The cause of NASH remains unclear. Early studies suggested NASH occurred only in female patients with obesity, diabetes, and/or hyperlipidemia. However, recent data suggest NASH may more frequently be present in males in the absence of obesity, diabetes, or hyperlipidemia. 1 These data raise the possibility that genetically determined alterations in fatty acid oxidation or very low density lipoprotein metabolism may contribute to the disease. This represents the second reported case of NASH resulting in orthotopic liver transplantation with recurrence in the allograft, 2 suggesting that extrahepatic factors importantly contribute to the development of NASH. Case PresentationA 42-year-old morbidly obese white man presented with a 1-month history of intermittent right upper quadrant pain and a 9-kg weight loss. His past medical history was notable for hypertriglyceridemia treated with gemfibrizol. He denied ethanol use. Laboratory evaluation revealed amylase of 3,800 U/L, lipase of 13,000 U/L, cholesterol of 188 mg/dL, triglycerides of 171 mg/dL, and elevated transaminases. Serologic studies for hepatitis A, B, and C were negative. A laparoscopic cholecystectomy for presumed gallstone pancreatitis was performed. An intraoperative cholangiogram was normal. An intraoperative liver biopsy was performed, and specimen revealed moderate steatosis with low-grade hepatocyte injury, focal collections of mononuclear inflammatory cells, minimal portal inflammation, and central pericellular fibrosis. A few hepatocytes contained Mallory's hyaline (Fig. 1A).The patient lost 33 kg in the 3 months after his operation due to anorexia and pain. In addition, he became jaundiced and pruritic; his only medication was ursodeoxycholate. Liver biopsy specimen revealed NASH and micronodular cirrhosis.The patient experienced continued weight loss and worsening fatigue. Nine months after his initial presentation, he underwent an orthotopic liver transplantation. The allograft donor was a previously healthy, slim, 15-year-old male who received a gunshot wound to the head while playing with a firearm. The donor patient had normal serum transaminases, glucose, and cholesterol. The donor liver appeared grossly normal.

Vertical transmission of HCV complicates up to 18% of pregnancies in HCV-positive, HIV-negative women and 6-36% in HCV-positive, HIV-positive women. The highest rates of vertical transmission of HCV were noted in women with high HCV RNA or concurrent HIV infection. Breast-feeding has not been associated with vertical transmission of HCV infection.

Cirrhosis and portal hypertension may be associated with pulmonary hypertension and pulmonary dysfunction. However, morphological pulmonary vascular lesions in patients with cirrhosis have not been well characterized morphometrically. We morphometrically evaluated pulmonary vessels in liver transplant recipients with pretransplantation cirrhosis and correlated our findings with pretransplantation cardiopulmonary function, postoperative course, and postmortem cardiopulmonary findings. Autopsy lung slides from 23 transplant recipients with pretransplantation cirrhosis were examined. External vessel diameter, intimal thickness, and arterial medial thickness were measured with a micrometer after pentachrome staining. The percent of total diameter comprised by intima or media was calculated for each vessel. Medical records were reviewed for smoking history, pretransplantation cardiopulmonary function testing, and postoperative course. Autopsy cases without liver or significant cardiopulmonary diseases, matched for age, sex, and smoking history, served as controls. Transplant recipients had significantly more pulmonary venous intimal thickening than matched controls (P F .0001). Sixty-five percent (15 of 23) of these patients had some degree of pretransplantation pulmonary dysfunction, defined by abnormalities in pulmonary function tests, oxygen saturation, and/or increased pulmonary artery pressures. However, the severity of venous intimal thickening did not correlate with the severity of pretransplantation pulmonary dysfunction. Arterial intimal and medial thickness were not statistically significantly different from controls. Pulmonary venous intimal thickening and resultant luminal impingement are morphological findings not previously described in this population. The arterial lesion, when present, is similar to that seen in pulmonary hypertension from other causes. These pulmonary vascular lesions may be implicated in pulmonary dysfunction in patients with cirrhosis and may be associated with increased posttransplantation cardiopulmonary morbidity and mortality. Copyright 1999 by the American Association for the Study of Liver Diseases S evere chronic liver disease, especially cirrhosis with concomitant portal hypertension, has been associated with numerous pulmonary abnormalities, including hypoxemia, decreased diffusion capacity, intrapulmonary and portopulmonary shunting, ventilation/perfusion mismatch, pleural vascular anomalies, and pulmonary hypertension. These pathological pulmonary conditions in patients with cirrhosis have been well documented in the absence of other intrinsic cardiac and pulmonary diseases. 1-7 Between 30% to 70% of the patients with cirrhosis are reportedly hypoxemic; 0.25% to 12.5% of the patients with advanced liver disease have clinical evidence of pulmonary hypertension, with higher percentages reported in studies using right cardiac catheterization. 1,4,[6][7][8][9][10] The natural history of this association between portal hypertension and pulmonary dysfunction in patients with c...

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Liver transplantation is complicated by specific medical problems. Diabetes mellitus occurs in 4-20% of patients undergoing liver transplantation. Patients with primary sclerosing cholangitis and ulcerative colitis experience up to a 13% incidence of colon cancer after transplantation. Lymphomas occur in 1-3% of patients after transplantation and account for 57% of malignancies occurring in adult patients. Atraumatic bone fractures occur in 22-38% of patients and neurological complications, including seizures, headache, and neuropathy occur in 19-47% of patients following liver transplantation. Patients undergoing liver transplantation may experience recurrence of their primary liver disease: hepatitis B, hepatitis C, primary biliary cirrhosis, autoimmune hepatitis, or primary sclerosing cholangitis. In patients not receiving immunoprophylaxis after transplantation for chronic hepatitis B, recurrent hepatitis B is seen in up to 90% of patients. This can be markedly reduced with hyperimmune globulin immunoprophylaxis. Recurrent hepatitis C is seen in the majority of patients; current treatment modalities are inadequate. Recurrence of primary biliary cirrhosis or primary sclerosing cholangitis in the allograft is infrequent. Autoimmune hepatitis may recur in up to 26% of patients following liver transplantation. Primary disease recurrence in the allograft and preventive strategies are discussed.