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Yukihiro Shimizu, Division of Internal Medicine, Center for Gastroenterology and Hepatology, Kyoto Katsura Hospital, 17 Yamada-Hirao, Nishikyo, Kyoto 615-8256, Japan Author contributions: Shimizu Y summarized and reviewed the previous reports on liver injury in systemic disease and wrote the manuscript alone. Correspondence to: Yukihiro Shimizu, MD, PhD, Division head, Division of Internal Medicine, Center for Gastroenterology and Hepatology, Kyoto Katsura Hospital, 17 Yamada-Hirao, Nishikyo, Kyoto 615-8256, Japan. yukihiro@katsura-hp.jp Telephone: +81-75-3915811 Fax: +81-75-3810090 Received: March 28, 2008 Revised: May 9, 2008 Accepted: May 16, 2008 Published online: July 14, 2008
Abstract Potential causes of abnormal liver function tests include viral hepatitis, alcohol intake, nonalcoholic fatty liver disease, autoimmune liver diseases, hereditary diseases, hepatobiliary malignancies or infection, gallstones and drug-induced liver injury. Moreover, the liver may be involved in systemic diseases that mainly affect other organs. Therefore, in patients without etiology of liver injury by screening serology and diagnostic imaging, but who have systemic diseases, the abnormal liver function test results might be caused by the systemic disease. In most of these patients, the systemic disease should be treated primarily. However, some patients with systemic disease and severe liver injury or fulminant hepatic failure require intensive treatments of the liver.
© 2008 The WJG Press. All rights reserved.
Key words: Abnormal liver function tests; Jaundice; Systemic disease
Peer reviewer: Guang-Cun Huang, MD, PhD, Nationwide Children’s Hospital and The Ohio State University, Center for Cell & Developmental Biology, The Research Institute at Nationwide Children’s Hospital and The Ohio State University, 700 Childrens Drive, Columbus OH 43205, United States
Shimizu Y. Liver in systemic disease. World J Gastroenterol 2008; 14(26): 4111-4119 Available from: URL: http://www.wjgnet.com/1007-9327/14/4111.asp DOI: http://dx.doi.org/10.3748/wjg.14.4111
INTRODUCTION Potential causes of abnormal liver function tests include viral hepatitis, alcohol intake, nonalcoholic fatty liver disease, autoimmune liver diseases and hereditary diseases such as hemochromatosis, a1-antitrypsin deficiency and Wilson’s disease. Many patients with liver injury are likely to be treated with several drugs, increasing the possibility that their liver injuries are drug-induced. Some patients with liver injury, however, have underlying systemic diseases, which may also affect their livers. Knowledge of liver involvement in systemic diseases is important for the accurate diagnosis of liver injury and to avoid unnecessary examination and treatment. This review will describe liver injury caused by various systemic diseases.
Cardiovascular diseases Ischemic hepatitis The pathophysiology of ischemic hepatitis, also known as “shock liver”, is poorly understood[1]. Patients usually show rapid (within 24-48 h) and dramatic transient increases in serum aminotransferase, lactate dehydrogenase (LDH) levels and bilirubin following periods of hemodynamic instability or hypoxia. Three features distinguish ischemic hepatitis from acute viral hepatitis: LDH elevation is more marked in ischemic than in viral hepatitis; serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) concentrations rapidly return to normal in ischemic hepatitis, usually within 7-10 d; and ischemic hepatitis is more often complicated by renal damage[2]. Ischemic hepatitis has several etiologies (Table 1)[2].
Liver congestion Liver congestion is caused by acute or chronic right-sided heart failure and is manifested by hepatomegaly (95%-99%), ascites (7%-49%), splenomegaly (12%-25%) and/or jaundice (< 20%)[3,4]. In addition, patients often show signs indicative of heart failure, including peripheral edema and pleural effusion. Liver function tests show that serum bilirubin is elevated, usually to 1-5 mg/dL and mostly in the unconjugated form, in 24%-81% of patients, depending on the severity of heart failure[3-5]. Bilirubin concentrations rapidly return to normal 3-7 d after improvement of right-sided heart failure. In addition, 3%-50% of patients with heart failure show elevated levels of serum aminotransferases, with the elevation of AST more marked than that of ALT[3-5]. Elevated serum alkaline phosphatase (ALP) is observed in 10%-20% of patients with right-sided heart failure, but these levels return to normal within 1 wk after improvement of heart failure[3-5].
Cardiac cirrhosis Cardiac cirrhosis may occur after longstanding hepatic congestion, but its incidence is relatively low. Although liver cirrhosis has no characteristic biochemical markers, a multivariate analysis found that elevated concentrations of AST and bilirubin are prognostic of poor outcome[6].
Heatstroke The liver is extremely sensitive to thermal injury and is a frequent site of tissue injury in patients with heatstroke, with almost all of these patients experiencing liver injury[7]. Elevated serum ALT concentration is the most common feature in patients with heatstroke, and may lead to acute hepatic failure[8]. Liver function tests usually return to normal after 2 wk, but may remain elevated after 1 mo[9].
Connective tissue diseases
Connective tissue
diseases often involve the liver, and various forms of hepatic
involvement have been reported. Laboratory markers and liver diseases
associated with connective tissue diseases are summarized in
Table 2[10,11].
Hematological Diseases Hodgkin disease Liver infiltration of malignant cells has been reported in 14% of patients with Hodgkin disease, and hepatomegaly in 9% of patients with stage Ⅰ-Ⅱ and in 45% of patients with stage Ⅲ-Ⅳ disease[17]. In addition, mild elevations of aminotransferases and moderate elevation of ALP can occur, due to tumor infiltration or extrahepatic bile duct obstruction[17]. However, cholestasis in zone 3, which was not associated with extrahepatic obstruction or tumor infiltration, has been described; this cholestasis may be due to vanishing bile duct syndrome[18].
Non-Hodgkin lymphoma Lymphoma cell infiltration of the liver is more common in non-Hodgkin than in Hodgkin disease, with 16%-43% of non-Hodgkin patients showing hepatic involvement[17]. Extrahepatic obstruction is also more common in non-Hodgkin than in Hodgkin disease. Moreover, hepatic infiltration is more common in low-grade B-cell lymphomas (small cell) than in high-grade (diffuse large B-cell, T-cell histiocytic) lymphomas[19]. Liver function tests show mild to moderate elevations in serum ALP, and hepatomegaly may occur[17]. Although liver involvement in both Hodgkin and non-Hodgkin lymphomas may present as acute hepatic failure[20-25], liver transplantation should be avoided[26]. Jaundice due to non-Hodgkin lymphoma can be distinguished from that due to viral hepatitis or drug hepatotoxicity by the presence of liver enlargement and lactic acidosis in lymphoma[27].
Chronic lymphoid leukemia (CLL) Patients with CLL often show mild to moderate liver enlargement and extensive lymphocytic infiltration in the portal tracts, with functional impairment of the liver in late stages[28,29].
Hairy cell leukemia Leukemia cells often infiltrate the liver, in both the portal tracts and sinusoids, and liver enlargement has been observed in up to 40% of patients with this disease[30].
Acute leukemia Although hepatic involvement in acute leukemia is usually mild and silent at the time of diagnosis[27], a post mortem study showed liver infiltration in > 95% of ALL and up to 75% of AML patients[31]. In ALL, infiltration was confined to the portal tracts, whereas, in AML, infiltration was observed in both portal tracts and sinusoids. Massive leukemic cell infiltration of the liver may present as fulminant hepatic failure[32]. In patients with acute leukemia, drug-induced liver injury and bacterial or fungal infections may also affect the liver.
Multiple myeloma Hepatomegaly has been observed in 15%-40% of patients with multiple myeloma and may sometimes be accompanied by splenomegaly[33,34].
Primary myelofibrosis Liver involvement is common in patients with primary myelofibrosis, and liver enlargement is observed in almost all patients. The mechanisms of liver involvement have been associated with extramedullary hematopoiesis, increased hepatic blood flow and hemosiderosis caused by multiple blood transfusions[27]. Ascites and esophageal varices secondary due to portal hypertension has been found in 7% of these patients[35,36] and nodular regenerative hyperplasia of the liver following obstruction of intrahepatic portal vein branches may augment the portal hypertension[37]. The most common liver function abnormality in patients with primary myelofibrosis is elevated ALP, which has a frequency of 40%-60% and which may be associated with the severity of sinusoidal dilatation[38].
Polycythemia vera Although direct liver involvement is uncommon, some patients may present with acute or chronic Budd-Chiari syndrome[39].
Chronic myeloid leukemia (CML) About 50% of patients with CML show mild to moderate hepatomegaly at presentation, with no liver function abnormalities[40]. At the time of blastic crisis, however, liver sinusoidal infiltration by immature cells may lead to liver enlargement and elevated serum ALP levels[41].
Myelodysplasias In patients with sideroblastic or refractory anemia, iron deposition in the liver may occur due to repeated transfusion or decreased iron utilization by bone marrow[27].
Sickle-cell disease The liver is commonly involved in sickle-cell disease. This may be due to iron overload caused by multiple blood transfusions, gallstones, or cardiac dysfunction due to secondary hemochromatosis[42].
Thalassemia The major cause of liver injury in patients with thalassemia is hemochromatosis due to ineffective erythropoiesis, with massive iron deposits found in the liver[27].
LUNG DISEASES Pneumonia Lobar pneumonia caused by Legionella pneumophila, Mycoplasma pneumoniae or Pneumococcus may be associated with elevated concentrations of serum aminotransferase and bilirubin[43]. Jaundice has been observed in 3%-25% of patients with Pneumococcus pneumonia[44], often developing between days 3 and 6 of illness. In Legionnaire’s disease, liver function tests are likely to show abnormalities, with elevated concentration of serum ALP and aminotransferase in up to 50% of patients[45]. Mycoplasma pneumoniae is a frequent cause of community-acquired pneumonia. Liver involvement is not common, but some patients may have elevated levels of serum aminotransferases[43]. Cholestatic hepatitis and mild hepatitis without pneumonia have been described[43]. Cytomegalovirus pneumonia can also result in jaundice and elevated levels of ALP and aminotransferases[46].
Chronic pulmonary disease Serum bilirubin, ALT, g-glutamyl transpeptidase (GGT) and ALP may be elevated in patients with chronic pulmonary disease or status asthmatics[47-49], and these liver abnormalities may be associated with secondary heart failure or hypoxia.
Renal diseases Even in the absence of liver metastasis, renal cancer causes hepatomegaly and abnormal liver function test results. Following tumor resection, however, these liver abnormalities return to normal, suggesting that the previously observed abnormalities were caused by a hepatotoxic hormone secreted from the tumor[50].
Systemic Infection-bacteremia and sepsis
Cholestasis is a
common complication in patients with extrahepatic bacterial infection
and sepsis, regardless of whether the infectious agent is gram-negative
(E.coli and Klebsiella) or gram-positive (S aureus)[51,52].
Proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-a)
and interleukin-6 (IL-6), as well as nitric oxide, are thought to induce
cholestasis by inhibiting the canalicular excretion of conjugated
bilirubin[53]. Liver biopsy may show mild portal
inflammation, but bile ducts often appear normal and there is usually no
cholangitis[54].
Laboratory findings in sepsis include mild elevation of ALP (mostly 1 to
3 times the ULN) and modest elevation of ALT. Peak serum bilirubin
concentrations typically range from 5 to 10 mg/dL, but levels as high as
30 to 50 mg/dL have been reported[31]. Importantly, the serum
concentrations of ALP and bilirubin may be discordant, with deeply
jaundiced patients often having normal ALP levels, while anicteric
patients may show marked elevation of ALP or GGT[55-57].
Compared with infected patients without bacteremia, those with
bacteremia had significantly higher serum levels of GGT and ALP and
significantly lower serum concentrations of albumin, cholesterol and
cholinesterase. These alterations were observed within several days
after the onset of bacteremia, but concentrations returned to normal
following adequate treatment of the infection[52]. Although
the major pathogens were S aureus and
LIVER DAMAGE IN INFECTION BY SPECIFIC PATHOGENS Clostridium perfringens infection C perfringens may directly affect the liver by forming an abscess or causing necrotizing massive gas gangrene of the liver, leading to fulminant hepatic failure[59].
Salmonella typhi infection While sepsis can cause liver dysfunction, it can also occur following Salmonella typhi infection, a condition known as Salmonella hepatitis[60]. Although severe elevation of liver function tests is rare, jaundice has been observed in 33% of these patients. Although the clinical features of Salmonella hepatitis may be identical to those of acute viral hepatitis, these diseases may be distinguished by the ALT/LDH ratio, which is < 4.0 in Salmonella hepatitis, significantly lower than the ratio in acute viral hepatitis, > 5.0[61].
Lyme disease Hepatic involvement is common in Lyme disease caused by Borrelia burgdorferi, and mild elevations of GGT and aminotransferase are commonly observed especially in patients with early stage disease[62,63].
Q fever Nearly 50% of patients with Q fever had accompanying hepatitis, but the liver function abnormalities were nonspecific. Although these patients usually show anicteric hepatitis, one third may have jaundice if the disease is prolonged[64].
Syphilis Acute cholestatic syphilitic hepatitis, sometimes accompanied by jaundice, has been reported in patients with secondary syphilis[65]. Patients with tertiary syphilis may present with gummas formation in the liver, which resemble metastatic tumors[66].
Campylobacter infection Mild to severe liver biochemical abnormalities have been observed following infection with Campylobacter organisms[67].
Chlamydia or Neisseria infection Perihepatitis has been observed in patients infected with Chlamydia trachomatis[68] and Neisseria gonorrhoeae[69], with the formation of liver granulomas in the former[65].
HIV infection Liver injury in patients with HIV infection can be caused by HIV itself, by coinfection with hepatitis viruses such as HBV and HCV, or by hepatic involvement of systemic infections, including M tuberculosis, M avium complex, Toxoplasma gondii, or Cryptosporidium. In addition, liver injury in HIV-infected patients may be due to the toxicities of drugs prescribed for the treatment of HIV or coinfected microbes. In addition, biliary tract injuries caused by tuberculosis, M.avium and Cryptosporidium have been reported[70].
Mycobacteria infection Liver involvement is frequent in patients with mycobacterial infections, not only with Mycobacterium tuberculosis infection, but also with M avium intracellulare or M genavense infection[65]. The clinical spectrum of liver disease due to Mycobacterium spp. ranges from the absence of symptoms to liver failure, with multiple granulomas in the parenchyma of the liver being the most common lesion[71]. These patients show elevated serum ALP concentrations and hepatomegaly. Although the number of intrahepatic granulomas is greater in patients with than without disseminated military tuberculosis, hepatic tuberculosis can occur, even in the absence of apparent tuberculosis elsewhere[72].
Fungal infection The liver is often involved in deep fungal infections, possibly due to enrichment of the blood flow through the liver or the invasion of fungi, including C albicans and C. tropicans, into the liver from the gut by penetrating through degenerated barriers of gastrointestinal mucosa[73]. Patients with liver involvement of fungal infection may show elevated serum concentrations of ALP and GGT, due to the formation of multiple small abscesses or granulomas in the liver. Liver involvement following deep fungal infections is summarized in Table 3[73].
ACUTE HEPATIC FAILURE CAUSED BY VIRUSES OTHER THAN HEPATITIS A TO E The major causes of acute hepatic failure include drugs, hepatitis A, hepatitis B, and hepatitis E. Although Epstein-Barr virus and cytomegalovirus can also cause severe hepatitis during primary infection, other microbes, which mainly affect other organs, can cause acute hepatic failure. Among these are Salmonella paratyphi A[74], herpes simplex virus[75,76], parvovirus B19[77], coxsackie virus B2[78], human herpesvirus-6[79], Varicella-Zoster virus[80], and Dengue virus[81]. Parvovirus B19 and human herpesvirus-6 are often found in patients with non-A to non-E acute hepatic failure.
TOTAL PARENTERAL NUTRITION (TPN) TPN may cause steatosis or cholestasis, and liver disease is more severe in infants than in adults. Elevated serum aminotransferase concentrations are common during the first 1-3 wk of TPN, and bilirubin increases in some adults after 10 wk or more of TPN[82-84]. Chronic cholestasis has been observed in 55% of patients receiving TPN for at least 2 years[85], and cholestasis can lead to acalculous and calculous cholecystitis or TPN-induced cholelithiasis[86].
Endocrine diseases Thyroid disease Patients with hyperthyroidism frequently experience liver injury, which may be caused by increased hepatocyte oxygen demand without an associated increase in hepatic blood flow. Liver injury can be either cholestatic or hepatocellular. Up to 64% of these patients show elevated serum ALP, and up to 35% show elevated ALT. Interestingly, only 17% of these patients show elevated GGT[17], and most of the increased ALP is bone-derived[87]. In contrast to hyperthyroidism, liver biochemistry abnormalities are less prominent in patients with hypothyroidism. However, modest elevations in serum AST and ALT have been reported in 84% and 60%, respectively, of patients with hypothyroidism[88]. Some patients may show low serum ALP[87], but their most characteristic symptom is ascites, which is caused by unknown mechanisms[87]. In addition, cholestatic jaundice has been described in case reports of patients with severe hypothyroidism[17].
Cushing syndrome Hypercortisolism causes fatty infiltration of the liver in half of the patients, which may progress to NASH. The prevalence of NASH in these patients has been estimated to be 20% to 50%[89].
Adrenal insufficiency Elevated serum aminotransferase concentrations have been reported in patients with adrenal insufficiency; these abnormalities usually resolve with appropriate hormone replacement[90,91].
Diabetes mellitus Elevated liver chemistries have been observed in 10%-20% of patients with DM[92,93], more frequently in patients with type 2 than type 1 DM[94]. One study reported that 16.5%, 9%, 11% and 6% of these patients had elevations in serum GGT, ALP, ALT and AST, respectively. Non-alcoholic fatty liver disease is a complication in 32% to 78% of patients with type 2 DM, and 50% of these patients may have non-alcoholic steatohepatitis (NASH)[95,96]. NASH in DM patients may lead to liver cirrhosis and eventually to hepatocellular carcinoma[94,97].
POSTOPERATIVE JAUNDICE Jaundice often occurs after surgery, especially after cardiac surgery; of the latter, approximately 26.5% show conjugated hyperbilirubinemia[98]. Factors thought to contribute to the development of jaundice after surgery include: (1) Liver congestion due to preexisting right-sided heart failure; (2) Degree of perioperative hypotension and hypoxia; (3) Destruction of transfused erythrocytes; (4) Hemolysis secondary to mechanical prostheses; (5) Type of operation-The incidence of postoperative jaundice is dependent on the type of operation. For example, patients who underwent mitral valve replacement or multiple valve surgery had a higher rate of jaundice than those who underwent coronary bypass graft surgery; (6) Perioperative infection; (7) Resorption of hematoma; (8) Worsening of jaundice in Gilbert’s syndrome-Gilbert’s syndrome is the most common form of inherited hyperbilirubinemia, with 5% to 10% of Caucasians and Japanese estimated to have this syndrome. Although serum bilirubin levels are usually below 3 mg/dL, with the unconjugated form being dominant, jaundice may be worsened by a stress caused by surgery or infection; (9) Total parenteral nutrition; (10) Drug-induced liver injury, and (11) Benign postoperative intrahepatic cholestasis. Postoperative jaundice usually occurs within 1-2 wk after major surgery. Serum concentrations of mainly conjugated bilirubin may increase to 40 mg/dL, but these resolve within a few days to weeks without specific treatment[99].
GASTROINTESTINAL DISEASES Abnormal liver function test results are observed in over 50% of patients with inflammatory bowel diseases requiring surgery. The hepatobiliary diseases accompanying ulcerative colitis and Crohn’s disease are shown in Table 4[100]. Patients who undergo jejunoileal resection for the treatment of severe obesity may experience liver damage[101]. The liver often shows NASH, leading to liver cirrhosis and liver failure. Similar liver injuries have been observed in patients undergoing gastrectomy via Billroth-Ⅱ reconstruction. Bacterial overgrowth in the blind-loop of the intestine can induce endotoxin and intrinsic ethanol[102,103], leading to Kupffer cell activation and hepatocyte damage.
GRANULOMA FORMATION IN THE LIVER Several systemic diseases and drugs have been shown to induce granulomas in the liver, causing liver enlargement. The most consistently abnormal liver biochemistry result is elevated serum ALP. The diagnosis and causes of hepatic granulomas may be determined by a histological examination of the liver. Five etiological categories have been identified[104]: (1) Immunological: Sarcoidosis, primary biliary cirrhosis, giant cell hepatitis, Wegener’s granulomatosis, chronic granulomatous disease and allergic granulomatosis; (2) Infectious: Hepatitis C virus, cytomegalovirus, Epstein-Barr virus, tuberculosis, Mycobacterium avium-intracellulare in patients with HIV infection, leprosy, brucellosis, typhoid fever, Whipple’s disease, tularaemia, yersiniosis, cat-scratch disease, histoplasmosis, blastomycosis, coccidiomycosis, candidiasis, Q fever, leishmaniasis, toxoplasmosis, syphilis, and schistosomiasis; (3) Medications: Penicillins, diphenylhydantoin and allopurinol; (4) Neoplastic: Hodgkin’s disease and hypernephroma, and (5) Foreign body: Beryllium, suture material used in operation and thorotrast.
AMYLOIDOSIS Hepatic involvement has been demonstrated in about one-fifth of patients with AA amyloidosis and about half of those with the AL type, and liver function tests can remain normal even in patients with substantial amyloid deposits and hepatomegaly. Elevated serum ALP and GGT occur first in patients with massive amyloid deposits, followed by modest elevations of serum AST and ALT[105].
CONCLUSION Abnormal liver function often occurs in patients without hepatitis virus infection and without excessive alcohol intake. Although US, CT or MR imaging should be used to assess the occurrence of fatty liver disease, hepatobiliary malignancies or infection and gallstones, diagnosis of autoimmune liver disease, especially with atypical presentation, is sometimes difficult. Moreover, intake of drugs including herbal medicines or supplemental nutrients may cause liver injury. However, abnormal liver function tests do not necessarily indicate serious liver disease. Asymptomatic patients with isolated, mild elevation of unconjugated bilirubin (e.g. Gilbert’s syndrome) or GGT generally do not have liver disease and do not require further examination[106]. In contrast, the liver may be involved in systemic diseases that mainly affect other organs. Therefore, in patients without etiology of liver injury by screening serology and diagnostic imaging, but who have systemic diseases, the abnormal liver function test results might be caused by the systemic disease. In most of these patients, the systemic disease should be treated primarily. However, some patients with systemic disease and severe liver injury or fulminant hepatic failure require intensive treatments of the liver.
REFERENCES
1 Kay PS, Keeffe EB. Cardiac disease and the liver. In: Gitlin N editor. The Liver and Systemic Disease. Hong Kong: Pearson Professional Limited, 1997: 1-16 2 Gitlin N, Serio KM. Ischemic hepatitis: widening horizons. Am J Gastroenterol 1992; 87: 831-836 PubMed 3 Richman SM, Delman AJ, Grob D. Alterations in indices of liver function in congestive heart failure with particular reference to serum enzymes. Am J Med 1961; 30: 211-225 PubMed DOI 4 Dunn GD, Hayes P, Breen KJ, Schenker S. The liver in congestive heart failure: a review. Am J Med Sci 1973; 265: 174- 5 Sherlock S. The liver in heart failure; relation of anatomical, functional, and circulatory changes. Br Heart J 1951; 13: 6 Tiukinhoy-Laing S, Blei AT, Gheorghiade M. The liver in cardiovascular disease. In: Rodés J, Benhaumou JP, Blei AT, Reichen J, Rizzetto M, editors. Textbook of Hepatology. 3rd ed. Oxford: Blackwell Publishing, 2007: 1609-1615 7 Rubel LR, Ishak KG. The liver in fatal exertional heatstroke. Liver 1983; 3: 249-260 PubMed 8 Weigand K, Riediger C, Stremmel W, Flechtenmacher C, Encke J. Are heat stroke and physical exhaustion underestimated causes of acute hepatic failure? World J Gastroenterol 2007; 13: 306-309 PubMed 9 Kew M, Bersohn I, Seftel H, Kent G. Liver damage in heatstroke. Am J Med 1970; 49: 192-202 PubMed DOI 10 Gitlin N. Connective tissue diseases and the liver. In: Gitlin N editor. The Liver and Systemic Disease. Hong Kong: Pearson Professional Limited, 1997: 115-135 11 Abraham S, Begum S, Isenberg D. Hepatic manifestations of autoimmune rheumatic diseases. Ann Rheum Dis 2004; 12 Runyon BA, LaBrecque DR, Anuras S. The spectrum of liver disease in systemic lupus erythematosus. Report of 33 histologically-proved cases and review of the literature. Am J Med 1980; 69: 187-194 PubMed DOI 13 Tojo J, Ohira H, Abe K, Yokokawa J, Takiguchi J, Rai T, Shishido S, Sato Y, Kasukawa R. Autoimmune hepatitis accompanied by systemic lupus erythematosus. Intern Med 2004; 43: 258-262 PubMed DOI 14 Usta Y, Gurakan F, Akcoren Z, Ozen S. An overlap syndrome involving autoimmune hepatitis and systemic lupus erythematosus in childhood. World J Gastroenterol 2007; 13: 2764-2767 PubMed 15 Iwai M, Harada Y, Ishii M, Tanaka S, Muramatsu A, Mori T, Nakashima T, Okanoue T, Hirohata S. Autoimmune hepatitis in a patient with systemic lupus erythematosus. Clin Rheumatol 2003; 22: 234-236 PubMed DOI 16 Lu MC, Li KJ, Hsieh SC, Wu CH, Yu CL. Lupus-related advanced liver involvement as the initial presentation of systemic lupus erythematosus. J Microbiol Immunol Infect 2006; 39: 471-475 PubMed 17 Ross A, Friedman LS. The liver in systemic disease. In: Bacon BR, O’Grady JG, Di Bisceglie AM, Lake JR, editors. Comprehensive Clinical Hepatology. 2nd ed. Philadelphia: Mosby Elsevier Ltd, 2006: 537-547 18 Hubscher SG, Lumley MA, Elias E. Vanishing bile duct syndrome: a possible mechanism for intrahepatic cholestasis in Hodgkin's lymphoma. Hepatology 1993; 17: 70-77 PubMed 19 Jaffe ES. Malignant lymphomas: pathology of hepatic involvement. Semin Liver Dis 1987; 7: 257-268 PubMed 20 Vardareli E, Dundar E, Aslan V, Gulbas Z. Acute liver failure due to Hodgkin's lymphoma. Med Princ Pract 2004; 13: 21 Dourakis SP, Tzemanakis E, Deutsch M, Kafiri G, Hadziyannis SJ. Fulminant hepatic failure as a presenting paraneoplastic manifestation of Hodgkin's disease. Eur J Gastroenterol Hepatol 1999; 11: 1055-1058 PubMed DOI 22 Rowbotham D, Wendon J, Williams R. Acute liver failure secondary to hepatic infiltration: a single centre experience of 18 cases. Gut 1998; 42: 576-580 PubMed 23 Emile JF, Azoulay D, Gornet JM, Lopes G, Delvart V, Samuel D, Reynes M, Bismuth H, Goldwasser F. Primary non- Hodgkin's lymphomas of the liver with nodular and diffuse infiltration patterns have different prognoses. Ann Oncol 2001; 24 Morali GA, Rozenmann E, Ashkenazi J, Munter G, Braverman DZ. Acute liver failure as the sole manifestation of relapsing non-Hodgkin's lymphoma. Eur J Gastroenterol Hepatol 2001; 13: 1241-1243 PubMed DOI 25 Yeshurun M, Isnard F, Garderet L, Rambeloarisoa J, Prevot S, Carbonell N, Najman A. Acute liver failure as initial manifestation of low-grade non-Hodgkin's lymphoma transformation into large-cell lymphoma. Leuk Lymphoma 2001; 26 Woolf GM, Petrovic LM, Rojter SE, Villamil FG, Makowka L, Podesta LG, Sher LS, Memsic L, Vierling JM. Acute liver failure due to lymphoma. A diagnostic concern when considering liver transplantation. Dig Dis Sci 1994; 39: 1351-1358
27 Bruguera M, Miquel R. The
effect of hematological and lymphatic diseases on the liver. In: Rodés
J, Benhaumou JP, 28 Schwartz JB, Shamsuddin AM. The effects of leukemic infiltrates in various organs in chronic lymphocytic leukemia. Hum Pathol 1981; 12: 432-440 PubMed DOI 29 Wilputte JY, Martinet JP, Nguyen P, Damoiseaux P, Rahier J, Geubel A. Chronic lymphocytic leukemia with portal hypertension and without liver involvement: a case report underlining the roles of increased spleno-portal blood flow and "protective" sinusoidal vasoconstriction. Acta Gastroenterol Belg 2003; 66: 303-306 PubMed 30 Yam LT, Janckila AJ, Chan CH, Li CY. Hepatic involvement in hairy cell leukemia. Cancer 1983; 51: 1497-1504
31
Thiele DL. Hepatic manifestations of systemic disease and other
disorders of the liver. In: Feldman M, Friedman LS, Science, 2002: 1603-1619 32 Litten JB, Rodriguez MM, Maniaci V. Acute lymphoblastic leukemia presenting in fulminant hepatic failure. Pediatr Blood Cancer 2006; 47: 842-845 PubMed DOI 33 Perez-Soler R, Esteban R, Allende E, Tornos Salomo C, Julia A, Guardia J. Liver involvement in multiple myeloma. Am J Hematol 1985; 20: 25-29 PubMed DOI 34 Barth C, Bosse A, Andus T. Severe acute cholestatic hepatitis by infiltration of monoclonal plasma cells in multiple myeloma. Z Gastroenterol 2005; 43: 1129-1132 PubMed DOI 35 Dubois A, Dauzat M, Pignodel C, Pomier-Layrargues G, Marty-Double C, Lopez FM, Janbon C. Portal hypertension in lymphoproliferative and myeloproliferative disorders: hemodynamic and histological correlations. Hepatology 1993; 17: 36 Alvarez-Larran A, Abraldes JG, Cervantes F, Hernandez-Guerra M, Vizzutti F, Miquel R, Gilabert R, Giusti M, Garcia- Pagan JC, Bosch J. Portal hypertension secondary to myelofibrosis: a study of three cases. Am J Gastroenterol 2005; 37 Wanless IR, Peterson P, Das A, Boitnott JK, Moore GW, Bernier V. Hepatic vascular disease and portal hypertension in polycythemia vera and agnogenic myeloid metaplasia: a clinicopathological study of 145 patients examined at autopsy. Hepatology 1990; 12: 1166-1174 PubMed DOI 38 Pereira A, Bruguera M, Cervantes F, Rozman C. Liver involvement at diagnosis of primary myelofibrosis: a clinicopathological study of twenty-two cases. Eur J Haematol 1988; 40: 355-361 PubMe 39 Valla D, Casadevall N, Lacombe C, Varet B, Goldwasser E, Franco D, Maillard JN, Pariente EA, Leporrier M, Rueff B. Primary myeloproliferative disorder and hepatic vein thrombosis. A prospective study of erythroid colony formation in vitro in 20 patients with Budd-Chiari syndrome. Ann Intern Med 1985; 103: 329-334 PubMed 40 Cervantes F, Rozman C. A multivariate analysis of prognostic factors in chronic myeloid leukemia. Blood 1982; 60: 1298-1304 PubMed 41 Ondreyco SM, Kjeldsberg CR, Fineman RM, Vaninetti S, Kushner JP. Monoblastic transformation in chronic myelogenous leukemia: presentation with massive hepatic involvement. Cancer 1981; 48: 957-963 PubMed DOI 42 Omata M, Johnson CS, Tong M, Tatter D. Pathological spectrum of liver diseases in sickle cell disease. Dig Dis Sci 1986; 43 Blei AT, Sznajder JI. The liver in lung diseases. In: Rodés J, Benhaumou JP, Blei AT, Reichen J, Rizzetto M, editors. Textbook of Hepatology, 3rd ed. Oxford: Blackwell Publishing, 2007: 1616-1621 44 Radford AJ, Rhodes FA. The association of jaundice with lobar pneumonia in the territory of Papua and New Guinea. Med J Aust 1967; 2: 678-681 PubMed 45 Kirby BD, Snyder KM, Meyer RD, Finegold SM. Legionnaires' disease: clinical features of 24 cases. Ann Intern Med 1978; 89: 297-309 PubMed 46 Amory JK, Rosen H, Sukut C, Wallace F, Saint S. Clinical problem-solving. A jaundiced eye. N Engl J Med 2006; 354: 1516-1520 PubMed 47 Colldahl H. A study of serum enzymes in patients suffering from periods of respiratory insufficiency, especially asthma and emphysema. Preliminary report. Acta Med Scand 1960; 166: 399-400 PubMed 48 El-shaboury AH, Thomas AJ, Williams DA. Serum transaminase activity in status asthmaticus. Br Med J 1964; 1: 1220- 1223 PubMed 49 Henrion J, Minette P, Colin L, Schapira M, Delannoy A, Heller FR. Hypoxic hepatitis caused by acute exacerbation of chronic respiratory failure: a case-controlled, hemodynamic study of 17 consecutive cases. Hepatology 1999; 29: 427- 50 Guevara M, Arroyo V, Rodés J . The liver in urogenital diseases. In: Rodés J, Benhaumou JP, Blei AT, Reichen J, Rizzetto M, editors. Textbook of Hepatology. 3rd ed. Oxford: Blackwell Publishing, 2007: 1653-1661 DOI 51 Chazouillères O, Housset C. Intrahepatic cholestasis. In: Rodés J, Benhaumou JP, Blei AT, Reichen J, Rizzetto M, editors. Textbook of Hepatology. 3rd ed, Oxford: Blackwell Publishing, 2007: 1481-1500 52 Kanai S, Honda T, Uehara T, Matsumoto T. Liver function tests in patients with bacteremia. J Clin Lab Anal 2008; 22: 53 Ding Y, Zhao L, Mei H, Huang ZH, Zhang SL. Alterations of biliary biochemical constituents and cytokines in infantile hepatitis syndrome. World J Gastroenterol 2006; 12: 7038-7041 PubMed DOI 54 Narita R, Murata M, Kihara Y, Abe S, Tabaru A, Yoshikawa I, Otsuki M. Sepsis presenting with severe jaundice. Am J Gastroenterol 2001; 96: 3214-3215 PubMed DOI 55 Fang MH, Ginsberg AL, Dobbins WO 3rd. Marked elevation in serum alkaline phosphatase activity as a manifestation of systemic infection. Gastroenterology 1980; 78: 592-597 PubMed 56 Miller DJ, Keeton DG, Webber BL, Pathol FF, Saunders SJ. Jaundice in severe bacterial infection. Gastroenterology 1976; 71: 94-97 PubMed 57 Neale G, Caughey DE, Mollin DL, Booth CC. Effects of intrahepatic and extrahepatic infection on liver function. Br Med J 1966; 1: 382-387 PubMed 58 Funada H, Matsuda T, Okada Y. Jaundice associated with Pseudomonas aeruginosa bacteremia complicating acute leukemia. Intern Med 1995; 34: 100-103 PubMed DOI 59 Bergert H, Illert T, Friedrich K, Ockert D. Fulminant liver failure following infection by Clostridium perfringens. Surg Infect (Larchmt) 2004; 5: 205-209 PubMed DOI 60 El-Newihi HM, Alamy ME, Reynolds TB. Salmonella hepatitis: analysis of 27 cases and comparison with acute viral hepatitis. Hepatology 1996; 24: 516-519 PubMed DOI 61 Gitlin N. Liver involvement in systemic infection. In: Gitlin N editor. The Liver and Systemic Disease. Hong Kong: Pearson Professional Limited, 1997: 229-236 62 Kazakoff MA, Sinusas K, Macchia C. Liver function test abnormalities in early Lyme disease. Arch Fam Med 1993; 2: 63 Horowitz HW, Dworkin B, Forseter G, Nadelman RB, Connolly C, Luciano BB, Nowakowski J, O'Brien TA, Calmann M, Wormser GP. Liver function in early Lyme disease. Hepatology 1996; 23: 1412-1417 PubMed DOI 64 Domingo P, Munoz C, Franquet T, Gurgui M, Sancho F, Vazquez G. Acute Q fever in adult patients: report on 63 sporadic cases in an urban area. Clin Infect Dis 1999; 29: 874-879 PubMed DOI 65 Gordon SC. Bacterial and systemic infections. In: Schiff ER, Sorrell MF, Maddrey WC, editors. Schiff’s Diseases of the Liver. 9th ed. Tokyo: Lippincott William & Wilkins, 2003: 1529-1545 66 Schlossberg D. Syphilitic hepatitis: a case report and review of the literature. Am J Gastroenterol 1987; 82: 552-553 67 Reddy KR, Farnum JB, Thomas E. Acute hepatitis associated with campylobacter colitis. J Clin Gastroenterol 1983; 5: 68 Tajiri T, Tate G, Iwaku T, Takeyama N, Fusama S, Sato S, Kunimura T, Mitsuya T, Morohoshi T. Right pleural effusion in Fitz-Hugh-Curtis syndrome. Acta Med Okayama 2006; 60: 289-294 PubMed 69 Cano A, Fernandez C, Scapa M, Boixeda D, Plaza G. Gonococcal perihepatitis: diagnostic and therapeutic value of laparoscopy. Am J Gastroenterol 1984; 79: 280-282 PubMed 70 Soriano V, Barreiro P, García-Samaniego J, Martín-Carbonero L, Núñez M. Human immunodeficiency virus and the liver. In: Rodés J, Benhaumou JP, Blei AT, Reichen J, Rizzetto M, editors. Textbook of Hepatology. 3rd ed. Oxford: Blackwell Publishing, 2007: 974-987 DOI
71 Sánchez-Tapias JM. Bacterial,
rickettsial and spirochaetal infections. In: Rodés J, Benhaumou JP, Blei
AT, Reichen J, 72 Mert A, Bilir M, Tabak F, Ozaras R, Ozturk R, Senturk H, Aki H, Seyhan N, Karayel T, Aktuglu Y. Miliary tuberculosis: clinical manifestations, diagnosis and outcome in 38 adults. Respirology 2001; 6: 217-224 PubMed DOI 73 Hay RJ. Fungal infections affecting the liver. In: Rodés J, Benhaumou JP, Blei AT, Reichen J, Rizzetto M, editors. Textbook of Hepatology. 3rd ed. Oxford: Blackwell Publishing, 2007: 1011-1019 DOI 74 Khan FY, Kamha AA, Alomary IY. Fulminant hepatic failure caused by Salmonella paratyphi A infection. World J Gastroenterol 2006; 12: 5253-5255 PubMed 75 Ichai P, Roque Afonso AM, Sebagh M, Gonzalez ME, Codes L, Azoulay D, Saliba F, Karam V, Dussaix E, Guettier C, Castaing D, Samuel D. Herpes simplex virus-associated acute liver failure: a difficult diagnosis with a poor prognosis. Liver Transpl 2005; 11: 1550-1555 PubMed DOI 76 Gruson D, Hilbert G, Le Bail B, Portel L, Boiron JM, Reiffers J, Gbikpi-Benissan G. Fulminant hepatitis due to herpes simplex virus-type 2 in early phase of bone marrow transplantation. Hematol Cell Ther 1998; 40: 41-44 PubMed 77 Ho JK, Tha SP, Coupland R, Dalal BI, Bowie WR, Sreenivasan GM, Krajden M, Yoshida EM. Parvovirus B19 in an immunocompetent adult patient with acute liver failure: an underdiagnosed cause of acute non-A-E viral hepatitis. Can J Gastroenterol 2005; 19: 161-162 PubMed 78 Wallot MA, Metzger-Boddien C, Auth M, Kehle J, Enders G, Dirsch O, Fiedler M, Voit T. Acute liver failure associated with Coxsackie virus B2 infection in a neonate. Eur J Pediatr 2004; 163: 116-117 PubMed DOI 79 Harma M, Hockerstedt K, Lautenschlager I. Human herpesvirus-6 and acute liver failure. Transplantation 2003; 76: 80 Dits H, Frans E, Wilmer A, Van Ranst M, Fevery J, Bobbaers H. Varicella-zoster virus infection associated with acute liver failure. Clin Infect Dis 1998; 27: 209-210 PubMed DOI 81 Gasperino J, Yunen J, Guh A, Tanaka KE, Kvetan V, Doyle H. Fulminant liver failure secondary to haemorrhagic dengue in an international traveller. Liver Int 2007; 27: 1148-1151 PubMed DOI 82 Grant JP, Cox CE, Kleinman LM, Maher MM, Pittman MA, Tangrea JA, Brown JH, Gross E, Beazley RM, Jones RS. Serum hepatic enzyme and bilirubin elevations during parenteral nutrition. Surg Gynecol Obstet 1977; 145: 573-580 PubMed 83 Lindor KD, Fleming CR, Abrams A, Hirschkorn MA. Liver function values in adults receiving total parenteral nutrition. JAMA 1979; 241: 2398-2400 PubMed DOI 84 Spiliotis JD, Kalfarentzos F. Total parenteral nutrition--associated liver dysfunction. Nutrition 1994; 10: 255-260 85 Cavicchi M, Beau P, Crenn P, Degott C, Messing B. Prevalence of liver disease and contributing factors in patients receiving home parenteral nutrition for permanent intestinal failure. Ann Intern Med 2000; 132: 525-532 PubMed 86 Koppe SWP, Buchman AL. Total parenteral nutrition-related liver disease. In Rodés J, Benhaumou JP, Blei AT, Reichen J, Rizzetto M, editors. Textbook of Hepatology. 3rd ed. Oxford: Blackwell Publishing, 2007: 1634-1641 DOI 87 Carithers RL. Endocrine disorders and the liver. In: Gitlin N, editor. The Liver and Systemic Disease. Hong Kong: Pearson Professional Limited, 1997: 59-72 88 Fong TL, McHutchison JG, Reynolds TB. Hyperthyroidism and hepatic dysfunction. A case series analysis. J Clin Gastroenterol 1992; 14: 240-244 PubMed 89 Sato T, Tajiri J, Shimada T, Hiramatsu R, Umeda T. Abnormal blood chemistry data in Cushing's syndrome: comparison with those for fatty liver. Endocrinol Jpn 1984; 31: 705-710 PubMed 90 Olsson RG, Lindgren A, Zettergren L. Liver involvement in Addison's disease. Am J Gastroenterol 1990; 85: 435-438 91 Boulton R, Hamilton MI, Dhillon AP, Kinloch JD, Burroughs AK. Subclinical Addison's disease: a cause of persistent abnormalities in transaminase values. Gastroenterology 1995; 109: 1324-1327 PubMed DOI 92 Salmela PI, Sotaniemi EA, Niemi M, Maentausta O. Liver function tests in diabetic patients. Diabetes Care 1984; 7: 93 Foster KJ, Griffith AH, Dewbury K, Price CP, Wright R. Liver disease in patients with diabetes mellitus. Postgrad Med J 1980; 56: 767-772 PubMed 94 Hashizume H, Sato K, Takagi H, Hirokawa T, Kojima A, Sohara N, Kakizaki S, Mochida Y, Shimura T, Sunose Y, Ohwada S, Mori M. Primary liver cancers with nonalcoholic steatohepatitis. Eur J Gastroenterol Hepatol 2007; 19: 827-834 95 Silverman JF, O'Brien KF, Long S, Leggett N, Khazanie PG, Pories WJ, Norris HT, Caro JF. Liver pathology in morbidly obese patients with and without diabetes. Am J Gastroenterol 1990; 85: 1349-1355 PubMed 96 Marchesini G, Brizi M, Morselli-Labate AM, Bianchi G, Bugianesi E, McCullough AJ, Forlani G, Melchionda N. Association of nonalcoholic fatty liver disease with insulin resistance. Am J Med 1999; 107: 450-455 PubMed DOI 97 Wei Y, Rector RS, Thyfault JP, Ibdah JA. Nonalcoholic fatty liver disease and mitochondrial dysfunction. World J Gastroenterol 2008; 14: 193-199 PubMed DOI 98 Mastoraki A, Karatzis E, Mastoraki S, Kriaras I, Sfirakis P, Geroulanos S. Postoperative jaundice after cardiac surgery. Hepatobiliary Pancreat Dis Int 2007; 6: 383-387 PubMed 99 Schmid M, Hefti ML, Gattiker R, Kistler HJ, Senning A. Benign postoperative intrahepatic cholestasis. N Engl J Med 1965; 100 Chapman RW, Angus PW. The effect of gastrointestinal diseases on the liver and biliary tract. In: Rodés J, Benhaumou JP, Blei AT, Reichen J, Rizzetto M, editors. Textbook of Hepatology. 3rd ed. Oxford: Blackwell Publishing, 2007: 1622- 1633 DOI 101 Peters RL, Gay T, Reynolds TB. Post-jejunoileal-bypass hepatic disease. Its similarity to alcoholic hepatic disease. Am J Clin Pathol 1975; 63: 318-331 PubMed 102 Peters RL. Patterns of hepatic morphology in jejunoileal bypass patients. Am J Clin Nutr 1977; 30: 53-57 PubMed 103 Baraona E, Julkunen R, Tannenbaum L, Lieber CS. Role of intestinal bacterial overgrowth in ethanol production and metabolism in rats. Gastroenterology 1986; 90: 103-110 PubMed 104 Maddrey WC. Granuloma of the liver. In: Schiff ER, Sorrell MF, Maddrey WC, editors. Schiff’s Diseases of the Liver. 9th ed. Tokyo: Lippincott Williams & Wilkins, 2003: 1563-1579 105 Hawkins PN. Amyloidosis. In: Rodés J, Benhaumou JP, Blei AT, Reichen J, Rizzetto M, editors. Textbook of Hepatology. 3rd ed. Oxford: Blackwell Publishing, 2007: 1702-1708 DOI 106 Johnston DE. Special considerations in interpreting liver function tests. Am Fam Physician 1999; 59: 2223-2230
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