Biochemical Evidence Of Liver Disease Research Articles

Case-control exercise challenge study on the pathogenesis of high serum gamma-glutamyl transferase activity in racehorses.

High serum γ-glutamyl-transferase (GGT) activity syndrome in racehorses has been associated with maladaption to exercise. Investigation of affected horses before and immediately after standard exercise may provide critical insight into the syndrome's pathophysiology. To investigate blood biomarker changes in actively competing racehorses with high GGT activity associated with an exercise challenge. Case-control study. High GGT case (age: 2-3 years) and normal GGT control (age: 2-7 years) pairs (3 Thoroughbred, 4 Standardbred pairs) at least 3months into their training/racing season were included. Horses with a recent history of high GGT activity (≥50 IU/L) without additional biochemical evidence of liver disease were identified by veterinarians. Horses were tested again in the week prior to a planned exercise challenge to confirm persistent increases in GGT activity. Controls from the same stable with similar training/racing intensity and serum GGT activity ≤36 IU/L were matched with each case. Blood samples were obtained immediately before, 15 and 120 min after exercise. Pre-exercise serum samples were analysed for baseline select serum chemistries, selenium and vitamin E concentrations. Cortisol concentration and markers of oxidative status were measured in serum or plasma for all time points. Individual serum bile acid and coenzyme Q10 concentrations, plasma lipid mediator (fatty acids, oxylipids, isoprostanes) concentrations and targeted metabolomics analyses were performed using liquid chromatography-mass spectrometry. Serum viral PCR for equine hepaci- and parvovirus was performed in each animal. Cases had higher baseline concentrations of total glutathione, taurocholic acid, cortisol and cholesterol concentrations and higher or lower concentrations of specific oxylipid and isoprostane mediators, but there were no case-dependent changes after exercise. Small sample size. Results indicated that glutathione metabolism was altered in high GGT horses. Enhanced glutathione recycling and mild cholestasis are possible explanations for the observed differences.

Associated Liver Disease in Alcoholic Chronic Pancreatitis

Background: Alcohol is a common etiological factor in the pathogenesis of both pancreatic and liver disease. The frequencies of associated liver histological change in patients with alcoholic chronic pancreatitis (AICP) vary from series to series. Significant proportion of patients with alcoholic pancreatitis does have histological changes in liver. Subjects and Methods: The study was conducted at Narayana Medical College & Hospital, Chintareddy Palem, Nellore, Andhra Pradesh on liver-biopsy specimens from 23 patients with chronic alcoholic pancreatitis subjected to operation for pain, from August 2015 to July 2016 and all the patients had undergone liver biopsy at the time of surgery for AICP. The patients were followed as part of a prospective study of 33 patients who had been treated for chronic pancreatitis. The pathologists were requested to report on alcohol related histological changes in the specimen. Results: There were 23 patients and all were men. Chronic pancreatitis was due to alcohol abuse in all patients. The median age at surgery was 39.8 years. The mean duration of alcohol abuse was 20.5 years (range 6-29 years).The average alcohol intake was 122gm 36gms/day. Three patients had jaundice for 3-6 months duration. None of the patients had any other risk factor for liver disease and none of them had clinical or biochemical evidence of liver disease. The histological reports were, 4 patients had alcoholic hepatitis, 2 severe steatohepatitis, 1 granulomatous hepatitis, 3 cholestasitc changes, one fatty liver and 12 had no significant pathology. None of the patients had cirrhosis. Thus significant alcoholic liver disease was present in 30.4% (7/23) of the patients. There was no increased incidence of post-operative mortality and morbidity in patients with liver pathology. Conclusion: As reported in many other series, chronic alcoholic pancreatitis is associated with histological changes in liver in significant proportion of patients. However its clinical significance and prognosis of these patients are unknown.

Protein Oxidation in Active and Abstinent Alcoholics in Comparison With Normal Controls

Background-Though there is much evidence in support of the hypothesis that acute or chronic alcohol toxicity is mediated primarily via the generation of damaging free radical species, only very few studies had analysed the effect of alcohol withdrawal on protein oxidation and antioxidant status in alcoholics. Also studies concentrating on alcoholics without any clinical or biochemical evidence of liver disease and eliminating other confounders such as smoking are less. Hence the present study aimed to measure carbonyl protein as an index of oxidative damage to proteins in alcoholics without liver disease and determine whether it is reversible on abstinence from alcohol. Methods- The study was conducted in patients with alcohol dependence attending the de-addiction facility in a tertiary care hospital in south India. The study group comprised of 30 male alcoholics in the age group 20-60 years who exhibited no clinical or biochemical evidence of severe liver disease. Blood sample collection was done in the study group immediately after admission and after one month of reported abstinence from alcohol (Groups 1&2, n=30 each).The control group (Group 3, n=30) included healthy male subjects in the same age group as alcoholics with no or occasional alcohol consumption only. Serum Protein carbonyl (PC) levels and plasma Vitamin C levels were estimated in the study and control groups..The confounding effect of smoking on the parameters of oxidative stress was eliminated by appropriate statistical methods and estimated marginal means calculated. Results-PC levels were found to decrease significantly on abstinence from alcohol. Both active alcoholics and abstinent alcoholics show significantly elevated PC levels compared to controls even after eliminating the effect of smoking. Serum Vitamin C levels were found to be lower in both the alcoholic subgroups compared to non-alcoholic controls, but there was no significant elevation of levels on abstinence from alcohol. Conclusion-Oxidative damage to proteins is increased in alcoholics without liver disease which comes down on abstinence. Antioxidant supplementation may be essential during the withdrawal phase to reverse this damage.

PWE-276 Validation of fibroscan as a screening tool for cystic fibrosis associated liver disease in an adult population

IntroductionCystic fibrosis (CF) associated liver disease affects up to 41% of CF sufferers and may progress to cirrhosis with associated complications.1 Diagnosis is frequently made without biopsy. A recent study...

Infección oculta por el virus de la hepatitis C

Occult hepatitis C virus (HCV) infection is characterized by the detection of HCV-RNA in liver in the absence of anti-HCV and serum HCV-RNA determined by conventional techniques. The development of a new enzyme immunoassay for the detection of antibodies against a conserved epitope in the HCV core protein, together with the detection of HCV-RNA in peripheral blood mononuclear cells and in serum after concentrating the viral particles by ultracentrifugation, allow diagnosis of more than 90% of patients with occult HCV without the need to perform a liver biopsy. Histological damage in occult HCV infection ranges from minimal changes to liver cirrhosis and hepatocellular carcinoma, although in general this disease is less severe than classical chronic hepatitis C. A significant prevalence of occult HCV infection has been identified in risk groups such as hemodialysis patients and the family members of patients with occult hepatitis C. This occult HCV infection can also be found in subjects without clinical or biochemical evidence of liver disease.

Management of occult hepatitis B virus infection: An update for the clinician

Occult hepatitis B virus (HBV) infection (OBI) is defined by the presence of HBV DNA in the liver tissue of individuals who test negative for hepatitis B surface antigen (HBsAg). Patients who have recovered from acute hepatitis B can carry HBV genomes for a long time and show histological patterns of mild necro-inflammation, even fibrosis, years after the resolution of acute hepatitis, without showing any clinical or biochemical evidence of liver disease. At least in conditions of immunocompetence, OBI is inoffensive itself, but when other relevant causes of liver damage are present it might make the course of the liver disease worse. The risk of HBV transmission through transfusion is related to blood donations negative for HBsAg that have been collected during the pre-seroconversion period or during chronic OBI. Use of HBV nucleic acid amplification testing and multivalent anti-HBs antibodies in the HBsAg assays is recommended for detection of true and false OBI, respectively. It is not known if prior hepatitis B immunization with an optimal anti-HBs response in cases of HBV transmission through organ transplantation can effectively modulate or abort the infection. Use of antiviral agents as prophylaxis in patients with serological evidence of past HBV infection prevents reactivation of OBI after transplantation in most cases. Reactivation of OBI has been observed in other conditions that cause immunosuppression, in which antiviral therapy could be delayed until the HBV DNA or HBsAg becomes detectable. OBI might contribute to the progression of liver fibrosis and hepatocellular carcinoma development in patients with chronic liver disease.

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Hepatic vasculitis presenting with multiple sterile liver abscesses in a patient with systemic lupus erythematosus

AbstractAlthough biochemical evidence of liver disease is common in patients with systemic lupus erythematosus (SLE), clinical liver disease is uncommon. We report on a 26‐year‐old woman who presented with acute febrile illness, right upper abdominal pain and multiple hypo‐dense lesions in the liver in a computed tomographic study that mimicked multiple liver abscesses. Multiple necrotizing hepatic granulomas and old occlusive hepatic arteritis were observed in the surgical liver specimen. She was later found to have SLE. This patient represented a rare case of SLE that had hepatic vasculitis with hepatic infarction mimicking multiple liver abscesses as an initial manifestation.

Comment on Mackenzie and Woodhouse: C-reactive protein concentrations during bacteraemia: a comparison between patients with and without liver dysfunction

Sir: With interest we read Mackenzie and Woodhouse's paper about serum C-reactive protein (CRP) levels in patients with and without liver dysfunction during bacteraemia [1]. The authors concluded that patients with biochemical evidence of liver disease show significantly lower serum CRP levels during bacteraemia than patients without liver dysfunction. This remarkable result was only achieved when patients with biopsy-proven liver cirrhosis were included in the analysis. When cirrhotic patients were excluded, however, and patients with liver dysfunction, defined as an elevated plasma bilirubin level and increased prothrombin time, were compared with controls, between-group differences did not reach statistical significance. Therefore, we feel that from the available data it cannot be concluded that patients with liver diseases, in general, generate lower serum CRP levels during bacteraemia. As multiple studies have shown greater CRP production in cirrhotic non-infected patients than in healthy controls [2, 3], it could be argued that cirrhotic patients produce less CRP during periods of infection. However, a recent large study in critically ill subjects reported that CRP levels during infection in cirrhotic patients did not significantly differ from CRP levels in non-cirrhotic patients [4]. Also, no differences were found in relation to the severity of the cirrhosis. Because interleukin-6 stimulates hepatocytes to produce CRP, an interesting study to aid the understanding of these apparently conflicting results would be to relate the interleukin-6 to CRP levels in cirrhotic patients. However, as far as we know, this has not been done. Finally, we believe that the use of CRP as a valuable screening test for infection in the ICU has certain limitations. The decision on starting antibiotics must be individualized and not be based on a certain CRP level. It should be based on suspicion of the presence of infection, the stability of the patient's clinical condition, the presence of comorbidity and the risk of death or complications.

C-reactive protein concentrations during bacteraemia: a comparison between patients with and without liver dysfunction

To evaluate the value of serum C-reactive protein (CRP) concentrations as a marker of sepsis in patients with biochemical evidence of liver dysfunction. A retrospective case-control comparison of serum CRP concentrations between patients with and those without liver dysfunction (prothrombin time over 18 s and serum bilirubin > or = 20 micromol/l) during their first episode of bacteraemia. The neurosciences and general adult intensive care units of a university teaching hospital. Any patient from the above settings with a first episode of bacteraemia (first isolate of pathogenic bacteria from blood cultures) over a 3-year period. After exclusions 126 first episodes of bacteraemia were identified, of which 33 were in patients with liver dysfunction. Serum CRP concentrations were significantly lower in patients with liver dysfunction (median 103 mg/l, IQR 29-204) than in those without (146 mg/l, 74, > 250). Patients with biochemical evidence of liver disease generate significantly lower serum CRP concentrations during bacteraemia than patients without liver dysfunction. Serum CRP concentrations should be interpreted with caution in patients with liver disease to diagnose and monitor bacterial sepsis.

The Anti-Myeloma Effect of Bortezomib Is Associated with Osteoblastic Activity.

Myeloma bone disease is characterized by osteolytic destruction associated with suppressed osteoblastic activity possibly through inhibition of the WNT signaling pathway. We already reported the association between increased alkaline phosphatase (ALP) and B but not dexamethasone response in myeloma patients (Zangari et al., BJH 2005, in press). To extend these observations, using data from the large APEX study, we have attempted to assess the relationship between quantitative alkaline phosphatase (ALP) changes during therapy with B and response and time to progression. We were interested in what threshold of increase in ALP (even within the normal laboratory range) might predict efficacy.Methods: A group of patients with no biochemical evidence of liver disease and creatinine clearances > 50 mL/minute treated with bortezomib 1.3 mg/m2 on days 1, 4, 8 and 11 for up to eight 3-week cycles followed by bortezomib 1.3 mg/m2 on days 1, 8, 15 and 22 for up to three 5-week cycles were studied. The percentage increase of ALP levels in responders and non-responders was analyzed at different thresholds and time points after baseline. Responses (the sum of CR plus PR) were based on EBMT criteria. The change from baseline ALP during therapy with B was compared in responders and non-responders.Results: There were 229 patients with a median age of 60 years. 59% were male; median B2M was 3.2 mg/L, myeloma subtypes included IgG 64%, IgA 24%; median time from diagnosis was 41 months. The median ALP elevation from baseline for bortezomib responding patients was approximately 25% but even a 10% ALP increment at week 6 from baseline was strongly associated with response (P=0.0001). The most powerful predictor of response was a 25% ALP elevation at week 6.Table 1Parameter25% ALP Elevation<25% ALP Elevationp-valueN64154CR n (%)10 (16)12 (8)0.0966PR n (%)35 (55)42 (27)<0.0001CR/PR n (%)45 (70)54 (35)<0.0001Cox regression analysis showed that ALP elevation of 25% was not only associated with response rate but was also positively correlated with time to progression (P=0.0022).For all bortezomib treated patients enrolled in the trial (n=333) regardless of their baseline (LFTs and creatinine), a 25% increase in ALP from the baseline to 6 week remained strongly associated with a very high response rate (p<0.0001) and longer time to progression (206 vs 169 days) p=0.01. [Display omitted] At the time of relapse after B therapy, the median ALP was 65.0 U/L and comparable to baseline level (65.5 U/L).Conclusion:During bortezomib treatment, markers of osteoblastic activation (such as ALP) may predict response and response duration in patients with multiple myeloma. In addition, this suggests that bone anabolism could affect myeloma growth. This observation needs to be confirmed prospectively.

The Importance of Liver Biopsy in the Investigation of Possible Mitochondrial Respiratory Chain Disease

The diagnosis of mitochondrial respiratory chain deficiency is usually made by analysis of mitochondrial respiratory chain activity in muscle biopsy. We describe 4 patients in whom the diagnosis was based on mitochondrial respiratory chain deficiency in liver alone. In 3 patients, liver complex IV activity was deficient, and the 4th patient had liver complex I deficiency (relative to citrate synthase and complex II activity). The enzyme activities in skeletal muscle biopsies from these patients were normal or equivocal. The age at presentation and the neurological symptoms differed from one patient to another. All 3 patients with complex IV deficiency had non-specific white matter changes on brain MRI. None of the patients had clinical or biochemical evidence of liver disease. These findings illustrate the wide variety of presentations associated with liver mitochondrial respiratory chain deficiency. They also demonstrate the importance of mitochondrial respiratory chain enzyme analysis in liver, in addition to muscle, even in cases where the primary clinical deficit is neurological and there is no liver disease.

Hepatitis C virus associated arthropathy in absence of clinical and biochemical evidence of liver disease - responding to interferon therapy

This commentary aims to provide Anaesthetists and Intensivists with an understanding of the viral hepatitides and their impact on clinical practice. This will include the modes and risks of transmission, clinical features and new options for disease treatment. Peri-operative management, safe clinical practice and needlestick injury will also be discussed.

Impairment of psychomotor responses after conscious sedation in cirrhotic patients undergoing therapeutic upper GI endoscopy

OBJECTIVES: The aim of this study was to determine whether the number connection test (NCT) times of a group of cirrhotic patients without clinically overt hepatic encephalopathy and a group of healthy patients without liver disease who were undergoing endoscopy were prolonged after sedation with short acting i.v. benzodiazepines. METHODS: All patients were administered the NCT in a standard fashion for 30 min before sedation for an upper GI endoscopy and then 2 h after sedation postprocedure. Two NCTs were carried out before and 2 h after sedation, and the mean of the tests pre- and postsedation calculated. Based on the upper limit of the 95% CI of the presedation NCT of patients without liver disease as the cut-off level for hepatic encephalopathy, the proportion of cirrhotic patients with subclinical encephalopathy before and after sedation were also determined. RESULTS: A total of 61 consecutive cirrhotic patients who underwent therapeutic upper GI endoscopy completed the study. The mean presedation NCT time was 43.5 s (95% CI = 39.0–48.1 s) and the mean postsedation NCT time 60.0 s (95% CI = 50.7–69.3 s). The difference between the mean pre- and postsedation NCT times was 16.4 s (95% CI = 9.8–23.1 s; p < 0.001). A total of 38 consecutive patients without clinical or biochemical evidence of liver disease who presented for upper GI endoscopy completed the NCT as described for the group of cirrhotic patients. The mean (± SD) baseline NCT time was 34.7 ± 7.9 s (95% CI = 32.1–37.2 s), whereas the mean postsedation NCT time was 33.7 ± 8.5 s (95% CI = 30.9–36.5 s). This difference was not statistically significant ( p = 0.177). Using the upper limit of the 95% CI of the mean (37.4 s) of the presedation time in the patients without liver disease as the cut-off between normal and encephalopathy, the number of cirrhotic patients with abnormal presedation NCT times was 33 patients (54.1%), and this number rose to 46 patients (75.4%) after sedation with midazolam. This increase in proportion of cirrhotic patients with prolonged NCT time was statistically significant ( p < 0.001). CONCLUSIONS: Sedation with i.v. midazolam prolongs NCT times in cirrhotic patients but not in healthy individuals without liver disease. The proportion of patients with prolonged NCT times increased in patients with cirrhosis following sedation, whereas this did not occur in those without liver disease.

Impairment of psychomotor responses after conscious sedation in cirrhotic patients undergoing therapeutic upper GI endoscopy.

The aim of this study was to determine whether the number connection test (NCT) times of a group of cirrhotic patients without clinically overt hepatic encephalopathy and a group of healthy patients without liver disease who were undergoing endoscopy were prolonged after sedation with short acting i.v. benzodiazepines. All patients were administered the NCT in a standard fashion for 30 min before sedation for an upper GI endoscopy and then 2 h after sedation postprocedure. Two NCTs were carried out before and 2 h after sedation, and the mean of the tests pre- and postsedation calculated. Based on the upper limit of the 95% CI of the presedation NCT of patients without liver disease as the cut-off level for hepatic encephalopathy, the proportion of cirrhotic patients with subclinical encephalopathy before and after sedation were also determined. A total of 61 consecutive cirrhotic patients who underwent therapeutic upper GI endoscopy completed the study. The mean presedation NCT time was 43.5 s (95% CI = 39.0-48.1 s) and the mean postsedation NCT time 60.0 s (95% CI = 50.7-69.3 s). The difference between the mean pre- and postsedation NCT times was 16.4 s (95% CI = 9.8-23.1 s; p < 0.001). A total of 38 consecutive patients without clinical or biochemical evidence of liver disease who presented for upper GI endoscopy completed the NCT as described for the group of cirrhotic patients. The mean (+/- SD) baseline NCT time was 34.7+/-7.9 s (95% CI = 32.1-37.2 s), whereas the mean postsedation NCT time was 33.7+/-8.5 s (95% CI = 30.9-36.5 s). This difference was not statistically significant (p = 0.177). Using the upper limit of the 95% CI of the mean (37.4 s) of the presedation time in the patients without liver disease as the cut-off between normal and encephalopathy, the number of cirrhotic patients with abnormal presedation NCT times was 33 patients (54.1%), and this number rose to 46 patients (75.4%) after sedation with midazolam. This increase in proportion of cirrhotic patients with prolonged NCT time was statistically significant (p < 0.001).

Concordance between anti HCV and HCV RNA among patients with and without biochemical evidence of liver disease

Concordance between anti HCV and HCV RNA among patients with and without biochemical evidence of liver disease

Assessment of Donor Fatty Livers for Liver Transplantation. Transplantation 2001; 71: 1221.

Assessment of Donor Fatty Livers for Liver Transplantation. Transplantation 2001; 71: 1221.

Autoimmune hepatitis/sclerosing cholangitis overlap syndrome in childhood: a 16-year prospective study.

To investigate whether sclerosing cholangitis with an autoimmune serology characteristic of autoimmune hepatitis (AIH) and AIH are distinct entities, we studied 55 consecutive children with clinical and/or biochemical evidence of liver disease and circulating antinuclear (ANA), anti-smooth muscle (SMA), and/or liver-kidney-microsomal type 1 (LKM1) autoantibodies. They underwent liver biopsy, direct cholangiography, sigmoidoscopy, and rectal biopsy at presentation. Twenty-eight were diagnosed as AIH in the absence and 27 autoimmune sclerosing cholangitis (ASC) in the presence of radiological features of cholangiopathy. Twenty-six ASC and 20 AIH had ANA and/or SMA; 1 ASC and 8 AIH LKM1 autoantibody. Similarities between the 2 conditions included most clinical and biochemical parameters and a lower frequency of HLA DR4. Inflammatory bowel disease and histological biliary changes were more common in ASC; coagulopathy, hypoalbuminemia, lymphocytic periportal hepatitis, and HLA DR3 were more common in AIH. Histological biliary changes were observed in 65% of ASC and 31% of AIH patients. Eighty-nine percent responded to immunosuppression. Follow-up liver biopsies from 17 ASC and 18 AIH patients had similarly reduced inflammatory activity and no progression to cirrhosis. Sixteen follow-up cholangiograms from AIH patients and 9 from ASC patients were unchanged, while 8 ASC patients showed a progressive cholangiopathy. One child with AIH and ulcerative colitis developed sclerosing cholangitis 8 years after presentation. At 2 to 16 years (median, 7 years) from presentation, all patients are alive, including 4 ASC patients who underwent liver transplantation. In conclusion, ASC and AIH are similarly prevalent in childhood; cholangiography is often needed to distinguish between these 2 entities, which are likely to lie within the same disease process.

The incidence of GB virus C / hepatitis G virus infection in Brazilian patients who received blood transfusion during cardiac surgery.

The incidence of GBV-C/hepatitis G virus (GBV-C/HGV) infection after blood transfusion is unknown in Brazil. Many studies have so far addressed its relationship with blood transfusion, but its association with liver disease was not confirmed. A prospective study was carried out between 1996 and 1999 in Rio de Janeiro. Ninety three patients who received blood transfusion during cardiac surgery were followed for six months and blood samples were drawn before and after surgery to determine antibodies to GBV-C/hepatitis G virus (anti-HGenv) using a step sandwich immunoassay and GBV-C/HGV-RNA using reverse transcriptase polymerase chain reaction. The alanine aminotransferase (ALT) levels were serially determined as well as clinical data compiled related to hepatitis. Prior to surgery, anti-HGenv was present in 35.5% (33/93) of patients and 4.3%(4/93) were found to be viremic. Seroconversion following transfusion was observed in 9 patients and 4 additional individuals became viremic for a total incidence of 23% (13/56). Six months after blood transfusion, only 4 of those nine patients previously antibody positive still had anti-HGenv detectable in serum. No patients had clinical or laboratory evidence of acute hepatitis and no correlation was found with GBV-C/HGV infection and number of blood units transfused (p = 0.37). This study highlights the importance of using both HGV-RNA PCR and anti-HGenv to accurately estimate the magnitude of GBV-C/HGV infection. The observed high prevalence and incidence rates show that this infection is common in Brazil; however, no clinical or biochemical evidence of liver disease was demonstrated in the period of study and longer longitudinal observation is needed to define any pathogenic effect.

Natural history of the TT virus infection through follow-up of TTV DNA–positive multiple-transfused patients

Little is known about the natural history and the pathogenicity of the TT virus (TTV). We present our findings of a cross-sectional study based on the TTV DNA screening of 173 multiple-transfused patients and a longitudinal study based on the follow-up of TTV DNA–positive patients. Overall, 48 patients (27.7%) tested positive for TTV DNA. The influence of the number of blood donor exposures on the prevalence of blood-borne viral infection indicates that TTV, hepatitis C virus (HCV), and an RNA virus known as GB virus C/hepatitis G virus (GBV-C/HGV) share a parenteral transmission, but that TTV, in contrast to the 2 other viruses, is also transmitted by at least another efficient means. The patients having a well-defined date of TTV infection were positive for TTV DNA during a mean period of 3.1 years. A chronic infection was observed in 31 cases (86%). TTV carriage appeared clinically benign in all patients. No clinical evidence of a disease potentially linked to the TTV infection was observed in patients with TTV DNA carriage over several years. The majority of TTV carriers had no biochemical evidence of liver disease. The prevalence of elevated serum alanine aminotransferase (ALT) level was higher in the TTV DNA–positive group, even in the absence of HCV infection, but the observed peaks of ALT level were most often transient and very mild. The prevalence of TTV DNA observed in blood recipients is consistent with that of TTV infection observed in blood donors. TTV infection frequently tends to persist. (Blood. 2000;95:347-351)