Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-three patients with nonspecific pleuritis were studied to determine clinical outcome. After a mean follow-up period of 6 months (1 to 36 months), a diagnosis was reached in 17 patients, while 6 patients remained unknown. The causes of the nonspecific pleuritis diagnosed on initial pleural biopsy were tuberculosis (11 patients, 48%), neoplasm (2 patients, 8.7%), parapneumonic effusion (1 patient), subphrenic abscess (1 patient), congestive heart failure (1 patients), and nephrotic syndrome (1 patient). The diagnosis was made by therapeutic trials (tuberculosis: 11 patients, parapneumonic effusion: 1 patient, congestive heart failure: 1 patient), by repeat pleural biopsy in 1 hepatoma, by open thoractomy in 1 lung cancer, by exploratory laparotomy in 1 subphrenic abscess, and by kidney biopsy in 1 nephrotic syndrome. The WBC counts (more than 2,000/mm3) and lymphocyte percentage (more than 60%) in the pleural fluid were significantly elevated in the patients with tuberculosis compared to those with malignant pleurisy, and other laboratory data were meaningless. As a result of this investigation, we suggest that tuberculous pleurisy is the most common cause of nonspecific pleuritis in Korea and that therapeutic trial with antituberculous medication for patients with high WBC count and lymphocyte percent in pleural fluid can help to locate the nonspecific pleuritis.
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PMID:Etiologic considerations of nonspecific pleuritis. 180 66

Ascitic fluid from tumour patients (hepatoma, gastric cancer, gallbladder cancer, colorectal cancer, ovarian cancer) and from non-malignant diseases (liver cirrhosis, congestive heart failure) were compared with respect to their content of determinants of the fibrinolytic system, tissue-type plasminogen activator antigen (t-PAag) and activity (t-PAact), urokinase-type plasminogen activator antigen (u-PA) and plasminogen activator inhibitor activity (PAI). Furthermore, SDS-polyacrylamide slab-gel electrophoresis (SDS-PAGE) was performed to evaluate molecular weight distribution of the detectable fibrinolytic parameters. In malignant ascites, PAI activity was three to four times higher, and increased complex formation of PAI with t-PA could be demonstrated, compared with non-malignant ascitic fluid. Tissue-type plasminogen activator antigen and activity showed a similar concentration in ascites of both study groups. Urokinase-type plasminogen activator antigen was detectable neither in ascites of malignant nor in ascites of non-malignant origin. It is concluded that t-PA is the physiological plasminogen activator in ascites and that increased PAI levels followed by increased complex formation between t-PA and PAI might reflect a reaction of the peritoneum.
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PMID:Plasminogen activators and plasminogen activator inhibitor in malignant and non-malignant ascitic fluid. 285 12

A 51-year-old woman with malignant ascites secondary to hepatocellular carcinoma had a peritoneovenous (LeVeen) shunt inserted with effective control of ascites and amelioration of symptoms. The results of 12 recent series evaluating the efficacy of peritoneovenous shunts in the treatment of 198 patients with malignant ascites were reviewed. Peritoneovenous shunts effectively controlled malignant ascites in 77% of patients. Complications occurred in 25%, although the majority of these were related to shunt occlusion and transient congestive heart failure.
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PMID:Peritoneovenous shunts in malignant ascites. 299 64

In this prospective study of 240 black patients with liver enlargement admitted to the medical wards of King Edward VIII Hospital, Durban, a cause for the hepatomegaly was found in 92.5% of cases (63.8% without recourse to biopsy, 28.7% after liver biopsy). The commonest cause was congestive heart failure (36.7%), followed by amoebic liver abscess (7.1%), hepatocellular carcinoma (5.8%) and cirrhosis (5.4%). Liver biopsy provided the diagnosis in 90.8% of patients with initial unexplained hepatomegaly. The diagnostic yield of liver biopsy was increased by submitting 3 biopsy specimens for histological examination. The 3 specimens are obtained using a single intercostal entry site and redirecting the biopsy needle, without increasing the risk of complications. Hepatic tuberculosis was present in 9.2% of patients who underwent biopsy. There were no consistent clinical findings in these patients. Therefore, in communities in which tuberculosis is endemic, all patients with unexplained hepatomegaly require liver biopsy since it provides the only means of making this diagnosis.
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PMID:Causes of hepatomegaly at King Edward VIII Hospital, Durban. A prospective study of 240 black patients. 300 36

Ceftizoxime (CZX), a parenteral cephalosporin derivative belonging to the so-called third generation cephalosporin is reported to have a broad antibacterial activity, particularly against Gram-negative aerobic bacilli and some anaerobes, such as Bacteroides fragilis and a good stability to beta-lactamases. Clinical study was performed on a total of 20 cases, 9 females (1 case had urinary tract infection 3 times) and 11 males, aged from 27 to 82 years. All patients had the underlying diseases. They were bronchial asthma in 3 cases, influenza in 1, chronic pulmonary emphysema in 1, pulmonary fibrosis in 1, chronic bronchitis with strongyloidiasis in 1, lung cancer in 3, esophagus cancer in 2, stomach cancer in 1, hepatoma with urolithiasis in 1, liver cirrhosis with diabetes mellitus in 1, alcoholism with strongyloidiasis in 1, cholelithiasis in 1 and congestive heart failure in 1, respectively. Clinical diagnoses for infections were 2-acute bronchitis, 2-exacerbation of chronic bronchitis, 2-broncho-pneumonia, 2-pneumonia including one suspected case, 1-obstructive pneumonia, 2-secondary pulmonary infection, 1-pulmonary infection, 3-urinary tract infection (UTI), 1-UTI with sepsis, 1-sepsis, 1-sepsis with purulent meningitis, 1-biliary tract infection and 1-infected bronchoesophageal fistula. CZX was given by intravenous drip infusion, at a dose of 1 to 2 g, twice daily for 3 to 15 days. Because of severity in infections and underlying diseases, some cases were treated either steroid, gamma-globulin preparations or other antibiotics in combination with CZX. Twelve out of 15 cases assessed clinically responded satisfactorily to the treatment and efficacy rate was 80.0%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effectiveness of ceftizoxime on various infections in patients with underlying diseases]. 609 Jul 23

The authors retrospectively investigated 62 diabetics who had received dialytic therapy at our department and our associated hospital over the past 10 years. We studied the complications and causes of death among the 62 subjects. Of the 62 patients (male 42, female 20), 27 (male 21, female 6), had died. The causes of death in the 27 cases included 7 from general weakness, 4 from gastrointestinal bleeding, 4 from cerebrovascular hemorrhage or thrombosis, 3 suicide, 3 congestive heart failure, 2 myocardial infarction, 2 hyperkalemia, 1 infection and 1 from hepatoma. With regard to diabetic retinopathy, 19 of the 62 patients suffered from bilateral blindness and 12 from unilateral blindness. In 8 patients, visual complications developed after hemodialysis, but 16 patients were already blind at the introduction of hemodialysis. There was no evidence that retinopathy was accelerated by dialysis and the authors suggest that the treatment of retinopathy is very important at the nondialyzed stage. With regard to other complications in dialyzed diabetics, unstable hypertension, diabetic gastroenteropathy, peripheral neuropathy, ischemic heart disease and gangrene were discovered in our population. Some rehabilitation was possible in all but 3 of the subjects (1 peripheral neuropathy, 2 leg amputation).
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PMID:Clinical study of complications in dialyzed diabetics. 668 May 16

Epirubicin is the 4' epimer of the anthracycline antibiotic doxorubicin, and has been used alone or in combination with other cytotoxic agents in the treatment of a variety of malignancies. Comparative and noncomparative clinical trials have demonstrated that regimens containing conventional doses of epirubicin achieved equivalent objective response rates and overall median survival as similar doxorubicin-containing regimens in the treatment of advanced and early breast cancer, non-small cell lung cancer (NSCLC), small cell lung cancer (SCLC), non-Hodgkin's lymphoma, ovarian cancer, gastric cancer and nonresectable primary hepatocellular carcinoma. Recently, dose-intensive regimens of epirubicin have achieved high response rates in a number of malignancies including early and advanced breast cancer and lung cancer. The major acute dose-limiting toxicity of anthracyclines is myelosuppression. In vitro and clinical studies have shown that, at equimolar doses, epirubicin is less myelotoxic than doxorubicin. The lower haematological toxicity of epirubicin, as well as the recent introduction of supportive measures such as colony-stimulating factors, has allowed dose-intensification of epirubicin-containing regimens, which is particularly significant because of the definite dose-response relationship of anthracyclines. Cardiotoxicity, which is manifested clinically as irreversible congestive heart failure and/or cardiomyopathy, is the most important chronic cumulative dose-limiting toxicity of anthracyclines. Epirubicin has a lower propensity to produce cardiotoxic effects than doxorubicin, and its recommended maximum cumulative dose is almost double that of doxorubicin, thus allowing for more treatment cycles and/or higher doses of epirubicin. In summary, dose-intensive epirubicin-containing regimens, which are feasible due to its lower myelosuppression and cardiotoxicity, have produced high response rates in early breast cancer, a potentially curable malignancy, as well as advanced breast, and lung cancers. Furthermore, there is evidence to suggest that improved response rates can improve quality of life in some clinical settings, but whether this leads to prolonged survival has not yet been determined. Recently implemented supportive measures such as colony-stimulating factors, prophylactic antimicrobials and peripheral blood stem cell support may help achieve other potential advantages of dose-intensive epirubicin-containing regimens such as reductions in morbidity and length of hospital admissions.
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PMID:Epirubicin. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in cancer chemotherapy. 768 69

Tumor in the right atrium creates a life-threatening condition and should be removed immediately. A cirrhotic patient who had recurrent hepatocellular carcinoma (HCC) over remnant liver with tumor thrombi extending to inferior vena cava (IVC) and right atrium presented with impending congestive heart failure. The recurrent tumor and its thrombi were successfully resected en-bloc using cardiopulmonary bypass and hypothermic circulatory arrest. Although the patient's disease-free and actual survival time were only 6 months and 14 months, respectively, he was rescued from heart failure. This aggressive surgical strategy creates further possibility to treat such advanced HCC cases. Further investigations regarding adjuvant therapies in these circumstances, however, are necessary.
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PMID:Surgical treatment for recurrent hepatocellular carcinoma with tumor thrombi in right atrium: using cardiopulmonary bypass and deep hypothermic circulatory arrest. 1095 24

Several age-related changes occur in the structure and functions of the liver. The volume of the liver decreases, despite an increase in the size of hepatocytes, suggesting loss of liver cells. There are decreases in hepatic blood flow, the synthesis of urea and cholesterol, and the metabolism of drugs. Moreover, the regenerative capacity of liver becomes less efficient. Certain caveats are important when treating older patients with liver disease. Strict dietary restrictions, such as a low protein diet, should be avoided in the elderly (unless the patient is encephalopathic) because these patients are often undernourished to start with. Similarly, strict salt restriction should be enforced with caution, since it makes food less palatable and may take away what little desire such patients have to eat. Diuretic doses should be adjusted carefully because of greater risks of azotaemia and electrolyte disturbances in the elderly. Extra vigilance should be exercised in the early detection of infections that are more likely to occur in patients with cirrhosis. For example, spontaneous bacterial peritonitis can be missed in the elderly because of poor systemic (fever, abdominal tenderness) and laboratory responses (leucocytosis). In patients presenting with acute variceal bleeding, it is better to err on the side of underhydration than overhydration because of the risk of congestive heart failure. Vasopressin should be avoided in the elderly, since this drug has a high probability of precipitating an ischaemic event. Older patients do not tolerate beta-blockers as well as younger individuals and may require other treatment strategies for the prevention of variceal rebleeding episodes. Hepatic encephalopathy, especially the milder form, needs careful assessment because it can be easily confused with senile dementia syndromes. Cirrhosis is a premalignant condition and patients are at increased risk of developing hepatocellular carcinoma (HCC), a tumour seen predominantly in the elderly. All patients with cirrhosis should be maintained on a lifelong screening programme consisting of a 6-monthly assessment of alpha-fetoprotein and an imaging study, since early detection provides the only hope for cure of HCC. The only definitive treatment of cirrhosis is liver transplantation. Advanced age is not a contraindication to transplantation, and survival in older patients (aged >60 years) is comparable to that in younger individuals.
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PMID:Drug treatment of the complications of cirrhosis in the older adult. 1158 44

Triamterene is a potassium-sparing diuretic used in the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and other diseases in which edema may occur. Toxicity and carcinogenicity studies were conducted by administering triamterene (greater than 99% pure) in feed to groups of male and female F344/N rats and B6C3F1 mice for 15 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium and Chinese hamster ovary cells. 15-day Studies: Groups of five male and five female rats were fed diets containing 0, 1,000, 3,000, 10,000, 30,000, or 60,000 ppm triamterene. The diets containing 10,000 ppm or more were unpalatable, and feed consumption by the 3,000 ppm groups was reduced. Rats exposed to 1,000 or 3,000 ppm triamterene received approximate doses of 80 or 60 mg/kg body weight per day (males) or 70 or 50 mg/kg per day (females). One male rat and two female rats receiving 3,000 ppm died during the second week of the study. The final mean body weights of 3,000 ppm male and female rats were significantly lower than those of controls. Rats in the 3,000 ppm groups had renal tubule regeneration and cytoplasmic vacuolization of the zona glomerulosa of the adrenal gland. Groups of five male and five female mice were fed diets containing 0, 300, 1,000, 3,000, 10,000, or 30,000 ppm triamterene, but the diets containing 10,000 or 30,000 ppm were unpalatable. All mice receiving 3,000 ppm died by day 6. Mice exposed to 300 or 1,000 ppm triamterene received approximate doses of 40 or 155 mg/kg body weight per day (males) or 45 or 170 mg/kg body weight per day (females). The final mean body weights of mice in the 300 and 1,000 ppm groups were similar to those of the controls. Renal tubule degeneration and necrosis were observed in the kidney of 3,000 ppm mice. 13-Week Studies: Groups of 10 male and 10 female rats were fed diets containing 0, 150, 300, 600, 1,200, or 2,400 ppm triamterene. All rats receiving 2,400 ppm died before the end of the study; all other rats survived to the end of the study. Rats exposed to 150, 300, 600, or 1,200 ppm triamterene received approximate doses of 10, 20, 40, or 70 mg/kg body weight per day (males) or 10, 20, 40, or 80 mg/kg per day (females). Body weight gains and final mean body weights of rats in the 1,200 ppm groups were significantly lower than those of controls. There were no biologically significant differences in hematologic, clinical chemistry, or urinalysis parameters among exposed and control rats. Calculi were observed in the renal pelvis of four male rats in the 1,200 ppm group. Chemical-related lesions were observed in the kidney and adrenal gland of rats in the 1,200 and 2,400 ppm groups. These consisted of degeneration and regeneration of the renal tubule epithelium and cytoplasmic vacuolization of cells of the zona glomerulosa of the adrenal cortex. Depletion of hematopoietic cells from the bone marrow and of lymphocytes from the spleen and thymus of rats in the 2,400 ppm groups may have been related to debilitation and reduced feed consumption rather than chemical exposure. Groups of 10 male and 10 female mice were fed diets containing 0, 100, 200, 400, 800, or 1,600 ppm triamterene. All mice receiving 1,600 ppm, one 800 ppm female, one 200 ppm male, and four 100 ppm males died before the end of the study. Mice exposed to 100, 200, 400, or 800 ppm triamterene received approximate doses of 15, 25, 50, or 90 mg/kg body weight per day (males) or 15, 25, 50, or 115 mg/kg per day (females). The body weight gain and final mean body weight of male mice receiving 800 ppm were significantly lower than those of the controls. The total leukocyte and lymphocyte counts of males receiving 800 ppm and of females receiving 100, 400, or 800 ppm were significantly lower than those of controls. No other differences in hematologic, clinical chemistry, or urinalysis parameters were considered to be biologically significant. Necrosis of Lymphocytes was observed in the lymph node, spleen, and thymus of mice in the 800 and 1,600 ppm groups groups. 2-Year Studies: The doses selected for the 2-year studies were based on lower body weights, mortality, and chemical-related lesions observed in exposed animals during the 13-week studies. Groups of 70 male and 70 female rats were fed diets containing 0, 150, 300, or 600 ppm triamterene and groups of 70 male and 70 female mice were fed diets containing 0, 100, 200, or 400 ppm. Ten animals from each group were included for interim evaluations at 3 and 15 months. Because of a dosing error involving the high-dose mice at week 40, a second study was conducted with groups of 60 male and 60 female mice fed diets containing 0 or 400 ppm triamterene. In the 2-year studies, rats exposed to 150, 300, or 600 ppm triamterene received approximately 5,10, or 25 mg/kg body weight per day (males) and 5, 15, or 30 mg/kg (females) and mice exposed to 100, 200, or 400 ppm received approximately 10, 25, or 45 mg/kg (males) and 15, 30, or 60 mg/kg (females) per day. 3-Month and 15-Month Interim Evaluations in the 2-Year Studies: There were no biologically significant differences in hematologic, clinical chemistry, or urinalysis parameters between exposed and control rats or mice at the 3- or 15-month interim evaluations. At necropsy, the mean body weights of exposed rats and mice were similar to those of the controls. There were no chemical-related lesions in exposed rats at 3 months or in exposed mice at 3 or 15 months. At the 15-month evaluation, basophilic, clear cell, and mixed cell foci of the liver occurred in exposed male rats. No chemical-related lesions were observed in female rats at 15 months. Survival, Body Weights, Clinical Findings, and Feed Consumption in the 2-Year Studies: Survival of exposed rats was similar to that of controls (males: 0 ppm, 25/47; 150 ppm, 25/50; 300 ppm, 19/50; 600 ppm, 27/50; females: 29/50, 34/50, 34/50, 29/50). The mean body weights of 600 ppm rats were consistently lower than, but within 5% of, those of controls after week 49. Feed consumption by male and female rats was similar among exposed and control groups throughout the studies. There were no clinical findings of toxicity. Survival of 400 ppm male mice in the first study was lower than that of controls because of the dosing accident at week 40. Survival of 100 and 200 ppm male mice and of all exposed groups of female mice in the first study and of exposed males and females in the second study was similar to controls (males: first study, 0 ppm, 47/50; 100 ppm, 45/50; 200 ppm, 46/50; 400 ppm, 46/60; second study, 0 ppm, 43/50; 400 ppm, 39/50; females: first study, 38/50; 43/50; 43/50; 43/60; second study, 40/50; 38/51). Mean body weights of exposed mice were similar to those of controls throughout the first study with one exception; in the week following the dosing error, the mean body weight of 400 ppm males was 16% lower than that of controls. In the second study, mean body weights of 400 ppm mice were slightly lower than those of controls during the final 8 weeks. Feed consumption by exposed mice was similar to that by controls throughout the studies. There were no clinical findings of toxicity in exposed mice. Neoplasms and Nonneoplastic Lesions in the 2-Year Studies: The incidences of mixed cell foci and focal hyperplasia of the liver were significantly increased in 300 and 600 ppm male rats, and the incidences of clear cell and mixed cell foci were significantly increased in 300 and 600 ppm female rats. Hepatocellular adenomas occurred in all groups of exposed male rats, but none occurred in controls; the incidence of hepatocellular adenoma in the 150 ppm males was significantly higher than that of controls (O ppm, 0/50; 150 ppm, 6/50; 300 ppm, 4/50; 600 ppm, 3/49). Hepatocellular adenomas were observed in two 600 ppm female rats, but not in the lower exposure groups or in controls. No hepatocellular carcinomas were seen in exposed or control rats. The incidences of nephropathy in exposed rats were similar to those of controls, but the average severity of the lesion was marginally increased in male rats receiving 300 ppm and in female rats receiving 600 ppm (males: 47/50, 2.4; 49/50, 2.7; 50/50, 3.0; 49/50, 2.8; females: 38/50, 1.1; 45/50, 1.2; 45/50, 1.3; 45/50, 1.4). Although in the first study the incidences of hepatocellular adenoma in exposed male mice were similar to that of controls, the incidences of multiple adenomas were greater in the exposed groups, and the incidence of hepatocellular carcinoma in the 400 ppm group was marginally greater (hepatocellular adenoma: 0 ppm, 17/50; 100 ppm, 22/50; 200 ppm, 19/50; 400 ppm, 20/60; hepatocellular carcinoma: 5/50; 7/50; 3/50; 13/60). In the second study, the incidence of hepatocellular adenoma in the 400 ppm males was significantly higher than that of controls (hepatocellular adenoma: 0 ppm, 21/50; 400 ppm, 36/50; hepatocellular carcinoma: 9/50; 11/50). The incidences of hepatocellular adenoma in exposed female mice in the first and second studies were significantly greater than those of controls (hepatocellular adenoma, first study: 10/50; 22/50; 23/50; 36/60; second study: 7/50; 28/51). The incidences of multiple adenoma were also increased in the exposed groups. Although the incidences of hepatocellular carcinoma were similar among exposed and control female mice in the first study, the incidence of hepatocellular carcinoma in the 400 ppm females in the second study was marginally greater than that of controls (hepatocellular carcinoma, first study: 4/50; 4/50; 3/50; 8/60; second study: 5/50; 11/50). In both studies, hepatocellular foci (basophilic, eosinophilic, clear cell, or mixed cell) also occurred more frequently in exposed female mice than in controls. The incidences of thyroid gland follicular cell hyperplasia in the 200 and 400 ppm males and in all exposed groups of females were significantly greater than those of controls in the first study. These findings were confirmed in the second study (follicular cell hyperplasia: males, first study, 3/50, 8/50, 16/50, 20/60; second study, 0/50,16/50; females, first study, 4/49,17/49,18/50, 28/60; second study, 9/50, 32/51). The incidences of follicular cell neoplasms were similar among exposed and control mice in both studies. The incidences (28/50, 36/50, 43/50, 49/60) and average severity (0.56, 0.80, 1.00, 1.07) of nephropathy were marginally higher in exposed female mice than in controls in the first study. In the second study, the differences in incidence (15/50, 21/50) and severity (0.38, 0.55) were not as great. It is uncertain if these increases were related to the ingestion of triamterene. The incidences and severity of nephropathy were similar among exposed and control male mice in both studies. Genetic Toxicology: Triamterene was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537 with or without exogenous metabolic activation (S9). It did not induce chromosomal aberrations in Chinese hamster ovary cells, with or without S9. Positive results were obtained for induction of sister chromatid exchanges in Chinese hamster ovary cells with and without S9. Conclusions: Under the conditions of these 2-year feed studies, there was equivocal evidence of carcinogenic activity of triamterene in male F344/N rats based on a marginal increase in the incidence of hepatocellular adenoma. There was no evidence of carcinogenic activity of triamterene in female F344/N rats administered 150, 300, or 600 ppm. There was some evidence of carcinogenic activity of triamterene in male B6C3F1 mice based on a marginal increase in the incidence of hepatocellular carcinoma in the first study and a significantly increased incidence of hepatocellular adenoma in the second study. There was some evidence of carcinogenic activity of triamterene in female B6C3F1 mice based on significantly increased incidences of hepatocellular adenoma and of adenoma and carcinoma (combined). Exposure to triamterene was associated with an increased incidence of hepatocellular foci, primarily mixed cell type, and an increase in the severity of nephropathy in female rats. In mice, exposure to triamterene was associated with an increased incidence of hepatocellular foci in females and an increased incidence of thyroid gland follicular cell hyperplasia in males and females. Synonyms: 6-Phenyl-2,4,7-pteridinetnamine; 6-phenyl-2,4,7-triaminopteridine; 2,4,7-triamino-6-phenypteridine; ademin; pterofen; pterophane; NSC-77625; SKF 8542 Trade names: Dyrenium, Dyazide, Dyren, Dytac, Jatropur, Maxzide, Noridyl, Triteren, Teriam, Urocaudal
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PMID:NTP Toxicology and Carcinogenesis Studies of Triamterene (CAS No. 396-01-0) in F344/N Rats and B6C3F1 Mice (Feed Studies). 1261 91


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