Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 52-year-old man was admitted to the General Surgical Service, with acute onset of left back and flank pain. Two weeks prior to admission he had been subjected to a 3G to 4G acceleration in an ejection seat training simulator. On the day of admission, he had performed a 100 yard swim in flight gear following a seven foot jump into water. He denied any injury during the above exercises or any other trauma. A falling hematocrit was demonstrated by serial determinations and a computerized tomography scan revealed a left retroperitoneal hematoma with normal bilateral renal function and no obvious renal injury. Continued hemorrhage resulted in laparotomy, which showed an 11 cm left adrenal tumor with massive hemorrhage into the retroperitoneum. Histologically the tumor was a benign non-functioning adrenal cortical adenoma.
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PMID:Massive retroperitoneal hemorrhage from an asymptomatic adrenal cortical adenoma. Report of a case. 271 7

The effects of phenobarbital (PB) on hepatocellular carcinogenesis in three strains of nitrosamine-initiated infant male mice were evaluated. Fifteen-day-old C57Bl/6NCrlBR (C57Bl), C3H/HeNCr1BR (C3H) and B6C3F1 mice were treated with a single i.p. injection of either diethylnitrosamine (DENA) (5 micrograms/body wt), dimethylnitrosamine (DMNA) (5 micrograms/body wt) or saline. One-half of the treated mice received PB via the drinking water (500 mg/l) for 24 weeks. The remaining treated mice were given deionized drinking water. Mice were killed at 28 weeks of age and hepatic lesions were evaluated. Only animals that received DENA or DMNA exhibited tumors. C3H mice treated with DENA + PB demonstrated a significant increase in hepatic adenoma number compared to C3H mice exposed to DENA only. Conversely, B6C3F1 males treated with DENA + PB exhibited a significant decrease in the number of hepatic adenomas compared to B6C3F1 males treated with DENA alone. No change was noted in adenoma size in B6C3F1 mice treated with DENA + PB from those receiving DENA only. Chronic PB exposure of C57Bl males previously treated with DENA had no effect on hepatic adenoma number or size. C3H mice treated with DMNA + PB displayed an increase in both adenoma size and adenoma number compared to C3H mice receiving DMNA only. Similarly, in B6C3F1 mice, PB treatment increased both the adenoma incidence and adenoma number in DMNA initiated mice. PB had no effect on hepatic adenoma incidence or number in DMNA-treated C57Bl mice. These data suggest that the ability of PB to promote hepatic tumorigenesis in the 15-day-old initiated mouse is dependent on both the strain of the mouse and the initiating chemical carcinogen.
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PMID:Strain differences in hepatic tumor promotion by phenobarbital in diethylnitrosamine- and dimethylnitrosamine-initiated infant male mice. 275 14

Chlorodibromomethane, a trihalomethane found in water supplies after chlorination, was administered by gavage in corn oil to male and female Fischer 344/N rats and B6C3F1 mice in toxicity studies of 13 weeks and 2 years duration. Doses used in the 13-week study were 0, 15, 30, 60, 125, and 250 mg/kg in rats and mice. At 250 mg/kg, hepatic and renal toxicity was produced in male and female rats and male mice, and mortality was increased in male and female rats. In the chronic study, male and female rats were administered the chemical at 0, 40, and 80 mg/kg. No adverse effects on survival in treated rats were observed. Male rats receiving 80 mg/kg had reduced body weight gains relative to controls. Fatty change and cytoplasmic changes were seen in the liver of treated male and female rats. The male and female mice in the chronic study received doses of 0, 50, and 100 mg/kg of chemical. A dosing accident rendered the number of low-dose male mice inadequate for statistical analysis. High-dose male mice had reduced survival relative to controls. Survival was similar in dosed and control female mice. Dosed male and high-dose female mice had reduced body weight relative to controls. Non-neoplastic hepatic lesions were seen in treated male mice (necrosis and hepatocytomegaly) and in treated female mice (calcification and fatty change); nephrosis was seen in treated male mice. The incidence of hepatocellular adenoma and carcinoma (combined) was increased in treated female mice, but only marginally so in treated male mice. Chlorodibromomethane, like chloroform, is toxic to liver and kidneys, and like chloroform induces hepatocellular tumors in mice.
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PMID:Toxicity and carcinogenicity of chlorodibromomethane in Fischer 344/N rats and B6C3F1 mice. 300 99

Female Swiss mice were exposed to cadmium in the drinking water at concentrations ranging from 0 to 50 ppm for 105 or 280 day time periods. In the 105 day study, the effect of cadmium on urethan-induced pulmonary adenoma formation was evaluated. Urethan-induced sleeping times observed following i.p. injection of urethan after 3 weeks of cadmium exposure were not affected by cadmium indicating that chronic cadmium exposure did not alter the elimination of urethan. Pulmonary adenoma formation which was evaluated 84 days later was not affected by cadmium. The size and number of tumors remained unchanged. This suggests that the immunosuppressive actions of cadmium do not influence urethan-induced adenoma formation. In the 280-day study, the effects of cadmium on the incidence of spontaneous murine lymphocytic leukemia was evaluated. Mortality from the leukemia virus was greater in the cadmium-exposed mice. Mice exposed to 10 or 50 ppm cadmium experienced 33% more deaths from the virus. The average time till death was unaffected. It appears that the immunosuppressive effects of cadmium impair immunosurveillance mechanisms that control expression of the murine lymphocytic leukemia virus.
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PMID:The effect of cadmium on chemical- and viral-induced tumor production in mice. 302 55

Female Swiss mice were exposed to lead in the drinking water at concentrations ranging from 0 to 1000 ppm for 105 or 280 day periods of time. The effect of lead on urethan-induced pulmonary adenoma formation was evaluated in the 105 day study. Urethan-induced sleeping times observed following ip injection of urethan (1.5 mg/g) after 3 weeks of lead exposure were not altered by lead indicating that lead did not affect the rate of urethan elimination. Pulmonary adenoma formation was evaluated 84 days later. Lead exposure did not affect the number of tumors produced, nor did it alter the mean tumor diameter in the lead treatment groups. This suggests that the immunosuppressive activity of lead does not enhance urethan-induced adenoma formation. In the 280 day study, the incidence of spontaneous murine lymphocytic leukemia was evaluated. Leukemia was observed in all treatment groups. Mortality was greater in the lead-exposed mice. Mice exposed to 50 or 1000 ppm lead had 41.6% and 58.3% more deaths associated with the virus. The median survival time was also reduced in the lead-exposed mice. It appears that the immunosuppressive effects of lead allow for increased expression of the murine lymphocytic leukemia virus.
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PMID:The effect of lead on chemical- and viral-induced tumor production in mice. 304 Aug 44

Patients with primary aldosteronism do not have distinctive clinical features. However, the associated hypertension is invariably high and often resistant to drug therapy. The recommended initial test in suspected primary aldosteronism is the determination of aldosterone excretion rate after salt loading. Patients in whom aldosterone excretion rates exceed 14.0 micrograms per 24 hours when the urinary sodium is at least 250 mEq per 24 hours are prime candidates for additional studies. The presence of hypokalemia and/or suppressed plasma renin activity provides corroborative evidence of primary aldosteronism, but the absence of either or both does not preclude the diagnosis. Spontaneous, moderately severe hypokalemia (less than 3.0 mEq per L), an anomalous postural decrease in plasma aldosterone concentration, and increased plasma 18-hydroxycorticosterone values (greater than 100 ng per dl) indicate the presence of an adenoma. For localization of an adenoma, an adrenal CT scan should be obtained first and is considered diagnostic if an adrenal mass is clearly identified. When the CT scan is inconclusive, adrenal venous sampling can be done for more definitive localization. In the presence of an adenoma, surgical excision is the recommended approach but only after pharmacologic normalization of arterial pressure and correction of metabolic abnormalities. Sustained salt and water depletion is the most important therapeutic goal for these patients, and cure can be achieved despite prolonged and severe hypertension.
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PMID:Primary aldosteronism. 306 43

Female Swiss mice were exposed to zinc chloride (0 to 500 ug/mL) or copper sulfate (0 to 200 ug/mL) in their drinking water for 15 weeks. After 3 weeks of the exposure period, the mice were administered urethan (1.5 mg/g) intraperitoneally. Urethan-induced pulmonary adenoma formation was evaluated 12 weeks later. Zinc exposure increased the number of adenomas produced but reduced the mean tumor diameter in the intermediate treatment groups, 50 and 200 ug/mL. Exposure to copper had no effect on tumor size or on tumor number. Weight gains in the mice were not affected by copper or zinc treatment, although a dose-dependent reduction in water consumption was observed with copper. Water consumption in mice exposed to zinc was elevated in one treatment group (50 ug/mL). Urethan-induced sleeping times, which reflect the rate of urethan excretion, were prolonged by zinc exposure but were unaffected by copper exposure. This finding suggests that zinc exposure impairs the elimination of urethan and enhances its carcinogenic activity, which is manifested by increased tumor formation.
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PMID:Influence of copper and zinc on urethan-induced adenoma development in mice. 324 Jul 18

Twenty-eight patients with resistant hypertension were found to have primary aldosteronism; 25 had solitary adenoma and 3 had adrenal hyperplasia. All were severely hypertensive despite receiving three or more antihypertensive agents, including conventional doses of diuretics, sympatholytics, and vasodilators. Hypervolemia (24 patients) or normovolemia (2 patients) despite severe diastolic hypertension was the hallmark in 26 patients. Adequate salt and water depletion alone with spironolactone (200 mg/day) and hydrochlorothiazide (50-100 ng/day) reduced arterial pressure in all. Twenty-two patients had surgical removal of a solitary adenoma. Over 1 to 2 years of follow-up, 13 were normotensive without medication, and six required hydrochlorothiazide and three hydrochlorothiazide plus a beta-blocker to normalize blood pressure. Blood pressure response to surgery had no relation to either duration or severity of hypertension. Six patients (three with hyperplasia, three with adenoma) have continued diuretic therapy and are normokalemic and normotensive. These results indicate that primary aldosteronism can be associated with sever and drug-resistant hypertension, that maintained hypervolemia is the reason for resistance to therapy, that sustained volume depletion is the most important therapeutic goal for these patients, and that cure can be achieved despite prolonged and severe hypertension.
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PMID:Clinical implications of primary aldosteronism with resistant hypertension. 334 59

Female Swiss mice were exposed to sodium selenite (3 micrograms/ml selenium content) and nickelous chloride (100 micrograms/ml nickel content) in the drinking water on alternate days for 15 weeks. After 3 weeks of metal exposure, the mice were administered urethan (1.5 mg/g) intraperitoneally. Pulmonary adenoma formation was evaluated 12 weeks later. Selenium exposure did not alter the tumor incidence (P = 0.059) or the tumour size (P = 0.98). Nickel exposure did not affect the tumour incidence (P = 0.25), but increased the average tumour size (P = 0.0025). Combined selenium and nickel exposure resulted in significant interactions associated with tumour size (P = 0.00075) and tumour number (P = 0.045). Urethan-induced sleeping times were reduced by selenium exposure (P = 0.0049), but were unaffected by nickel exposure (P = 0.99). Combined metal exposure did not influence urethan-induced sleeping times (P = 0.48).
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PMID:Alterations in urethan-induced adenoma formation in mice exposed to selenium and nickel. 342 64

The carcinogenic activities of sodium chlorite in B6C3F1 mice were examined. Sodium chlorite was given at concentrations of 0 (control), 0.025% (low dose), or 0.05% (high dose) in the drinking water of 150 female and 150 male mice for 80 weeks, after which time the animals were returned to distilled water without sodium chlorite. All mice were sacrificed 85 weeks from the beginning of the experiment. The incidence of tumor-bearing animals was 32% (control), 34% (low dose), and 26% (high dose) in female mice, and 46% (control), 57% (low dose), and 53% (high dose) in male mice. The types and incidence of neoplasms that occurred frequently in each group of both sexes were similar to those observed spontaneously in B6C3F1 mice. The incidence of lymphomas/leukemias in the high dose group of females (2%), however, was lower than that in the control group (15%). Furthermore, the incidence of pulmonary adenomas in the high dose group of males (12%) was higher than that in the control group (0%), but neither dose-related increases in the adenoma incidences nor increased incidences of the adenocarcinomas were observed. These results indicated no clear evidence of a carcinogenic potential of sodium chlorite in B6C3F1 mice.
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PMID:Studies of carcinogenicity of sodium chlorite in B6C3F1 mice. 344


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