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PubMed1991

The relation between fibrosis of hilar lymph glands and the development of parenchymal silicosis.

The necropsy findings on the cardiorespiratory organs of 849 South African gold miners were analysed to test the hypothesis that fibrosis of the hilar lymph glands predisposes to the development of parenchymal silicotic nodules. Four hundred and eighty three cases had fibrosed glands, 34% of which also had parenchymal silicosis. By comparison, of 238 cases with silicosis, 88% had fibrosed glands. The proportion of cases with both silicosis and fibrosed glands, as well as those with gland fibrosis only, increased with increasing duration of exposure. As far as can be ascertained from a necropsy series such as this, it is possible that fibrosis of the lymph glands may predispose to the development of lung parenchymal silicosis.

Fibrosis↗
PubMed1997

Decreased nitric oxide in the exhaled air of patients with systemic sclerosis with pulmonary hypertension.

BACKGROUND: Systemic sclerosis (SSc) may be complicated by pulmonary hypertension (PHT), which can occur both in the setting of fibrosing alveolitis or as lone pulmonary vascular disease. Nitric oxide (NO) is a powerful vasodilator and is produced by various cells in the respiratory tract including pulmonary vascular endothelial cells and can be measured in expired air. A study was undertaken to test the hypothesis that exhaled NO levels would be decreased in patients with SSc with PHT and to assess the utility of this measurement in discriminating between patients with and without PHT, regardless of concurrent fibrosing alveolitis. METHODS: Exhaled NO was measured with a chemiluminescence analyser in 23 patients with SSc (six with PHT, 17 subjects without) and in 67 normal individuals. Doppler echocardiography was used to assess pulmonary artery pressure in subjects with SSc, and lung function tests were performed at the same visit as NO measurements. Thin section CT scans were analysed for the presence of abnormality consistent with fibrosing alveolitis. RESULTS: Patients with SSc with PHT had a greater reduction in arterial oxygen tension (PaO2) and carbon monoxide gas transfer (TLCO) than patients with SSc without PHT. Exhaled NO was significantly higher in patients with SSc without PHT than in normal individuals, and was significantly decreased in patients with SSc with PHT (mean (SD) 20 (6) ppb) compared with 149 (19) ppb in those with SSc without PHT (mean difference 129 (95% CI 112 to 146) ppb) and 80 (7) ppb in normal individuals (mean difference 60 (95% CI 54 to 66) ppb). CONCLUSION: Exhaled NO is decreased in patients with SSc with PHT compared with both normal individuals and patients with SSc without PHT.

Adult↗
PubMed1998

Role of urokinase in the fibrogenic response of the lung to mineral particles.

The lung plasminogen activator (PA) response was examined in four different models of particle-induced pulmonary lesions in NMRI mice (single intratracheal administration, 0.75 to 5 mg/mouse). Sequential changes in cellular (total and differential counts) and biochemical markers of alveolitis (lactate dehydrogenase [LDH], total proteins) were monitored in bronchoalveolar fluid (BALF) and the fibrotic lung response was assessed histologically. An intense but spontaneously resolving alveolitis was produced by manganese dioxide (MnO2) and a fibrosing alveolitis was elicited by crystalline silica (DQ12). Minimal and noninflammatory responses were obtained after instillation of titanium dioxide (TiO2) and tungsten carbide (WC), respectively. The comparison between the resolving and the fibrosing alveolitis model was especially taken into consideration in an attempt to identify fibrinolytic changes associated with the development of fibrosis. At the alveolitis stage, similarly increased BALF PA activities were measured in both the resolving and the fibrosing alveolitis models whereas only slight and no PA modifications were noted after administration of TiO2 and WC, respectively. Persistently (up to 120 d) increased BALF PA activity was selectively associated with the progression to fibrosis (DQ12), suggesting that PA is involved in the fibrotic process. ELISA measurements demonstrated that the changes in BALF PA activity were exclusively related to changes in urokinase (uPA), not tissue-type PA. A rapid and persisting (up to Day 30) upregulation of cell-associated PA activity occurred after DQ12, MnO2, and TiO2 treatment only. Cellular PA activity was however significantly higher in fibrogenic inflammatory cells recovered from DQ12 than from MnO2-treated mice suggesting that the intensity of cellular PA upregulation may represent an early indicator of the progression to fibrosis. The implication of urokinase in the pathogenesis of silica-induced fibrosis was demonstrated by the use of a uPA knockout mice. The acceleration of the fibrotic process in uPA-deficient compared with the wild type animals demonstrated the contribution of uPA to limit the fibrotic process.

Animals↗
PubMed1991

Structural features of interstitial lung disease in systemic sclerosis.

Most studies of lung histology in systemic sclerosis have been based on autopsy specimens and consequently emphasize end-stage fibrotic disease. Although occasional pathologic descriptions of open-lung biopsies have recognized the presence of inflammatory cells, suggesting a similarity to "lone" cryptogenic fibrosing alveolitis, the two conditions have never been formally compared. In this study we describe the morphologic features of 49 open-lung biopsies from 34 systemic sclerosis patients with interstitial lung disease, many of whom had their lung disease diagnosed at an early stage. None had pulmonary hypertension. Examination of lung tissue by light microscopy showed the earliest changes to include patchy lymphocyte and plasma cell infiltration of the alveolar walls, interstitial fibrosis, and increased macrophages but only occasional polymorphonuclear cells and lymphocytes in the alveolar spaces. Alveolitis was not observed without fibrosis. Comparison of 22 biopsies with a similar number from patients with lone cryptogenic fibrosing alveolitis, matched for age and sex, revealed no qualitative or quantitative differences, other than a higher prevalence of focal lymphoid hyperplasia (follicular bronchiolitis) in the systemic sclerosis patients than in the lone cryptogenic fibrosing alveolitis controls (23 and 5%, respectively). There was an inverse correlation between the extent of interstitial inflammation and patients' age (p less than 0.05), disease duration (p less than 0.05), and age at onset of systemic sclerosis (p less than 0.01). There was also an inverse correlation between DLCO and interstitial fibrosis (p less than 0.01) and loss of lung architecture (p less than 0.05). Ultrastructural studies of eight systemic sclerosis biopsies showed evidence of endothelial and epithelial injury together with interstitial edema and excess collagen deposition. Occasional mast cells were observed, often in close contact with interstitial fibroblasts, but there were no tubuloreticular structures or evidence of immune complexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

KL-6, a human MUC1 mucin, is chemotactic for human fibroblasts.

KL-6 in serum and bronchoalveolar lavage fluid has been reported to be a sensitive marker indicating the activity of fibrosing lung diseases. The molecule is clustered in MUC1 mucin according to the findings of immunohistochemical and cytometric studies. To elucidate the pathogenic role of KL-6 in fibrosing lung disease, we characterized its biochemical properties and examined whether purified KL-6 is chemotactic for human fibroblasts in vitro using modified Boyden chambers. Biochemical properties of purified KL-6 were similar to those of other MUC1 mucins previously reported. KL-6 promoted the migration of 5 of 5 human lung fibroblasts and 3 of 4 human skin fibroblasts. Checkerboard analysis revealed that KL-6 was chemotactic as well as chemokinetic. Though platelet-derived growth factor, fibroblast growth factor, or fibronectin were also chemotactic for fibroblasts in the experimental system, only fibronectin augmented KL-6-induced chemotaxis. These observations indicate that KL-6 is one of the chemotactic factors for most fibroblasts and that the increased KL-6 in the epithelial lining fluid in small airways may cause the intra-alveolar fibrosis in fibrosing lung diseases.

Antigens↗
PubMed1999

Soluble tumor necrosis factor (TNF) receptors p55 and p75 and interleukin-10 downregulate TNF-alpha activity during the lung response to silica particles in NMRI mice.

We have found reduced activity of tumor necrosis factor (TNF)-alpha accompanying resolving and fibrosing alveolitis induced in NMRI mice by mineral particles (MnO2 and SiO2, respectively), which is in apparent contradiction to the well-recognized proinflammatory and profibrotic activities of this cytokine. The objective of this study was to examine the mechanisms involved in this paradoxical response in NMRI mice. Although lung tissue messenger RNA (mRNA) levels for TNF-alpha were transiently (up to 15 d) and persistently (up to 120 d) upregulated in the resolving and fibrosing models, respectively, these changes were not accompanied by a parallel release of TNF-alpha protein, which was respectively transiently and persistently downregulated in bronchoalveolar lavage fluid and bronchoalveolar lavage cell cultures. The downregulation of the TNF-alpha protein was concurrent with the accumulation of recruited polymorphonuclear neutrophils (PMNs) in alveoli, and coculture experiments showed that PMN explanted from the lungs of mice treated with silica particles were able to downregulate the expression of TNF-alpha protein by naive alveolar macrophages. In addition, PMN depletion prevented the downregulation of TNF-alpha induced by silica, further establishing the role of PMNs in the downregulation of TNF-alpha. The possible degradation of TNF-alpha by proteolytic enzymes could be excluded. Marked increases in soluble p55 and p75 TNF receptors (sTNF-R), as well as in interleukin (IL)-10, paralleled the downregulation of TNF-alpha protein. The role of these mediators in the observed reduction of TNF-alpha activity was confirmed by immunoneutralizing the activity of p55 and p75 sTNF-R and by using IL-10-deficient animals. Because IL-10 also exerts profibrotic activity in addition to its antiinflammatory activity, the protracted overproduction of IL-10 observed in fibrosing alveolitis may help the understanding of why, in NMRI mice treated with silica particles, lung fibrosis develops in association with a downregulation of TNF-alpha.

Animals↗
PubMed1997

The source and role of RANTES in interstitial lung disease.

The chemokine "regulated on activation, normal T-cell expressed and secreted" (RANTES) is a potent eosinophil and lymphocyte attractant with particular preference for CD45RO+ T-cells and eosinophils. These cells accumulate in the lungs of patients with sarcoidosis and fibrosing alveolitis. The purpose of this study was to determine whether RANTES mediates the inflammatory cell influx in these diffuse lung diseases. Cell types and number of bronchoalveolar cells expressing RANTES protein were investigated by immunocytochemistry using lavage cells obtained from 22 patients and 11 control subjects. Subsequently, RANTES messenger ribonucleic acid (mRNA) was semiquantitated using reverse transcription polymerase chain reaction (RT-PCR) methodology in unseparated lavage cell pellets in 26 patients and 13 control subjects. Cells expressing RANTES mRNA were identified by in situ hybridization. RANTES protein expression in lower respiratory tract (LRT) cells was identified in all study groups. The percentage of RANTES+ lavage cells in sarcoidosis was higher than in controls. RANTES was localized in the cytoplasm, mainly in alveolar macrophages (CD68+ cells) in sarcoidosis, and both in alveolar macrophages and eosinophils in fibrosing alveolitis. The same cell types which expressed RANTES protein expressed RANTES mRNA, as assessed by in situ hybridization. Sarcoidosis patients had higher levels of RANTES mRNA than the other groups. RANTES protein was higher in individuals with abnormal lymphocyte numbers: RANTES protein and mRNA expression was significantly correlated with lavage CD45RO+ lymphocyte numbers. These results indicate that RANTES may mediate T-lymphocyte influx in diffuse lung disease, particularly sarcoidosis. Moreover, they suggest that the cellular source of RANTES is the alveolar macrophage in sarcoidosis, and both macrophages and eosinophils in fibrosing alveolitis.

Bronchoalveolar Lavage Fluid↗
PubMed1976

Ultrastructural changes in hypertrophied myocardium of spontaneously hypertensive rats.

In seven arbitrarily selected groups of 3-, 5-, 9-, 11-, 15-, and 21-week and one-year-old spontaneously hypertensive rats (SHR) (F25-26), qualitative as well as quantitative light and electron microscope studies were conducted on the myocardium in the left ventricular papillary muscle and lateral wall. Age-and body-weight-matched groups of normotensive Wistar-Kyoto rats were employed as controls. In the strain of SHR used in this study blood pressure was significantly higher than in the controls in the 7th week of age, reached sustained levels (approximately 180 mmHg) in the 15th week of age and remained higher thereafter. The heart weight/body weight ratio gradually increased in SHR after the 15th week of age. In 3-week-old SHR, there was no significant difference in fine structure of the myocardium in comparison with control animals. The cardiocytes were small in size and rapidly growing. Myofibrillogenesis seemed to occur in association with juvenile forms of intercalated discs, subsarcolemmal dense mats, occasional Z band expansions and unorganized filamentous structures in the periphery of preexisting myofibrils. In 5- and 9-week-old SHR, the muscle fiber diameters in the papillary muscle were significantly larger than those in control animals of the same age. Subcellular structures of many cardiocytes were, however, apparently equal in both papillary muscle and lateral wall of the left ventricle in SHR and control animals. In 11-week-old SHR, the cardiocytes were moderately hypertrophied in both papillary muscle and lateral wall. The myofibrils were significantly increased in mass in association with altered intercalated discs, extended subsarcolemmal dense mats and unorganized filamentous structures in the periphery of preexisting myofibrils. Focal interstitial fibroses occurred in in the myocardium, and tunnel capillaries appeared in some hypertrophied cardiocytes. In 15-week-old SHR, the cardiocytes had markedly hypertrophied in accordance with the establishment of sustained hypertension. The intracellular volume ratios of myofibrils and T system had increased significantly whereas the mitochondrial volume had markedly decreased resulting in a significant increase in the myofibril/mitochondria volume ratio. There were marked changes in the intercalated discs associated with numerous immature sarcomers, and frequent abnormal Z band expansions. Interstitial fibroses had markedly increased in number and extent. In 21-week-old SHR, in addition to findings similar to those in 15-week-old SHR, heterogeneous changes of the contractile material, mitochondria and sarcoplasmic matrix were more prominent, suggesting heterogeneous malfunctions in later stages of cardiac hypertrophy. In one-year-old SHR, subcellular changes in many cardiocytes qualitatively resembled those in 21-week-old SHR. Interstitial fibroses and tunnel capillaries were also increased in extent and number...

Age Factors↗
PubMed1985

CT in the diagnosis of interstitial lung disease.

The computed tomographic (CT) appearance of interstitial lung disease was assessed in 23 patients with known interstitial disease. These included seven patients with fibrosing alveolitis, six with silicosis, two with hypersensitivity pneumonitis, three with lymphangitic spread of tumor, two with sarcoidosis, one with rheumatoid lung disease, and two with neurofibromatosis. The CT appearance of the interstitial changes in the different disease entities was assessed. Nodules were a prominent CT feature in silicosis, sarcoidosis, and lymphangitic spread of malignancy. Distribution of nodules and associated interlobular septal thickening provided further distinguishing features in these diseases. Reticular densities were the predominant CT change in fibrosing alveolitis, rheumatoid lung disease, and extrinsic allergic alveolitis. A marked peripheral predominance of the interstitial densities was seen in all seven cases of fibrosing alveolitis and in the patient with rheumatoid lung, in marked contrast with the two cases of hypersensitivity pneumonitis in whom a central distribution of the changes was seen. The observed patterns correlate with the pathologic findings and provide information that at times cannot be obtained from the chest radiograph. CT can be useful in the investigation of selected instances of interstitial pulmonary disease.

Alveolitis, Extrinsic Allergic↗
PubMed2002

[A clinicopathologic study of nonspecific interstitial pneumonia].

OBJECTIVE: To investigate the clinicopathologic features of nonspecific interstitial pneumonia (NSIP). METHODS: The clinical and pathological data of 8 cases with NSIP confirmed by open or video-assisted thoracoscopic lung biopsy were reviewed retrospectively. RESULTS: NSIP occurred more in female (male:female 1:3, 2/6), and the patients' average age was 48 years. The clinical manifestation was progressive dyspnea, cough and sputum, crackles over both lungs and restrictive ventilating abnormalities. Reticular changes and patchy ground-glass attenuation in lower lung fields were the main findings on high resolution computed tomography. The pathological characteristic was uniform interstitial inflammation and fibrosis. Three cases showed fibroblast foci, was BOOP like changes in 4 and honeycombing in 1 case. of the 8 patients, 6 had cellular and fibrosing patterns; 2 had fibrosing patterns only; the former showed better response to glucocorticoid therapy than the latter. CONCLUSIONS: The histologic patterns of NSIP correlated closely with the therapeutic effect of glucocorticoids. It is difficult to differentiate pathologically the fibrosing pattern of NSIP from usual interstitial pneumonia, therefore clinical data are indispensable in the diagnosis.

Adult↗
PubMed1990

Bypass of superior vena cava. Fifteen years' experience with spiral vein graft for obstruction of superior vena cava caused by benign disease.

Nine patients had operations for obstruction of the superior vena cava with superior vena caval syndrome caused by benign disease. Three patients had fibrosing mediastinitis, four had fibrosing mediastinitis with caseous necrosis, one had thrombosis of the superior vena cava around a pacemaker electrode, and one had spontaneous thrombosis of the superior vena cava. Patients ranged in age from 25 to 68 years. All bypass operations were performed with a composite spiral vein graft constructed from the patient's own saphenous vein, split longitudinally and wrapped around a stent in spiral fashion. The edges of the vein were sutured together to form a large conduit ranging in diameter from 9.5 to 15.0 mm. Six grafts were from the left innominate vein and three grafts were from the internal jugular vein. The grafts were placed into the right atrial appendage in all except one case, in which the graft was to the distal superior vena cava. Follow-up extends from 1 to 15 years. One patient required reoperation at 4 days for thrombosis at the innominate vein-graft anastomosis. Resection of the anastomosis and reconstruction of the graft rendered the patient symptom free. Two grafts closed during the first year after operation. One patient had advancing fibrosing mediastinitis, and a second bypass graft from the external jugular veins remain patent. Another patient had recurrence of spontaneous venous thrombosis. Thus seven of nine grafts remain patent for up to nearly 15 years and all but one patient is free of superior vena caval syndrome. These data show that bypass of the obstructed superior vena cava with a spiral vein graft relieves superior vena caval syndrome and demonstrate long-term patency of the graft.

Adult↗
PubMed1989

Diffuse fibrosis of the pancreas: a peculiar pattern of pancreatitis in alcoholic cirrhosis.

In order to evaluate the effects of chronic alcohol consumption on pancreas morphology we reviewed the autopsy data of 530 patients: 148 with liver alcoholic cirrhosis (group I), 39 with non alcoholic cirrhosis (group II), 47 autopsies of chronic alcohol drinkers without liver cirrhosis (group III) and 296 non alcoholic patients with normal liver, age and sex-matched with group I (group IV). In the control group (group IV) lipomatosis and intralobular fibrosis were common (57 percent and 40 percent) and increased with age. The prevalence of five elementary lesions (protein plug, dilatation of duct, epithelial atrophy, canalicular regression and perilobular fibrosis) and of one pathologic diagnosis (diffuse fibrosing pancreatitis) were higher in group I than in group IV. Duct lesions (protein plugs, canalicular regression and epithelial atrophy) were also significantly higher in drinkers without cirrhosis (group III) than in group IV. Chronic calcifying pancreatitis was rare (2 cases in group I). Thirty-six cases were classified as diffuse fibrosing pancreatitis. This constituted an homogeneous histopathologic group, significantly more frequent in the group of alcoholic cirrhosis, and was always discovered incidentally at autopsy. Because diffuse fibrosing pancreatitis might easily be confused with the morphological changes of chronic calcifying pancreatitis, we suggest to include this histopathologic entity into the Marseille's classification of pancreatitis.

Acute Disease↗
PubMed1987

[Pulmonary function of patients with bird-breeders' exogenous allergic alveolitis].

A total of 59 bird fanciers suffering from alveolitis were examined, of them 23 with alveolitis of bronchitis type, 24 with alveolitis of pneumonic type and 11 alveolitis of fibrosing type. In all 3 variants of a course of alveolitis the obstructive syndrome was the main sign of functional disturbances. Intrapulmonary gas exchange disturbances slightly expressed in alveolitis of bronchitis type and pneumonic type, acquired greater importance in fibrosing alveolitis. The absence of restrictive changes in the patients could result from weakly expressed fibrosing of the pulmonary tissue, its combination with emphysematous-dystrophic changes as well as with lung hyperinflation as a result of disturbances in bronchial permeability.

Adult↗
PubMed1984

The morphogenesis and classification of diffuse interstitial lung diseases: a clinicopathological approach, based on tissue reaction patterns.

This account gives a clinicopathological overview and classification of diffuse interstitial lung diseases, emphasising the interstitial pneumonias. The morphogenesis and progression of fibrosing alveolitis are discussed in relation to the normal cellular and extracellular components of the pulmonary interstitium, with the alveolar macrophage playing a pivotal role. So-called desquamative interstitial pneumonia is considered to represent an early steroid-responsive cellular exudative phase of fibrosing alveolitis, most of the intra-alveolar cells being macrophages rather than type II pneumocytes. The distinction between fibrosing alveolitis and diffuse alveolar damage, and their possible pathogenetic relationships to each other, are also discussed. Throughout this presentation it is stressed that inflammatory interstitial disorders such as the "desquamative" alveolopathies constitute stereotyped patterns of tissue reaction to a variety of injurious agents, which should always be taken into account in reaching a definitive clinicopathological diagnosis, especially in fibreoptic biopsies where histomorphological discriminants may not be present because of the small amount of tissue sampled.

Adult↗
PubMed1996

Evidence for two patterns of inheritance of sensitivity to induction of lung fibrosis in mice by radiation, one of which involves two genes.

We showed previously that autosomal recessive determinants control the development of pulmonary fibrosis in mice during the early and late phases after irradiation. The extent of fibrosis was inversely correlated with the intrinsic lung activity of both plasminogen activator (PLA) and angiotensin-converting enzyme (ACE). To test these observations further, two groups of mice were given a dose of 15 Gy to the thorax: offspring of a backcross between C57L/J ("fibrosing mice") and the F1 of CBA/J ("non-fibrosing in the early phase") x C57L/J, and additional F1 individuals of CBA/J x C57L/J. Mice were euthanized upon developing a substantial respiratory deficiency (50% reduction in carbon monoxide uptake) during the early phase (14-25 weeks postirradiation). Seventeen mice from the backcross were heavily fibrosed, 38 were classed as intermediate, and 15 contained no fibrosis. No evidence of sex linkage was seen. These data strongly support our earlier conclusions and suggest that two autosomal genes which function additively determine the extent of the principal type of fibrosis in these strains. As no indication of a bimodal distribution of lung PLA or ACE activity was obtained, it is unlikely that one of the genes controls the level of either enzyme. The F1 mice unexpectedly showed small amounts of an unusual type of fibrosis which was not associated with hyaline material or fibrin deposits, in contrast to all previous reports of fibrosis during the early phase in mice. Similar, fibrin-free fibrosis was found during the early phase in mast cell-deficient WBB6F1/J mice (and their normal siblings). In the F1 mice this unusual fibrosis appears to be regulated independently by two additional genes, one of which is sex-linked.

Animals↗
PubMed1977

[Heart and pericardial metastases resulting from bronchial carcinoma. Side effects of radiotherapy (author's transl)].

A brief survey of bibliography on heart and pericardial metastases resulting from bronchial carcinoma is followed by a report on our autopsy findings in 110 patients suffering from bronchial carcinoma. In 29 cases, i.e. 26 p.c., heart and pericardial metastases were found. In three cases, only the heart was affected, in 16 cases only the pericardium, and in 10 cases both heart and pericardium were involved. In 27 cases, they were spread by way of the blood and were mostly part of a general formation of hematogenous metastases. In-growth exclusively from primary tumour regions was found only in two cases. In 19 cases, metastases were both hematogenous and grown-in per continuitatem. Anatomicopathologically, 18 patients had a small cell carcinoma, 10 a squamous cell carcinoma, and one showed an adenocarcinoma. While 15, i.e. 14%, of our 110 patients, on whom we performed an autopsy, had died from arrosion bleeding, this was true only in one case in the group of 29 patients with heart and pericardial metastases. Radiation side effects in the form of lung and pericardial fibroses in the patients, who had generally been treated with cobalt 60 gamma rays, were confirmed by autopsy findings only in one third in both cases as compared with the findings by X-ray diagnosis during life. Lung fibroses were found in 16 cases (14%), and pericardial fibroses in 6 cases (5.5%). They were not strictly dependent on the dose.

Adenocarcinoma↗
PubMedDate not supplied

In vivo pulmonary toxicity of cellulose in rats.

Cellulose after a single intratracheal dose (15 mg per animal) brought about fibrosing granulomatous alveobronchiolitis and an increase of IgA production in the bronchoalveolar lavage. Fibrosing alveolitis showed moderate progression as a function of time. With different morphological methods, injury of type I pneumocytes and the incomplete repair of type II pneumocytes were detected. The damage of the alveolar epithelium initiated and activated a series of processes that led to definite pulmonary alterations: pulmonary fibrosis leading to the disintegration of the alveolo-capillary morphological functional unit.

Animals↗
PubMed1982

Relationships between steroid receptor and epithelial cell proliferation in benign fibrocystic disease of the breast.

Tissue specimens from 27 patients with mammary fibrocystic disease were assayed for estrogen (ER) and progestin (PR) receptors. Seventeen patients (63%) had ER-positive lesions (greater than 5 fmol/mg protein). A progression in ER presence was noted from fibrocystic disease (35%) and fibrosing adenosis (50%) to lobular and ductal hyperplasia (85%). Similarly, ER content increased from 14.5 +/- 13 fmol/mg cytosol protein in fibrocystic disease and fibrosing adenosis to 31.5 +/- 23 fmol/mg protein in epithelial hyperplastic lesions. Furthermore, the ER-PR couple was only encountered in lobular and ductal hyperplasia. The authors' data indicate that the incidence of steroid receptor parallels the intensity of hyperplasia in benign breast disease.

Adult↗