Gallbladder abnormalities

Avila NA, Shawker TH, Roach P, Bradford MH, Skarulis MC, Eastman R. Sonography of gallbladder abnormalities in acromegaly patients following octreotide and ursodiol therapy incidence and time course. J Clin Ultrasound 1998 26(6) 289-94. 

Biliary tract Nine subjects with Prader-Willi syndrome (mean age 15 years) received either octreotide 30 mg or saline intramuscularly every 4 weeks for 16 weeks. After a 24-week wash-out period, they then received the alternative therapy. Three developed gallbladder abnormalities on ultrasound by the end of the octreotide phase two went on to have cholecystectomy 12-24 months later [39 ]. 

In patients with normal gallbladder function, effective agents for eradication of chronic carriage include amoxicillin (3 g divided three times a day in adults for 3 months), trimethoprim-sulfamethoxazole (one double-strength tablet twice a day for 3 months), and ciprofloxacin (750 mg twice daily for 4 weeks). In patients with anatomic abnormalities, such as biliary or kidney stones, surgery combined with antibiotic therapy is indicated. 

Results obtained in this way were helpful, but of limited value. The analyses told us whether or not the bile was supersaturated with cholesterol, but did not tell us whether the abnormality was due to too much cholesterol, too few bile acids, too few phospholipids or to some combined defect. The next step, therefore, was to measure the hour-by-hour bile lipid-secretion rates using marker-corrected perfusion techniques. These assume that, in response to the perfusion stimulus (such as an intra-duodenal amino acid mixture), the gallbladder remains tonically contracted throughout and steady-state conditions ensue. 

Flepatic or severe renal dysfunction, including primary biliary cirrhosis, and patients with unexplained persistent liver function abnormality preexisting gallbladder disease hypersensitivity to fenofibrate. 

Transient abnormalities in liver function tests (eg, elevation in serum bilirubin, alkaline phosphatase, serum transaminases), and reduced biliary excretion of contrast media used for visualization of the gallbladder have also been observed. Drug/Food interactions Food interferes with the absorption of rifampin, possibly resulting in decreased peak plasma concentrations. Take on an empty stomach with a full glass of water. 

Examine liver, gallbladder (mouse), stomach, spleen, pancreas, intestines, kidneys, adrenal gland, ureters, bladder, umbilical artery, genital organs, dorsal aorta, and caudal vena cava. Possible abnormalities that can be observed include absent renal papilla, dilated ureter(s), and displaced testis. 

A. An influx of abnormal phospholipids in the gallbladder as a result of ileal disease... 

Molecular alterations of gallbladder adenomas are fairly different than those observed in the conventional dysplasia-carcinoma sequence. Mutations of the p53 gene are virtually nonexistent in gallbladder adenomas and only rarely detected in EHBD tumors. In contrast, p53 abnormalities are quite common in flat dysplasia and invasive carcinoma. Similarly, mutation of the KRAS oncogene is detected in only 25% of gallbladder adenomas. In contrast, mutations of the -catenin gene, which are uncommon in invasive biliary carcinomas, have been detected in 60% of adenomas, mostly the pyloric gland type, and less commonly the papillary or intestinal typesA ... 

Wistuba II, Miquel JF, Gazdar AF, Albores-Saavedra J. Gallbladder adenomas have molecular abnormalities different from those present in gallbladder carcinomas. Hum Pathol. 1999 30 21-25. 

Wistuba II, Albores-Saavedra J. Genetic abnormalities involved in the pathogenesis of gallbladder carcinoma. J Hepatobiliary Pancreat Surg. 1999 6 237-244. 

Spiro Site s red blood cells are deficient in spectrin. This deficiency impairs ) the ability of his erythrocytes to maintain the redundant surface area neces- sary to maintain deformability. Mechanical stresses in the circulation cause progressive loss of pieces of membrane. As membrane components are lost, Spiro Site s red blood cells become spherical and unable to deform. Elis spleen is enlarged because of the large number of red blood cells that have become trapped within it. His erythrocytes are lysed by mechanical stresses in the circulation and by macrophages in the spleen. Consequently, this hemolytic process results in an anemia. His gallstones were the result of the large amounts of bilirubin that were produced and stored in the gallbladder as a result of the hemolysis. The abnormally rounded red cells seen on a blood smear are characteristic of hereditary spherocytosis. 

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