Background The extent of serious complications in people whohave acquired chronic hepatitis C after a blood transfusionis unclear.
Methods We studied 131 patients with chronic post-transfusionhepatitis C who were referred to our center between February1980 and June 1994. Eighty-two other patients were excludedbecause they had multiple transfusions, hemophilia, intravenousdrug use, human immunodeficiency virus infection, hepatitisB infection, hemochromatosis, or alcoholic liver disease. Liverbiopsies were performed in 101 patients; biopsies were not performedin the other 30 patients, all with signs of cirrhosis, becausethe results of coagulation tests were abnormal.
Results The mean age of the patients was 57 years (range, 21to 81) at the time of our initial evaluation. The mean age atthe time of the blood transfusion was 35 years (range, 1 to76). The mean duration of follow-up after presentation to uswas 3.9 years (range, 1 to 15). Eighty-eight of the patients(67.2 percent) initially had fatigue, and 89 (67.9 percent)had hepatomegaly. Twenty-seven patients (20.6 percent) initiallyhad chronic hepatitis, 30 (22.9 percent) had chronic activehepatitis, 67 (51.1 percent) had cirrhosis, and 7 (5.3 percent)had hepatocellular carcinoma. Hepatocellular carcinoma developedin an additional seven patients an average of 36 months (range,7 to 121) after the initial visit. During follow-up, 20 patients(15.3 percent) died: 8 from complications of cirrhosis (1 aftera liver transplantation); 11 from hepatocellular carcinoma;and 1, with chronic active hepatitis, from pneumonia.
Conclusions In a group of patients seen at a referral center,chronic post-transfusion hepatitis C was a progressive diseaseand, in some patients, led to death from either liver failureor hepatocellular carcinoma.
Serologic testing for antibodies to hepatitis C virus (HCV)has shown that over 90 percent of cases of post-transfusionnon-A, non-B hepatitis in the United States are caused by HCV.Acute HCV infection is usually not detected clinically. Lessthan one third of infected patients have jaundice after receivinga transfusion.1,2 Sustained elevations of serum aminotransferaseconcentrations for six months or longer have been noted in upto 60 percent of people with post-transfusion non-A, non-B hepatitis.These people have been considered to have chronic hepatitis.2,3In a recent study, the detection of HCV RNA in serum from patientswith HCV antibodies and concomitant elevations of aminotransferaseconcentrations after a transfusion confirmed HCV as the principalcause of chronic hepatitis.4
The natural history of chronic HCV infection acquired througha blood transfusion is unclear. One report suggested that thereis a sequential but slow progression from acute HCV infectionto chronic infection, cirrhosis, and eventually, hepatocellularcarcinoma.5 In one study, clinical evidence of cirrhosis waspresent in 20 percent of patients with chronic HCV infection16 years after the initial blood transfusion.6 In another study,very few patients had complications of chronic infection afteran average follow-up of 18 years.7 Thus, the progression ofHCV infection acquired from a blood transfusion remains unclear.To elucidate the clinical course of post-transfusion HCV infection,we studied a group of patients referred to a tertiary care center.
Methods
Patients
Between February 1980 and June 1994, 213 patients with chronichepatitis C and a history of a blood transfusion were evaluatedat the Liver Center at Huntington Memorial Hospital. All thepatients had positive tests for antibodies to HCV, accordingto the methods described below. Eighty-two patients were excludedfrom the study because they had received multiple blood transfusionsor had hemophilia, coexisting intravenous drug abuse, coinfectionwith the human immunodeficiency virus, or coexisting chronicliver disease (hepatitis B, hemochromatosis, or alcoholic liverdisease). The remaining 131 patients with chronic post-transfusionHCV infection were enrolled in the study.
The year of the blood transfusion was documented according tothe patient's recollection. During interviews, all patientsrecalled the year of either surgery or a medical illness leadingto a blood transfusion. Six of the patients (4.6 percent) wereself-referred because of an abnormal alanine aminotransferaseconcentration or a positive test for antibodies to HCV aftera blood donation; the other 125 patients (95.4 percent) hadbeen referred by their private physicians. Of the 131 patients,118 (90.1 percent) had been referred because of abnormal resultsof liver-function tests or positive tests for antibodies toHCV, 8 (6.1 percent) because of chronic liver disease, and 5(3.8 percent) because of a liver mass.
Liver biopsies were performed in 101 patients. Biopsies werenot performed in the other 30 patients, all of whom had signsof cirrhosis, because the results of coagulation tests wereabnormal. Liver-biopsy specimens were evaluated according toestablished histologic criteria for four categories of liverdisease: chronic hepatitis, chronic active hepatitis, cirrhosis,and hepatocellular carcinoma.8 Chronic hepatitis, previouslyreferred to as chronic persistent hepatitis, was diagnosed ifthe histologic features included portal lymphoid hyperplasia,focal hepatocytolysis, and preservation of the limiting plate.9Chronic active hepatitis was characterized by piecemeal necrosisand parenchymal inflammation with or without bridging necrosis.Cirrhosis was diagnosed when nodular formation was present inaddition to the above changes. Hepatocellular carcinoma wasdiagnosed on the basis of histologic findings or elevated alpha-fetoproteinlevels and ultrasonographic or radiographic changes consistentwith hepatocellular carcinoma.10 During follow-up, all patientswere screened for hepatocellular carcinoma by means of alpha-fetoproteintests performed at six-month intervals and yearly ultrasoundexamination of the liver.
Laboratory Tests
Serum samples from the 131 patients were tested for HCV antibodieswith assays from Chiron (Emeryville, Calif.).11 The antigensused were the C25 fusion protein; C22, C100-3, and C33c in asecond-generation assay; and the individual HCV recombinantproteins C22, E1, E2, NS3, C100-3, and NS5. The liver tests,which included determinations of serum albumin, bilirubin, aspartateaminotransferase, and alanine aminotransferase, were performedwith the Hitachi 747 analyzer (Boehringer–Mannheim, Indianapolis).Alpha-fetoprotein levels were measured by radioimmunoassay atthe Nichols Institute (San Juan Capistrano, Calif.); the upperlimit of normal was 18 ng per milliliter. All data are reportedas means ±SD.
Results
At the time of the initial evaluation at our hospital, the averageage of the 131 patients was 57 years (range, 21 to 81). Themean age at the time of the blood transfusion was 35 years (range,1 to 76). There were 81 women and 50 men; 101 of the patientswere white, 22 were Asian, and 8 were African American (Table 1).Nineteen patients recalled a period of jaundice after theblood transfusion. The mean duration of follow-up after theinitial visit to our hospital was 3.9 years (range, 1 to 15).
Table 1. Types of Liver Disease According to Race and Ethnic Group among 131 Patients with Transfusion-Associated Hepatitis C.
The presenting symptoms and signs are shown according to diseasecategory in Table 2. Fatigue was the most common symptom (occurringin 67.2 percent of the patients), followed by abdominal pain(in 19.8 percent), anorexia (in 14.5 percent), and weight loss(in 6.1 percent). Jaundice was noted in only 2 of the 67 patientswith cirrhosis. Hepatomegaly and splenomegaly were detectedin 67.9 and 21.4 percent of the 131 patients, respectively.The initial mean laboratory values were as follows: albumin,4 g per deciliter (range, 2.4 to 5.4); bilirubin, 0.96 mg perdeciliter (16.4 µmol per liter) (range, 0.2 to 6.0 mgper deciliter [3.4 to 103 µmol per liter]); aspartateaminotransferase, 105 U per liter (range, 20 to 550); and alanineaminotransferase, 132 U per liter (range, 13 to 670).
Table 2. Presenting Symptoms and Signs in 131 Patients with Transfusion-Associated Hepatitis C.
All 131 patients had antibodies to the chimeric protein C25.The most frequent antibodies to individual recombinant HCV proteinswere antibodies to NS3 (in 97.0 percent of the patients), C22(in 95.4 percent), NS5 (in 71.8 percent), and C100-3 (in 65.7percent). Antibodies to E1 and E2 were detected in 51.2 and35.9 percent of the patients, respectively.
Twenty-seven patients (20.6 percent) had chronic hepatitis,30 (22.9 percent) had chronic active hepatitis, 67 (51.1 percent)had cirrhosis, and 7 (5.3 percent) had hepatocellular carcinoma(Table 2). Fatigue was present in more than 50 percent of thepatients with chronic or chronic active hepatitis, in 75 percentof those with cirrhosis, and in all the patients with hepatocellularcarcinoma (Table 2). One patient with a histologic diagnosisof chronic hepatitis also had lymphoma. Splenomegaly in thispatient may have been due to the lymphoma. Of the 67 patientswith cirrhosis, 54 (80.6 percent) had thrombocytopenia (meanplatelet count, 80,900 per cubic millimeter; range, 27,000 to107,000) with splenomegaly, 28 (41.8 percent) had ascites, 12(17.9 percent) had esophageal varices, and 12 (17.9 percent)had hepatic encephalopathy. Only 12 patients (17.9 percent)had none of the clinical signs that we studied. The incidenceof cirrhosis and hepatocellular carcinoma, according to ethnicor racial background, is shown in Table 1.
Five of the 14 patients with hepatocellular carcinoma were initiallyreferred to our unit for evaluation of a liver mass. Two otherpatients had elevated serum alpha-fetoprotein levels and radiologicfindings consistent with hepatocellular carcinoma within a monthafter the first visit. Hepatocellular carcinoma developed inan additional seven patients an average of 36 months (range,7 to 121) after the initial visit. These seven patients areincluded in the group with hepatocellular carcinoma in Table 1.All the patients with hepatocellular carcinoma also had clinicalor histologic evidence of cirrhosis. The mean serum alpha-fetoproteinlevel in the patients with hepatocellular carcinoma was 22,730ng per milliliter (range, 7.4 to 183,915). The mean alpha-fetoproteinlevel in the patients without hepatocellular carcinoma was 7.7ng per milliliter (range, 1.6 to 58). Serum alpha-fetoproteinlevels were normal on repeated determinations in all patientswith chronic or chronic active hepatitis and above the normalrange in six of the patients who had cirrhosis without hepatocellularcarcinoma.
The mean interval between the time of the blood transfusionand the diagnosis of chronic hepatitis, chronic active hepatitis,cirrhosis, or hepatocellular carcinoma is shown in Figure 1.The mean interval was 13.7 years (range, 1 to 42) for chronichepatitis, 18.4 years (range, 1 to 37) for chronic active hepatitis,20.6 years (range, 3 to 42) for cirrhosis, and 28.3 years (range,8 to 42) for hepatocellular carcinoma.
Figure 1. Mean (±SD) Interval from Blood Transfusion to the Diagnosis of Diseases Associated with Hepatitis C in 131Patients.
A total of 103 patients received a transfusion before the ageof 50 years (average age, 29.2 years), and 28 patients receiveda transfusion when they were 50 or older (average age, 58.5years). These two groups had similar or identical percentagesof patients with chronic hepatitis (20 and 21 percent, respectively),chronic active hepatitis (23 and 21 percent, respectively),cirrhosis (46 percent in both groups), and hepatocellular carcinoma(11 percent in both). Among the patients who were 50 or olderat the time of the transfusion, the average time from the transfusionto the development of chronic hepatitis, chronic active hepatitis,cirrhosis, and hepatocellular carcinoma was 6.3, 10.7, 9.8,and 14.7 years, respectively. Among the younger patients, theaverage time to the development of these diseases was 15.9,20.4, 23.6, and 31.5 years, respectively.
During follow-up, 20 patients died, including 8 from complicationsof cirrhosis (1 of whom underwent a liver transplantation) and11 from hepatocellular carcinoma. One patient with chronic activehepatitis died from pneumonia. Three patients with cirrhosisunderwent orthotopic liver transplantation and were alive asof April 1, 1995.
Discussion
The 213 patients considered for this study represented approximatelyone third of the patients with HCV antibodies referred for evaluationduring the study period. We have no information on the poolof patients receiving transfusions (i.e., the denominator) fromwhich these 213 patients were drawn. Before the identificationof HCV, from 5 to 12 percent of patients in the United Statesmay have contracted acute non-A, non-B hepatitis after receivinga transfusion, and 91 percent of these infections may have beencaused by HCV.1 The Centers for Disease Control and Preventionhave estimated that 20 percent of acute HCV infections progressto chronic active hepatitis or cirrhosis.4
In our study, 104 patients had chronic active hepatitis, cirrhosis,or hepatocellular carcinoma. Using these estimates and assumingthat we saw all the patients with serious liver disease relatedto post-transfusion HCV in the population of patients referredto our center, we calculated that the pool from which our patientswere drawn included approximately 4700 to 11,400 people witha history of a transfusion. Since our institution is a tertiarycare center, many of the patients may have been referred afterthey had already been evaluated elsewhere and had become seriouslyill. Therefore, we may have seen a larger proportion of chronicallyill patients with HCV infection and liver disease than mightbe seen in other settings.
A majority of the patients with HCV infection had symptoms andsigns of chronic liver disease when they were evaluated initially.Both fatigue and hepatomegaly were frequent findings, especiallyin the patients with cirrhosis and hepatocellular carcinoma(Table 2). Other investigators have reported that most patientswith chronic infection from post-transfusion non-A, non-B hepatitisor hepatitis C had few clinical symptoms and signs of liverdisease.6,7 Only about one sixth of the patients we studiedrecalled being jaundiced after the transfusion. This proportionis consistent with the range in other studies (15 to 41 percent).6,12At the time of presentation, the mean serum bilirubin levelamong the 131 patients in our study was 0.96 mg per deciliter(16.4 µmol per liter). Only two patients with cirrhosishad clinical jaundice. In contrast, patients with chronic activehepatitis B are often jaundiced during periods of clinical exacerbation.13
The mean time between the transfusion and our initial evaluationwas 22 years. The mean time from the transfusion to the diagnosisof liver disease was 20.6 years for the patients with cirrhosisand 28.3 years for those with hepatocellular carcinoma. We havereported elsewhere the development of hepatocellular carcinomain both Asian and white patients with anti-HCV antibodies, regardlessof the route of transmission.10 In other reports in which fewpatients with HCV infection after a transfusion had complications,the mean follow-up times were 16 and 18 years for the two diagnoses,respectively.6,7 The incidence of serious liver disease maybe higher over a longer period. In our study, the mean timesto the progression of liver disease were similar to those ina previous report from Japan.5 In that study of 89 patients,the mean times from the transfusion to the development of chronichepatitis, cirrhosis, and hepatocellular carcinoma were 10.0,21.2, and 29.0 years, respectively.
Twenty of the 131 patients referred to us died, all but 1 fromcomplications of cirrhosis or hepatocellular carcinoma. In aprevious report of post-transfusion non-A, non-B hepatitis,only 3.3 percent of the deaths were considered to be relatedto the underlying liver disease.7 In that study, 78 percentof the patients who died also had a history of alcoholic liverdisease. We excluded patients with a history of excessive alcoholintake.
In summary, in a group of patients referred to a tertiary carecenter, we found that HCV infection was a progressive diseaseand, in some patients, led to death from either liver failureor hepatocellular carcinoma. Screening of blood products forhepatitis C before transfusion will substantially reduce theincidence of post-transfusion HCV infection. For people whoare already infected with HCV, our findings support the useof antiviral therapy to eradicate the virus and halt the progressionof chronic liver disease.
We are indebted to Drs. George Kuo and David Chien of the ChironCorporation for performing the assays of anti-HCV antibodies,and to Ms. Tina Jordan for assistance in the preparation ofthe manuscript.
Source Information
From the Liver Center, Huntington Memorial Hospital, 744 Fairmount Ave., Pasadena, CA 91105, where reprint requests should be addressed to Dr. Tong.
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