Dysplastic nodules frequently develop into hepatocellular carcinoma in patients

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Cancer. 2005 Dec 20; [Epub ahead of print]

Dysplastic nodules frequently develop into hepatocellular carcinoma in

patients with chronic viral hepatitis and cirrhosis.

Kobayashi M, Ikeda K, Hosaka T, Sezaki H, Someya T, Akuta N, Suzuki F,

Suzuki Y, Saitoh S, Arase Y, Kumada H.

Department of Gastroenterology, Toranomon Hospital, Tokyo, Japan.

BACKGROUND: Advances in imaging technology have enhanced the detection of

small nodular lesions during the course of chronic liver disease. METHODS:

Between 1995 and 2002, the authors examined 154 consecutive patients with

small hepatic nodules without hepatocellular carcinoma (HCC) over a median

duration of 2.8 years. The median size of these nodules was 14 mm (range,

7-40 mm). The initial histopathologic diagnosis included high-grade

dysplastic nodule (HGDN) (n = 13), low-grade dysplastic nodule (LGDN) (n =

42), and regenerative nodule (RN) (n = 99). RESULTS: A total of 29 (18.8%)

nodules developed into HCC during the observation period. Cumulative HCC

development rates at the first, third, and fifth year were 46.2%, 61.5%, and

80.8% for HGDN; 2.6%, 30.2%, and 36.6% for LGDN; and 3.3%, 9.7%, and 12.4%

for RN, respectively. The rate of HCC development was significantly higher

in the HGDN group than for other types (P < 0.001). Multivariate analysis

disclosed that histopathologic diagnosis (P < 0.001) and findings on

computed tomographic arterial portography (CT-AP) (P = 0.004) were

significantly associated with future HCC development. The hazard ratios of

HGDN and LGDN were 16.8 (95% confidence interval [CI], 6.19-45.6) and 2.96

(95% CI, 1.20-7.31), respectively. A decrease in portal blood flow also

showed a significantly high hazard ratio of 3.04 (95% CI, 1.42-6.50).

Approximate annual development rate to HCC was 20% in patients with HGDN and

10% in LGDN. CONCLUSION: HGDN should be considered a precancerous lesion

when it appears during follow-up of chronic viral hepatitis or cirrhosis.

Reduced portal blood flow in the nodule on computed tomography-AP is also an

important predictor for development of hepatocellular carcinoma. Cancer

2006. © 2005 American Cancer Society.

PMID: 16369988 [PubMed - as supplied by publisher]

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[Guest guest]

Cancer. 2005 Dec 20; [Epub ahead of print]

Dysplastic nodules frequently develop into hepatocellular carcinoma in

patients with chronic viral hepatitis and cirrhosis.

Kobayashi M, Ikeda K, Hosaka T, Sezaki H, Someya T, Akuta N, Suzuki F,

Suzuki Y, Saitoh S, Arase Y, Kumada H.

Department of Gastroenterology, Toranomon Hospital, Tokyo, Japan.

BACKGROUND: Advances in imaging technology have enhanced the detection of

small nodular lesions during the course of chronic liver disease. METHODS:

Between 1995 and 2002, the authors examined 154 consecutive patients with

small hepatic nodules without hepatocellular carcinoma (HCC) over a median

duration of 2.8 years. The median size of these nodules was 14 mm (range,

7-40 mm). The initial histopathologic diagnosis included high-grade

dysplastic nodule (HGDN) (n = 13), low-grade dysplastic nodule (LGDN) (n =

42), and regenerative nodule (RN) (n = 99). RESULTS: A total of 29 (18.8%)

nodules developed into HCC during the observation period. Cumulative HCC

development rates at the first, third, and fifth year were 46.2%, 61.5%, and

80.8% for HGDN; 2.6%, 30.2%, and 36.6% for LGDN; and 3.3%, 9.7%, and 12.4%

for RN, respectively. The rate of HCC development was significantly higher

in the HGDN group than for other types (P < 0.001). Multivariate analysis

disclosed that histopathologic diagnosis (P < 0.001) and findings on

computed tomographic arterial portography (CT-AP) (P = 0.004) were

significantly associated with future HCC development. The hazard ratios of

HGDN and LGDN were 16.8 (95% confidence interval [CI], 6.19-45.6) and 2.96

(95% CI, 1.20-7.31), respectively. A decrease in portal blood flow also

showed a significantly high hazard ratio of 3.04 (95% CI, 1.42-6.50).

Approximate annual development rate to HCC was 20% in patients with HGDN and

10% in LGDN. CONCLUSION: HGDN should be considered a precancerous lesion

when it appears during follow-up of chronic viral hepatitis or cirrhosis.

Reduced portal blood flow in the nodule on computed tomography-AP is also an

important predictor for development of hepatocellular carcinoma. Cancer

2006. © 2005 American Cancer Society.

PMID: 16369988 [PubMed - as supplied by publisher]

_________________________________________________________________

Don’t just search. Find. Check out the new MSN Search!

http://search.msn.click-url.com/go/onm00200636ave/direct/01/

[Guest guest]

Cancer. 2005 Dec 20; [Epub ahead of print]

Dysplastic nodules frequently develop into hepatocellular carcinoma in

patients with chronic viral hepatitis and cirrhosis.

Kobayashi M, Ikeda K, Hosaka T, Sezaki H, Someya T, Akuta N, Suzuki F,

Suzuki Y, Saitoh S, Arase Y, Kumada H.

Department of Gastroenterology, Toranomon Hospital, Tokyo, Japan.

BACKGROUND: Advances in imaging technology have enhanced the detection of

small nodular lesions during the course of chronic liver disease. METHODS:

Between 1995 and 2002, the authors examined 154 consecutive patients with

small hepatic nodules without hepatocellular carcinoma (HCC) over a median

duration of 2.8 years. The median size of these nodules was 14 mm (range,

7-40 mm). The initial histopathologic diagnosis included high-grade

dysplastic nodule (HGDN) (n = 13), low-grade dysplastic nodule (LGDN) (n =

42), and regenerative nodule (RN) (n = 99). RESULTS: A total of 29 (18.8%)

nodules developed into HCC during the observation period. Cumulative HCC

development rates at the first, third, and fifth year were 46.2%, 61.5%, and

80.8% for HGDN; 2.6%, 30.2%, and 36.6% for LGDN; and 3.3%, 9.7%, and 12.4%

for RN, respectively. The rate of HCC development was significantly higher

in the HGDN group than for other types (P < 0.001). Multivariate analysis

disclosed that histopathologic diagnosis (P < 0.001) and findings on

computed tomographic arterial portography (CT-AP) (P = 0.004) were

significantly associated with future HCC development. The hazard ratios of

HGDN and LGDN were 16.8 (95% confidence interval [CI], 6.19-45.6) and 2.96

(95% CI, 1.20-7.31), respectively. A decrease in portal blood flow also

showed a significantly high hazard ratio of 3.04 (95% CI, 1.42-6.50).

Approximate annual development rate to HCC was 20% in patients with HGDN and

10% in LGDN. CONCLUSION: HGDN should be considered a precancerous lesion

when it appears during follow-up of chronic viral hepatitis or cirrhosis.

Reduced portal blood flow in the nodule on computed tomography-AP is also an

important predictor for development of hepatocellular carcinoma. Cancer

2006. © 2005 American Cancer Society.

PMID: 16369988 [PubMed - as supplied by publisher]

_________________________________________________________________

Don’t just search. Find. Check out the new MSN Search!

http://search.msn.click-url.com/go/onm00200636ave/direct/01/

[Guest guest]

Cancer. 2005 Dec 20; [Epub ahead of print]

Dysplastic nodules frequently develop into hepatocellular carcinoma in

patients with chronic viral hepatitis and cirrhosis.

Kobayashi M, Ikeda K, Hosaka T, Sezaki H, Someya T, Akuta N, Suzuki F,

Suzuki Y, Saitoh S, Arase Y, Kumada H.

Department of Gastroenterology, Toranomon Hospital, Tokyo, Japan.

BACKGROUND: Advances in imaging technology have enhanced the detection of

small nodular lesions during the course of chronic liver disease. METHODS:

Between 1995 and 2002, the authors examined 154 consecutive patients with

small hepatic nodules without hepatocellular carcinoma (HCC) over a median

duration of 2.8 years. The median size of these nodules was 14 mm (range,

7-40 mm). The initial histopathologic diagnosis included high-grade

dysplastic nodule (HGDN) (n = 13), low-grade dysplastic nodule (LGDN) (n =

42), and regenerative nodule (RN) (n = 99). RESULTS: A total of 29 (18.8%)

nodules developed into HCC during the observation period. Cumulative HCC

development rates at the first, third, and fifth year were 46.2%, 61.5%, and

80.8% for HGDN; 2.6%, 30.2%, and 36.6% for LGDN; and 3.3%, 9.7%, and 12.4%

for RN, respectively. The rate of HCC development was significantly higher

in the HGDN group than for other types (P < 0.001). Multivariate analysis

disclosed that histopathologic diagnosis (P < 0.001) and findings on

computed tomographic arterial portography (CT-AP) (P = 0.004) were

significantly associated with future HCC development. The hazard ratios of

HGDN and LGDN were 16.8 (95% confidence interval [CI], 6.19-45.6) and 2.96

(95% CI, 1.20-7.31), respectively. A decrease in portal blood flow also

showed a significantly high hazard ratio of 3.04 (95% CI, 1.42-6.50).

Approximate annual development rate to HCC was 20% in patients with HGDN and

10% in LGDN. CONCLUSION: HGDN should be considered a precancerous lesion

when it appears during follow-up of chronic viral hepatitis or cirrhosis.

Reduced portal blood flow in the nodule on computed tomography-AP is also an

important predictor for development of hepatocellular carcinoma. Cancer

2006. © 2005 American Cancer Society.

PMID: 16369988 [PubMed - as supplied by publisher]

_________________________________________________________________

Don’t just search. Find. Check out the new MSN Search!

http://search.msn.click-url.com/go/onm00200636ave/direct/01/