Recurrent biliary cystadenoma: MR imaging appearance.

The authors report the case of a 37-year-old woman with a biliary cystadenoma that mimicked a liver cyst. The magnetic resonance (MR) imaging features of this rare lesion were correlated with the pathologic findings, showing the potential of MR imaging for depicting and aiding in the diagnosis of biliary cystadenoma and its recurrence.

Cholestatic hepatitis leading to hepatic failure in a patient with organ-transmitted hepatitis C virus infection.

A 51-year-old heart transplant recipient who developed subfulminant hepatic failure because of organ-transmitted hepatitis C virus (HCV) infection is described. He presented with a predominantly cholestatic liver damage after heart transplantation. An extensive evaluation, including abdominal ultrasound and computed tomography scan and endoscopic retrograde cholangiopancreatography was unrevealing. Liver biopsy, however, was suggestive of a large duct obstruction with prominent portal and pericellular fibrosis, marked cholestasis, pericholangitis with marked ductular proliferation, and diffuse hepatocyte degeneration. Antibody to HCV (anti-HCV) was initially negative. He deteriorated in the ensuing 3 months. A repeat enzyme immunoassay-2 test for anti-HCV 4 months after initial presentation was weakly positive. Quantitation of serum HCV RNA by branched DNA assay revealed high level viremia, 547 x 10(6) genome equivalents per milliliter. Using in situ polymerase chain reaction, HCV RNA was detected in the cytoplasm in > 80% of the hepatocytes. The patient underwent interferon alfa therapy, and serum HCV RNA levels were reduced 20-fold after four doses. Unfortunately, the patient developed pulmonary aspergillosis and died. This case illustrates that in immunosuppressed patients anti-HCV is not a good marker for the diagnosis of HCV infection, and HCV can cause a progressive form of cholestatic liver disease mimicking a large duct obstruction.

Fibrosing cholestatic hepatitis in a transplant recipient with hepatitis B virus precore mutant.

A patient with hepatitis B virus (HBV) precore mutant (seropositive for hepatitis B surface antigen [HBsAg], anti-hepatitis B e antigen [HBeAg], and HBV DNA) who underwent orthotopic liver transplantation for end-stage liver disease is described. Sequencing of the HBV precore region of the pretransplant serum sample confirmed the presence of the precore stop-codon mutant (G-->A mutation in codon 1896) only. The patient received HBV immunoglobulin prophylaxis for 6 months but HBV recurred thereafter with a mild hepatitic flare, and he remained seropositive for HBsAg, anti-HBe, and HBV DNA. The initial hepatitic illness resolved in 3 months. The patient remained well for another 16 months before presenting with fibrosing cholestatic hepatitis (FCH). During his entire initial hepatitic flare, quiescent period, and final FCH phase, he remained seropositive for HBsAg, anti-HBe, and HBV DNA. Moreover, sequencing of the serum HBV DNA in final FCH phase showed the presence of the identical HBV precore mutant. Immunohistochemical staining showed extensive expression of HBsAg/pre-S1, pre-S2, and hepatitis B core antigen, but HBeAg was scarcely detectable. This case illustrates that (1) recurrence of HBV precore mutant infection can occur in liver; (2) it can give rise to FCH; and (3) hepatic accumulation of HBeAg is not essential for the development of FCH.

Acute fatty liver of pregnancy in a patient with chronic active hepatitis and associated hepatocyte alpha 1-antitrypsin inclusions.

BACKGROUND: Acute fatty liver of pregnancy is a rare, potentially fatal condition that shares many of the signs and symptoms of severe preeclampsia. Early reports of this condition noted alarmingly high fetal and maternal mortality rates. However, recent reports have described more favorable outcomes due to prompt recognition and aggressive treatment. We here describe a patient with acute fatty liver of pregnancy superimposed on chronic active hepatitis. CASE: A 27-year-old woman, para 0-1-2-1, presented at 36 weeks' gestation with a 2-week history of malaise, nausea, emesis, diarrhea, and an 18-lb weight loss. The serum concentrations of transaminase enzymes, bilirubin, and alkaline phosphatase were increased, and a mild coagulopathy was present. The patient underwent repeat cesarean delivery and intraoperative needle biopsy of the liver. Histologic examination of the biopsy demonstrated the characteristic changes of acute fatty liver of pregnancy and chronic active hepatitis with associated alpha 1-antitrypsin hepatocyte inclusions. The serum alpha 1-antitrypsin level was mildly elevated and the phenotype was normal (PiMM), excluding alpha 1-antitrypsin deficiency. Viral and autoimmune etiologies for chronic hepatitis were excluded by laboratory studies. The woman experienced rapid resolution of symptoms and laboratory abnormalities in the immediate postoperative period. CONCLUSION: Acute fatty liver of pregnancy may occur in patients with underlying chronic liver disease. Prompt delivery is necessary to reduce the risk of fetal and maternal mortality.

Oral glutamine accelerates healing of the small intestine and improves outcome after whole abdominal radiation.

The healing effects of glutamine given orally for 8 days as a single amino acid nutrient after treatment with whole abdominal radiation (10 Gy) were studied. Rats received isonitrogenous and isovolumic diets containing 3% glutamine or 3% glycine. Control rats were not irradiated but were given identical diets. In irradiated animals, survival was 100% in animals receiving glutamine compared with 45% in animals receiving glycine. Glutamine ingestion diminished bloody diarrhea and the incidence of bowel perforation. Arterial glutamine level was higher in animals receiving glutamine in the diet, as were gut glutamine extraction (35% +/- 8% vs 12% +/- 7%) and intestinal glutaminase activity. These metabolic improvements were associated with a marked increase in villous height, villous number, and the number of mitoses per crypt in rats receiving glutamine. Glutamine was not beneficial in control nonirradiated animals. The data demonstrated that provision of oral glutamine after abdominal radiation supported gut glutamine metabolism, improved mucosal morphometrics, and decreased the morbidity and mortality associated with this abdominal radiation model.

Prophylactic glutamine protects the intestinal mucosa from radiation injury.

Glutamine may be an essential dietary component, especially for the support of intestinal mucosal growth and function. This study evaluated the effects of a glutamine-enriched elemental diet, administered before whole-abdominal radiation on gut glutamine metabolism, mucosal morphometrics, and bacterial translocation. Rats were randomized to receive a nutritionally complete elemental diet that was glutamine-enriched or glutamine-free for 4 days. The animals were then subjected to a single dose of 1000 cGy x-radiation to the abdomen. After irradiation, all animals received the glutamine-free diet. Four days later the animals underwent laparotomy for sampling of arterial and portal venous blood, culture of mesenteric lymph nodes, and removal of the small intestine for microscopic examination. There was no difference in arterial glutamine or gut glutamine extraction between the two groups, but body weight loss was significantly diminished in the glutamine-fed rats. Rats receiving the glutamine-enriched elemental diet before radiation had a significant increase in jejunal villous number, villous height, and number of metaphase mitoses per crypt. Scanning electron microscopy confirmed the presence of an intact gut epithelium in eight of eight rats receiving prophylactic glutamine compared to one of eight animals in the glutamine-free group. Three of eight rats fed glutamine had culture positive mesenteric lymph nodes compared with five of seven rats receiving the glutamine-free diet. Glutamine exerts a protective effect on the small bowel mucosa by supporting crypt cell proliferation effect on accelerate healing of the acutely radiated bowel.

Glutamine-enriched diets support muscle glutamine metabolism without stimulating tumor growth.

Glutamine is a principal fuel utilized by rapidly growing tumors. Advanced malignant disease results in muscle glutamine depletion and weight loss. Concern exists about providing dietary glutamine to the host with cancer since it may stimulate tumor growth. This study examined the effects of oral glutamine on muscle glutamine metabolism and tumor growth. Twenty-four rats with large sarcomas were pair fed a glutamine-enriched or glutamine-free elemental diet. Diets were isonitrogenous and isocaloric. After 6 days of feeding, the animals were anesthetized and arterial glutamine, hindquarter glutamine flux, muscle glutamine content, tumor weight, tumor DNA content, tumor glutaminase activity, and number of metaphase mitoses/high power field (HPF) in the tumor were determined. There was no difference in arterial glutamine between the two groups, but provision of a glutamine-enriched diet increased muscle glutamine content by 60% (2.31 +/- 0.21 mumole/g tissue vs 1.44 +/- 0.22 mumol/g tissue, P less than 0.05), which supported muscle glutamine release. There were no differences among tumor DNA content, tumor glutaminase activity, or tumor weight and there was no difference histologically in the number of metaphase mitoses/HPF. Glutamine-enriched oral diets may replete host glutamine stores and support muscle glutamine metabolism without stimulating tumor growth.

Intestinal glutamine metabolism after massive small bowel resection.

Gut glutamine utilization after massive small bowel resection was studied to gain further insight into the alterations and adaptations in intestinal glutamine metabolism that occur during the development of post-resectional hyperplasia. After resection of the middle 60% of the small intestine in the rat, gut glutamine metabolism was studied immediately and 1, 2, and 3 weeks later. Whole gut glutamine extraction was 22% in sham controls and it acutely declined to 12% (p less than 0.01) after bowel resection. Extraction increased to 31% 1 week later (p less than 0.05) and then returned to normal by week 2. Gut ammonia release decreased after massive small bowel resection, whereas intestinal alanine release increased. The increase in gut glutamine extraction at 1 week occurred at a time when jejunal and ileal DNA and protein content were markedly increased (p less than 0.01). Intestinal glutaminase content declined initially and then increased by the third week after bowel resection (p less than 0.01). With time, increases in gut cellularity and glutaminase content are associated with gut glutamine utilization in the shortened small bowel that is equal to that of the intact unresected intestine.