Absorption of Iron in Cirrhosis of Liver

Callender, Sheila T.; Malpas, J. S.

doi:10.1136/bmj.2.5371.1516

Cited by 62 publications

(28 citation statements)

References 10 publications

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“…All 16 subjects with positive hepatic iron staining had underlying hepatocellular causes of cirrhosis and 15 (94%) were men. Subjects with positive iron staining had higher Child-Pugh scores (10 [5-13] vs. 6 [5][6][7][8][9][10][11][12][13][14], respectively, P ϭ .003) compared with subjects with negative iron staining. Seven (44%) patients had acanthocytes.…”

Section: Resultsmentioning

confidence: 99%

“…Within the cirrhosis group, subjects with hepatocellular cirrhosis had more severe liver disease than subjects with cholestasis-induced cirrhosis. This finding was reflected in a higher Child-Pugh score (9 [5][6][7][8][9][10][11][12][13][14] vs. 5 [5][6][7][8][9], P ϭ .004), a higher MELD score (15.3 Ϯ 6.3 vs. 10.0 Ϯ 3.9, P ϭ .02), increased prothrombin time (15.3 Ϯ 4.2 vs. 11.6 Ϯ 2.2, P ϭ .006), and a lower serum albumin level (28.7 Ϯ 6.4 vs. 35.5 Ϯ 5.0, P ϭ .003).…”

Section: Resultsmentioning

confidence: 99%

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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: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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

et al. 2004

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“…In hepatitis C patients, increased iron absorption in cirrhosis and difficulty in excreting iron from the body contribute to development of iron overload [38] . There is growing evidence that iron overload enhances the amount of liver injury and progression to cirrhosis and HCC.…”

Section: Iron Overloadmentioning

confidence: 99%

Hepatitis C comorbidities affecting the course and response to therapy

El-Zayadi¹

2009

WJG

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Several studies have demonstrated that the outcome of chronic hepatitis C (CHC) infection is profoundly influenced by a variety of comorbidities. Many of these comorbidities have a significant influence on the response to antiviral therapy. These comorbidities negatively affect the course and outcome of liver disease, often reducing the chance of achieving a sustained virological response with PEGylated interferon and ribavirin treatments. Comorbidities affecting response to antiviral therapy reduce compliance and adherence to inadequate doses of therapy. The most important comorbidities affecting the course of CHC include hepatitis B virus coinfection, metabolic syndrome, and intestinal bacterial overgrowth. Comorbidities affecting the course and response to therapy include schistosomiasis, iron overload, alcohol abuse, and excessive smoking. Comorbidities affecting response to antiviral therapy include depression, anemia, cardiovascular disease, and renal failure.

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“…It is possible that the increased iron absorption may be due to the pancreatic insufficiency which is known to occur in many patients with cirrhosis (Sobel and Waye, 1963). Several groups have reported a reduction in the increased iron absorption found in cirrhotic patients following the administration of pancreatin or duodenal juice (Callendar and Malpas, 1963;Linscheer et al, 1964;Davis and Biggs, 1964).…”

Section: Cirrhosis With Siderosismentioning

confidence: 99%

Iron Metabolism in Haemochromatosis

Dymock

1970

Ann Clin Biochem

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Absorption of Iron in Cirrhosis of Liver

Cited by 62 publications

References 10 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

Hepatitis C comorbidities affecting the course and response to therapy

Iron Metabolism in Haemochromatosis

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