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PubMed2006

Histologic findings in recurrent HBV.

KEY CONCEPTS: 1. The histopathologic presentation of hepatitis B (HB) infection in liver allografts is generally similar to that seen in the nonallografts. 2. An atypical pattern of recurrent HB, i.e., fibrosing cholestatic hepatitis (FCH) occurs in a small number of patients. These patients present with a severe cholestatic syndrome, which may clinically resemble acute or chronic rejection. 3. There are several other possible causes of acute and chronic hepatitis in liver allografts that may need to be considered. 4. Hepatitis B virus (HBV) infection in the liver allograft can easily be confirmed by performing immunohistochemical stains for hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg). The expression pattern of these HBV antigens varies and is sometimes helpful in determining whether the liver injury is mainly from the HBV or from other causes in coexistence with the HBV infection. 5. Histological grading of the necroinflammatory activity and staging of the fibrosis should only be applied when the changes are related to the recurrent HB. 6. The pathology of liver transplantation is complex; therefore, clinical correlations remain extremely important in arriving at the final and correct diagnosis.

Acute Disease↗
PubMed2007

Immunosuppression with calcineurin inhibitors with respect to the outcome of HCV recurrence after liver transplantation: results of a meta-analysis.

A controversy exists over whether the outcome of a hepatitis C virus (HCV)-infection-related liver transplant differs based on the calcineurin inhibitor (CNI) used. We have performed a systematic review and a subsequent meta-analysis evaluating tacrolimus (Tac)-based vs. cyclosporine A-based immunosuppression in HCV-infected liver transplant recipients. Searches were conducted to locate randomized controlled trials comparing Tac vs. cyclosporine A. Data on HCV liver transplant recipients were obtained, independently of whether the study was specifically designed for patients with this disease or not. A fixed effects model was used for statistical pooling of the relative risks (RR) for the different outcomes. A total of 5 articles (366 patients) fulfilled the inclusion criteria. Statistically significant differences between Tac-based vs. cyclosporine A-based therapies were not found for mortality (P = 0.11; RR = 0.72; 95% confidence interval [CI], 0.49-1.08), graft survival (P = 0.37; RR = 0.86; 95% CI, 0.61-1.21), biopsy-proven acute rejection (P = 0.65; RR = 0.91; 95% CI, 0.61-1.36), corticoresistant acute rejection (P = 0.26; RR = 2.25; 95% CI, 0.55-9.29), and fibrosing cholestatic hepatitis (P = 0.92; RR = 0.96; 95% CI, 0.41-2.26). In 1 study, no differences were detected regarding severe fibrosis at 1 yr. In conclusion, patient and graft survivals in HCV-positive liver transplant patients are similar independently of the CNI selected as basic immunosuppressant. Unfortunately, data on the severity of recurrence and effect on viremia are scarce. Well-designed randomized prospective studies are needed to determine whether there are differences between the 2 CNIs regarding these specific variables.

Biopsy↗
PubMed1985

Experimental study of lymphatic contractility in lymphedema and its clinical significance.

Fifty-four rats that had been used as models for lymphedema were divided into nine groups to observe the changes of lymphatic contractility in pathologic conditions at varying postoperative days. The changes of the lymphatic contractility were divided into three stages in this paper: In the first stage, the lymphatic contractility was impaired by high intralymphatic pressure, but the morphology of its wall was normal and it could recover its function if the pressure was decreased. In the second stage, the blocked lymphatic lost its contractile function partially or completely because its wall thickened and fibrosed, but the newborn lymphatics possessed contraction function and could be anastomosed. In the third stage, most lymphatics had lost their contractile function because of severe fibrosis. The fibrosis of the tissue even blocked the growth of the newborn lymphatics. In this stage, therefore, it was unsuitable to do a lymphatic-venous anastomosis. It can be concluded from the experiment that lymphatic contractility should be considered before performing a lymphatic-venous anastomosis. The lymphatic that still has contractile function should be selected for lymphatic-venous anastomosis.

Animals↗
PubMed2003

hnRNP B1 expression in benign and malignant lung disease.

Evidence is accumulating to suggest that hnRNP B1 expression may be a useful tool in the early diagnosis of lung cancer. This study examined the immunohistochemical expression of hnRNP B1 in archived sections of resected lung cancers and compared the patterns of expression with those seen in similar archived sections of non-neoplastic lung. Particular attention was paid to the expression of hnRNP B1 in the benign bronchial cells in both cases, to establish if overexpression of this protein in respiratory epithelial cells is specific for malignancy. Nineteen cases of different types of non-small cell carcinoma were examined (eight squamous cell, six adenocarcinomas, two carcinosarcomas, two undifferentiated large cell carcinomas, and one mucoepidermoid carcinoma) and compared with sections from 16 open lung biopsies (three cases of cryptogenic fibrosing alveolitis, two cases of sarcoidosis, two cases of organizing pneumonia, and one case each of tuberculosis, extrinsic allergic alveolitis, non-specific interstitial pneumonitis, pneumocystis pneumonia, aspergilloma, respiratory bronchiolitis-interstitial lung disease, mineral dust disease, Sjögren's syndrome and systemic sclerosis vascular variant). All the tumours showed positive staining, with the vast majority, 16/19 (84%), showing strong diffuse nuclear staining. The background cells of these cases showed positive staining in alveolar macrophages, lymph node germinal centres, bronchial mucous glands, and bronchial epithelial cells. No significant difference was seen in the percentage of positive bronchial epithelial cells in bronchi adjacent to the tumour compared with the resection margins. In the benign lung cases, positive bronchial epithelial cells were seen in a small percentage, 3/16 (18%), of cases, but the majority of cases showed no or very focal staining. The levels of expression between benign epithelial cells of malignant cases, compared with benign, showed a significant difference when the staining was assessed in percentage of positive nuclei (p = 0.001, Fisher's exact test). The results confirm that hnRNP B1 is widely expressed in a range of lung carcinomas; that expression is seen in benign bronchial epithelial cells and inflammatory cells; and that expression in background bronchial epithelial cells appears to be higher in malignant than in benign lung disease. It is feasible that this biomarker may be of use in the detection of early lung cancer, provided that levels of expression can be accurately quantified.

Adenocarcinoma↗
PubMed2003

Expression of the developmental Sonic hedgehog (Shh) signalling pathway is up-regulated in chronic lung fibrosis and the Shh receptor patched 1 is present in circulating T lymphocytes.

During pulmonary development, Sonic hedgehog (Shh) and transforming growth factor beta1 (TGF-beta1) signalling both contribute to branching morphogenesis. In interstitial lung disease, the complex alveolar structure of the lung is disrupted and remodelled, which leads to fibrosis, loss of respiratory surface, morbidity, and mortality. It is well documented that TGF-beta1 is involved in fibrosis. However, little is known about Shh signalling in damaged epithelia. This study examined whether or not components of the Shh signalling pathway, as well as TGF-beta1, are expressed in human fibrotic lung disease (cryptogenic fibrosing alveolitis and bronchiectasis) and in murine experimental models of fibrotic and non-fibrotic chronic pulmonary inflammation. Using immunohistochemistry, it was observed that Shh, like TGF-beta1, is up-regulated in epithelial cells at sites of fibrotic disease but not non-fibrotic inflammation. The Shh receptor patched was detected in infiltrating mononuclear cells and alveolar macrophages, as well as normal resting peripheral blood T lymphocytes. Neither Shh nor patched is expressed by hyperproliferative goblet cells in inflammatory epithelium. This study demonstrates that patched is present in human peripheral CD4 and CD8 lymphocytes at both protein and mRNA levels. Taken together, these results suggest that components of the highly conserved Shh signalling pathway may play a role in the remodelling of damaged pulmonary epithelium and that damaged epithelium and cells of the immune system may communicate via this pathway.

Animals↗
PubMed2001

Upregulation of tenascin and TGFbeta production in a type II alveolar epithelial cell line by antibody against a pulmonary auto-antigen.

Type II alveolar epithelial cells express a 70-90 kDa antigen to which circulating auto-antibodies have been previously identified in patients with cryptogenic fibrosing alveolitis (CFA). In vitro experiments have been conducted with a rabbit polyclonal antibody raised to this auto-antigen, and the type II epithelial cell line A549. This study examined possible effects that interaction of this antibody with type II epithelial cells might have on the production of cytokines and extracellular matrix components that may be important in the pathogenesis of CFA. There was a significant increase in TGFbeta and tenascin, but not IL4, production by the A549 cells after culture with the immune serum. Further experiments showed that after 72 hours in culture, the antibody decreased A549 cell number in a complement-dependent process, which appeared to be cytostatic rather than cytolytic. These results indicate in vitro biological activity for this antibody and suggest a possible in vivo role for auto-antibody to type II epithelial cells in the pathogenesis of CFA.

Animals↗
PubMed2005

National differences in reporting 'pneumonia' and 'pneumonia interstitial': an analysis of the WHO International Drug Monitoring Database on 15 drugs in nine countries for seven pulmonary conditions.

PURPOSE: Increased post-marketing reports of 'interstitial pneumonia' as an adverse drug reaction (ADR) from the use of gefitinib, irinotecan, or leflunomide among patients in Japan have not been noted in other countries. The WHO International Drug Monitoring Database was analyzed to examine Japan's pattern of reporting the term 'pneumonia interstitial' for 15 selected drugs with a mixed history of association with pulmonary ADRs. METHODS: ADR counts from the WHO Database for 1992-2001 were obtained for 15 disparate drugs (three androgen blockers, eight cytotoxics, one proton pump inhibitor, one monoclonal antibody, and two anti-epileptics) from nine countries (Australia, France, Germany, Italy, Japan, Spain, Thailand, U.K., and U.S.A.) for seven pulmonary ADR terms (alveolitis fibrosing, pneumonia, pulmonary fibrosis, lung fibrosis interstitial, pulmonary infiltration, interstitial lung disease, and pneumonia interstitial). Statistical analyses included estimating Poisson-distributed expected rates, observed/expected (O/E) ratios, and 95% confidence intervals (CI). The overlapping nature and changes in definition over time of these terms in medical texts and in the WHO-ART, COSTART, J-ART, and MedDRA coding systems is also noted. RESULTS: Compared to other countries, both Japan and France did not have higher O/E reporting ratios for all seven pulmonary ADRs combined, but did have higher O/E ratios for 'pneumonia interstitial' and lower O/E ratios for 'pneumonia' for the same drugs. CONCLUSIONS: Japan and France were found to preferentially use the term 'pneumonia interstitial' for ADR where other countries used 'pneumonia.' This cultural pattern coincides with the fact that 'pneumonia interstitial' in older versions of COSTART, J-ART, and MedDRA were subsumed under infectious pulmonary diseases.

Adverse Drug Reaction Reporting Systems↗
PubMed2001

Development of progressive pulmonary interstitial and intra-alveolar cholesterol granulomas (PICG) associated with therapy-resistant chronic systemic juvenile arthritis (CJA).

A girl aged 5 years with therapy-resistant chronic systemic juvenile arthritis (CJA) developed progressive fibrosing lung disease. Histology of an open lung biopsy revealed pulmonary interstitial and intra-alveolar cholesterol granulomas (PICG). Since treatment with steroids and immunosuppressive drugs did not prevent progression of lung fibrosis, an experimental treatment with a tumor necrosis factor alpha (TNF alpha) antagonist etanercept was started. Although development of chronic changes in the lung parenchyma could not be prevented, this treatment brought considerable relief and markedly improved the child's physical capacity. By ruling out other causes for development of PICG, we concluded that the primary disease had caused the development of cholesterol granulomata by macrophage activation. We suggest, therefore, that a trial with etanercept in children with otherwise therapy-resistant CJA should be considered, especially if pulmonary complications have developed.

Arthritis, Juvenile↗
PubMed1992

Technique and use of transbronchial biopsy in children and adolescents.

Since July 1988, a total of 92 transbronchial biopsies (TBB) have been performed in 18 patients (aged 3-16 years). Twelve patients (67%) were heart-lung transplant (HLT) recipients undergoing surveillance for pulmonary graft rejection and infection. The remainder included immunocompromised patients at risk of opportunistic infections (n = 4), patients with fibrosing alveolitis (n = 1) and a collagen vascular disorder with suspected lung involvement (n = 1). TBB was performed through either a fiberoptic (n = 50) or a rigid (n = 41) bronchoscope, all under general anesthesia. On one occasion a cardiac bioptome was used through an endotracheal stent. The sensitivity of TBB for diagnosing acute and chronic rejection in HLT patients was 88% and 60%, respectively (specificity, 91% and 100%). Definitive diagnoses were made in 4 (67%) of the non-HLT group. Bronchoalveolar lavage (BAL) was performed during each procedure for microbiological and cytological examination. Thirty-four pathogenic organisms including Pseudomonas aeruginosa (16/34), Staphylococcus aureus (8/34), and Candida albicans (5/34) were isolated from BAL culture. Complications included pneumothorax (8%), transient pyrexia (7%), and dyspnea (2%).

Acquired Immunodeficiency Syndrome↗
PubMed2006

Diagnosis and treatment of intestinal malabsorption in cystic fibrosis.

Intestinal malabsorption is severe and of early onset in virtually all people who have cystic fibrosis. The main cause is deficiency of pancreatic enzymes. Bicarbonate deficiency, abnormal bile salts, mucosal transport problems, motility differences, and anatomical structural changes are other contributory factors. Effective treatment should allow a normal to high-fat diet to be taken, control symptoms, correct malabsorption, and achieve a normal nutritional state and growth. Appropriate pancreatic enzyme replacement therapy will achieve normal or near-normal absorption in most people with cystic fibrosis. Early identification and treatment of intestinal malabsorption is critical to achieving optimal nutritional status. The occurrence of fibrosing colonopathy in a few patients on very high doses of those enzymes which have the copolymer Eudragit L30 D55 in their covering resulted in guidelines in the UK to avoid doses equivalent to more than 10,000 IU lipase per kg per day, and also to avoid preparations containing this copolymer in children and adolescents. For patients not responding to 10,000 IU lipase per kg per day review of adherence to treatment, change of enzyme preparation, variation in time of administration, and reduction in gastric acid may improve absorption. The importance of early investigation to exclude other gastrointestinal disorders as a cause of the patient's symptoms, rather than merely increasing the dose of enzymes, is stressed. With modern pancreatic enzymes in doses up to or only slightly in excess of 10,000 IU lipase per kg per day, adequate control of gastrointestinal symptoms and absorption can be achieved, and a normal nutritional state and growth rate maintained in most people with cystic fibrosis.

Adolescent↗
PubMed2000

Immune stimulation in scleroderma patients treated with thalidomide.

Scleroderma (SSc) is a fibrosing connective tissue disease that is poorly responsive to any treatment, including immune suppression. SSc shares many characteristics with chronic graft-versus-host disease (GVHD). Because the immunomodulatory drug thalidomide has proven beneficial in chronic GVHD, we studied the immune response and clinical effects of thalidomide in SSc patients. We treated 11 SSc patients with thalidomide in an open label, dose escalating, 12 week study. Histologic comparison of skin biopsies showed changes in skin fibrosis and an increase in epidermal and dermal infiltrating CD8(+) T cells with thalidomide treatment. In thalidomide-treated SSc patients, plasma levels of IL-12 and TNF-alpha increased, while plasma IL-5 and IL-10 levels remained unchanged. These changes were associated with clinical effects, including dry skin, dermal edema, transient rashes, decreased gastroesophageal reflux symptoms, and healing of digital ulcers. When SSc PBMCs activated by anti-CD3 mAb were exposed to thalidomide, increases in both production of IL-2, IL-3, GM-CSF, and IFN-gamma and T cell expression of CD40L were observed. Thalidomide therefore appears to induce immune stimulation in SSc patients in association with clinical changes. However, it remains to be shown whether long-term enhancement of immune responses in SSc patients is clinically beneficial.

Adjuvants, Immunologic↗
PubMed1996

Angiotensin converting enzyme and myofibroblasts during tissue repair in the rat heart.

Following left coronary artery ligation in the rat, markedly increased angiotensin converting enzyme (ACE) binding appears at the site of myocardial infarction (MI). This is also the case in fibrosed visceral pericardium that follows pericardiotomy alone (without MI). Immunohistochemical ACE labeling, using a monoclonal antibody, indicates fibroblast-like calls express ACE at each of these sites of tissue repair. It is unknown, however, whether these cells are phenotypically transformed fibroblasts containing alpha-smooth muscle actin (i.e. myofibroblasts). This study was therefore undertaken to determine whether myofibroblasts appear at the site of MI and pericardial fibrosis and their relationship to ACE expression. MI was created by left coronary artery ligation. Fibrosis of the visceral pericardium was induced by pericardiotomy alone. Hearts were studied on postoperative day 3, week 1, 2, 4 and 8. In serial sections of the same heart: immunohistochemistry (anti alpha-smooth muscle actin antibody and monoclonal ACE antibody, 9B9) was used to detect myofibroblasts and cells expressing ACE, respectively. We found that at sites of MI and pericardial fibrosis, myofibroblasts began to appear on day 3 and became abundant at week 1, 2, 4 and remained in these repairing sites for at least 8 weeks. Myofibroblasts at sites of MI and pericardial fibrosis are positively labeled by ACE antibody. Thus in these models of tissue repair involving either MI or pericardial fibrosis, myofibroblasts are associated with ACE expression. These findings suggest that myofibroblast ACE may play a role in the fibrogenic response of tissue repair in the rat myocardium by regulating local concentrations of substances involved in healing and matrix remodeling.

Animals↗
PubMed1995

Lung toxicity of hard metal particles and production of interleukin-1, tumor necrosis factor-alpha, fibronectin, and cystatin-c by lung phagocytes.

Hard metal alloys (WC-Co) are made of a mixture of cobalt (Co; 6%) and tungsten carbide (WC; 94%) particles. Chronic inhalation of hard metal dust can lead to the development of a fibrosing alveolitis, the pathogenesis of which is still undefined. The present investigation was undertaken to assess the effect of Co, WC, and WC-Co particles on the release by lung phagocytes of interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), fibronectin, and cystatin-c. The responses were compared with those induced by two other lung toxicants, i.e., crystalline silica (DQ12) and arsenic trioxide (As2O3). IL-1 and TNF-alpha activities produced in the presence and absence of LPS stimulation were measured with the aid of bioassays while fibronectin and cystatin-c were determined by latex immunoassays. In vitro, maximal noncytotoxic doses of As2O3, Co, WC, or WC-Co did not significantly affect the production of these mediators by rat alveolar macrophages. In contrast, DQ12 enhanced the production of TNF-alpha (with and without LPS stimulation) and IL-1 (after LPS stimulation) and decreased cystatin-c release (in the absence of LPS). Following a single intratracheal instillation of the different test preparations in the rat, the response of the lung phagocytes obtained by bronchoalveolar lavage (BAL) 24 hr later was examined. We were unable to detect any consistent effect of Co (0.06 mg/100 g body wt), WC (1 mg/100 g body wt), or WC-Co treatment (1 mg/100 g body wt) on the production of the above mediators. In contrast, after LPS stimulation, As2O3 (0.5 mg/100 g body wt) and DQ12 (1 mg/100 g body wt) stimulated the production of TNF-alpha and IL-1. In the absence of LPS, As2O3 stimulated fibronectin and cystatin-c production and DQ12 stimulated cystatin-c release. Since the dose of WC-Co used in vivo (1 mg/100 g body wt) caused pronounced lung inflammation (increased LDH, protein, and albumin levels in BAL fluid), we conclude that the acute lung toxicity of WC-Co particles is not mediated through enhanced production of the examined mediators by lung phagocytes.

Alloys↗
PubMed1995

Retinal and choroidal responses to panretinal photocoagulation: an ultrastructural perspective.

BACKGROUND: There have been few histological or ultrastructural studies of the outer retina and choriocapillaris following panretinal photocoagulation therapy. This investigation examines the long-term morphological effects of panretinal photocoagulation in two patients with type II diabetes who had received laser treatment more than 6 months prior to death. METHODS: Regions of retina and choroid from each patient were fixed in 2.5% glutaraldehyde, dissected out and examined using light microscopy and scanning and transmission electron microscopy. RESULTS: After removing the neural retina, scanning electron microscopy of non-photocoagulated areas of the eye cups revealed normal cobblestone-like retinal pigment epithelial (RPE) cells. Regions with laser scars showed little RPE infiltration into the scar area, although large rounded cells often appeared in isolation within these areas. Sections of the retina and choroid in burn regions showed a complete absence of the outer nuclear layer and photoreceptor cells, with the inner retinal layers lying in close apposition to Bruch's membrane. Non-photocoagulated regions of the retina and choroid appeared normal in terms of both cell number and cell distribution. The RPE layer was absent within burn scars but many RPE-like cells appeared markedly hypertrophic at the edges of these regions. Bruch's membrane always remained intact, although the underlying choriocapillaris was clearly disrupted at the point of photocoagulation burns, appearing largely fibrosed and non-perfused. Occasional choroidal capillaries occurring in this region were typically small in profile and had plump non-fenestrated endothelium. CONCLUSIONS: This study outlines retinal and choroidal cell responses to panretinal photocoagulation in diabetic patients and demonstrates an apparent reduction in the capacity of these tissues to repair laser damage.

Aged↗
PubMed1992

Hyaluronan (hyaluronic acid) in lung lavage of asbestos-exposed humans and sheep.

The concentration of hyaluronan was measured in the bronchoalveolar lavage fluid (BALF) of 18 control subjects and 27 workers from the asbestos mills and mines of Québec, 9 without asbestosis and 18 with asbestosis. Hyaluronan was also measured in the BALF of 9 control sheep exposed to 100 ml phosphate-buffered saline (PBS) at 10 day intervals for 39 months, and 13 sheep exposed at the same intervals to 100 mg chrysotile in 100 ml PBS for 24 months. At month 24, the asbestos-exposed sheep were classified into 3 groups: (A) 4 sheep exposed to PBS alone, (B) 4 sheep exposed to 10 mg chrysotile asbestos every 10 days, and (C) 5 sheep exposed to 100 mg chrysotile asbestos every 10 days for 15 months. The BALF hyaluronan averaged 53.9 +/- 7.4 ng/ml in human controls, 67.5 +/- 10.3 ng/ml in asbestos-exposed workers without asbestosis, and 206 +/- 83 ng/ml in workers with asbestosis (p less than 0.05 vs. normal). In the control sheep, BALF hyaluronan was 34.7 +/- 6.9 ng/ml, and it was 31.5 +/- 17.8 ng/ml in the low-dosage asbestos-exposed group (A), 83.0 +/- 27.7 ng/ml in the intermediate-dose group (B), and 248.0 +/- 134.7 ng/ml in the high-dosage group (C) (p less than 0.05 vs. controls). In contrast, the release of plasminogen activator, a protease that may play a role in limiting the fibrotic process, was increased in group A, but not in groups B and C. In conclusion, BALF hyaluronan constitutes an indicator of lung interstitial tissue changes that may reflect the activity of the fibrosing alveolitis associated with chronic asbestos exposure.

Adult↗
PubMed1995

Alveolar macrophages from bronchoalveolar lavage of patients with pulmonary histiocytosis X: determination of phenotypic and functional changes.

In recent years the alveolar macrophage has been found to play a central role in interstitial lung disease. Pulmonary histiocytosis X is characterized by infiltrating fibroblasts, mononuclear cells, and CD-1-positive Langerhans cells. Bronchoalveolar lavage (BAL) fluid displays an increase of CD-1-positive cells and a remarkable exaggeration of the total cell count with only slight changes in the differential cell count. Changes of alveolar macrophage phenotype and functional activity occurring in pulmonary histiocytosis X have not yet been characterized. The BAL fluid of nine patients with histologically proven isolated pulmonary histiocytosis X was compared with that of 16 control patients. Immunophenotyping of alveolar macrophages by monoclonal maturation and differentiation markers of monocyte/macrophage lineage cells [Ki-M2, Ki-M6 (CD-68), Ki-M8, Ki-M1 (CD-11c)] revealed a significant increase of immature macrophages with a more monocyte-like phenotype. The proliferation marker Ki-67 revealed an increased proportion of proliferating macrophages. Functional analysis by measuring oxygen radical release revealed an increase both in baseline and stimulated luminol-enhanced chemiluminescence. Fibronectin production was elevated in alveolar macrophage supernatants from pulmonary histiocytosis X patients. These findings are consistent with phenotypic changes of alveolar macrophages in other interstitial lung diseases such as sarcoidosis and idiopathic pulmonary fibrosis. Local proliferation and the fresh influx of blood monocytes seem to be responsible for the increase in immature and functionally activated alveolar macrophages. The increase in oxygen radical release and fibronectin production suggests an augmented tissue injuring and fibrosing capacity of alveolar macrophages in pulmonary histiocytosis X.

Adult↗
PubMed1996

Molecular variants of fibronectin and laminin: structure, physiological occurrence and histopathological aspects.

This review deals with biological and pathological aspects of various isoforms of the matrix molecules fibronectin and laminin. They are generated by different molecular mechanisms: ED-A+ and ED-B+ fibronectin by alternative splicing of pre mRNA, de novo-glycosylated fibronectin by alternative post-translational O-linked glycosylation of the IIICS region, and the laminin isoforms by exchange of single chains of the heterotrimeric molecule. In contrast to the "common" fibronectin, the distribution of ED-B+ and de novo-glycosylated fibronectin is restricted to embryonic tissues; they subsequently reappear in granulation tissue, in fibrosing processes and in tumour stroma. The expression of these so-called oncofetal fibronectins is stimulated by growth factors (TGF beta). The association of the ED-B+ fibronectin with proliferative activity and newly formed vessels identifies this fibronectin variant as a marker of cellular activity in the process of fibrosis and as a suitable agent for the evaluation of tumour angioneogenesis. Initial results suggest a correlation between the amount of ED-B+ and de novo-glycosylated fibronectin in tumour stroma and the behaviour of carcinomas with regard to their invasiveness and propensity for metastatic dissemination. The current nomenclature of the laminin molecule family is presented. The laminin chain constitution of basement membranes switches from embryonic or proliferatively active to adult terminally differentiated tissues [disappearance of the laminin beta 2 (s) chain] and depends on the tissue type. The discrepancy between the loss of basement membranes (multiple basement membrane defects) in carcinomas and the recently reported increased laminin chain synthesis in these tumours may be explained by abundant laminin chain deposition outside the basement membrane in the carcinoma invasion front, possibly associated with enhanced adhesion of budding tumour cells.

Animals↗
PubMed1995

Hypophysitis in surgical and autoptical specimens.

We present the clinical and histological findings of 11 cases of inflammatory anterior pituitary lesions, 8 of which were obtained during surgery and 3 of which were obtained from autopsies. Additionally, we extended the conventional classification of pituitary inflammatory disease by the new entity " secondary hypophysitis". Of the surgically obtained specimens 5 consisted of inflammatory extension into the pituitary gland out of the surrounding tissue. In all of these patients the inflammation originated from an additional tumor in the sellar region (4 craniopharyngiomas, 1 prolactinoma). These will be referred to as "secondary hypophysitis", an entity which has not yet been mentioned in the literature. Of the remaining 6 cases, 2 were granulomatous hypophysitis, 2 pituitary abscesses, 1 lymphocytic hypophysitis, and 1 showed extensive scarring of the anterior pituitary lobe due to preceeding lymphocytic hypophysitis. At histological examination the basic structure of the anterior pituitary was maintained in all cases. Relative counts of hormone-producing cells were normal. In secondary hypophysitis, the affected area was composed of fibrous tissue and granulation tissue. B and T lymphocytes were present in equal amounts. Granulomas were not found. Inflammatory infiltrates, granulation tissue and fibroses were seen in different proportions. Based on our results and three other cases reported in the literature so far, we think that the presently used classification of pituitary inflammatory diseases lacks an entity which describes a non-abscess-forming inflammation of the pituitary gland originating from an associated pathological process. Therefore, we introduced the term secondary hypophysitis to describe this fourth entity of pituitary inflammatory disease.

Adult↗