Hulkova H,Luksan O,Sauer M,Wunschova-Moudra I,Novotny J,Jirsa Mdoi
10.3748/wjg.v19.i6.946subject
Has Abstractpub_date
2013-02-14 00:00:00pages
946-50issue
6eissn
1007-9327issn
2219-2840journal_volume
19pub_type
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