Bile Cast Research Articles

Histochemical and ultrastructure study of bile cast in liver transplantation patients

To investigate the histological components and solubility of the bile-cast, and to study the pathological course of bile cast formation. HE staining, bilirubin staining (Gmelin reaction), Masson's staining, alcian blue staining and fibrin staining (weigert's) were performed on the formalin-fixed paraffin-embedded section of the bile cast. Ultrastructure was examined under the scanning electron microscope. Solubility test was also conducted using chymotrypsin, heparin, trypsin solution, HCl and NaOH solution to dissolve the bile-cast. The major components of the bile-cast were bilirubin crystals and collagen fibers. Between the mass of collagen fibers there was certain blood vessel structure. Necrosis bile duct structure was not found in the cast. Under the scanning electron microscope, four kinds of crystal morphologies were viewed. There were some mucoid mass and necrosis defluvium epithelial cells in the bile cast. Solubility test showed that the bile cast could be partial dissolved in NaOH solution (pH = 12.5). No dissolution was found in HCl solution (pH = 5.0), chymotrypsin solution, heparin and trypsin solution. Collagen fibers work as framework in the bile cast with bilirubin crystal filling between the framework. The emergence of fibroblast and blood vessels indicated the formation of bile cast might be the course of exudation and organization due to bile duct epithelium damage. Bile cast could be partially dissolved in alkaline solution, but could not be dissolved in acid solution, or in chymotrypsin, heparin and trypsin solutions.

Bile cast syndrome after orthotopic liver transplantation

Bile cast syndrome after orthotopic liver transplantation

Renal function and structure in subacute hepatic failure

Subacute hepatic failure (SHF) is a fatal complicaton of acute viral hepatitis. Renal failure has been implicated as the main cause of death in this disease. However, renal functional and structural evaluation in such patients have not been performed. The present prospective study evaluated the renal functional and structural abnormalities in patients with subacute hepatic failure. Fourteen consecutive patients with SHF, 11 with acute liver failure (ALF) and 15 with cirrhosis of the liver (Child's B or C) were included in the present study. All 40 patients had liver disease caused by hepatitis viruses. The glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) estimations were measured in all patients by the use of technetium-99m diethylenetriaminepentaacetic acid and [131I]-labeled ortho-iodohippuric acid, respectively. Ante-mortem or post-mortem liver biopsies were performed in all patients. In three patients with SHF, post-mortem kidney biopsies were also performed. Thirty six percent (5/14) of patients with SHF, 18% (2/11) of patients with ALF and 20% (3/15) of patients with cirrhosis had renal failure. Seven patients with SHF, seven with ALF and nine with cirrhosis died. All the patients with renal failure in each of the three groups were among the deceased patients. Glomerular function was markedly affected among patients with SHF, which was shown by significantly higher (P < 0.05) proteinuria levels (0.367 +/- 0.38 g/24 h) compared to levels in patients with ALF (0.178 +/- 0.11 g/24 h) and cirrhosis (0.212 +/- 0.133 g/24 h). The GFR in SHF (56 +/- 27 mL/min per 1.73 m2) and cirrhotic patients (58 +/- 36 mL/min per 1.73 m2) was significantly lower compared to those in ALF patients (102 +/- 51 mL/min per 1.73 m2; P < 0.05). A significantly higher proportion (P < 0.05) of patients with SHF and cirrhosis (64 and 73%, respectively) had a GFR below 80 mL/min per 1.73 m2 compared to patients with ALF (18%). The GFR value among the deceased SHF patients (46 +/- 26 mL/min per 1.73 m2) was significantly lower (P < 0.05) than those SHF patients who survived (65 +/- 25 mL/min per 1.73 m2). However, similar features could not be documented among patients with ALF or cirrhosis. Subtle structural changes in the glomerulus were also noted in patients with SHF. These included mesangial proliferation and thickening, basal membrane thickening and increased cellularity with interstitial edema. The ERPF was markedly reduced (P = 0.058) among patients with SHF (347 +/- 131 mL/min per 1.73 m2) and cirrhosis (395 +/- 137 mL/min per 1.73 m2) in comparison to ERPF documented among patients with ALF (436 +/- 217 mL/min per 1.73 m2). Such a reduction in renal tubular blood flow, along with histologic documentation of hyaline presence, bile and grannular cast in the tubule, indicated a possible tubular dysfunction in patients with SHF. It is concluded that glomerular and tubular dysfunction with subtle structural abnormalities does occur in patients with SHF. These are similar to renal changes in cirrhosis and may have similar pathogenetic mechanisms that require further evaluation.

Liver transplantation and bile analysis: a parallel evolution.

Liver transplantation and bile analysis: a parallel evolution.

A Total Bile Cast of the Biliary Tree

A Total Bile Cast of the Biliary Tree

A Total Bile Cast of the Biliary Tree

Summary The development of a complete bile cast of the biliary tree in a 70-year-old man with recurrent episodes of cholecystitis and choledocholithiasis is reported. A review of the literature has failed to reveal similar examples of this entity. A mechanism for the development of the cast is suggested.

Limy bile cast of gallbladder.

N INFREQUENT AND INTFIIESTING CONDITION of the gallbladder is due to the presence of bile containing a high concentration of calcium carbonate, with the result that the gallbladder is radiographically visible even without the administration of dye. The earliest report of calcium bile was made in 1911, by Churchman, z who found a material in the gallbladder which had the consistency of toothpaste. Chemical analysis revealed that this material consisted largely of soaps of calcium salts. The term "milk of calcium" bile was originated by Volkmann," who, in 1926, reported 2 eases in which the gallbladders removed at operation contained a white fluid which proved to be calcium carbonate. In 1931, Phemister and his co-workers 3 reported 7 eases with calcium earbonate gallstones. Knutsson/in 1933, reported 12 eases of calcium carbonate deposits in the gallbladder, and introduced the term "limy bile" in preference to "milk of calcium" bile because he showed that the amorphous material in the gallbladder not ahvays was a thin, milky fluid, but was often a semisolid paste or solid concretion. In 1935, Kornblum and Hall 5 gathered 5 eases, including 1 of their own, in a discussion of the radiographic findings. In 1942, McCall and Tuggle G reported a study of 15 patients with calcium bile. The most reeent report 7 was of a ease of a densely opaque gallbladder fortuitously visualized during a gastrointestinal x-ray series.

Congenital biliary atresia with emphasis on the skeletal abnormalities.

Congenital biliary atresia is a developmental defect resulting in the complete exclusion of bile from the intestinal tract. The severe hepatic damage consequent upon the biliary obstruction produces polyclinical abnormalities which have been reported in numerous publications (29, 33, 34). As far as can be determined, however, there has been no clear distinction made between the two varieties of osseous dystrophy found in this condition. The following two cases are presented to illustrate these differences, as well as many of the other abnormalities found in biliary atresia. Report Of Cases Case I: D. P., a colored female, was born on July 29, 1952, and was first admitted to the Cincinnati General Hospital on Sept. 23, 1952, because of jaundice which had not been present at birth. The mother stated that the baby passed on the average four yellow stools daily and the urine was never dark. Physical examination was normal except for scleral icterus. The stools were clay-colored and the urine dark. Serum bilirubin was 9.0 mg./l0 c.c. Since there was a discrepancy between the mother's observations concerning the color of the urine and feces and that of the examining physician, the possibility of one of the “inspissated bile syndromes” was considered. Despite the institution of a hydrocholeretic regimen to increase the flow of bile, the signs of obstructive jaundice persisted. Laparotomy on Oct. 28 demonstrated a large cirrhotic liver and complete absence of the extrahepatic ducts and gallbladder. Since definitive surgery was impossible, a liver biopsy was obtained to ascertain the condition of the intrahepatic ducts and the abdomen was then closed. On histologic examination the liver showed stasis of bile pigment with bile cast formation in the small biliary radicles. No large biliary ducts could be found. There were marked distortion of the hepatic architecture and perilobular fibrosis. In the surrounding stroma, numerous lymphocytes and a few neutrophils were seen. The microscopic diagnosis was “obstructive biliary stasis with acute and chronic cholangitis and early biliary cirrhosis.” The patient's history over the next three years was one of numerous respiratory infections interspersed with periods of comparative well-being. The serum calcium varied between 3.7 and 5.3 mEq/1 (7.4 to 10.6 mg./100 c.c), the serum phosphorus between 1.1 and 2.1 mEq/1 (1.9–3.6 mg./ 100 c.c), and the serum alkaline phosphatase between 14 and 26 Bodansky units. Moderately severe mental and physical retardation was noted, but the general state of nutrition was good. Hepatosplenomegaly was progressive, ascites became severe, and there were epistaxis and melena. Roentgen examination (Fig. 1) revealed large esophageal varices.