The Anemia of Liver Disease: Observations on Its Mechanism 1

Jandl, James H.

doi:10.1172/jci103087

Cited by 230 publications

(64 citation statements)

References 26 publications

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“…4 -10,30 Anemia is a frequent finding in chronic liver disease and, in most cases, is multifactorial. 31 In our study, anemia was present in 24 subjects with cirrhosis, but DMT1 and Ireg1 expression in these subjects was similar to the 22 subjects without anemia. The expression of DMT1 or Ireg1 in the 46 subjects with cirrhosis did not correlate with hemoglobin levels as it did in controls, suggesting that the degree of anemia was not a significant factor causing increased expression of these iron transport genes in cirrhosis.…”

Section: Discussionsupporting

confidence: 48%

“…Iron deficiency-an important cause of increased iron absorption and intestinal iron transporter expression 19,22,28 -is common in patients with cirrhosis and frequently is occult. 10,31 Iron deficiency was diagnosed in four subjects with cirrhosis and the expression of the iron transport genes in these four subjects was similar to that observed in the iron-deficient controls. In the 42 non-iron-deficient subjects with cirrhosis, the levels of DMT1 and Ireg1 expression remained significantly elevated compared with iron-replete controls.…”

Section: Discussionmentioning

confidence: 62%

“…However, in a few patients, spur cell anemia may develop. 31,32 Of nine subjects in our study with acanthocytes, only three fulfilled the criteria for a diagnosis of spur cell anemia. 24 The levels of DMT1 and Ireg1 expression in these nine patients were similar to the levels observed in all 46 patients with cirrhosis.…”

Section: Discussionmentioning

confidence: 93%

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Increased duodenal expression of divalent metal transporter 1 and iron-regulated gene 1 in cirrhosis

et al. 2004

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Hepatic hemosiderosis and increased iron absorption are common findings in cirrhosis. It has been proposed that a positive relation exists between intestinal iron absorption and the development of hepatic hemosiderosis. The current study investigated the duodenal expression of the iron transport molecules divalent metal transporter 1 (DMT1 [IRE]), ironregulated gene 1 (Ireg1 [ferroportin]), hephaestin, and duodenal cytochrome b (Dyctb) in 46 patients with cirrhosis and 20 control subjects. Total RNA samples were extracted from duodenal biopsy samples and the expression of the iron transport genes was assessed by ribonuclease protection assays. Expression of DMT1 and Ireg1 was increased 1.5 to 3-fold in subjects with cirrhosis compared with iron-replete control subjects. The presence of cirrhosis per se and serum ferritin (SF) concentration were independent factors that influenced the expression of DMT1. However, only SF concentration was independently associated with Ireg1 expression. In cirrhosis, the expression of DMT1 and Ireg1 was not related to the severity of liver disease or cirrhosis type. There was no correlation between the duodenal expression of DMT1 and Ireg1 and the degree of hepatic siderosis. In conclusion, the presence of cirrhosis is an independent factor associated with increased expression of DMT1 but not Ireg1. The mechanism by which cirrhosis mediates this change in DMT1 expression has yet to be determined. Increased expression of DMT1 may play an important role in the pathogenesis of cirrhosis-associated hepatic iron overload. (HEPATOLOGY 2004;39: 492-499.)

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Section: Discussionsupporting

confidence: 48%

Section: Discussionmentioning

confidence: 62%

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Increased duodenal expression of divalent metal transporter 1 and iron-regulated gene 1 in cirrhosis

et al. 2004

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“…Because of the high continuing transfusion rejaundice. Laboratory studies showed the following: Hgb, 9 g/dL; WBC, 4,800/mm 3 ; platelets, 75,000/mm 3 . quirement that continued beyond 90 days, the patient was listed for liver transplantation and underwent Peripheral smear exam showed increased macrocytosis with some basophilic stippling, and increased aniso-transplantation 145 days after TIPS with resolution of hemolysis.…”

Section: Methodsmentioning

confidence: 98%

“…7,8,11 The red cell life-span is shorter in patients with cirrhosis compared with normal subjects. 3,4,20,21 individual laboratory parameters used to make the diagnosis. A liver ultrasound or computed tomography Severe liver disease is associated with alterations in hepatic cholesterol metabolism 22 and the cholesterol/ scan were used to exclude an intrahepatic or perihepatic hematoma as a source for indirect hyperbilirubi-phospholipid ratio in red cell membranes.…”

Section: White Blood Cell and Platelet Changesmentioning

confidence: 99%

The hematologic consequences of transjugular intrahepatic portosystemic shunt

et al. 1996

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jects. However, it is self-limited and rarely requires SEE EDITORIAL ON PAGE 177.intervention. Potential mechanisms of such hemolysis are discussed. TIPS is also not recommended as a means of improving platelet counts in patients with Transjugular intrahepatic portosystemic shunts (TIPS) severe hypersplenism. (HEPATOLOGY 1996;23:32-39.) are a recent innovation in the management of portal hypertension. In 1992, we had previously described anCirrhosis is associated with a number of hematologic instance of severe hemolysis associated with this procedure. This study was undertaken to define and quan-abnormalities. 1-3 Anemia may result from gastrointestify the true incidence of TIPS-associated hemolysis tinal bleeding and iron deficiency 4 or directly as a conand its clinical spectrum, as well as to test the hypothe-sequence of severe liver disease. Anemia due to liver sis that portal decompression by TIPS would amelio-disease is characterized by macrocytosis 5 and the develrate hypersplenism in patients with portal hyperten-opment of target 5,6 and spur cells. [7][8][9] In some patients sion. A total of 60 patients undergoing TIPS for with alcoholic liver disease, an acute hemolytic anemia prevention of recurrent variceal hemorrhage (n Å 40) may also develop. 10 Additionally, the cause of liver disor refractory ascites (n Å 20) were studied. Forty pa-ease may also be associated with anemia, e.g., alcoholtients with cirrhosis who were followed concurrently induced bone marrow suppression. 11 Finally, portal hyserved as controls. At entry, both groups were compapertension, a principal complication of cirrhosis, leads rable with the exception of increased ascites in the TIPS group. A total of 7 instances of intravascular he-to splenic engorgement with consequent enlargement molysis were identified in 60 TIPS patients, whereas and hypersplenism. 4,12 none occurred in controls. Of these, 4 patients were Although hypersplenism may cause pancytopeasymptomatic and detected on routine laboratory test-nia, 13,14 thrombocytopenia frequently dominates the ing. Hemolysis led to a greater than 4-g/dL decrease in clinical presentation. Whereas the degree of thrombohemoglobin in 2 patients, 2-to 3-g/dL decrease in 2 cytopenia only occasionally leads to severe spontaneous others and a 3-to 4-gm/dL decrease in 1 patient. Two mucosal bleeding, it has other important clinical consepatients were able to compensate for hemolysis and quences. Specifically, it may contribute to the bleeding did not develop anemia. In all but 1 case, the findings diathesis 4 after even minor surgery, e.g., tooth extracof hemolysis subsided by 12 to 15 weeks; in 1 patient, tion, as well as during episodes of variceal hemorrhage. orthotopic liver transplantation was associated with resolution of the hemolysis. Overall, no significant Thrombocytopenia also precludes therapy with interchanges in white blood cell or platelet counts were feron-a 2 in some patients with hepatitis C and otherobserved in patients undergoing TIPS despite ade-wise well-compensated...

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Megaloblastic Anemia in "Alcoholic" Cirrhosis

Krasnow¹

1957

Arch Intern Med

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The Anemia of Liver Disease: Observations on Its Mechanism 1

Cited by 230 publications

References 26 publications

Increased duodenal expression of divalent metal transporter 1 and iron-regulated gene 1 in cirrhosis

Increased duodenal expression of divalent metal transporter 1 and iron-regulated gene 1 in cirrhosis

The hematologic consequences of transjugular intrahepatic portosystemic shunt

Megaloblastic Anemia in "Alcoholic" Cirrhosis

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