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At least 703 records · Page 39Linked to original sources
PubMed1995

Monoclonality of parathyroid tumors in chronic renal failure and in primary parathyroid hyperplasia.

The pathogeneses of parathyroid disease in patients with uremia and nonfamilial primary parathyroid hyperplasia are poorly understood. Because of multigland involvement, it has been assumed that these common diseases predominantly involve polyclonal (non-neoplastic) cellular proliferations, but an overall assessment of their clonality has not been done. We examined the clonality of these hyperplastic parathyroid tumors using X-chromosome inactivation analysis with the M27 beta (DXS255) DNA polymorphism and by searching for monoclonal allelic losses at M27 beta and at loci on chromosome band 11q13. Fully 7 of 11 informative hemodialysis patients (64%) with uremic refractory hyperparathyroidism harbored at least one monoclonal parathyroid tumor (with a minimum of 12 of their 19 available glands being monoclonal). Tumor monoclonality was demonstrable in 6 of 16 informative patients (38%) with primary parathyroid hyperplasia. Histopathologic categories of nodular versus generalized hyperplasia were not useful predictors of clonal status. These observations indicate that monoclonal parathyroid neoplasms are common in patients with uremic refractory hyperparathyroidism and also develop in a substantial group of patients with sporadic primary parathyroid hyperplasia, thereby changing our concept of the pathogenesis of these diseases. Neoplastic transformation of preexisting polyclonal hyperplasia, apparently due in large part to genes not yet implicated in parathyroid tumorigenesis and possibly including a novel X-chromosome tumor suppressor gene, is likely to play a central role in these disorders.

Adult↗
PubMed1996

Prevention of intimal hyperplasia by irradiation. An experimental study in rabbits.

PURPOSE: This experimental study was designed to investigate the effect of irradiation in prevention of intimal hyperplasia. MATERIAL AND METHODS: Twenty rabbits were divided into 4 groups, which were irradiated with 2, 5, 10 and 20 Gy, respectively. The intima of both femoral arteries was injured by air-drying, and irradiation was performed on the unilateral side. The contralateral+ femoral artery served as a control. Angiograms as well as histologic specimens were obtained 1 month later. RESULTS: Marked intimal hyperplasia was observed in all control sites. There were no significant differences in thickness of intimal hyperplasia between irradiated and control sites in groups irradiated with 2 and 5 Gy. However, in the 10-Gy- and 20-Gy-irradiated groups, intimal hyperplasia of the irradiated site was significantly suppressed. Medial thinning and dilation of the lumen were observed in the 20-Gy-irradiated group. CONCLUSION: Radiation may prevent intimal hyperplasia. Further investigation of the optimal dose, timing of irradiation, and long-term patency of irradiated vessels may be needed.

Animals↗
PubMed1987

Oral leukoplakia and costochondral hyperplasia induced by diethylnitrosamine in hamsters exposed to cigarette smoke with or without dietary vitamin C.

Male Syrian golden hamsters receiving 12 weekly subcutaneous injections of diethylnitrosamine (DEN) were subjected to cigarette smoke-inhalation and fed a diet or without 1% vitamin C supplement for a period of 58 weeks. Another group was a sham-smoked control and was not fed vitamin C. Tissues of the oral cavity and costal cartilage were examined by light and/or scanning electron microscopy. Oral leukoplakia and costochondral hyperplasia occurred with high frequency in all groups treated with DEN. Leukoplakic lesions were found in the palate, tongue, and pharynx; the early change was focal erosion with mild epithelial hyperplasia and inflammatory cell infiltration. Advanced lesions had marked mucosal thickening due to acanthosis, parakeratosis, hyperkeratosis, and submucosal infiltration of lymphocytes and plasma cells. Precancerous lesions were noted in tongue and pharynx. Scanning electron microscopy of tongues revealed destruction of filiform papillae. The incidence of leukoplakic lesions were higher in smoke-exposed hamsters than in controls, but the incidence in vitamin C-supplemented hamsters was low when compared with the smoke-exposed hamsters without vitamin C. Costochondral hyperplasia was initiated by thickening of the perichondrium followed by proliferation of chondrocytes. Costochondral hyperplasia appeared earlier, and the incidence was higher in the vitamin C-supplemented hamsters. It could not be determined whether costochondral hyperplasia was the primary lesion induced by DEN or secondary change.

Animals↗
PubMed1993

Adenomatous hyperplasia of equine allantoic epithelium.

Adenomatous hyperplasia with or without cystic formation of allantoic epithelium was observed in 63/954 equine placentas examined from 1 February 1988 to 31 January 1990. In 61/63 placentas, the adenomatous hyperplasia was associated with other placental lesions: 49 with chronic or chronic-active placentitis, six with placental edema, three with fetal diarrhea, one with placentitis and fetal diarrhea, one with fetal diarrhea and placental edema, and one with hyperplasia of chorionic epithelium. When lesions were less severe, the hyperplastic lesions were not grossly visible, but when lesions were severe, nodular, tumorous, cystic masses were observed at or near the insertion site of umbilical blood vessels. Histologically, lesions classified as stage 1 were characterized by hypertrophy and hyperplasia of epithelial cells and formation of intraepithelial glands (lumina). Lesions classified as stage 2 were characterized by the presence of fibro-adenomatous changes in the allantoic stroma. Lesions classified as stage 3 were characterized by the formation of the nodular masses, which were composed of glandular or cystic structures of various sizes lined by cuboidal or low to medium columnar epithelium. These glands or cysts were empty or contained amphophilic secretion, a mixture of neutrophils and secretion material, or neutrophils. The cause of adenomatous hyperplasia of the equine allantois is not certain; however, there is a close connection between chronic placental disorders and this hyperplastic lesion.

Allantois↗
PubMed1991

Learning disabilities in children with congenital adrenal hyperplasia.

Early exposure to androgens may be a cause of the higher incidence of learning disabilities among males. To test this hypothesis, we determined the frequency of learning disabilities, as measured by extent of Wechsler Verbal-Performance IQ discrepancy, among female patients with congenital adrenal hyperplasia, who are exposed in utero to excess androgens for their sex. A significantly larger Verbal-Performance IQ discrepancy (10.1 vs 7.7) was found for the 18 female patients than for 27 unaffected female siblings (P = .045, one-tailed). The Verbal-Performance IQ discrepancy of the females with congenital adrenal hyperplasia is in the male range (10.4 to 13.4), similar to males with congenital adrenal hyperplasia (n = 20) and unaffected male siblings (n = 31). In addition to the sex effect, there is an effect of the type of congenital adrenal hyperplasia on the frequency of learning disabilities. Simple virilizers are more likely to be learning disabled than salt-wasters (P = .04, one-tailed). However, salt-waster patients have a lower IQ (104 vs 117) than simple virilizer patients (P = .005, one-tailed). Presumably, this is because some salt-waster patients suffer brain injury from episodes of hypotension and hyponatremia. The diffuse insult to the central nervous system may overide the androgen effect and result in a general cognitive impairment. Because of this confounding effect on IQ in the salt-waster form of congenital adrenal hyperplasia, the simple virilizer female versus unaffected female siblings reprsents the best test of the hypothesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2003

Differential effects of peroxisome proliferator activator receptor-alpha and gamma ligands on intimal hyperplasia after balloon catheter-induced vascular injury in Zucker rats.

BACKGROUND: Patients with type 2 diabetes mellitus have a higher rate of restenosis following angioplasty. Peroxisome proliferator activator receptor-alpha (PPAR) and gamma ligands such as fenofibrate and rosiglitazone, respectively, have been shown to have protective effects on the vessel wall. We studied the effect of fenofibrate and rosiglitazone on intimal hyperplasia in the Zucker rat, a model for insulin resistance and type 2 diabetes mellitus, following balloon catheter-induced injury. METHODS AND RESULTS: Three groups of 13-week-old female fatty Zucker rats were administered an aqueous suspension of either 3 mg/kg/d rosiglitazone (n=7) or 150 mg/kg/d fenofibrate (n=6) by gavage, or served as controls (n=9). In addition, two groups of 13-week-old female lean Zucker rats were either administered 3 mg/kg/d rosiglitazone (n=6) or served as controls (n=6). Carotid balloon injury was induced 1 week after the drugs were started. The drug administration was continued for 3 weeks. A 2-mm balloon catheter was introduced through the femoral artery to the left carotid. The balloon was inflated to 4 atmospheres for 20 seconds and then was deflated to 2 atmospheres and dragged down to the aorta. The rats were killed 3 weeks after the injury. The carotid intima/media ratio was calculated. Intimal hyperplasia after carotid balloon-induced injury in the fatty Zucker rats was significantly reduced in the group treated with rosiglitazone (0.18 +/- 0.29) compared with the untreated group (0.97 +/- 0.13; P<.01). Plasma glucose, triglyceride, and insulin levels were elevated, indicative of the presence of insulin resistance; rosiglitazone treatment significantly reduced insulin and triglyceride levels without decreasing glucose. Rosiglitazone treatment also reduced, but to a lesser extent, the intimal hyperplasia in the lean Zucker rats (0.57 +/- 0.10 vs 1.06 +/- 0.12 treated and untreated, respectively; P<.01); however, it had no effect on insulin, triglyceride, or glucose levels in this group. The intimal hyperplasia in the fatty Zucker rats treated with fenofibrate was not reduced compared with controls (0.84 +/- 0.26 vs 0.97 +/- 0.13, respectively); fenofibrate reduced insulin and triglyceride, but not glucose levels, in these animals. CONCLUSIONS: The PPAR-gamma ligand rosiglitazone, but not the PPAR-alpha ligand fenofibrate, decreases intimal hyperplasia following balloon injury in both fatty and lean Zucker rats. This effect of the PPAR-gamma ligand was independent of glycemia, insulin, and lipid levels, and was more pronounced in insulin-resistant rats.

Animals↗
PubMed1984

Testicular androgen and estrogen secretion and benign prostatic hyperplasia in the beagle.

The natural history of benign prostatic hyperplasia (BPH) in the dog is characterized by a slow progression through two phases. The early phase of the disease process is characterized by glandular hyperplasia and occurs as early as 2.5 yr of age. The late phase of the disease is characterized by cystic hyperplasia and occurs after 4 yr. The results of the present study are the first to compare Leydig cell structure and steroidogenic function in dogs with BPH with those in age-matched controls. It was discovered that glandular BPH can occur in young dogs (2.5 yr) in which Leydig cell mass and ultrastructure and maximally stimulated androgen secretion are indistinguishable from those in age-matched controls. These results support the concept that the early phase of BPH (glandular hyperplasia) is not related temporally to some defect in the Leydig cell. In contrast, the late phase of BPH (cystic hyperplasia) in beagles 6 yr of age is associated with diminished smooth endoplasmic reticulum in the Leydig cell and with diminished production of androgens by perfused testes in vitro. During the course of these studies, we discovered that the testes of young beagles with BPH, but not age-matched controls or old beagles with BPH, secrete an unidentified molecule (putative estrogen). This molecule was characterized partially in that it is extractable from testicular venous effluent with diethyl ether, elutes in a discrete fraction in several different high performance liquid chromatographic systems, reacts with an antibody that recognizes 17 beta-estradiol, estrone, and estriol, and competes with 17 beta-[3H]estradiol for the rat uterine estrogen receptor. Based on the elution volume from high performance liquid chromatography, the unknown molecule (putative estrogen) is not estriol, estradiol, or estrone.

Androgens↗
PubMed2003

Germline succinate dehydrogenase subunit D mutation segregating with familial non-RET C cell hyperplasia.

C cell hyperplasia is associated with medullary carcinoma of the thyroid in the inherited MEN2 syndromes, in which the great majority of cases have been shown to be due to a mutation in the RET oncogene. We report a study of a family with C cell hyperplasia and hypercalcitoninemia in which no cases of medullary carcinoma have yet occurred and which lacked an identifiable causative RET mutation. Four of the family members showed hypercalcitoninemia, and marked C cell hyperplasia was present in each of the three in whom thyroidectomy has been performed. We investigated the possible involvement of the SDHD gene, because somatic and germline mutations in this gene have been found in a variety of tumors of neural crest-derived tissue. A germline mutation in exon 2 of the SDHD gene (c149 A-G, His 50 Arg) was found in six members of the family; all the four available members with hypercalcitoninemia possessed the mutation. One of the five available members without hypercalcitoninemia, an 18-yr-old female, also showed the mutation. We conclude that we have identified a new syndrome, characterized by familial non-RET C cell hyperplasia. Our studies suggest that a mutation in SDHD may be causative. These observations have implications for apparently incidental cases of hypercalcitoninemia or C cell hyperplasia.

Adult↗
PubMed1984

Primary adrenal hyperplasia: a new subset of primary hyperaldosteronism.

The existence of a new subset of primary hyperaldosteronism that combines the morphology of bilateral hyperplasia with the biochemical and therapeutic responses typical of adenoma recently was suggested. The following is the first detailed case report of that subset. The patient had severe hypokalemia and hypertension responsive to spironolactone, and elevated supine plasma aldosterone and 18-hydroxycorticosterone values that did not increase after ambulation. Surgical removal of 75% of both adrenal glands decreased mineralocorticoid levels into the low normal range and allowed the return of normal renin-angiotensin function, although plasma aldosterone was still unresponsive to postural change. Glucocorticoid reserve remained normal. Histology showed bilateral cortical hyperplasia. The results support the existence of a new subset of adrenal hyperplasia, termed primary adrenal hyperplasia, in which biochemical parameters and response to surgery mimic those of adrenal adenomas. The existence of such a subset indicates that morphological categorization alone is insufficient to rule out a possible therapeutic response to surgery in patients with aldosterone-secreting adrenal hyperplasia.

Adenoma↗
PubMed1986

Myeloid hyperplasia in the SENCAR mouse: differentiation from granulocytic leukemia.

The term myeloid hyperplasia has been used interchangeably with many other terms to describe an increased production of granulocytes, megakaryocytes, and erythrocytes in the spleen and other organs in the mouse. This process is occasionally misdiagnosed as granulocytic leukemia. This paper reviews some of the terms used interchangeably with myeloid hyperplasia and describes criteria that can be used to differentiate myeloid hyperplasia from granulocytic leukemia. Additionally, the results of a study in which myeloid hyperplasia was induced following the formation of skin tumors in SENCAR mice is discussed. In this study, positive correlations were found between skin lesions, the spleen weight, and histologic appearance of the spleen. The liver rarely showed microscopic changes of myeloid hyperplasia unless the spleen weighed at least 1.0% of the body weight.

Animals↗
PubMed2002

The pathophysiology of benign prostatic hyperplasia.

The development of human benign prostatic hyperplasia and its related signs and symptoms clearly requires a combination of testicular androgens and aging. Although the role of androgens as a causative factor for human benign prostatic hyperplasia is debated, they undoubtedly play at least a permissive role. The principle prostatic androgen is dihydrotestosterone. Two isoenzymes of 5-alpha reductase have been discovered. Type 2 is dominant in the genital issue. Testosterone is reduced by the 5-a reductase to dihydrotestosterone. Benign prostatic hyperplasia is predominantly due to stromal hyperplasia of the gland and affects more than 70% of men of 70 years or older with or without obstruction. Recent studies identified transforming growth factor-b, fibroblast growth factor and insulin-like growth factor family members as key regulators of cell proliferation and extracellular matrix turnover with interrelated activities. Furthermore, estrogens, andenergic signaling and inflammatory processes have been shown to have an impact. Without a solid understanding of the physiology and pathophysiology of benign prostatic hyperplasia it can be difficult to interpret the results of clinical trials and symptoms.

Aging↗
PubMed2006

Testicular adrenal rest hyperplasia due to 21-hydroxylase deficiency: a case report.

Bilateral testicular tumors are a rare complication of congenital adrenal hyperplasia. It can be extremely difficult to distinguish histologically between Leydig cell tumors and adrenocortical rest hyperplasia, which may lead in some cases to unnecessary orchidectomy. A 7-yr-old boy was admitted because of precocious puberty and enlargement of testicles. Hormonal studies established the diagnosis of congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Testicular biopsy revealed interlacing strands, cords, and rests of cells resembling interstitial (Leydig) cells but with no Reinke crystalloids. Here we report a case of testicular adrenal rest hyperplasia in congenital adrenal hyperplasia and discuss the pathological and clinical features and origin of this rare lesion by using immunohistochemical evaluation.

Adrenal Hyperplasia, Congenital↗
PubMed2004

Adrenocortical hyperplasia associated with ACTH-dependent Cushing's syndrome: comparison of the size of adrenal glands with clinical and endocrinological data.

Diffuse or nodular hyperplasia of adrenal glands is associated frequently with ACTH-dependent Cushing's syndrome. We carried out a retrospective analysis of 28 patients with ACTH-dependent Cushing's syndrome admitted to our institution between 1984 and 1999 in order to clarify the incidence of adrenal hyperplasia in ACTH-dependent Cushing's syndrome and also to determine the correlation between adrenal gland images and clinical, biochemical and endocrinological data. Of the 28 patients, 16 (57%) showed diffuse adrenal hyperplasia while only 3 had focal adrenal nodules in the hypertrophied adrenals. There was a positive, significant correlation between the width of the adrenal glands measured on CT and circulating plasma ACTH, cortisol levels and urinary free cortisol (UFC) levels. Duration of the disease also correlated positively with adrenal width. No correlation was found between age and adrenal size and there was no difference in the prevalence of diffuse hyperplasia between normotensive and hypertensive patients. These results suggest that chronic ACTH hypersecretion may lead to diffuse adrenal hyperplasia in patients with ACTH-dependent Cushing's syndrome.

ACTH Syndrome, Ectopic↗
PubMed1985

Concurrent endometrial hyperplasia with carcinoma of the corpus uteri.

Using 117 uteri which were extirpated in cases of carcinoma of the corpus uteri, a study was made to investigate the relationship between the site of the cancer and the site of associated endometrial hyperplasia. It was found that 75% of the cases had carcinomas of the upper portion of the uterus primarily of the uterine fundus. About 50% of the cancers were associated with adenomatous or atypical hyperplasia, and these two types of hyperplasia were frequently found in the fundus or upper portion of the uterus. In contrast, there was no site of particular prevalence in cases with concurrent cystic hyperplasia. About 70% of the cases had adenomatous or atypical hyperplasia on one or both of the histological blocks adjacent to the cancer.

Endometrial Hyperplasia↗
PubMed1983

Risk factors in phenytoin-induced gingival hyperplasia.

A survey was carried out into the degree of gingival hyperplasia in 68 patients receiving phenytoin in a hospital for the mentally handicapped. Comparisons of degree of gingival hyperplasia exhibited by the patients were made with a range of parameters by analysis of variance and Chi square tests. The severity of the hyperplasia increased with increasing dose, increasing dose per unit body weight and serum levels of phenytoin and also with decreasing age and weight of the patients. No significant relationship (P less than 0.2) was found between serum folate levels and degree of hyperplasia. Poor oral hygiene predisposed patients to hyperplasia.

Adolescent↗
PubMed1985

Nifedipine-induced gingival hyperplasia. A histochemical and ultrastructural study.

Gingival hyperplasia induced by nifedipine (Procardia), a calcium channel-blocking agent used as an anti-anginal drug, was studied. In recent months, the role of nifedipine in the etiology of gingival hyperplasia has attracted interest. The purpose of this study was to determine the causal relationship and compare nifedipine to other drug-induced (phenytoin) and nondrug-induced gingival hyperplasias. Histochemical studies revealed increased numbers of fibroblasts containing strongly sulfated mucopolysaccharides in the nifedipine- and phenytoin- (Dilantin) induced gingival hyperplasias as compared to the nondrug-induced cases. Numerous secretory granules were also noted in the fibroblast cytoplasm in the nifedipine-treated case studied by electron microscopy. These results imply that there is an increase in acid mucopolysaccharide production in the nifedipine- and phenytoin-induced gingival hyperplasias. The potential significance and comparisons of the drugs' effects at the cellular level are discussed.

Acid Phosphatase↗
PubMed2003

Recurrent recalcitrant gingival hyperplasia and plasminogen deficiency: a case report.

BACKGROUND: Recurrent gingival hyperplasia due to plasminogen deficiency is a rare condition due to fibrin deposition in the connective tissue. Only eight cases have previously been reported in the English literature, and all cases were diagnosed before the age of 35 years. This paper presents an older patient with recurrent gingival hyperplasia due to plasminogen deficiency (hypoplasminogenemia). METHODS: A 59-year-old woman presented with recurrent gingival swelling of 6 years' duration. Multiple biopsies performed at various time periods were histologically reported to be gingival hyperplasia with chronic inflammation. Routine hematoxylin and eosin (H & E) staining and direct immunofluorescence were performed. RESULTS: H & E-stained sections showed subepithelial, eosinophilic, amorphous, acellular deposits. Direct immunofluorescence showed positive staining for fibrin, immunoglobulin (Ig) G, IgA, and IgM. Functional plasminogen and plasminogen activator inhibitor-1 assays were done and found to be deficient. A diagnosis of gingival hyperplasia due to plasminogen deficiency (hypoplasminogenemia) was rendered. CONCLUSIONS: Recurrent gingival hyperplasia due to plasminogen deficiency (hypoplasminogenemia) is a newly recognized and rare condition. H & E staining, direct immunofluorescence, and assessment of functional plasminogen levels are essential to differentiate this condition from other conditions in which subepithelial, eosinophilic, amorphous materials are deposited.

Deficiency Diseases↗
PubMed2004

Fas ligand gene therapy for vascular intimal hyperplasia.

Fas, a member of the tumor necrosis factor receptor super-family, is expressed in all cell types examined, while physiologic expression of Fas ligand (FasL) is found predominantly in activated T-lymphocytes, vascular endothelial cells, and "immune-privileged" tissues. Activation of Fas following FasL binding activates caspases, which results in apoptosis. In the vasculature, there may be a delicate balance between cell proliferation and apoptosis in vascular smooth muscle cells. Shifts in this balance could account for the accumulation of vascular smooth muscle cells in response to arterial injury, a major feature of vascular intimal hyperplasia. Intimal hyperplasia occurs in more than a third of patients receiving percutaneous transluminal balloon angioplasty. Stenting with or without coating significantly reduces the incidence rate of angiographic restenosis and that of target vessel revascularization. However, "in-stent" intimal hyperplasia/restenosis remains a challenge for clinical cardiologists. Although both the cell types and mechanisms that contribute to intimal hyperplasia in response to vascular injury remain controversial, vascular smooth muscle cell migration and proliferation appear to play an important role in the process. In animal models, cytotoxic and cytostatic gene therapy strategies targeted at the vascular smooth muscle cells have shown therapeutic potential for the treatment of vascular intimal hyperplasia. However, Fas ligand-based gene therapy appears to offer several advantages. In this review article, we will discuss the mode of FasL/Fas signaling in vascular smooth muscle cells and its therapeutic implications. We will also compare the relative merits of FasL with other cytotoxic and cytostatic gene therapy approaches for the treatment of intimal hyperplasia.

Animals↗