Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

UFT was administered preoperatively in 20 cases of primary hepatocellular carcinoma, and tegafur, 5-fluorouracil (5-FU), uracil, total thymidylate synthase (TS) and free TS in blood and liver tissue were determined. The results were as follows. 1. Tegafur level was significantly high in blood, while the levels of 5-FU and uracil were high in the liver tissue. The 5-FU level in the cancerous area was 0.099 micrograms/g, higher than the effective level regardless of the presence or not of complication with liver cirrhosis. 2. Total TS, FdUMP (computed as total TS-free TS) and TS inhibition rate [(computed as (TS-free TS)/TS x 100 (%)] were significantly higher in the cancerous liver tissue than in the non-cancerous area. In the cases where determination was made simultaneously for the cancerous liver and non-cancerous liver tissues, the FdUMP level and TS inhibition rate in the cancerous liver tissue were high in 14 out of 17 cases (82.4%) and 13 out of 17 cases (76.5%) respectively. Therefore, UFT seems to have selective toxicity. 3. No correlation was found between 5-FU level, total TS, FdUMP in the liver tissue on the one hand and TS inhibition rate on the other. 4. UFT yielded sufficient 5-FU levels in the cancerous area regardless of the presence or not of complication with cirrhosis and therefore is expected to inhibit DNA synthesis selectively in the cancerous tissue.
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PMID:[Study on the pharmacokinetics of UFT in patients with hepatocellular carcinoma associated with cirrhosis]. 255 Dec 51

Tegafur fine granule preparation orally administered to the patients with primary hepatoma and liver cirrhosis, and the concentration of tegafur and 5-fluorouracil in the blood were determined. The concentration of tegafur in blood was maintained well in the injured liver, and remained same 3 weeks after administration of tegafur fine granules. The concentration of 5-fluorouracil in the blood decreased distinctly when the dysfunction of the liver was severe (KICG less than 0.070). In the case of malignant disease with the injured liver, oral administration or tegafur might be less effective. However, the concentration of 5-fluorouracil in the blood did not decrease 3 weeks after administration of tegafur fine granules. No cases showed noticeable clinical effects by only oral administration.
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PMID:[Sequential changes in blood concentrations of tegafur and 5-FU during oral administration of fine granules of tegafur in patients with primary liver cancer]. 630 83

A 55 year-old man was admitted with massive ascites. Although the laboratory data on admission were compatible with hepatic cirrhosis and remarkable esophageal varices were observed during endoscopy, the imaging findings such as computed tomography and ultrasonographic examination did not confirm hepatic cirrhosis. The patient had no history of alcohol abuse, blood transfusions or acute hepatitis. Serological markers related to viral and autoimmune hepatitis were all negative. Seven years ago, the patient had undergone an operation for colon cancer and has been taking tegafur since then for a total of 55 months. Tegafur was suspected as the causative agent for the liver dysfunction of this patient and the administration of tegafur was stopped. His laboratory data improved gradually and the ascites vanished. The first liver biopsy performed 6 months after discontinuation of tegafur still revealed chronic active hepatitis. However, at the liver biopsy performed 18 months after withdrawal of tegafur, inflammatory activity had subsided and the third liver biopsy, performed 34 months thereafter, revealed further improvement of the pathological changes that had occurred in the liver. We therefore conclude that the administration of tegafur may have caused chronic active liver injury with portal hypertension manifested as ascites and esophageal varices.
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PMID:Chronic liver failure induced by long-term administration of tegafur: a case report. 995 26

A 35-year-old female received right hemicolectomy for a poorly differentiated adenocarcinoma of the ascending colon with lymph node metastasis (1/28) in February 1997. CEA was 1.68 ng/microl prior to colectomy. Adjuvant chemotherapy with weekly 5-FU and leucovorin intravenously was started following surgery and discontinued after 17 doses in May 1997. She received bilateral salpingo-ophorecctomy for metastatic cancer in August 1999. Intravenous chemotherapy was resumed with weekly 5-FU and leucovorin intravenously in August 1999. CEA was 93.8 ng/microl in November 1999. Intravenous chemotherapy was discontinued after 20 doses and oral chemotherapy with futraful and leucovorin was started in January 2000. CEA was found to be 240.3 ng/microl in December 1999 and then elevated to 1521.3 ng/microl in June 2001, which was 10 months after resection of metastatic ovarian cancer. No metastatic lesions could be detected, however, with image studies. The CEA decreased to 396.6 ng/microl three months later. Futraful was switched to uracil-tegafur (UFUR) in September 2001. The CEA for the patient ranged from 68.5 to 298.9 ng/microl for the following 5 years without aggressive chemotherapy. No evidence of recurrence could be demonstrated by imaging studies. The patient is not a smoker and denied exposure to a smoking environment. She was also not known to have persistent infections, inflammatory bowel disease, pancreatitis, cirrhosis of the liver, or any benign tumors. The current case suggested that: (i) elevation of CEA is not necessarily well correlated with presence of metastatic colon cancer; (ii) some patients may live with elevated CEA for years without evidence of recurrence or metastasis; (iii) aggressive chemotherapy may not be necessary in patients with only elevated CEA.
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PMID:Unusual elevation of CEA in a patient with history of colon cancer. 1706 Apr 6