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)

Nitrofurantoin was studied and evaluated because of its widespread use as a drug for treating urinary tract infections in humans, its structural relationship to known carcinogenic 5-nitrofuran compounds, and the lack of adequate studies to assess its carcinogenicity. Toxicology and carcinogenesis studies of nitrofurantoin were conducted by administering nitrofurantoin (greater than 99% pure) in feed to groups of F344/N rats and B6C3F1 mice of each sex for 14 days, 13 weeks, or 2 years. Fourteen-Day and Thirteen-Week Studies: None of the rats (at dietary concentrations up to 20,000 ppm) died before the end of the 14-day studies. Rats that received 5,000, 10,000, or 20,000 ppm lost weight. Four of five male and 4/5 female mice that received 10,000 ppm and 1/5 females that received 5,000 ppm nitrofurantoin died before the end of the studies. Mice that received 5,000 ppm and male mice that received 10,000 ppm lost weight. In the 13-week studies, final mean body weights of rats that received 2,500, 5,000, or 10,000 ppm were 10%, 34%, or 47% lower than that of the controls for males and 15%, 31%, or 41% lower for females. Feed consumption by dosed and control rats was generally similar. Degeneration of the germinal epithelium of the seminiferous tubules of the testis was observed in male rats that received 2,500 to 10,000 ppm nitrofurantoin. Necrosis of the ovarian follicles was observed in 8/10 female rats that received 10,000 ppm, in 3/10 females that received 5,000 ppm, and in 1/10 that received 2,500 ppm. For mice, final mean body weights of the 5,000-ppm groups were 13% lower than that of the controls for males and 15% lower for females. Two of 10 male mice that received 5,000 ppm and 1/10 males that received 300 ppm died before the end of the 13-week studies. Estimated feed consumption was similar for dosed and control groups. Degeneration of the germinal epithelium of the testis was observed in males that received 1,300 to 5,000 ppm; necrosis of the ovarian follicles was observed in females that received 5,000 ppm but not in the lower dose groups. Necrosis of the renal tubular epithelium was observed in 2/9 males that received 5,000 ppm. Based on these results, 2-year studies of nitrofurantoin were conducted by feeding diets containing 0, 1,300, or 2,500 ppm nitrofurantoin to groups of 50 male F344/N rats and to groups of 50 male and female B6C3F1 mice for 103 weeks. Groups of 50 female F344/N rats were fed diets containing 0, 600, or 1,300 ppm nitrofurantoin on the same schedule. Body Weight and Survival in the Two-Year Studies: Mean body weight and average daily feed consumption of dosed male and female rats were similar to those of the controls throughout the studies. The average amount of nitrofurantoin consumed per day was estimated to be 60 and 110 mg/kg for low and high dose male rats and 30 and 60 mg/kg for low and high dose female rats. No significant differences in the number of rats surviving to the end of the studies were observed between any groups of rats of either sex (male: control, 24/50; low dose, 27/50; high dose, 26/50; female: 25/50; 26/50; 31/50). Mean body weights of high dose male and female mice were up to 12% lower than those of the controls throughout most of the studies. The average daily feed consumption by dosed mice ranged from 93% to 100% that by controls. The average amount of nitrofurantoin consumed per day was estimated to be 280-300 mg/kg and 570-580 mg/kg for low and high dose mice. The survival of the control group of female mice was lower than that of the dosed groups (control, 19/50; low dose, 37/50; high dose, 37/50). The decrease in survival was most likely related to the increase in microbial infection in the reproductive tract observed in the controls. Groups of male mice had similar survival (28/50; 29/50; 34/50). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Organs showing toxicity from nitrofurantoin exposure identified in the short-term studies were the testis in male rats and mice, the ovary in female rats and mice, and the kidney in male mice. Lesions oband mice, the ovary in female rats and mice, and the kidney in male mice. Lesions observed in the 2-year studies were in the testis in male rats and mice, ovary in female mice, and kidney in male rats. Chronic nephropathy was observed in nearly all rats, but the severity of the lesions was judged to be greater in dosed male rats. Hyperplasia of the transitional cell epithelium (control, 0/50; low dose, 5/50; high dose, 2/50) and hydronephrosis of the renal pelvis (0/50; 5/50; 2/50) were also observed in dosed male rats. In the standard single sections of the left and right kidney from each rat, tubular cell adenomas were observed in one low dose and two high dose males; a tubular cell carcinoma was observed in another high dose male. Because the number of renal tubular cell neoplasms identified by standard procedures in the dosed male rats was low, additional step-sections of the kidney were evaluated. The incidences of tubular cell adenomas derived from the step-sections and original sections (combined) were significantly increased in dosed male rats (adenomas: 3/50; 11/50; 19/50); tubular cell carcinomas occurred in two high dose males only. Lesions considered to be associated with the nephropathy and nitrofurantoin exposure were observed in male rats and included hyperplasia of the parathyroid glands (3/49; 18/47; 23/49), fibrous osteodystrophy of the bone (0/50; 5/50; 5/50), and mineralization of the glandular stomach (1/49; 8/50; 14/50). Atypical cells of the epididymis (0/50; 0/50; 12/50) and degeneration of the testis (0/50; 0/50; 36/50) were observed in high dose male rats. Fibrinoid necrosis of arterioles (1/50; 8/50; 15/50) and perivascular infiltration of mononuclear cells (3/50; 9/50; 19/50) were also observed in the testis of male rats. Interstitial cell adenomas of the testis occurred with a negative trend (47/50; 45/50; 21/50), and no adenomas or carcinomas of the preputial gland were seen in high dose male rats (12/48; 11/50; 0/47). The incidence of clitoral gland neoplasms was increased in low dose female rats (5/44; 10/38; 4/42). Osteosarcomas were observed in the bone of one low dose and two high dose male rats. The historical incidence of osteosarcomas in untreated male F344/N rats is 8/1,937 (0.4%). The incidences of subcutaneous tissue neoplasms in dosed male rats were greater than that in the controls (1/50; 7/50; 5/50). No neoplastic lesions in dosed female rats or male mice were considered to be compound related at the doses of nitrofurantoin administered. For female mice, ovarian atrophy was observed in 48/50 low dose and 49/50 high dose mice but not in controls. Tubular cell adenomas of the ovary (0/50; 0/50; 5/50), benign mixed tumors (tubular and stromal) (0/50; 0/50; 4/50), and granulosa cell tumors (0/50; 3/50; 2/50)) were observed in dosed female mice. One granulosa cell tumor in the high dose group was malignant. Ovarian abscesses (18/50) and suppurative inflammation of the uterus (11/50) were observed in control female mice but not in dosed female mice and are believed to be related to indigenous microbial infections and most likely were the cause of early deaths in this group. Adenocarcinomas of the uterus were seen in one low dose and in one high dose mouse. Testicular aspermatogenesis (1/49; 1/49; 16/50), degeneration of the germinal epithelium (0/49; 3/49; 23/50), and atypical cells (0/50; 0/49; 26/50) and depletion (1/50; 1/49; 15/50) of the epididymis were observed at increased incidences in high dose male mice. Spindle cell hyperplasia of the adrenal cortex was observed in dosed female mice (3/50; 41/50; 45/50). A spindle cell adenoma (adrenal capsule adenoma) was seen in one low dose female mouse, and a spindle cell carcinoma (adrenal capsule carcinoma) was seen in one low dose male mouse. Mineralization of the renal medulla (male: 0/50; 0/50; 17/50; female: 0/50; 0/50; 7/50) and dilatation of the renal tubules (male: 0/50; 0/50; 14/50) were observed in high dose mice. Hepatocellular neoplasms (adenomas or carcinomas, combined) were observed at an increased incidence in high dose female mice (2/50; 2/50; 8/50). An Ito cell tumor of the liver was observed in one low dose and one high dose female mouse. Malignant lymphomas occurred in female mice (12/50; 19/50; 24/50). Genetic Toxicology: Nitrofurantoin was mutagenic in Salmonella typhimurium strains TA98 and TA100, with and without metabolic activation, but was not mutagenic for strains TA1535 or TA1537. Nitrofurantoin induced forward mutations at the TK+/- locus of L5178Y mouse lymphoma cells in the absence of metabolic activation (it was not tested with activation). Nitrofurantoin induced increased numbers of sister chromatid exchanges and chromosomal aberrations in cultured Chinese hamster ovary cells with and without metabolic activation. Results of the sex-linked recessive lethal assay in Drosophila were negative after administration of nitrofurantoin by feeding or by injection. Conclusions: Under the conditions of these 2-year feed studies, there was some evidence of carcinogenic activity of nitrofurantoin for male F344/N rats as shown by increased incidences of uncommon kidney tubular cell neoplasms. Uncommon osteosarcomas of the bone and neoplasms of the subcutaneous tissue were observed in dosed male rats. Incidences of interstitial cell adenomas of the testis and neoplasms of the preputial gland were decreased in the 2,500-ppm group of male rats. There was no evidence of carcinogenic activity of nitrofurantoin for female F344/N rats fed diets containing 600 ppm or 1,300 ppm for 2 years. Female rats may have been able to tolerate higher doses. There was no evidence of carcinogenic activity of nitrofurantoin for male B6C3F1 mice fed diets containing 1,300 ppm or 2,500 ppm for 2 years. There was clear evidence of carcinogenic activity of nitrofurantoin for female B6C3F1 mice as shown by increased incidences of tubular adenomas, benign mixed tumors, and granulosa cell tumors of the ovary. Nonneoplastic lesions considered related to nitrofurantoin exposure were chronic nephropathy and associated lesions (hyperplasia of the parathyroid gland, fibrous osteodystrophy of the bone, and mineralization of the glandular stomach) in male rats and testicular degeneration in male rats and mice. Ovarian atrophy and hyperplasia of the adrenal cortex spindle cells were observed in dosed female mice. Synonyms: 1-(((5-nitro-2-furanyl)methylene)amino-2,4-imidazolidinedione); 1-(5-nitro-2-furfurylideneamino)-hydantoin; N-(5-nitro-2-furfurlidene)-1-aminohydantoin; 1-((5-nitrofurfurylidene)amino)hydantoin Trade Names: Benkfuran; Benkfurin; Chemiofuran; Cyantin; Dantafur; Furadantin; Furadantine; Furadantoin; Furadonin; Furadonine; Furantoin; Furatoin; Furobactina; Ituran; Macrodantin; Nifurantin; NSC 2107; N-Toin; Orafuran; Parafuran; Urizept; USAF EA-2; Welfurin; Zoofurin
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PMID:NTP Toxicology and Carcinogenesis Studies of Nitrofurantoin (CAS No. 67-20-9) in F344/N Rats and B6C3F1 Mice (Feed Studies). 1272 84

Benzene ranks 16th in production volume for chemicals produced in the United States, with approximately 9.9 billion pounds being produced in 1984, 9.1 billion pounds in 1983, and 7.8 billion pounds in 1982. This simplest aromatic chemical in used in the synthesis of styrene (polystyrene plastics and synthetic rubber), phenol (phenolic resins), cyclohexane (nylon), aniline, maleic anhydride (polyester resins), alkylbenzenes (detergents), chlorobenzenes, and other products used in the production of drugs, dyes, insecticides, and plastics. Benzene, along with other light, high-octane aromatic hydrocarbons, such as toluene and xylenes, is a component of motor gasoline. Benzene is also used as a solvent, but for most applications, it has been replaced by less hazardous solvents. During the 17-week studies, groups of 10 or 15 male and female F344/N rats and B6C3F1 mice were gavaged 5 days per week with benzene in corn oil (5 ml/kg) at doses of 0 to 600 mg/kg. No benzene-related deaths occurred; in rats that received benzene, final mean body weights were 14%-22% lower compared with vehicle controls and in mice, slight dose-related reductions were observed (less than 10% differences). Doses for the 2-year studies were selected based on clinical observations (tremors in higher dosed mice), on clinical pathologic findings (lymphoid depletion in rats and leukopenia in mice), and on body weight effects. Two-year toxicology and carcinogenesis studies of benzene (greater than 99.7% pure) were conducted in groups of 50 F344/N rats and 50 B6C3F1 mice of each sex and for each dose. Doses of 0, 50, 100, or 200 mg/kg body weight benzene in corn oil (5 ml/kg) were administered by gavage to male rats, 5 days per week, for 103 weeks. Doses of 0, 25, 50, or 100 mg/kg benzene in corn oil were administered by gavage to female rats and to male and female mice for 103 weeks. Ten additional animals in each of the 16 groups were killed at 12 months and necropsies were performed. Hematologic profiles were performed at 3-month intervals. These studies were designed and conducted because of large production volume and potential human exposure, because of the epidemiologic association with leukemia, and because previous experiments were considered inadequate or inconclusive for determining potential carcinogenicity in laboratory animals. In the 2-year studies, mean body weights of the 200 mg/kg male rats (-23%) and the 100 mg/kg mice (-14% to -19%) were lower than those of the vehicle controls, and survival of dosed groups decreased with increasing dose (rats--male: vehicle control, 32/50; low dose, 29/50; mid dose, 25/50; high dose, 16/50; female: 46/50; 38/50; 34/50; 25/50; mice--male: 28/50; 23/50; 18/50; 7/50; female: 30/50; 26/50; 24/50; 18/50). At week 92 for rats and week 91 for mice, survival was greater than 60% in all groups; most of the dosed animals that died before week 103 had neoplasia. Compound-related nonneoplastic or neoplastic effects on the hematopoietic system, Zymbal gland, forestomach, and adrenal gland were found both for rats and mice. Further, the oral cavity was affected in rats, and the lung, liver, harderian gland, preputial gland, ovary, and mammary gland were affected in mice. Significantly increased (P<0.05) incidences of neoplasms were observed at multiple sites for male and female rats and for male and female mice. Primary neoplasms observed in rats and mice are summarized in Table 1 (see page 12 of the Technical Report). Hematologic data from vehicle control and dosed rats and mice were obtained at 3-month intervals from 0 to 24 months. Reliably identifiable hematologic effects were limited to lymphocytopenia and associated leukocytopenia in benzene-dosed rats and mice. These effects were seen from 3 to 18 months in dosed male rats and in dosed male mice; a similar but less pronounced response was observed in dosed female rats during this same time period. The effect in female mice was limited to 12-18 months. The technical quality of certain of these data was questionable; thus, more detailed analyses (e.g., investig questionable; thus, more detailed analyses (e.g., investigation of the association between hematologic and pathologic changes) are deemed inappropriate for these data. Benzene increased the frequency of micronucleated normchromatic peripheral erythrocytes in male and female mice (rats were not examined); males were more sensitive than females. The hematopoietic system of rats and mice of each sex was affected by benzene in the 2-year studies. The incidences of malignant lymphomas in all dosed groups of mice were greater than those in the vehicle controls (male: 4/49; 9/48; 9/50; 15/49; female: 15/49; 24/45; 24/50; 20/49). Lymphoid depletion of the splenic follicles (rats) and thymus (male rats) was observed at increased incidences. Bone marrow hematopoietic hyperplasia was observed at increased incidences in dosed mice of each sex (male: 0/49; 11/48; 10/50; 25/49; female: 3/49; 14/45; 8/50; 13/49). The incidences of Zymbal gland carcinomas in mid and high dose male rats and in dosed female rats were greater than those in the vehicle controls (male: 2/32; 6/46; 10/42; 17/42; female: 0/45; 5/40; 5/44; 14/46). The incidences of Zymbal gland carcinomas in mid and high dose male mice and in high dose female mice were greater than those in the vehicle controls (male: 0/43; 1/34; 4/40; 21/39; female: 0/43; 0/32; 1/37; 3/31). In mid and high dose male mice and in high dose female mice, the incidences of epithelial hyperplasia of the Zymbal gland were also increased (male: 0/43; 3/34; 12/40; 10/39; female: 1/43; 1/32; 2/37; 6/31). Hyperplasia of the adrenal capsule was observed at increased incidences in dosed mice of each sex (male: 2/47; 32/48; 14/49; 4/46; female: 5/49; 19/44; 34/50; 30/48). The incidence of pheochromocytomas in mid dose male mice was greater than that in the vehicle controls (male: 1/47; 1/48; 7/49; 1/46), whereas the incidences in dosed female mice were lower than that in the vehicle controls (female: 6/49; 1/44; 1/50; 1/48). Hyperplasia of the zona fasciculata of the adrenal cortex was observed at increased incidences in low dose rats of each sex (male: 0/50; 13/49; 0/48; 2/49; female: 0/50; 17/50; 0/47; 0/49). Benzene was associated with increased incidences of neoplasms of the skin and oral cavity of rats. The incidences of squamous cell papillomas and squamous cell carcinomas of the skin in high dose male rats were greater than those in the vehicle controls (squamous cell papilloma: 0/50; 2/50; 1/50; 5/50; squamous cell carcinoma: 0/50; 5/50; 3/50; 8/50). Increased incidences of uncommon squamous cell papillomas or squamous cell carcinomas (combined) of the oral cavity were observed in dosed male and female rats (male: 1/50; 9/50; 16/50; 19/50; female: 1/50; 5/50; 12/50; 9/50). Incidences of squamous cell papillomas or carcinomas (combined) (male: 2/45; 2/42; 3/44; 5/38; female: 1/42; 3/40; 6/45; 5/42), hyperkeratosis, and epithelial hyperplasia of the forestomach were increased in some dosed groups of male and female mice; incidences of hyperkeratosis and acanthosis were increased in high dose male rats. Compound-related effects in the lung, harderian gland, preputial gland, ovary, mammary gland, and liver were seen in mice but not in rats. Administration of benzene was associated with increased incidences of alveolar epithelial hyperplasia in mid and high dose mice (male: 2/49; 3/48; 7/50; 10/49; female: 1/49; 1/42; 9/50; 6/49). Increased incidences of alveolar/bronchiolar carcinomas and alveolar/bronchiolar adenomas or carcinomas (combined) were observed in high dose male mice (carcinomas: 5/49; 11/48; 12/50; 14/49; adenomas or carcinomas: 10/49; 16/48; 19/50; 21/49). Alveolar/bronchiolar adenomas were seen at increased incidences in high dose female mice (4/49; 2/42; 5/50; 9/49), as were alveolar/bronchiolar carcinomas (0/49; 3/42; 6/50; 6/49) and alveolar/bronchiolar adenomas or carcinomas combined (4/49; 5/42; 10/50; 13/49) in mid and high dose female mice. The incidences of focal or diffuse hyperplasia of the harderian gland were increased in dosed mice of each sex (male: 0/49; 5/46; 11/49; 7/48; female: 6/48; 10/44; 11/50; 10/47). The incidences of harderian gland adenomas (0/49; 9/46; 13/49; 11/48) in dosed male mice were greater than that in the vehicle controls. A marginal increase in the incidence of adenomas or carcinomas (combined) of the harderian gland was seen in high dose female mice (5/48; 6/44; 10/50; 10/47). The administration of benzene to male mice was associated with increased incidences of hyperplasia (1/21; 18/28; 9/29; 1/35) and squamous cell carcinomas (0/21; 3/28; 18/29; 28/35) of the preputial gland. Increased incidences of mammary gland carcinomas were found in mid dose and high dose female mice (0/49; 2/45; 5/50; 10/49) and carcinosarcomas in high dose female mice (0/49; 0/45; 1/50; 4/49). Increased incidences of various uncommon neoplastic and nonneoplastic lesions of the ovary (papillary cystadenoma, luteoma, granulosa cell tumor, tubular adenoma, benign mixed tumor, epithelial hyperplasia, and senile atrophy) were associated with the administration of benzene to female mice. In mid and high dose female mice, the incidences of granulosa cell tumors (1/47; 1/44; 6/49; 7/48) and benign mixed tumors (0/47; 1/44; 12/49; 7/48) were greater than those in the vehicle controls. Increased incidences of hepatocellular adenomas were observed in low dose female mice (1/49; 8/44; 5/50; 4/49) and hepatocellular adenomas or carcinomas (combined) in low dose and mid dose female mice (4/49; 12/44; 13/50; 7/49). An audit of the experimental data was conducted for these 2-year carcinogenesis studies on benzene. No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year gavage studies, there was clear evidence of carcinogenicity of benzene for male F344/N rats, for female F344/N rats, for male B6C3F1 mice, and for female B6C3F1 mice. For male rats, benzene caused increased incidences of Zymbal gland carcinomas, squamous cell papillomas and squamous cell carcinomas of the oral cavity, and squamous cell papillomas and squamous cell carcinomas of the skin. For female rats, benzene caused increased incidences of Zymbal gland carcinomas and squamous cell papillomas and squamous cell carcinomas of the oral cavity. For male mice, benzene caused increased incidences of Zymbal gland squamous cell carcinomas, malignant lymphomas, alveolar/bronchiolar carcinomas and alveolar/bronchiolar adenomas or carcinomas (combined), harderian gland adenomas, and squamous cell carcinomas of the preputial gland. For female mice, benzene caused increased incidences of malignant lymphomas, ovarian granulosa cell tumors, ovarian benign mixed tumors, carcinomas and carcinosarcomas of the mammary gland, alveolar/bronchiolar adenomas, alveolar/bronchiolar carcinomas, and Zymbal gland squamous cell carcinomas. Dose-related lymphocytopenia was observed for male and female F344/N rats and male and female B6C3F1 mice. Synonyms: benzol, cyclohexatriene, pyrobenzol
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PMID:NTP Toxicology and Carcinogenesis Studies of Benzene (CAS No. 71-43-2) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1274 14

Increase of the Prostatic Specific Antigen (PSA) is a non-invasive, sensitive and specific markers for prostatic diseases, including prostatic cancer. However, age-related Benign Prostatic Hyperplasia (BPH), as well as prostatitis, may at the same time alter PSA values. The aim of this study was to evaluate the relationship between ageing and PSA, and whether age-specific upper normal limits of PSA should be considered for elderly patients. We evaluated 569 consecutive subjects aged 60 years or more (mean age 74.2 years) who were free from malignant prostatic disease, without clinical evidence of prostatic phlogosis and who were not receiving PSA levels affecting drugs. All patients underwent Digital Rectal Examination (DRE) and Trans-Rectal Ultrasonography (TRU), with determination of the three prostatic diameters, the Maximum Adenoma Diameter (MAD) and calculation of the prostatic volume (PV) by the ellipsoid formula. PSA was determined in all patients before DRE and TRU, and the PSA free ratio was determined in those with total PSA values >4 ng/ml. The PSA density was calculated according to the formula PSA/PV. One hundred and seventy-nine subjects (31.6%) were found to have PSA values >4 ng/ml: among them, 26 (14.5%) had values exceeding 10 ng/ml. Age was slightly correlated with PV (P<0.05), but not with PSA values. On the contrary, PSA values were strongly related with PV and MAD (P<0.01 both). Mean PSA-free ratio was 16.3+/-6.0% and most of patients had values in the so-called 'grey zone' of discrimination between benignity and malignity. Elevated PSA levels are common in older subjects without evidence of prostatic malignancy; PSA values are poorly affected by age itself and strongly correlated with increasing PV. These results suggest the possibility to consider as indicative of benignity PSA values between 4 and 10 ng/ml, when these values are associated with relevant increase of PV and with PSA-free ratio greater than 10%.
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PMID:Relationship between Prostatic Specific Antigen (PSA) and volume of the prostate in the Benign Prostatic Hyperplasia in the elderly. 1296 96

Most space occupying lesions of the sellar region are tumors (e.g., pituitary adenomas, craniopharyngiomas, but also meningiomas). In approximately 8% of patients with sellar mass lesions, non-neoplastic disorders (e.g., inflammations, cysts, hyperplasia) are causal. Cystic lesions of the pituitary region are classified as Rathke's cysts, colloid cysts, arachnoidal cysts and epidermoid cysts. These have to be differentiated from cystic craniopharyngeomas or cystic pituitary adenomas. Autochthonous inflammations (lymphocyctic hypophysitis, idiopathic granulomatous hypophysitis, xanthomatous and peritumorous hypophysitis) have to be distinguished from generalized diseases involving the pituitary (e.g., sarcoidosis, tuberculosis). Hyperplasia can result in a doubling of pituitary size. Lactotroph and corticotroph hyperplasia are the most common and may be of a diffuse and nodular type. The nodular form of pituitary hyperplasia may show transition into adenoma. Other hyperplasias may be found adjacent to adenomas or other tumours. Furthermore, vascular (aneurysms) and bony lesions (especially fibrous dysplasia) can appear as space occupying lesions of the sellar region.
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PMID:[Space occupying processes of the sellar region with emphasis on tumor-like lesions]. 1451 70

The effects of aerosol budesonide and dietary myo-inositol on progression of benzo[alpha]pyrene (B[alpha]P) induced carcinogenesis were studied in A/J mouse lung. First, we determined when to intervene in the carcinogenesis process by exposing several animals to B[alpha]P at 100 and 150 mg/kg of body wt. Groups of these animals were necropsied from 1 to 36 weeks post-carcinogen. The presence of different categories of lung tumors was noted over the 36 week time period. Hyperplasia first appeared approximately 6 weeks post-carcinogen followed by adenoma at 9 weeks, then by carcinoma at 26 weeks. From this temporal sequence we determined we could test for effects of preventive agents on progression to hyperplasia by intervening at 3 weeks, for effects on progression to adenoma by intervening at 6 weeks and for effects on progression to carcinoma by intervention at 12 weeks. Intervention at 3 weeks post-carcinogen with aerosolized budesonide delayed both hyperplasia and adenoma formation. Once hyperplasia appeared in budesonide treated animals, however, it increased at the same rate as in control animals, indicating a delay in progression. Progression from adenoma to carcinoma was reduced when budesonide was given 12 weeks post-carcinogen. Dietary myo-inositol failed to suppress progression from adenoma to carcinoma when started 12 weeks post-carcinogen. In summary, budesonide is a chemopreventive agent that has inhibitory effects on B[alpha]P induced carcinogenesis of the lung in A/J mice at all stages of progression from hyperplasia formation to cancer.
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PMID:Effect of chemopreventive agents on separate stages of progression of benzo[alpha]pyrene induced lung tumors in A/J mice. 1457 61

Benign Prostatic Hyperplasia is a common entity among the aging male population. Its prevalence is increasing with age and is around 80% in the over 80-years old. The androgen-estrogen ratio changes in favor of the estrogens, which leads to a growth of prostatic tissue, presenting histologically as hyperplasia. BPH can cause irritative or obstructive symptoms or both. Nowadays we speak of bladder storage or bladder voiding symptoms, summarised as LUTS (Lower Urinary Tract Symptoms). LUTS has a structural and a functional component, the structural being caused by the size of the adenoma itself the functional depending on the muscle tone of the bladder neck and the prostatic urethra. To investigate LUTS, we use validated symptom scores, sonography for residual urine and eventually a urodynamic evaluation. There are 3 grades of BPH. The indication for an interventional therapy is relative in BPH II, and absolute in BPH III. Prior to treatment, other diseases mimicking the same symptoms, have to be ruled out and adequatly treated. Electro-resection of the prostate (TUR-P) remains the standard therapy and the benchmark any new technology has to compete with. TUR-P has good short- and longterm results, but can be associated with a considerable perioperative morbidity, and the learning curve for the operator is long. The most promising of the newer techniques is the Holmium-Laser-Enucleation of the prostate (Laser-TUR-P), showing at least identical short- and median-term results, but a lower perioperative morbidity than TUR-P For several minimally-invasive techniques, indications are limited. TUMT TUNA, WIT and laser-coagulation all produce a coagulation necrosis of the prostatic tissue by thermic damage with secondary tissue shrinking. Urodynamic results however, are not comparable to TUR-P or Laser-TUR-P, and significantly more secondary interventions within 2 to 5 years are required. Minimal-invasive techniques present a favorable alternative for younger patients without complications of BPH, and for older patients with relevant comorbidities, and can usually be performed under local anaesthesia. The morbidity is low and further therapies remain possible later, if necessary.
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PMID:[Old and new interventional therapies in the treatment of symptomatic benign prostate hyperplasia (BPH)]. 1651 65

Most frequent causes of androgenic manifestation are Cushing's syndrome, PCO, benign and malignant androgen-secreting non adrenal tumors and iatrogenic hirsutism. Hyperplasia or neoplasms of ectopic adrenocortical gland are rare. We report a case of a 63-year old female with hirsutism and alopecia. Laboratory data highlighted increased levels of androgens. Diagnostic imaging revealed normal morphology of adrenocortical gland and ovaries. In view of the clinical picture and suspected diagnosis of extra-adrenal cause, she underwent bilateral salpingo-oophorectomy. Histologic examination showed an ectopic adrenal gland with adenoma in the ovarian and peri-ovarian tissue. At six months of follow up, the patients has no sign of hyperandrogenism. In case of hyperandrogenism in postmenopausal women and in the absence of the adrenocortical gland abnormality, ovarian origin should be considered in the differential diagnosis.
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PMID:Hyperandrogenism in a postmenopausal woman: a rare case of ectopic adrenal cortical gland. 2810 88

Ectopic adrenocortical tissue may be present in many anatomical localizations. Hyperplasia, adenoma or carcinoma can occasionally develop from the ectopic adrenal tissue. Therefore, it should be surgically excised when it is detected. Adrenocortical tumors are the most common type of adrenal neoplasms. Ectopic adrenocortical adenomas are rarely seen. A total of 34 cases of ectopic adrenocortical adenoma (14 of which are oncocytomas) have been reported at different localizations in English literature. Most of them are non-functional. Differential diagnosis is required with other benign or malign oncocytic neoplasms. We report a 56-year-old male patient, who presented with a retroperitoneal mass. Our case is the seventh case of ectopic retroperitoneal adrenal adenoma with oncocytic cells.
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PMID:Incidental retroperitoneal oncocytoma (Ectopic oncocytic adrenocortical adenoma): Case report and review of the literature. 3070 78


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