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PubMed2003

Nuclear morphometric changes and therapy monitoring in patients with endometrial hyperplasia: a study comparing effects of intrauterine levonorgestrel and systemic medroxyprogesterone.

OBJECTIVE: To show that local application of the levonorgestrel intrauterine device was a better therapy for endometrial hyperplasia (EH) compared to per-oral gestagen treatment based on subjective (WHO criteria) and objective (prognostic data-based morphometric and stereological method/D score, predicting the risk of cancer development for each single patient) evaluation. METHODS: Women between 30 and 70 years with EH and D score > 0 were treated with levonorgestrel intrauterine device (n = 26) and the results compared to a historic group of women treated with per-oral gestagen (n = 31). In both treatment groups only patients with low risk (D score > 1) and uncertain risk (D score = 0-1) of cancer development were included. Endometrial specimens were investigated prior to treatment and after 3 months of therapy. The endometrial samples from the two groups were examined by light microscopy and objective data-based morphometry to assess tissue characteristics and to evaluate nuclear size variation. RESULTS: After 3 months all patients treated with levonorgestrel intrauterine device showed regression of hyperplasia, whereas 14 of 31 patients in the per-oral group still had persisting disease. The objective morphometric analysis showed reduction in nuclear size for both treatment groups, including the D score > 1 as well as the D score 0-1 patients. However, the reduction was most obvious for the levonorgestrel intrauterine device-treated patients with initial D score of 0-1. CONCLUSION: The present study indicates that levonorgestrel intrauterine device is a superior alternative to per oral treatment of endometrial hyperplasia. By using objective morphometric treatment monitoring we have shown that the hyperplasia patients with the highest malignant potential (D score = 0-1) were those taking most benefit from local high-dose levonorgestrel therapy.

Adult↗
PubMed2005

Development of metastatic endometrial endometrioid adenocarcinoma while on progestin therapy for endometrial hyperplasia.

BACKGROUND: Conservative treatment with progestins is a reasonable treatment option for endometrial complex atypical hyperplasia and, in the experimental setting, for some women with grade 1 endometrial endometrioid adenocarcinoma. The risk of progression to a high-stage endometrial cancer is quite low, with only two previously reported cases in the English literature. CASE: A 40-year-old woman with endometrial complex atypical hyperplasia diagnosed by dilatation and curettage was managed conservatively with progestin therapy (initially, megesterol acetate; then, a combination oral contraceptive). More than 2 years after her original diagnosis, she developed endometrial endometrioid adenocarcinoma, FIGO grade 2, with lymph node metastasis. The tumor was microsatellite instability-high due to methylation of MLH1 and loss of MLH1 protein. CONCLUSION: Currently, there are no good criteria for predicting which patients with complex atypical hyperplasia/grade 1 endometrioid adenocarcinoma will optimally respond to progestin therapy. There is some evidence that endometrial complex hyperplasia demonstrating loss of MLH1 protein by immunohistochemistry is strongly related to subsequent or concurrent endometrial cancer, especially tumors of higher grade and stage. In a woman with a biopsy diagnosis of endometrial hyperplasia, evaluation of MLH1 protein status by immunohistochemistry may provide useful information when medical management is being considered.

Adult↗
PubMed2000

Relation between vascular morphologic changes during stent implantation and the magnitude of in-stent neointimal hyperplasia.

Intimal hyperplasia usually occurs after balloon overstretch injury or wire coil stimuli to coronary arteries. We examined whether the degree of vessel wall stretch during coronary stent placement could predict the amount of in-stent neointimal hyperplasia after a 6-month follow-up. Serial (preintervention, postballooning, poststent implantation, and a follow-up after 6 months) intravascular ultrasound (IVUS) was used to study 457 consecutive cross-sectional areas in 28 patients. IVUS imaging, using a motorized pullback system at 0.5 mm/s, allowed 1-mm axial increment measurements of the total vascular, stent, and lumen cross-sectional areas. The mean total vascular area changed from 10.89 +/- 2.50 mm2 before to 11.27 +/- 2.49 mm2 after ballooning, to 12.80 +/- 2.59 mm2 after stenting, and to 12.58 +/- 2.41 mm2 at follow-up (p < 0.0001). The mean lumen area changed from 3.36 +/- 1.95 mm2 before to 4.21 +/- 1.65 mm2 after ballooning, to 5.16 +/- 1.09 mm2 after stenting, and to 3.57 +/- 1.23 mm2 at follow-up (p < 0.0001). The mean stent area decreased from 5.25 +/- 1.17 mm2 after stenting to 5.09 +/- 0.90 mm2 at follow-up (p < 0.0001). Stepwise logistic regression analysis showed that delta total vascular area (after stent implantation - before intervention) was a strong predictor of the amount of intimal hyperplasia (r = 0.57, p < 0.0001). Vascular overstretch caused by the stenting procedure promotes intimal hyperplasia in proportion to the degree of sectional vascular stretch.

Aged↗
PubMed2003

Relative contributions of intimal hyperplasia and vascular remodeling in early cardiac transplant-mediated coronary artery disease.

The relative contribution of intimal hyperplasia and vascular remodeling in early transplant coronary artery disease (TxCAD) is unknown. This study was designed to determine the contributions of vascular remodeling and intimal hyperplasia in the initial year after transplantation by intravascular ultrasound (IVUS). Twenty-five patients underwent baseline (<6 weeks after transplant) and 1-year angiography and IVUS to evaluate total vessel, luminal, and intimal + medial areas in >or=3 segments of the coronary artery. Nine patients had donor atherosclerotic disease on baseline study (23% of segments), and at 1-year, 21 patients (84%) had intimal hyperplasia (70% of segments). Fourteen patients had positive remodeling in all arterial segments, whereas the remaining 11 had positive and negative remodeling in the same vessel. Mean plaque area and total vessel area increased significantly (p = 0.0001) in proximal, mid, and distal segments, whereas total vessel area was most pronounced in distal segments. Luminal area did not change over time. Of the 87 segments evaluated, 68 (78%) had an increase in total vessel area, 57 (66%) had intimal growth, and 54 (62%) had an increase in luminal area. Although changes in total vessel and luminal area were closely correlated, a decrease in luminal area was associated with positive and negative remodeling. In conclusion, luminal area is generally maintained during the initial transplant year despite significant intimal hyperplasia due to positive remodeling. Reduction in the luminal area results from either inadequate positive remodeling or negative remodeling without intimal growth and often occurs in the same artery.

Adult↗
PubMed1978

Focal nodular hyperplasia of the liver and oral contraceptives.

The increased incidence of liver tumors in women of childbearing age who have been using oral contraceptives for many years suggests an environmental causation. The causative agent may be the steroidal oral contraceptives. Two lesions are recognized: focal nodular hyperplasia and hepatic adenoma. This paper concentrates on focal nodular hyperplasia, with two cases added to the four previously described cases. It is postulated that the estrogen component causes vascular lesions characterized by myointimal hyperplasia and thrombosis, leading to infarct, necrosis, and subsequent nodular hepatic regeneration. The clinical feature highlighted is the long history of gastrointestinal disturbance associated with negative gastrointestinal investigation with the possible exception of cholelithiasis. It is suggested that gray-scale ultrasonography is an effective screening method that also aids in a definitive diagnosis. As these tumors are often incidental findings it is emphasized that the liver should always be inspected at laparoscopy. Ultimately, diagnosis by biopsy or excision is essential as it may well be possible to treat cases of focal nodular hyperplasia of the liver conservatively, once oral contraceptives have been discontinued.

Adult↗
PubMed2003

Absence of caveolin-1 sensitizes mouse skin to carcinogen-induced epidermal hyperplasia and tumor formation.

Caveolin-1 is the principal protein component of caveolae membrane domains, which are located at the cell surface in most cell types. Evidence has accumulated suggesting that caveolin-1 may function as a suppressor of cell transformation in cultured cells. The human CAV-1 gene is located at a putative tumor suppressor locus (7q31.1/D7S522) and a known fragile site (FRA7G) that is deleted in a variety of epithelial-derived tumors. Mechanistically, caveolin-1 is known to function as a negative regulator of the Ras-p42/44 MAP kinase cascade and as a transcriptional repressor of cyclin D1, possibly explaining its transformation suppressor activity in cultured cells. However, it remains unknown whether caveolin-1 functions as a tumor suppressor gene in vivo. Here, we examine the tumor suppressor function of caveolin-1 using Cav-1 (-/-) null mice as a model system. Cav-1 null mice and their wild-type counterparts were subjected to carcinogen-induced skin tumorigenesis, using 7,12-dimethylbenzanthracene (DMBA). Mice were monitored weekly for the development of tumors. We demonstrate that Cav-1 null mice are dramatically more susceptible to carcinogen-induced tumorigenesis, as they develop skin tumors at an increased rate. After 16 weeks of DMBA-treatment, Cav-1 null mice showed a 10-fold increase in tumor incidence, a 15-fold increase in tumor number per mouse (multiplicity), and a 35-fold increase in tumor area per mouse, as compared with wild-type littermate mice. Moreover, before the development of tumors, DMBA-treatment induced severe epidermal hyperplasia in Cav-1 null mice. Both the basal cell layer and the suprabasal cell layers were expanded in treated Cav-1 null mice, as evidenced by immunostaining with cell-type specific differentiation markers (keratin-10 and keratin-14). In addition, cyclin D1 and phospho-ERK1/2 levels were up-regulated during epidermal hyperplasia, suggesting a possible mechanism for the increased susceptibility of Cav-1 null mice to tumorigenesis. However, the skin of untreated Cav-1 null mice appeared normal, without any evidence of epidermal hyperplasia, despite the fact that Cav-1 null keratinocytes failed to express caveolin-1 and showed a complete ablation of caveolae formation. Thus, Cav-1 null mice require an appropriate oncogenic stimulus, such as DMBA treatment, to reveal their increased susceptibility toward epidermal hyperplasia and skin tumor formation. Our results provide the first genetic evidence that caveolin-1 indeed functions as a tumor suppressor gene in vivo.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1999

Frequent genetic alterations in simple urothelial hyperplasias of the bladder in patients with papillary urothelial carcinoma.

In order to understand the origin of bladder cancer, very early urothelial lesions must be investigated in addition to more advanced tumors. Tissue from 31 biopsies of 12 patients with urothelial hyperplasias and simultaneous or consecutive superficial papillary tumors were used to microdissect urothelium from 15- microm sections of biopsies. The biopsies were obtained with the recently developed highly sensitive diagnostic method of 5-aminolevulinic acid-induced fluorescence endoscopy (AFE). Besides flat and papillary urothelial neoplasms, the method of photodynamic diagnostics also detects simple urothelial hyperplasias as fluorescent positive lesions. In addition, 12 fluorescence-positive biopsies showing histologically normal urothelium were investigated. Fluorescence in situ hybridization was done using a dual color staining technique of biotinylated centromeric probes of chromosomes 9 and 17 and digoxigenin-labeled gene-specific P1 probes for chromosomes 9q22 (FACC), 9p21(p16/CDKI2), and 17p13(p53). Ten of 14 hyperplasias (70%) showed deletions of chromosome 9. In 7 out of 8 patients with genetic alterations in the hyperplasias the genetic change was also present in the papillary tumor. Six out of 12 samples of microdissected normal urothelium also showed genetic alterations on chromosome 9. Microdissection of urothelial lesions, obtained during AFE, has led to the first unequivocal documentation of genetic changes in urothelial lesions diagnosed as normal in histopathology. Thus, this technical approach is important to provide insight into the earliest molecular alterations in bladder carcinogenesis.

Adult↗
PubMed2001

A novel organ culture method to study intimal hyperplasia at the site of a coronary artery bypass anastomosis.

BACKGROUND: Intimal hyperplasia or restenosis at the site of a coronary artery bypass anastomosis contributes to early graft failure, and growth factor release in response to construction of the anastomotic site strongly influences this process. Due to the difficulties in studying restenosis after coronary artery bypass graft surgery, we have tested whether an organ culture model we have developed can simulate the early events associated with intimal hyperplasia. METHODS: End-to-side anastomosis of porcine radial artery to porcine coronary artery were constructed. The vessels were trimmed and incubated under standard tissue culture conditions for 14 days. Appropriate controls were treated similarly. The vessels were frozen, cryosectioned, and immunostained for the expression of the proliferation marker proliferating cell nuclear antigen (PCNA). A proliferative index (PCNA positive nuclei/total nuclei) was calculated for comparative purposes. RESULTS: Limited PCNA staining was observed in noncultured vessel segments (0.046+/-0.045). A slight increase in this index was observed in vessels that had been placed into culture without manipulation (0.230+/-0.141) and in vessels subjected to an arteriotomy (0.462+/-0.249). However, the most significant increase was obtained after construction of an anastomosis (4.98+/-6.66). No change in total cell number was evident over the course of the experiment or in relation to the treatment. CONCLUSIONS: Culture conditions and incision slightly stimulate cell proliferation in porcine coronary artery segments when compared with basal conditions of a native artery. In contrast, construction of an anastomosis increases proliferation 108-fold. Therefore, surgical manipulation of arterial conduits during construction of an anastomotic site is the primary trigger for intimal hyperplasia, independent of dissection and incision of the vessel. Furthermore, these data indicate the organ culture model we have developed will be useful for examining the cellular and molecular mechanisms that mediate intimal hyperplasia at the site of a coronary artery bypass graft anastomosis.

Anastomosis, Surgical↗
PubMed1986

Comparison of cod-liver oil and aspirin-dipyridamole for the prevention of intimal hyperplasia in autologous vein grafts.

The combination of aspirin and dipyridamole is currently used to prevent intimal hyperplasia and to improve long-term vein graft patency following myocardial revascularization. Preliminary studies indicate that cod-liver oil, rich in eicosapentaenoic acid, an unsaturated fatty acid, may also be effective in the prevention of intimal hyperplasia. Twenty-four mongrel dogs were used to compare the effectiveness of aspirin-dipyridamole and cod-liver oil on vein graft intimal hyperplasia following arterial bypass. Forty-eight segments of undistended autologous external jugular vein were interposed between bilaterally divided femoral arteries. All animals received a 2% cholesterol diet for 1 week before and 6 weeks after operation. Eight controls received the diet alone. Eight other animals received dipyridamole (2.5 mg per kilogram of body weight) two days before operation and dipyridamole (2.5 mg/kg) and aspirin (30 mg/kg) daily for 6 weeks after operation. Another 8 animals received cod-liver oil containing 1.8 gm of eicosapentaenoic acid daily 1 week before and for 6 weeks following operation. Serum cholesterol increased similarly in all groups; it rose from 4.5 +/- 0.2 mm/L to 8.3 +/- 0.8 mm/L in the controls, to 7.2 +/- 0.5 mm/L in the aspirin-dipyridamole group, and to 7.1 +/- 0.5 mm/L in the cod-liver oil group (p less than 0.01). Prothrombin time, partial thromoboplastin time, total platelet counts, and bleeding times were unchanged. Intimal hyperplasia was measured at 6 weeks with a Zeiss computerized microscope; 376 +/- 25 measurements were made from each graft. The intima increased from 4.5 +/- 0.2 to 83 +/- 10 micron in the control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

A missense mutant myostatin causes hyperplasia without hypertrophy in the mouse muscle.

Myostatin, which is a member of the TGF-beta superfamily, is a negative regulator of skeletal muscle formation. Double-muscled Piedmontese cattle have a C313Y mutation in myostatin and show increased skeletal muscle mass which resulted from an increase of myofiber number (hyperplasia) without that of myofiber size (hypertrophy). To examine whether this mutation in myostatin gene affects muscle development in a dominant negative manner, we generated transgenic mice overexpressing the mutated gene. The transgenic mice exhibited dramatic increases in the skeletal muscle mass resulting from hyperplasia without hypertrophy. In contrast, it has been reported that a myostatin mutated at its cleavage site produces hypertrophy without hyperplasia in the muscle. Thus, these results suggest that (1) the myostatin containing the missense mutation exhibits a dominant negative activity and that (2) there are two types in the dominant negative form of myostatin, causing either hypertrophy or hyperplasia.

Amino Acid Substitution↗
PubMed1992

Transurethral hyperthermia for benign prostatic hyperplasia patients with retention.

From 1989 to 1990, 32 poor surgical risk patients with urinary retention were treated with transurethral microwave hyperthermia at the department of urology, University of Leuven in Belgium. Mean patient age was 73 years (range 58 to 90 years) and mean duration of retention was 4 weeks (range 3 to 12 weeks). Followup ranged from 13 to 82 weeks, with a mean of 31 weeks. Bilobar or trilobar hyperplasia was diagnosed in 25 patients (78%), while 7 (22%) had median lobe or median bar hypertrophy. The mean prostatic volume was 52 cc (range 25 to 150 cc). Transurethral microwave hyperthermia was given with a helical antenna at 915 MHz. once or twice per week. The mean number of transurethral microwave hyperthermia sessions was 8.9 (range 5 to 10). Each session consisted of a 60-minute treatment at a mean maximum temperature of 45.4C (range 43.7 to 47.2C), average temperature 43.9C (range 42.7 to 45.5C) and minimum temperature 42.0C (range 40.2 to 43.0C). The temperature was continuously monitored, including thermal mapping in all patients. Of the 25 patients who presented with bilobar or trilobar hyperplasia 18 (72%) were catheter-free for the duration of followup. Of the 7 median lobe or median bar patients 1 (14%) showed sufficient improvement to warrant catheter removal. This patient, however, had recurrent retention 4 months after transurethral microwave hyperthermia. In patients with bilobar and trilobar hyperplasia a strong correlation was observed among maximum temperature (p = 0.0006), average temperature (p = 0.0033) and treatment response. As expected, no such correlation existed between minimum temperature and response to treatment (p = 0.56). Our study has again demonstrated therapeutic activity in patients with benign prostatic hyperplasia treated with transurethral microwave hyperthermia. A new finding was a strong correlation between temperature and response.

Aged↗
PubMed1991

Characterization of prostate cancer, benign prostatic hyperplasia and normal prostates using transrectal 31phosphorus magnetic resonance spectroscopy: a preliminary report.

We assessed the ability of 31phosphorus (31P) transrectal magnetic resonance spectroscopy to characterize normal human prostates as well as prostates with benign and malignant neoplasms. With a transrectal probe that we devised for surface coil spectroscopy we studied 15 individuals with normal (5), benign hyperplastic (4) and malignant (6) prostates. Digital rectal examination, transrectal ultrasonography and magnetic resonance imaging were used to aid in accurate positioning of the transrectal probe against the region of interest within the prostate. The major findings of the in vivo studies were that normal prostates had phosphocreatine-to-adenosine triphosphate (ATP) ratios of 1.2 +/- 0.2, phosphomonoester-to-beta-ATP ratios of 1.1 +/- 0.1 and phosphomonoester-to-phosphocreatine ratios of 0.9 +/- 0.1. Malignant prostates had phosphocreatine-to-beta-ATP ratios that were lower (0.7 +/- 0.1) than those of normal prostates (p less than 0.02) or prostates with benign hyperplasia (1.1 +/- 0.2, p less than 0.01). Malignant prostates had phosphomonoester-to-beta-ATP ratios (1.8 +/- 0.2) that were higher than that of normal prostates (p less than 0.02). Using the phosphomonoester-to-phosphocreatine ratio, it was possible to differentiate metabolically malignant (2.7 +/- 0.3) from normal prostates (p less than 0.001), with no overlap of individual ratios. The mean phosphomonoester-to-phosphocreatine ratio (1.5 +/- 0.5) of prostates with benign hyperplasia was midway between the normal and malignant ratios, and there was overlap between individual phosphomonoester-to-phosphocreatine ratios of benign prostatic hyperplasia glands with that of normal and malignant glands. To verify the in vivo results, we performed high resolution magnetic resonance spectroscopy on perchloric acid extracts of benign prostatic hyperplasia tissue obtained at operation and on a human prostatic cancer cell line DU145. The extract results confirmed the differences in metabolite ratios observed in vivo. We conclude that transrectal 31P magnetic resonance spectroscopy can characterize metabolic differences between the normal and malignant prostate.

Adult↗
PubMed1989

Prenatal fetal adrenal suppression following in utero diagnosis of congenital adrenal hyperplasia.

Congenital adrenal hyperplasia due to 21-hydroxylase deficiency can result in marked virilization of the external genitalia of affected female subjects. Theoretically, suppression of the fetal pituitary-adrenal axis with glucocorticoid during gestational weeks 9 to 17 should prevent the development of ambiguous genitalia in the female fetus. Prenatal diagnosis of congenital adrenal hyperplasia can be made on elevated amniotic fluid 17-hydroxyprogesterone and adrenal androgen concentrations, and HLA typing of cultured amniotic fluid cells. However, these tests cannot be completed before 16 to 17 weeks of gestation, and maternal therapy would have to be instituted before the exact genetic status of the fetus is known. Chorionic villus sampling during the first trimester provides an alternative to second trimester diagnosis in patients who are at risk for bearing offspring with congenital adrenal hyperplasia. We report the use of dexamethasone suppression at 8 weeks of gestation in a 34-year-old woman whose son had congenital adrenal hyperplasia due to severe salt-losing 21-hydroxylase deficiency and whose biopsy revealed a 46XX chromosomal pattern. Cultured cells from the biopsy confirmed the fetus to be of identical HLA haplotype to the previous affected sibling. At 41 weeks the patient delivered a female neonate with minimal prominence of the clitoris, mildly rugated labia, a single perineal opening and minimal posterior labial fusion. Postnatal tapering of maternal steroids was performed with no long-term sequelae.

Adrenal Hyperplasia, Congenital↗
PubMed1990

Local microwave hyperthermia of benign prostatic hyperplasia.

Recently, hyperthermia has been used for treatment of benign prostatic hyperplasia. The preliminary results reported were promising. However, apart from patients with total urinary retention, objective voiding parameters have not been reported in detail for patients with prostatism. In a phase II study we treated 30 patients with benign prostatic hyperplasia by local microwave hyperthermia (915 MHz.). The prostate was heated transrectally to 42 to 43C, with the treatment consisting of 8 sessions of 60 minutes each given twice a week. To assess the results of treatment several parameters were determined before and 4 weeks after hyperthermia therapy, including transrectal ultrasound of the prostate with volumetry, urinary flow rate and residual volume. Of the patients 28 could be evaluated and only 2 showed a relevant improvement. Neither the voiding parameters nor the size of the prostate could be changed significantly by hyperthermia. The success rate of 7.1% is even lower than the spontaneous temporary regression rate of benign prostatic hyperplasia. Thus, we believe that hyperthermia cannot be regarded as an effective treatment for benign prostatic hyperplasia comparable to transurethral resection.

Aged↗
PubMed1979

Light microscopic stereological analysis of the normal human prostate and of benign prostatic hyperplasia.

Normal prostate glands from 6 men less than 30 years old and enucleated tissue of benign prostatic hyperplasia were analyzed by stereological methods. Studies on the relative volumetric amount of fibromuscular (stromal) and glandular areas of the gland reveal no statistically significant difference between the inner and outer parts of the normal prostate and between the inner part of the normal prostate and benign prostatic hyperplasia. However, in benign prostatic hyperplasia there is a significant increase in the volumetric amount of the fibromuscular tissue and a decrease in the glandular area compared to the outer part of the normal prostate and the whole normal prostate (sum of the inner and the outer parts). These stereological data are discussed with respect to the pathogenesis of benign prostatic hyperplasia.

Adult↗
PubMed1975

Prostatic fluid lactic dehydrogenase isoenzyme patterns of prostatic cancer and hyperplasia.

LDH isoenzyme patterns were determined in prostatic fluid from 286 patients with a prostate gland judged to be normal, the site of benign hyperplasia on clinical evidence or the site of benign hyperplasia or carcinoma on the basis of histologic evidence. Fluid from 12 of 15 patients (80 per cent) with carcinoma representing all stages and grades of disease showed an LDH-V/I ratio of more than 3. This ratio was exceeded in only 6 of 57 (11.8 per cent) and 14 of 97 (14.4 per cent) patients in whom the diagnosis of benign prostatic hyperplasia without evidence of infection was established histologically or clinically, respectively. An LDH-V/I ratio exceeding 3 was seen commonly in patients with a diagnosis of benign prostatic hyperplasia with a recent history suggesting infection and more than 10 WBCs per high power field on microscopic examination of the prostatic fluid. These observations suggest that an LDH-V/I ratio exceeding 3 in the prostatic fluid in the absence of a history of infection and more than 10 WBCs per high power field on microscopic examination should be regarded as an indication of a high risk of the presence or development of a malignancy of the prostate. The results obtained also support the concept that, in the presence of malignancy, expressed prostatic fluid provides an adequate sample of cells with altered metabolism.

Adenocarcinoma↗
PubMed2000

Norethindrone acetate and estradiol-induced endometrial hyperplasia.

OBJECTIVE: To identify the lowest effective continuous dose of norethindrone acetate that significantly reduces 12-month incidence of endometrial hyperplasia associated with unopposed 17beta-estradiol (E2), 1 mg. METHODS: In a double-masked, randomized, multicenter study, 1176 healthy postmenopausal women 45 years of age or older without evidence of endometrial abnormalities were given 12 months of treatment with unopposed E2, 1 mg, or continuous-combined regimens of E2, 1 mg, and norethindrone acetate, 0.1 mg, 0.25 mg, or 0.5 mg. Endometrial histology was evaluated at the end of the treatment period. RESULTS: Continuous-combined E2-norethindrone acetate regimens significantly reduced 12-month incidence of endometrial hyperplasia compared with unopposed E2 1 mg (P <.001). Endometrial hyperplasia occurred in 14.6% of women treated with unopposed E2 1 mg, whereas in all continuous-combined groups, the rate decreased to less than 1%. Among patients who received E2-norethindrone acetate 0.1 mg, incidence was 0.8%; among those who received 0.25 mg and 0.5 mg, it was 0.4%. CONCLUSION: Continuous norethindrone acetate at doses as low as 0.1 mg combined with E2 1 mg effectively negated risk for endometrial hyperplasia associated with unopposed E2 1 mg, at least for the first year of therapy.

Climacteric↗
PubMed1980

Adrenal medullary hyperplasia: a clinicopathologic study of four cases.

This study presents the clinicopathologic findings in four new cases of adrenal medullary hyperplasia. The patients presented with episodic hypertension frequently associated with palpitations, headache, and diaphoresis. All four had elevated urinary catecholamine levels during attacks, and were thought clinically to have a pheochromocytoma. In each case laparotomy revealed a diffusely enlarged adrenal gland without a discrete tumor. Histologic examination of the adrenals demonstrated a diffuse and nodular expansion of the medulla confirmed by morphometric study. Of the four patients, three underwent unilateral and one bilateral adrenalectomy. Two patients who underwent unilateral adrenalectomy have been free of symptoms for three years. Thus, it would appear that adrenal medullary hyperplasia may occur unilaterally or asynchronously in the two glands. The bilaterally adrenalectomized patient has had persistent attacks, suggesting that the stimulus to adrenal medullary hyperplasia may possible affect other chromaffin tissues. On the basis of our cases and a review of the literature, we propose the following criteria for the diagnosis of adrenal medullary hyperplasia: a clinical history of episodic attacks suggesting pheochromocytoma (generally with associated increased urinary catecholamine levels), an adrenal gland showing diffuse expansion of the medulla into the alae or tail of the gland with or without nodule formation, a medulla composed of enlarged cells with or without pleomorphism, and, most important, an increased medulla/cortex ratio, together with an increased calculated medullary weight as determined by morphometric analysis.

Adrenal Cortex↗