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Nodular hyperplasia

Nodular hyperplasia of the prostate is usually associated with a normal serum acid phosphatase activity. Complications such as acute urinary obstruction or prostatic infarction will elevate this serum activity for several days as will cystoscopy and catheterization (98). Digital palpation of the prostate may result in an elevation which subsides within a few hours. [Pg.215]

Tartrate is a most widely used inhibitor of prostatic acid phenylphosphatase activity. With this inhibitor Bonner and associates detected five cases of unsuspected carcinoma of the prostate in 221 hospital patients and clarified the diagnoses in another four patients (98). Nonetheless, the diagnostic specificity of an elevated 1-tartrate inhibited activity is not absolute, as Fishman et. al found it elevated in 48 of 1,190 males without cancer. Whitmore and associates also observed this activity to be elevated in 3 of 20 patients with uncomplicated nodular hyperplasia (102). Hill compared the total versus the "prostatic" serum activities in 20 patients with localized untreated carcinoma of the prostate and observed... [Pg.215]

Dose-related incidence of hepatic nodular hyperplasias in the 25 and 50 mg/kg diets and an increased incidence of hepatomas in the male 5- and 25-mg/kg groups. Controls experienced a high incidence of premature deaths (Epstein 1976)... [Pg.871]

Wakefield AJ, Murch SH, Anthony A, et al. Ileal-lymphoid-nodular hyperplasia, non-specific colitis and pervasive developmental disorder in children. Lancet 1998 351 637-A1. [Pg.452]

Hepatic lesions (adenomas, focal nodular hyperplasia, hepatocellular carcinoma, etc) Rarely, benign and malignant hepatic adenomas have been associated with the use of hormonal contraceptives. Severe abdominal pain, shock, or death may be due to rupture and hemorrhage of a liver tumor. [Pg.217]

B artolozzi C, Lencioni R, Paolicchi A, et al. Differentiation of hepatocellular adenoma and focal nodular hyperplasia of the liver comparison of power Doppler imaging and conventional color Doppler sonography. EurRadiol 1997 7 1410-1415. [Pg.375]

Oral contraceptives, estrogens, and benign liver tumors The effects of oral contraceptives on the liver include not only benign liver tumors (focal nodular hyperplasia, hepatic adenoma, and hemangioma) (74) and hepatocellular carcinoma, but also peliosis hepatis (75), sinusoid dilatation (76), and such probably unrelated shorter-term complications as jaundice and gallstones. [Pg.179]

Marks WH, Thompson N, Appleman H. Failure of hepatic adenomas (HCA) to regress after discontinuance of oral contraceptives. An association with focal nodular hyperplasia (FNH) and uterine leiomyoma. Ann Surg 1988 208(2) 190-5. [Pg.195]

Benign liver tumors (hepatocellular adenoma and focal nodular hyperplasia) are extremely rare conditions that appear to be related to oral contraceptive use (212). [Pg.230]

A dose-related trend towards portal sclerosis and bile duct proliferation was observed in rats given doses of from 0.3 to 6.2 mg/kg/day triphenyltin hydroxide for 52 and 104 weeks there was no corresponding increase in liver weight (Tennekes et al. 1989a). The dose-related trend was stronger in females (p<0.0005) than in males (p<0.005). In mice this same compound was associated with a 35%-40% increase in liver weight and nodular hyperplasia at doses of 15.2 mg/kg/day for males and 20.2 mg/kg/day for females but not at lower doses (Tennekes et al. 1989b). [Pg.79]

Tumors were also present in mice given diets containing 0.9-20.2 mg/kg/day triphenyltin hydroxide. After sacrifice at 80 weeks, examination of the tissue revealed an increased incidence of hepatocellular adenomas in both sexes. These tumors were consistent with the nodular hyperplasia seen in the livers of the treated animals. As was the case with the rat study, the females appeared to be more sensitive than the males. There was decrease in survival for the females at the highest dose. Only 50% of the females receiving this dose were alive at the termination of the study as opposed to 70% of the males in the same dose group and 74% of the female control animals. [Pg.88]

Wakefield AJ, Murch SH, Anthony A, Linnell J, Casson DM, Malik M, Berelowitz M, Dhillon AP, Thomson MA, Harvey P, Valentine A, Davies SE, Walker-Smith JA. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet 1998 351 (9103) 637 U. [Pg.713]

ACTH-independent Cushing s syndrome shows increased cortisol, but the ACTH is not elevated but rather decreased due to negative feedback. It can be caused by exogenous administration of glucocorticoids or by adrenal adenoma, carcinoma or nodular hyperplasia. [Pg.198]

In delayed-phase imaging, the signal increase in the liver parenchyma does not necessarily increase the conspicuity or detection of lesions because residual hepatocytes of a tumor of hepatocytic origin, such as hepatocellular carcinoma (HCC) and focal nodular hyperplasia, may influence the contrast enhancement. Gd-BOPTA is effective for use with delayed-phase MRI to detect metastases [130]. In cirrhosis, liver functioning is impaired and the number of normal hepatocytes is reduced. The entry of Gd-BOPTA into cirrhotic hepatocytes decreases, but the accumulation in the liver increases due to reduced biliary excretion [131]. As a consequence, contrast enhancement is reduced and the window of acquisition is widened. The contrast enhancement of a cirrhotic liver is therefore different from that observed in normal liver parenchyma. [Pg.424]

The carcinogenicity of PCTs was demonstrated in a study with mice which were treated with a 250 mg/kg and 500 mg/kg PCT diet for 24 weeks [58]. A significantly higher incidence of nodular hyperplasia of the liver was found in the PCT exposed mice. Also the exposed group had a higher incidence of hepatocellular carcinomas. A combination of HCB and PCTs in the diet of the mice considerably enhanced the occurrence of nodules and carcinomas. [Pg.57]

The following lesions may be hypoechoic (7.) metas-tases, (2.) liver cell carcinoma, (3.) adenomas, (4.) focal nodular hyperplasia, (5.) abscesses, (6.) haematomas, (7.) early liver infarction, (S.) foci showing reduced fatty infiltration, (9.) lymphomas, and (10.) lipomas. In individual cases, differentiation between a benign and a malignant structural defect may cause considerable difficulties. (59) (s. fig. 9.4)... [Pg.132]

Focal nodular hyperplasia (see chapter 36.4.2) — as a benign hepatocellular tumour - is mostly hypoechoic. Occasionally, it can be differentiated as a protruding contour or a pediculate liver tumour. Compression of the surrounding liver tissue may be the cause of a visible capsule , which actually has no anatomical structure of its own. At a size of > 3 cm, fibrous septa and arteries... [Pg.133]

Focal nodular hyperplasia On MRI scans (as with CT), FNH shows the characteristic central venous star. Otherwise, the signal intensity of FNH is homogeneously isointense (Ti) or slightly hyperintense (T2). Immediately following the i.v. administration of CM (Gd-DTPA), a distinct but rapidly fading enhancement is observed. (65, 95, 100, 102, 110, 118)... [Pg.178]

In 80-90% of cases, focal nodular hyperplasia shows a typical, radial (spoke-like) arrangement of coiled vessels in the area of the tumour, which originate from a circular artery. Occasionally, fine a.v. shunts are present. The smooth-edged lesion is hypervascular. The parenchymal phase, with its homogeneous concentration of contrast medium, allows the lesion to be clearly demarcated from healthy liver tissue. (156) Hepatic adenoma is generally hypervascular. Displaced vessels are frequently visible. [Pg.180]

Hepatic adenomas and focal nodular hyperplasia dynamic CT study Radiology 1986 160 53-58... [Pg.187]

Procacd, C., Fngazzola, C., Onquino, M., Mangiante, G., Zonta, L., Bergamo Andreis, JA., NicoB, N., Rstolesi, G.F. Contribution of CT to characterization of focal nodular hyperplasia of the liver. Gastrointest. Radiol. 1992 17 63-73... [Pg.187]

Shamsi, K., De Schepper, A., Degryse, H., Deckers, F. Eocal nodular hyperplasia of the liver radiologic findings. Abdom Imaging 1993 18 32-38... [Pg.187]

Butch, R.J., Stark, D., Malt, R.A. Magnetic resonance imaging of hepatic focal nodular hyperplasia. J. Comput. Assist. Tomogr. 1986 10 874-877... [Pg.188]

Mahfonz, A.-E., Hamm, B., Taupitz, M., Wolf, K.-J. Hypervascular hver lesions differentiation of focal nodular hyperplasia from malignant tumors with dynamic gadolinum-enhanced MR imaging. Radiology 1993 186 133-138... [Pg.189]

Vilgrain, V., Flejou, J.-F., Arrive, L., Belghiti, J.,Najmark, D., Menu, Y., Zins, M., Vidlierme, M.-R, Nahum, H. Focal nodular hyperplasia of the hver MR imaging and pathologic correlation in 37 patients. Radiology 1992 184 699-703... [Pg.189]


See other pages where Nodular hyperplasia is mentioned: [Pg.216]    [Pg.203]    [Pg.63]    [Pg.73]    [Pg.92]    [Pg.84]    [Pg.50]    [Pg.68]    [Pg.88]    [Pg.883]    [Pg.1242]    [Pg.1320]    [Pg.178]    [Pg.915]    [Pg.137]    [Pg.150]    [Pg.161]    [Pg.173]    [Pg.187]    [Pg.188]    [Pg.189]    [Pg.190]    [Pg.191]    [Pg.194]    [Pg.194]   
See also in sourсe #XX -- [ Pg.303 ]




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Focal nodular hyperplasia

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Hyperplasia

Hyperplasia nodular lymphoid

Nodular regenerative hyperplasia

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