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PubMed2001

Prognostic value of morphometry in patients with normal breast tissue or usual ductal hyperplasia of the breast.

Women with usual ductal hyperplasia have a relative risk of 1.6-1.9 of subsequent breast cancer development. This slightly increased risk is generally not considered sufficiently high to justify (chemo)preventive therapy. It is therefore important to identify high-risk ductal hyperplastic lesions that would benefit from such a treatment. Nuclear morphometric features have been shown in previous work to be useful for objectively describing morphologic features associated with high risk in (pre)invasive breast lesions. The aim of this study was to evaluate whether such morphometric features can also predict subsequent invasive cancer development in patients with the common pattern of usual ductal hyperplasia or a normal breast biopsy. The present case-control study included 423 women with normal breast biopsies (n = 89) or biopsies containing usual ductal hyperplasia (n = 334). Of these 423 women, 132 developed invasive breast cancer during follow-up (mean 16.7 +/- 7.0 years). On the original hematoxylin and eosin-stained sections, nuclear morphometry was performed with a digitizing video overlay system, and mitotic and apoptotic indices were assessed. Patients with mean nuclear feature values for area, perimeter, diameter or longest axis above the 75th percentile had 1.6-1.7 times the breast cancer risk of women with mean nuclear feature values below this value. Pairwise combinations of these features yielded slightly higher cancer risks for the fourth quartile patients, with the highest risk (1.9) for patients with SD of nuclear area and perimeter values above the 75th percentile. The number of apoptotic or mitotic cells had no prognostic value for patients with apparently normal tissue or usual ductal hyperplasia. Our results give a first indication that normal breast tissue or usual ductal hyperplasia harbor nuclear morphologic changes that, when assessed by morphometry, may be used to predict breast cancer development. It is worthwhile studying this further in independent groups of patients with long-term follow-up.

Adolescent↗
PubMed1991

Effect of low molecular weight heparin on intimal hyperplasia.

Intimal hyperplasia is a significant cause of vascular graft failure. To investigate the potential uses of low molecular weight heparins (LMWHs) as prophylactic agents against graft thrombosis in humans, the anti-proliferative effects of a regimen of subcutaneous LMWH have been studied in an experimental model. Aortic intimal hyperplasia was created in 30 New Zealand White rabbits by endothelial denudation using an embolectomy balloon catheter technique. Three groups of ten animals were randomized to act as controls or to be treated with subcutaneous LMWH once or twice daily for 4 weeks. At 4 weeks all animals were killed and the aortas were harvested for analysis. The degree of intimal hyperplasia was measured using a computerized image analysis system and was expressed as an intimal:medial area ratio and also as percentage luminal reduction. A 60 per cent reduction in the degree of intimal hyperplasia was seen following treatment with LMWH. Heparin-treated animals had considerably less luminal reduction (daily LMWH 8 per cent and twice-daily LMWH 10 per cent) compared with untreated controls (26 per cent) (P less than 0.001). There was a similar difference seen in the intima:media area ratios, daily LMWH 0.38, and twice-daily LMWH 0.44, versus controls, 1.11 (P less than 0.001). In an experimental model, subcutaneous LMWH therapy effectively inhibits intimal hyperplasia.

Animals↗
PubMed1992

Long-term reduction of intimal hyperplasia by the selective alpha-1 adrenergic antagonist doxazosin.

Studies have shown that alpha 1-adrenergic blockade reduces intimal hyperplasia in the rabbit aorta. In this study a selective alpha 1-adrenergic antagonist, doxazosin, has been used to examine whether this effect is persistent and dose dependent. Forty-eight New Zealand White rabbits underwent endothelial denudation of the abdominal aorta using a Fogarty balloon catheter. Test rabbits were given low-dose (2 mg) or high-dose (8 mg) doxazosin daily and all animals killed at either 1 or 12 weeks after the procedure. The aortas were harvested after fixation in situ with 4 per cent glutaraldehyde and neointimal hyperplasia was measured, using an x-y digitizer, as the percentage reduction in luminal cross-sectional area. At 1 week after surgery, rabbits receiving the low dose had a median area reduction of 7.7 per cent and those receiving the high dose a reduction of 8.2 per cent; both had significantly less intimal hyperplasia than control rabbits, which had a median area reduction of 14.8 per cent (P < 0.01). However, at 12 weeks, when compared with the 32.6 per cent reduction in the control group, only those rabbits receiving high-dose doxazosin had significantly less intimal hyperplasia, with a reduction of 5.5 per cent (P < 0.001). It is concluded that selective alpha 1-adrenergic blockade significantly reduces neointimal hyperplasia, that this effect is dose dependent, and that it persists for at least 3 months.

Animals↗
PubMed2006

Impact of age, benign prostatic hyperplasia, and cancer on prostate-specific antigen level.

BACKGROUND: The distribution of prostate-specific antigen (PSA) values for men with or without prostate carcinoma are confounded because of verification bias. Correcting for verification bias, the means and variances of PSA values were estimated in specific clinical scenarios. METHODS: Existing receiver operating characteristic (ROC) curves, adjusted for the presence of verification bias in a screening population, were used to estimate the mean and variance of PSA values for men with or without prostate carcinoma, stratified by age and the presence or absence of benign prostatic hyperplasia. Men with a suspicious digital rectal exam (nodular) were excluded from analysis. RESULTS: Among men with cancer and the absence of benign prostatic hyperplasia, mean PSA values were 2.05 ng/mL and 2.66 ng/mL for younger (<60 yr) and older (> or =60 yrs) men, respectively. These estimates were 2.56 ng/mL and 3.90 ng/mL in the presence of benign prostatic hyperplasia for younger and older men, respectively. For men without prostate carcinoma, these values were 0.78 ng/mL and 1.23 ng/mL for younger and older men, respectively, among those without benign prostatic hyperplasia, and 0.97 ng/mL and 1.75 ng/mL for younger and older men, respectively, among those with benign prostatic hyperplasia. CONCLUSIONS: Accurate estimates of the mean and variance of PSA values for men with or without cancer may provide PSA thresholds for biopsy that are specific for age and prostate size as assessed by digital rectal exam. Therefore, the current threshold of 4.0 ng/mL should not be applied indiscriminately.

Age Factors↗
PubMed1983

Hyperplasia in the spinal sensory system of the frog. I. Plasticity in the most caudal dorsal root ganglion.

Increases in the amount of periphery available for innervation have been achieved by the unilateral removal of hindlimb dorsal root ganglion (DRGs) in Rana pipiens, a procedure which generally results in a compensatory cell number increase (hyperplasia) in the DRGs which remain. We have found that the hyperplastic response is extremely variable, and we have investigated various factors which might control its production. Our findings indicate, however, that the pattern of DRGs removed, the animal's age at the time of removal, and the survival period are not strictly related to the production of hyperplasia in hindlimb DRGs. Special emphasis has been placed on DRG 10, the caudalmost DRG which normally innervates the cloaca and sends a small projection to the hindlimb. This DRG displayed dramatic cell number increases of up to 564%. In addition, several unique features of the hyperplastic response have been observed in DRG 10. This DRG showed increases in cell number on both the operated and the unoperated sides. It showed hyperplasias in animals subjected to ganglionectomy past metamorphosis as well as during larval development. Finally the production of DRG 10 hyperplasias exclusively occurred in male pre- and postmetamorphic animals. To account for these distinctive features of DRG 10 hyperplasia, baseline studies of the normal course of proliferation and cell death in DRG 10 were undertaken. They reveal no fundamental developmental differences between DRG 10 and other hindlimb DRGs. Other mechanisms responsible for these unusual features of developmental plasticity in DRG 10 are discussed.

Animals↗
PubMed1997

Role of ischemia in causing apoptosis, atrophy, and nodular hyperplasia in human liver.

Ischemia is known to be a cause of hepatocellular apoptosis and atrophy in experimental animals, but the effect of vascular obstruction on such lesions in the normal or cirrhotic human liver has not been studied. The purpose of this study was to investigate the role of ischemia in the development of apoptosis, atrophy, and nodular hyperplasia in cirrhotic and noncirrhotic human livers. Apoptosis, focal atrophy, and nodular hyperplasia were semiquantitated in 203 liver specimens obtained at transplantation, segmental resection, or autopsy. These parameters were correlated with etiology, stage, activity, and acute and healed portal vein thrombosis (PVT). Large numbers of apoptotic cells were found in livers with acute PVT (17.2/medium-power field [MPF]) and in infarcts of Zahn caused by obstruction of portal veins (PVs) by tumor (16.4/MPF). Smaller numbers of apoptotic cells were found in cirrhosis of various etiologies (3.8-10.0/MPF) and rarely in normal livers (0.16/MPF). Evidence of healed PVT was found in 47% of cirrhotic livers and was associated with nodular hyperplasia (58% vs. 32%, P < .01) and focal atrophy (79% vs. 49%, P < .002). Apoptotic cells were found equally in those with and without healed PVT (40% vs. 38%, not significant). These observations suggest that apoptosis is a transient response to acute ischemia and that atrophy and nodular hyperplasia are chronic responses to ischemia. Vascular obstruction may be an important cause of the apoptosis and atrophy, which are found in nodular regenerative hyperplasia (NRH), infarct of Zahn, chronic hepatitis, and cirrhosis.

Apoptosis↗
PubMed1995

Nuclear and cytoplasmic bcl-2 expression in endometrial hyperplasia and adenocarcinoma.

The bcl-2 proto-oncogene, which inhibits programmed cell death (apoptosis), has recently been found to be cyclically expressed in human endometrium. In order to investigate its role in endometrial hyperplasia and neoplasia, bcl-2 expression was studied in 25 cases of endometrial carcinoma and 20 cases of endometrial hyperplasia (eight simple, two complex, and ten atypical hyperplasias). Uniform intense cytoplasmic bcl-2 expression was found in all cases of non-atypical hyperplasia, and less strong positivity in eight out of ten cases of atypical hyperplasia. In well-differentiated carcinomas, nine out of ten showed weak to moderate bcl-2 expression, whereas six out of seven poorly differentiated carcinomas were bcl-2-negative. Moderately differentiated tumours were an intermediate group, with six out of eight being positive. Widespread localization of bcl-2 protein to the chromosomes of dividing cells was also demonstrated, regardless of cytoplasmic bcl-2 expression, with rare staining of interphase nuclei. Our findings suggest a role for bcl-2 in the natural history of endometrial neoplasia and studies are needed to determine its usefulness as a prognostic marker. The finding of bcl-2 localization to chromosomes has important implications for its mode and site of action.

Adenocarcinoma↗
PubMed1996

bcl-2 expression in endometrial hyperplasia and carcinoma.

The bcl-2 gene codes for a protein which functions to inhibit apoptotic cell death. bcl-2 overexpression was originally described in follicular lymphoma, but more recently bcl-2 expression has been observed in a variety of other human neoplasms. In this study we used immunohistochemistry to examine bcl-2 protein expression in endometrial hyperplasia and carcinoma. bcl-2 protein was observed in 4/4 cases of complex hyperplasia, 1/4 cases of complex atypical hyperplasia, and 10/29 cases of carcinoma. The staining observed in the cases of complex atypical hyperplasia and carcinoma was focal and less intense than the reactivity of normal proliferative endometrium. We conclude that bcl-2 protein is seldom overexpressed in complex atypical hyperplasia or carcinoma of the endometrium. Rather, in many cases of endometrial carcinoma bcl-2 expression appears to be decreased.

Adenocarcinoma, Clear Cell↗
PubMed1997

Treatment of endometrial hyperplasias with gonadotropin-releasing hormone agonists: pathological, clinical, morphometric, and DNA-cytometric data.

On the basis of the recently reported observation that gonadotropin-releasing hormone agonists (GnRH-a) can affect endometrial cell proliferation, both indirectly, through the hormonal axis, and directly, by acting on the GnRH-a receptors, we investigated how far GnRH-a can be used as a new treatment mode for endometrial hyperplasias. Forty-two women, aged 28-60 years, with histologically confirmed simple (n = 30) or complex (n = 12, 2 with atypias) hyperplasia of the endometrium were involved in the study. According to the protocol they were treated for 6 months with GnRH-a (leuprolide acetate or triptorelin), and each patient underwent uterine curettage in the third and the sixth month of treatment, and 6 and at least 12 months after cessation of the treatment, for histological examination and morphometric and DNA-cytometric evaluation of the endometrium (mean pathological follow-up, 19.2 months; mean clinical follow-up, 30.7 months). During treatment, most of the women first revealed endometrial atrophy, and, after cessation of the treatment, again an atrophic or mainly functional endometrium; in 7 women, all with initial diagnosis of simple hyperplasia, the endometrial hyperplasia reappeared, which led in all 7 cases to hysterectomy. The mean values of almost all morphometric and DNA-cytometric parameters during and after treatment showed statistically significant changes in relation to pretreatment values, indicating a decrease in the proliferative activity of the endometrial cells; the GnRH-a antiproliferative effect was still active for a long time after cessation of the therapy. Our results, based for the first time not only on histological but also on serial nuclear morphometric and DNA-cytometric examinations of the endometrial cells and on the longest follow-up time, support the view that in cases of endometrial hyperplasia, especially of complex type, the use of GnRH agonists, which decrease the proliferative tendency of endometrial cells, could represent an alternative conservative therapeutic approach, which, however, requires close monitoring of the endometrium.

Adult↗
PubMed2000

Apoptosis may be an early event of progestin therapy for endometrial hyperplasia.

OBJECTIVE: The aim of this study was to investigate the role of apoptosis during progestin therapy for the treatment of endometrial hyperplasia. METHODS: Pre- and posttreatment paraffin-embedded endometrial tissue samples from 19 women with endometrial hyperplasia were examined for changes in glandular cellularity and apoptotic activity related to the administration of progestins. Twelve patients were successfully treated with progestin therapy and 7 patients failed treatment. Glandular cellularity was assessed based on calculating the average number of cells per gland obtained on histologic examination of hematoxylin and eosin stained tissue sections. Apoptotic activity was assessed on the same tissue sections by counting the average number of apoptotic cells per 10 high power fields (hpf) using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) assay. The effects of progesterone on apoptotic activity in a low-grade endometrial adenocarcinoma cell line (Ishikawa cells) was also examined using an ELISA cell death detection kit. RESULTS: Glandular cellularity significantly decreased with progestin therapy in both treatment outcome groups. The reduction in cells per gland was significantly greater in the group of successfully treated cases compared to the treatment failures (P = 0.005). However, within the successfully treated group, in situ detection of apoptotic cells using the TUNEL assay showed no statistical difference between pre- and posttreatment endometrial samples. Interestingly, a significant decrease in apoptosis was found in posttreatment samples of the group with persistent hyperplasia. The average number of apoptotic cells detected in 10 hpf was reduced from 7.9 prior to treatment to 3.1 after progestin therapy (P = 0.03). In the progesterone-treated Ishikawa cell line, an increase in apoptotic activity started at 24 h, reached a peak at 48 h, and continued up to 72 h of hormone treatment. At 48 h, apoptotic activity was 42.6% greater than in the untreated control (P = 0.04). By 72 h of progesterone treatment, apoptosis was 37.2% greater in the treated cells compared to the noninoculated cells (P = 0.04). CONCLUSIONS: Progestin-induced apoptosis may occur during the early period of treatment for endometrial hyperplasia. Compared to the fully responsive group, persistent endometrial hyperplasia may have intrinsically different molecular mechanisms in response to progestin therapy.

Adult↗
PubMed1997

B-cell deficiency does not abrogate development of cutaneous hyperplasia in mice inheriting the defective fibrillin-1 gene.

Tight-skin (TSK) mouse, the experimental model for scleroderma, develops cutaneous hyperplasia, cardiac hypertrophy, pulmonary emphysema and autoimmunity against scleroderma target autoantigens. The cutaneous hyperplasia is associated with the accumulation of microfibrils and elastic fibers in the middle and deep dermis. Fibrillin-1 (Fbn-1) is a major component of the 10-12 nm microfibrils found in the extracellular matrix. In this study we report the identification of a genetic marker in the Fbn-1 gene that can distinguish the mutant phenotype. TSK mice exhibit an unique polymorphism in the Fbn-1 gene. RNA analysis, PCR analysis and sequence determination of the mutant gene showed that the Fbn-1 gene polymorphism is due to intragenic duplication of a segment of the gene coding for 3.0 Kb of mRNA sequence (10 Kb of the genome). Histological analysis of skin samples from F1 progeny obtained by crossing TSK mice with JH-/-, RAG2-/- or vit/vit showed a significant correlation between the inheritance of the defective Fbn-1 gene and the development of cutaneous hyperplasia. Further, our results also show that in mice deficient in mature B cells inheriting the defective Fbn-1 gene, development of cutaneous hyperplasia is not abrogated. Thus, production of autoantibodies or the presence of mature B lymphocytes do not play an integral role in the pathogenesis of cutaneous hyperplasia.

Amino Acid Sequence↗
PubMed1998

Expressions and activities of cell cycle regulatory molecules during the transition from myocyte hyperplasia to hypertrophy.

The role of cell cycle dependent molecules in controlling the switch from cardiac myocyte hyperplasia to hypertrophy remains unclear, although in the rat this process occurs between day 3 and 4 after birth. In this study we have determined (1) cell cycle profiles by fluorescence activated cell sorting (FACS); and (2) expressions, co-expressions and activities of a number of cyclins, cyclin-dependent kinases (CDKs) and CDK inhibitors by reverse transcriptase-polymerase chain reaction (RT-PCR), immunoblotting and in vitro kinase assays in freshly isolated rat cardiac myocytes obtained from 2, 3, 4 and 5-day-old animals. The percentage of myocytes found in the S phase of the cell cycle decreased significantly during the transition from hyperplasia to hypertrophy (5.5, 3.5, 2.3 and 1.9% of cells in 2-, 3-, 4- and 5-day-old myocytes, respectively,P<0.05), concomitant with a significant increase in the percentage of G0/G1 phase cells. At the molecular level, the expressions and activities of G1/S and G2/M phase acting cyclins and CDKs were downregulated significantly during the transition from hyperplasia to hypertrophy, whereas the expressions and activities of G1 phase acting cyclins and CDKs were upregulated significantly during this transition. In addition, p21(CIP1)- and p27(KIP1)- associated CDK kinase activities remained relatively constant when histone H1 was used as a substrate, whereas phosphorylation of the retinoblastoma protein was upregulated significantly during the transition from hyperplasia to hypertrophy. Thus, there is a progressive and significant G0/G1 phase blockade during the transition from myocyte hyperplasia to hypertrophy. Whilst CDK2 and cdc2 may be pivotal in the withdrawal of cardiac myocytes from the cell cycle, CDK4 and CDK6 may be critical for maintaining hypertrophic growth of the myocyte during development.

3T3 Cells↗
PubMed1996

The temporal sequence of G-protein expression in intimal hyperplasia.

The universal response of a blood vessel to intimal injury is the development of intimal hyperplasia. The etiology of this lesion is not fully understood but is assumed to involve stimulation of receptors on smooth muscle cells with their subsequent proliferation. Many receptor-mediated processes are coupled to G-proteins but little information exists regarding the expression of G-proteins during the development of intimal hyperplasia. This study examines the kinetics of G-protein expression in experimental vein grafts. Male New Zealand White rabbits had a right carotid interposition bypass graft using the ipsilateral external jugular vein. These were harvested on days 1, 3, 5, 7, 14, and 28 postoperatively for histology (n = 3), for in vitro isometric tension studies of potassium chloride, serotonin, bradykinin, and histamine (n = 3), or for Western blot analysis (n = 3) of the G-protein subunits (alpha(i1), alpha(i2), alpha(i3), alpha(S) and beta). The results show that expression of alpha(i3) developed de novo, was detectable by day 1, and continued to increase through day 7, paralleling the development of intimal hyperplasia. The expression of alpha(S) (52 kDa) increased significantly by day 1 and also continued to increase until day 7. In contrast, expression for alpha(i2), alpha(S) (45 kDa) and beta subunits increased at a much slower rate from 1 to 7 days and remained constant thereafter. No alpha(i1) was detected. The contractile response to potassium chloride was significantly reduced (36% of the response in the jugular vein) over the first 7 days and increased to 196% of the jugular vein response at 14 and 28 days. There was minimal response to serotonin, bradykinin, and histamine over the first 7 days. Contractile responses to serotonin increased while those to bradykinin and histamine decreased from 7 to 28 days. This study demonstrates that there are specific changes in alpha(i) and alpha(S) subunits within 24 hr of grafting and that increases in all G-proteins occur in a time dependent manner up to 7 days postoperatively. Microscopic development of intimal hyperplasia occurs from days 3 to 5 and increases rapidly between 7 and 14 days. Changes in the expression of G-proteins in the vein grafts, particularly the alpha(i3) subunit, parallel this formation of intimal hyperplasia. These alterations in G-protein expression do not appear to correlate with G-protein-mediated, contractile responses in the vein grafts.

Animals↗
PubMed1998

The quantitative distinction of hyperplasia from hypertrophy in hepatomegaly induced in the rat liver by phenobarbital.

A histological method utilizing the optical dissector principle has been developed for determining the absolute numbers of rat hepatocytes in the liver after treatment with phenobarbital (PB). The optical dissector is a technique derived from the "new stereology" used to measure the number of features, in this case hepatocyte nuclear profiles, that are present in a reference volume of tissue. The method has been applied to distinguish between the hepatomegaly that commonly occurs in rodents after treatment with chemicals, due to an increase in the number of cells caused by cell division (hyperplasia), rather than the size of cells (hypertrophy). In the case of PB treatment, the hepatomegaly was found to be partly due to hypertrophy and partly to hyperplasia after 2 weeks of treatment. While the increase in the absolute number of hepatocytes was not significant after 2 weeks, after 12 weeks of treatment with PB the number of hepatocytes was significantly increased, compared to the controls at that time point. PCNA labeling index measurements of liver hepatocytes confirmed that there was a significant increase in the growth fraction of hepatocytes during PB treatment. The induction of hyperplasia can be associated with an increased risk of eventual liver tumor formation, and the distinction of hyperplasia from hypertrophy, using a purely histological method, for the determination of increases in absolute hepatocyte cell numbers, will be useful in assessing whether treatment-related sustained hyperplasia is occurring in the liver, although this methodology could be applied to any organ.

Animals↗
PubMed1994

Nodular regenerative hyperplasia: a controversial indication for orthotopic liver transplantation.

Nodular regenerative hyperplasia of the liver is an uncommon cause of portal hypertension. Patients with nodular regenerative hyperplasia have signs and symptoms of portal hypertension, without evidence of hepatocellular failure or encephalopathy. We report the case of a 44-year-old woman with recurrent esophageal bleeding and refractory ascites who had a history of hemosiderosis, hepatitis C, and chronic renal allograft rejection. Our preoperative diagnosis was cirrhotic end-stage liver disease and end-stage renal disease for which the patient underwent combined hepatic and renal transplantation. Her portal hypertension symptoms resolved, and her renal function has been normal for 18 months of follow-up. Histologic examination of the liver revealed nodular regenerative hyperplasia, and a review of the literature regarding the surgical management of patients with nodular regenerative hyperplasia revealed that various shunting procedures are generally recommended. After the failure of medical management in patients with nodular regenerative hyperplasia, portosystemic shunting may be indicated before proceeding to hepatic transplantation.

Adult↗
PubMed1981

Relationship between diseases of the pancreas and hyperplasia of Brunner's glands.

Examination of 105 duodeno-pancreatectomy specimens showed that 75% of the cases of chronic pancreatitis (n = 74) manifested diffuse hyperplasia of Brunner's glands. In pancreatitis involving part of the pancreas in the presence of ducts of the embryonic type (n = 6), in segmental pancreatitis (n = 16), and in pancreatic cancer (n = 23), no significant difference in the thickness of the layer of Brunner's glands was found as compared with normal specimens. There was no statistically significant correlation between the degree of hyperplasia of Brunner's glands and the degree of scarring of the exocrine pancreatic parenchyma. Nor was there any correlation between existence and extent of scarring of the duodenal wall, inflammatory infiltration of the duodenal mucosa, duration of disease, consumption of alcohol and history of gall stones and ulcers in patients with and without hyperplasia of Brunner's glands. Diffuse hyperplasia of the duodenal glands is probably an adaptive reaction to the exocrine insufficiency of the pancreas or the changes in gastric function (hyperacidity, accelerated emptying of the stomach) caused by chronic pancreatitis. A fact which supports this statement is that the inhibitor hormone urogastrone--an inhibitor of gastric acid secretion--is formed in Brunner's glands. The question is also discussed whether chronic pancreatitis and hyperplasia of Brunner's glands might not also develop simultaneously in the presence of disturbances of the gastrointestinal hormones, themselves either primary or due to alcohol consumption.

Alcoholism↗
PubMed1996

Prognosis of orbital lymphoid hyperplasia.

BACKGROUND: Orbital lymphoid hyperplasia can be associated with systemic non-Hodgkin lymphoma (NHL), even when polyclonal proliferation is found in the orbit. Although irradiation is recommended, some orbital lymphoid hyperplasias are treated by steroids (when inflammation is clinically presumed) or left untreated. METHODS: The incidence of concurrent NHL and the incidence of future NHL after oral prednisone, radiotherapy, or no treatment were retrospectively evaluated in 33 cases of lymphoid hyperplasia (22 benign lymphoid hyperplasias, BLH, and 11 atypical lymphoid hyperplasias, ALH), after follow-up of 2-13 years. RESULTS: NHL occurred in 12 of 33 cases (36.4%). In seven patients it was concurrent; in five patients it occurred 2-6 years later. In the actuarial curve, at 5 years 55% of patients were free of lymphoma, at 10 years, 46%. NHL was more commonly observed when the lacrimal gland was involved (57% vs 21%; P = 0.03). Of the 13 patients treated with oral steroids, 46% had complete response, 39% partial response, and 15% future NHL. Of the seven irradiated patients, five (71%) had complete response, two (29%) partial response, and none future NHL. Of the eight untreated patients, five (63%) had partial response and three (37%) future NHL. Irradiated lacrimal gland BLHs only achieved partial response, one having radiation-induced orbital inflammation. CONCLUSION: Because of a high risk of NHL, in all orbital lymphoid tumors systemic staging and follow-up are mandatory. The advised management is irradiation, except for Sjögren syndrome, an initially inflammatory lacrimal gland BLH, where a course of steroid is suggested before considering radiotherapy.

Anti-Inflammatory Agents↗
PubMed1994

Primary aldosteronism: difference in clinical presentation and long-term follow-up between adenoma and bilateral hyperplasia of the adrenal glands.

Since 1974 primary aldosteronism has been diagnosed in 71 patients in our outpatient clinic. Thirty-four patients had a unilateral aldosterone-producing adenoma, whereas bilateral adrenal hyperplasia was diagnosed in 37 patients. Although at the time of diagnosis the mean potassium values were lower and mean aldosterone levels were higher in patients with an adenoma, as compared to those with bilateral hyperplasia, these laboratory data did not allow us to differentiate between the two leading causes of primary aldosteronism in the individual patient due to pronounced overlap of laboratory values between the two groups. During the first few years, a successful differential diagnosis was made by adrenal phlebography and separate sampling of plasma aldosterone in both adrenal veins; later non-invasive imaging techniques such as computed tomography and radionuclide scanning were used. The best results were obtained in patients with adenoma who underwent adrenalectomy. Fifty-six percent of these patients were clinically and biochemically cured; 28% were improved and had normal blood pressure values during drug treatment. In contrast, patients with bilateral hyperplasia were treated pharmacologically, but only in half of the patients could normal blood pressure values be achieved. Two thirds of the male patients developed gynecomastia during spironolactone treatment. As expected, unilateral adrenalectomy was unsuccessful in the 7 patients with bilateral hyperplasia who underwent surgery. Our results confirm that surgical treatment of adrenal adenomas and drug treatment of bilateral hyperplasias are the appropriate therapy in primary aldosteronism. A differential diagnosis cannot be made on the basis of clinical and non-invasive laboratory data alone; imaging techniques have to be included in the diagnostic process.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗