Biomedical subjects
Publications and source records attributed to J Boitnott.
Recurrent hepatocellular carcinoma is well described following liver transplantation. However, de novo hepatocellular carcinoma in the allograft is rare. We describe the clinical and pathological features of a case of de novo hepatocellular carcinoma arising in a cirrhotic allograft 9 years following transplantation for chronic hepatitis B.
Recurrence of primary sclerosing cholangitis (PSC) after liver transplantation is very uncommon. The true incidence of recurrence is unknown, mainly because of the difficulty in differentiating ischemic strictures from that of recurrent disease. Primary sclerosing cholangitis and ischemic strictures have identical histopathologic and cholangiographic features. We report a young man who had recurrence of PSC in two allografts and report our experience in 32 patients who had liver transplantation for PSC. Six patients (18%) had evidence of non-anastomotic strictures and, of these, only one patient (reported here) had unequivocal evidence of true recurrence. The strictures in other five patients happened because of ischemia. The recurrence of the disease in two allografts in an immunosuppressed patient, in the absence of ischemia, chronic rejection, or any known pathogen, raises the question of the role of an unidentified infectious agent in the etiopathogenesis of PSC.
CONTEXT: Hepatitis C virus (HCV) infection may resolve (viral clearance), persist without complications, or cause end-stage liver disease (ESLD). The frequency and determinants of these outcomes are poorly understood. OBJECTIVE: To assess the incidence and determinants of viral clearance and ESLD among persons who acquired HCV infection from injection drug use. DESIGN AND SETTING: Community-based prospective cohort study with enrollment in 1988-1989 and a median follow-up of 8.8 years. SUBJECTS: A total of 1667 persons aged 17 years or older with a history of injection drug use and an HCV antibody-positive test result during follow-up. MAIN OUTCOME MEASURES: Viral clearance was assessed in a subset of 919 patients and defined as failure to detect HCV RNA in at least 2 consecutive samples collected 5 or more months apart. End-stage liver disease was assessed at semiannual visits and by review of medical records and death certificates and defined by the presence of ascites, esophageal varices, or hepatic encephalopathy, or when ESLD was stated as a cause of death. RESULTS: Viral clearance was observed in 90 persons who were compared with 722 with persistent viremia, while the viremia of 107 was not resolved. Viral clearance occurred more often in nonblacks (adjusted odds ratio [OR], 5.15; 95% confidence interval [CI], 2.60-10.17) and those not infected with human immunodeficiency virus (HIV) (adjusted OR, 2.19; 95% CI, 1.26-3.47). Forty cases of ESLD were observed throughout follow-up (incidence, 3.1 per 1000 person-years). In a multivariate model, risk of ESLD was higher for persons aged 38 years or older at enrollment (adjusted relative incidence, 3.67; 95% CI, 1.96-6.88) and who reported ingestion of more than 260 g of alcohol per week (adjusted relative incidence, 3.60; 95% CI, 1.73-7.52). Of 210 patients without ESLD randomly selected for biopsy, only 2 had cirrhosis. CONCLUSIONS: Our results indicate that although HCV infection can be self-limited or associated with ESLD, the majority of adults have persistent viremia without clinically demonstrable liver disease. Further research is needed to explain the less frequent clearance of HCV infection among black persons and to improve utilization of treatment for those infected in the context of injection drug use. JAMA. 2000;284:450-456
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The relationship between pyridoxal phosphate deficiency and activities of serum and liver aminotransferases was studied in 12 patients with alcoholic hepatitis. Plasma pyridoxal phosphate and the activities of liver aminotransferases were initially decreased in the patients, as compared with mean values in controls with normal hepatic histology. Addition of pyridoxal phosphate to liver homogenates increased liver alanine aminotransferase, but not aspartate aminotransferase, in all patients with initially low plasma pyridoxal phosphate. After 1 mo of abstinence from alcohol, with intake of an adequate diet and pyridoxine supplementation, plasma pyridoxal phosphate increased in all patients with initially low values (p less than 0.02). Serum aspartate aminotransferase decreased, whereas serum alanine aminotransferase increased, resulting in a decrease in their ratio in serum (p less than 0.001). Liver alanine aminotransferase increased (p less than 0.005), whereas liver aspartate aminotransferase remained unchanged. These data suggest that pyridoxal 5'-phosphate depletion is partially responsible for the low serum alanine to aspartate aminotransferase ratio that is typical of patients with alcoholic hepatitis.
Twelve patients with the Budd-Chiari syndrome have been managed surgically. Ten of the patients were female, two were male, with a mean age of 40 years. Three of the patients had polycythemia vera, two had pre-existing cirrhosis, one had ingested estrogens, one had an occult tumor, and in four there were no associated factors. Ten patients presented with ascites and two with bleeding esophageal varices. The diagnosis was confirmed in all 12 patients by liver biopsy and hepatic vein catheterization. Inferior vena cavography revealed the abdominal vena cava to be thrombosed in six patients. The superior mesenteric vein was used to decompress the congested liver in all 12 patients. In five patients, a mesocaval shunt (MCS) was performed and in seven patients, a mesoatrial shunt (MAS) was carried out. There were four hospital deaths (two MCS, two MAS). One late death (MAS) occurred from liver failure following shunt thrombosis. Two additional patients (one MCS, one MAS) re-developed ascites immediately following surgery and angiography revealed a thrombosed shunt. Ascites has been controlled with a LeVeen shunt in these two patients, but liver biopsies showed progression to cirrhosis. The remaining five patients (three MAS, two MCS) did well, and angiography revealed patent shunts. Two of these patients, however, re-developed ascites at 4 and 10 months following MAS and required a second MAS. Follow-up ranges from 6 to 68 months. In three of the patients (two MCS, one MAS) with patent shunts, liver biopsy shows a remarkable return toward normal liver architecture and histology.
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Two hundred four volunteer blood donors with hepatitis B surface antigen found in their blood were followed for 3 to 44 months. The annual clearance rate of this antigen was 1.7%. Liver enzyme levels (aminotransferase) were elevated in 45 (22.1%) on at least one occasion, in 26 (12.7%) for one month or more, and in 13 for more than six months. Liver biopsies were performed on 17 chronic carriers with normal enzymes and nonspecific histologic abnormalities were found in 14 and mild diffuse hepatitis in three. Seventeen carriers with abnormal enzymes were biopsied, and specimens revealed chronic active hepatitis (CAH) in seven, including two with bridging necrosis and three with cirrhosis. CAH was found in 7 of 26 (26.9%) carriers with abnormal liver enzymes persisting for at least one month and 4 of 13 (30.8%) with abnormal liver enzymes for more than six months.
In this report, we present a 41-year-old woman who developed rapidly progressive "giant cell hepatitis" that lead to end-stage liver disease. She underwent a successful liver transplantation in 1989. However, the giant cell hepatitis recurred in the allograft, resulting in cirrhosis within 4 years. She underwent a second liver transplantation in 1993. After 2 years of a relatively stable course, she again developed cirrhosis and was awaiting liver transplantation at the time of this report. The histopathologic features in the two allografts were identical to her original disease. Despite extensive investigations, no etiology for her liver disease could be found.