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Biomedical subjects

M C Cid

Publications and source records attributed to M C Cid.

At least 37 records · Page 2Linked to original sources
PubMed1997

Clinical features in patients with permanent visual loss due to biopsy-proven giant cell arteritis.

The objective was to determine associated clinical findings in patients with visual loss due to giant cell arteritis (GCA) by means of a record review of 146 patients with biopsy-proven GCA. Twenty-three (15.75%) patients had lost vision. All of these patients complained of classical GCA cranial symptoms for an average of 1.3 months, 34.8% had an apparent isolated polymyalgia rheumatica for an average of 10.8 months and 65.2% had premonitory visual symptoms before visual loss for an average of 8.5 days. A clear delay in diagnosis and treatment was present in 15 patients (65.2%) who complained of at least two classical cranial symptoms for longer than 3 weeks and/or who had presented premonitory visual symptoms for longer than 72 h before blindness. Two additional patients lost vision while receiving standard steroid therapy. In conclusion, a high proportion of patients with permanent visual loss have a delayed diagnosis and treatment. A wider recognition of the disease would potentially reduce the prevalence of irreversible visual loss among GCA patients.

Biopsy↗
PubMed1996

Expression of an estrogen receptor by human coronary artery and umbilical vein endothelial cells.

BACKGROUND: Premenopausal women have much lower susceptibility to coronary artery disease than do men or postmenopausal women. It has been proposed that estrogen plays a role in cardioprotection, but little information is available regarding the mechanism by which estrogen may help to protect the vasculature. Here, we describe an estrogen receptor (ER) in human coronary artery and umbilical vein endothelial cells. METHODS AND RESULTS: Human umbilical vein endothelial cells and human coronary artery endothelial cells were cultured in hormone-free medium for 48 hours before experiments. Estradiol (3.7 nmol/L) added to cultures promoted proliferation by a mechanism that is inhibited by the specific ER antagonist ICI182,780. Estradiol-treated cells incorporated twice the [3H]thymidine of hormone-free cells; this increase was prevented by ICI182,780. Endothelial cells from both sources stained in a nuclear pattern with an ER-specific antibody. Ribonuclease protection assay detected mRNA for the ER. Ligand-binding studies estimated 2 x 10(4) to 8 x 10(4) receptors per cell and a Kd of approximately 5 nmol/L. Interaction of ERs with a consensus estrogen response element was shown by an electrophoretic mobility shift assay. In addition, an antibody against the ER supershifted the protein-DNA complex. CONCLUSIONS: These studies define the presence of an ER in human coronary artery and umbilical vein endothelial cells. They support the hypothesis that cardioprotective effects of estrogen are mediated, at least in part, through a classic steroid hormone receptor mechanism.

Arteries↗
PubMed1996

Polyarteritis nodosa in human immunodeficiency virus infection: report of four cases and review of the literature.

Four patients with HIV infection were diagnosed as having panarteritis nodosa type vasculitis in muscle samples taken by biopsy. Fever, weight loss and neuromuscular symptoms were the major complaints. All but one were successfully treated with a low dose of prednisone. The other patient refused treatment, but her muscular complaints did not worsen during 9 months of follow-up. Previously reported cases in the literature are reviewed.

Adult↗
PubMed1996

New developments in the pathogenesis of systemic vasculitis.

Over the past few years, novel pathogenic mechanisms leading to vascular inflammation and injury have been discovered. Circumstantial evidence that supports a pathogenic role for antineutrophil cytoplasmic antibodies (ANCA) in mediating vessel damage includes in vitro studies showing that ANCA promote neutrophil activation and endothelial injury. In addition, several animal models of ANCA-induced vasculitis and glomerulonephritis have been developed. The role of T cell-mediated immune mechanisms in vasculitis has been strengthened by molecular studies demonstrating clonal expansion of selected T cell populations in inflammatory foci, possibly recognizing a disease-relevant antigen. There is also increasing awareness of the important role that adhesion molecules may play in the development of vascular inflammatory infiltrates. The putative participation of cytokines and growth factors, released by inflammatory cells, in vessel occlusion and organ dysfunction, is a focus of increasing research activity.

Animals↗
PubMed1996

Expression of intercellular adhesion molecule-3 (ICAM-3/CD50) in malignant lymphoproliferative disorders and solid tumors.

ICAM-3/CD50 is a recently described LFA-1 counter receptor that seems to play an important role in the initiation of immune responses. In this study we have examined the expression of ICAM-3/CD50 in a large series of human neoplasms including 101 Non-Hodgkin's lymphomas (NHL), 26 Hodgkin's disease, and 38 solid tumors to define the distribution patterns of this molecule in malignant neoplasms and their possible correlation with clinical and pathological characteristics of the patients. In NHL, ICAM-3/CD50 was expressed in almost all the tumors with a tendency to be lost in high grade lymphomas. Reed-Sternberg cells and their variants in Hodgkin's disease were always negative independently of the histological subtype of the disease. No expression was observed in tumor epithelial cells of the 38 solid tumors examined. Strong endothelial cell staining was observed in 31% of the NHL and 31% of Hodgkin's disease. ICAM-3 expression in these cases was restricted to small tumor vessels. ICAM-3 expression in endothelial cells of NHL was significantly more frequent in high grade (40%) than in low grade lymphomas (14%) (p = 0.012). In addition, tumor vessels were also positive in 29% of solid tumors independently of the histological type. No correlation was observed between ICAM-3 expression in tumor or endothelial cells and other clinical and pathological characteristics of the patients. These findings indicate that ICAM-3 expression in human tumors is restricted to hematological neoplasms with a tendency to be lost in high grade lymphomas and Hodgkin's disease. ICAM-3 is also expressed by endothelial cells from tumor-associated neovascularization in both lymphoid and solid tumors.

Animals↗
PubMed1996

Oestrogen and endothelial cell angiogenic activity.

1. Increasing evidence suggests that oestrogens protect women from cardiovascular disease during their reproductive years. Although most studies by others have examined the effect of oestrogen on vascular smooth muscle cells, we have evaluated the effect of oestrogen on the angiogenic behaviour of endothelial cells. 2. Oestrogen enhances endothelial cell attachment, proliferation, migration and organization into capillary-like structures in vitro. In vivo, oestrogen augments experimental angiogenesis. 3. As the same endothelial cell behaviours that are important in angiogenesis in small vessels are also important in the healing response to injury of large vessels, it is likely that the effect of oestrogen on these endothelial cell functions contributes significantly to the cardioprotective effects of oestrogen in women.

Animals↗
PubMed1996

Von Willebrand factor in the outcome of temporal arteritis.

OBJECTIVE: To determine fluctuation in circulating von Willebrand factor (vWF) in the outcome of patients with temporal arteritis. METHODS: Plasma vWF antigen concentrations were measured in 65 patients with biopsy proven temporal arteritis at different disease activity stages, in 12 with isolated polymyalgia rheumatica, and in 16 controls. Fourteen temporal arteritis patients underwent serial determinations during the course of their disease. RESULTS: vWF concentrations were significantly raised in temporal arteritis (mean 220 [arbitrary units], range 96 to 720) and in polymyalgia rheumatica (mean 196, range 103 to 266) compared with healthy controls (mean 98, range 75 to 137) (P < 0.05). Although vWF values tended to be higher in temporal arteritis, no significant differences were found between temporal arteritis and polymyalgia rheumatica patients nor between temporal arteritis patients with ischaemic complications (mean 269, range 130 to 720) and those who presented with polymyalgia rheumatica or constitutional symptoms only (mean 179, range 140 to 220). The highest levels were obtained in patients with associated, mainly infectious, diseases (mean 631, range 240 to 1680). Raised vWF values found in active temporal arteritis patients (mean 220, range 96 to 720) persisted within the first two years after the beginning of treatment (mean 244, range 102 to 510) but tended to normalise in patients in long term remission (mean 143, range 50 to 260). CONCLUSIONS: Persistent elevation of vWF during early remission of temporal arteritis might represent an endothelial activation status induced by a remaining inflammatory microenvironment rather than a marker of endothelial cell injury. In long term remission, decreasing vWF concentrations might reflect progression of inflammatory lesions to a healing stage.

Acute Disease↗
PubMed1996

Cell adhesion molecule expression in cutaneous lesions of dermatomyositis.

Chronic inflammation seems to play a major role in skin and muscle cell damage in dermatomyositis. Adhesion molecules and their ligands are fundamental in regulating inflammation. We have carried out an immunohistochemical analysis of different activation-inducible adhesion markers in 15 biopsy specimens from dermatomyositis skin lesions. Consistent findings were the increased expression of intercellular adhesion molecule-1 (ICAM-1) on endothelial cells, inflammatory cells and focally grouped keratinocytes in contact with subepidermal inflammatory infiltrates. Immunoreactivity for vascular cell adhesion molecule-1 (VCAM-1) was predominant on endothelial cells of the upper reticular dermis and dermal stellate-shaped cells. E-selectin (endothelial leukocyte adhesion molecule-1) immunoreactivity was less extensive, detected mostly on segments of vessels of the papillary dermis and upper reticular dermis, and sometimes independent of inflammation. This pattern of adhesion molecule expression is similar to that described in other immunemediated dermatoses. The up-regulation of the adhesion molecules appears to play a role in the development and perpetuation of dermatomyositis skin lesions.

Adolescent↗
PubMed1996

[Incidence of diabetic nephropathy in the province of Badajoz along the period from 1990 to 1994].

Current registries provide information only on the number of diabetic patients with end-stage renal failure, more detailed information on the incidence of diabetic nephropathy with incipient renal failure is currently not available. The Nephrology Service of Hospital Infanta Cristina in Badajoz serves a population of approximately 650,000. In the time span between 1.1.90 and 31.12.94 the outpatient clinic and the renal ward had 1,717 admissions for evaluation of renal illness, 166 due to diabetic nephropathy (9.7% of total. Twelve (7.2%) were type I diabetics (mean age, 29.9 +/- 6.2 years), and 154 were type II diabetics (mean age 63.4 +/- 9.8 years). The annual incidence increased from 41.5/mio in 1990 to 61.5/mio in 1994. In parallel, 286 patients were admitted for renal replacement therapy, i.e. 88/mio/year. Of this group 60 patients had diabetes: type I, 8 patients (13.3%, mean age 3.7 +/- 6.4); type II, 52 patients (86.7%, mean age 66.0 +/- 6.6 years). This corresponds to an admission rate for dialysis of 18.5/mio/year (19.6% of all patients), with a increasing incidence rate from 13.8/mio in 1990 to 23.1/mio in 1994. This incidence of diabetic nephropathy is more than two-fold greater than the previously reported incidence by the EDTA registry for Spain, it is six-fold greater that the figure recorded for our region. Although the rates of incidence and prevalence of renal failure due to diabetic nephropathy founded in this study seems still to be lower than those of other developed european countries, it is detected a trend toward an increase of these figures in the latter years.

Diabetic Nephropathies↗
PubMed1996

Leucocyte/endothelial cell adhesion receptors in muscle biopsies from patients with idiopathic inflammatory myopathies (IIM).

Interactions between leucocytes and endothelial cells through specific adhesion receptors play an increasingly recognized crucial role in the development of inflammatory infiltrates in chronic inflammatory diseases. In this study we investigated adhesion molecule expression in muscle biopsies from 18 dermatomyositis, six polymyositis, five inclusion-body myositis patients and from eight normal controls. Immunohistochemical detection of leucocyte integrins LFA-1 and VLA-4, their endothelial counter-receptors intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and the endothelial cell markers CD31 and von Willebrand factor-related antigen (vWFAg) was performed using specific MoAbs and an alkaline phosphatase anti-alkaline phosphatase technique. ICAM-1 expression was up-regulated and VCAM-1 induced in muscle capillaries of dermatomyositis samples. In both dermatomyositis and polymyositis, endothelial cells from vessels surrounded by inflammatory infiltrates strongly expressed ICAM-1 and VCAM-1. Infiltrating leucocytes were intensively LFA-1- and VLA-4-positive. These data suggest that leucocyte/endothelial cell interactions mediated by the receptor/ligand pairs LFA-1/ICAM-1 and VLA-4/VCAM-1 actively participate in the development of muscle inflammatory infiltrates in the major inflammatory myopathies. In addition, ICAM-1 and VCAM-1 over-expression by capillary endothelial cells in dermatomyositis supports the hypothesis that capillary activation and/or injury is a major feature in this disease.

Adolescent↗
PubMed1995

Estrogen promotes angiogenic activity in human umbilical vein endothelial cells in vitro and in a murine model.

BACKGROUND: Angiogenesis is a critical event in wound healing, tumor growth, and the inflammatory vasculitides. Since women have a higher incidence of many vasculitic diseases, we examined the effects of female sex steroids, particularly estradiol, on human umbilical vein endothelial cell (HUVEC) behavior in vitro and on angiogenesis in vivo. METHODS AND RESULTS: HUVECs were grown in estrogen-free medium before each assay. Exogenous 17 beta-estradiol (1 to 5 nmol/L) increased cell attachment to laminin, types I and IV collagen, and fibronectin, as well as to tissue culture plastic. After a confluent monolayer of cells was "wounded" by scraping, estradiol-treated (10(-8) mol/L) cells migrated into the wound three times faster than untreated cells. Cell proliferation on plastic and on laminin increased threefold to fivefold, respectively, in the presence of estradiol. Estradiol also enhanced the ability of HUVECs to organize into tubular networks when plated on a reconstituted basement membrane, Matrigel. Estradiol effects on both the "wounding" assay and tube formation were blocked by the specific estrogen receptor antagonist ICI 182,780. Ovariectomy markedly decreased in vivo vascularization of Matrigel plugs coinjected with basic fibroblast growth factor in mice. With estrogen replacement, angiogenesis was increased to the levels observed in nonovariectomized mice. CONCLUSIONS: These studies demonstrate that, in vitro and in vivo, estradiol enhances endothelial cell activities important in neovascularization and suggest a promoting influence of estrogens on angiogenesis.

Animals↗
PubMed1995

Membrane attack complex deposits in cutaneous lesions of dermatomyositis.

BACKGROUND AND DESIGN: The presence of membrane attack complex of complement (MAC) deposits in the intramuscular vasculature of biopsy specimens taken from patients with dermatomyositis (DM) has been implicated in the pathogenesis of this myopathy. The purpose of this study was to investigate the presence of MAC deposition in the skin lesions of patients with DM. Using immunohistochemical methods, we examined 22 biopsy specimens from lesional skin, six biopsy specimens from uninvolved skin, and 12 muscle biopsy specimens from patients with DM for the presence of MAC and vitronectin and CD59, two regulatory proteins of complement. RESULTS: The deposition of MAC was demonstrated in a large percentage of biopsy specimens obtained from the lesional skin of patients with DM. Deposits were found along the dermoepidermal junction in 19 (86%) of 22 biopsy specimens. Deposits on the vessel walls of the dermis were found in 17 (77%) of 22 biopsy specimens; but only in six of these biopsy specimens (27%) were deposits present in more than 10% of blood vessels. In contrast, deposits along the dermoepidermal junction and the vessel walls of the dermis were absent in specimens from uninvolved skin. In 12 muscle biopsy specimens obtained simultaneously from these patients, MAC deposits were found on the vessel walls in nine (75%), but only in six (50%) were deposits found in more than 10% of the intramuscular vessels. The pattern of vitronectin immunoreactivity in skin and muscle biopsy specimens obtained from patients with DM was similar to MAC deposits. The expression of CD59 was normal in all skin and muscle biopsy specimens. CONCLUSIONS: The deposition of MAC was found in a high percentage of biopsy specimens from the lesional skin of patients with DM; it was absent in uninvolved skin. These findings suggest that the complement system may be involved in the pathogenesis of the skin lesions of DM.

Adolescent↗
PubMed1995

Effect of the mode of calcitriol administration on PTH-ionized calcium relationship in uraemic patients with secondary hyperparathyroidism.

To assess the effect of the different modes of calcitriol administration on PTH-ionized calcium relationship we conducted a prospective clinical trial in 33 patients on chronic haemodialysis with secondary hyperparathyroidism (four times upper normal limit intact PTH) who were randomly assigned, with stratification to PTH levels, to receive daily oral, intermittent oral, or intermittent intravenous calcitriol at the same dose of 0.045 micrograms/kg/weekly. PTH-iCa curves were generated by inducing hypo- or hypercalcaemia in sequential haemodialysis 1 week apart, before and after 10 weeks on treatment. All patients were dialysed against a dialysate calcium concentration of 2.5 mEq/l throughout the study period. After drop-outs, 26 patients completed the study: 11 on intravenous calcitriol (mean basal PTH +/- SD: 666 +/- 280 pg/ml), eight on intermittent oral calcitriol (mean basal PTH: 831 +/- 361), and seven on daily oral calcitriol (mean basal PTH: 719 +/- 280). Serum ionized calcium and phosphorus significantly increased in intravenous and daily oral groups after calcitriol treatment, but not in the intermittent oral group. Basal PTH did not significantly change in the three groups after 10 weeks on treatment. Maximal PTH significantly decreased in intravenous group (1449 +/- 660 versus 1122 +/- 691 pg/ml, P = 0.0085) and at the limit of statistical significance in the intermittent oral group (1701 +/- 774 versus 1445 +/- 634, P = 0.12), but it did not change in the daily oral group. Minimal PTH did not modify in the three groups. In all three groups, a shift to the right in the PTH-iCa relationships were observed, with significant changes in the set point of calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Haemodynamic changes induced by the correction of anaemia by erythropoietin: role of antiplatelet therapy.

BACKGROUND: In a retrospective study, antiplatelet therapy has been shown to be associated with a decreased incidence of erythropoietin-induced hypertension. In order to ascertain the role of antiplatelet drugs in the haemodynamic response to the correction of anaemia by rHuEpo, 18 patients on chronic haemodialysis who started rHuEpo therapy were prospectively studied. METHODS: The subjects were randomly assigned to receive or not, one of the following antiplatelet drugs: ditazole (3 patients), ticlopidine (3 patients) or aspirin plus dipyridamole (3 patients). Cardiac index (CI) by echo-Doppler, total peripheral resistance (TPR) and mean arterial pressure (MAP) were determined at baseline 10 and 20 weeks following the initiation of rHuEpo therapy. rHuEpo therapy was administered subcutaneously at the same dose (40 U/kg thrice weekly) during the first 10 weeks. Ten uraemic patients on haemodialysis who had never received rHuEpo therapy served as the control group. RESULTS: One patient in the group without antiplatelet drugs discontinued the study due to the development of severe hypertension after 12 weeks on rHuEpo therapy. There were no significant differences in the haemodynamic parameters at baseline. At 10 weeks, MAP was higher in patients without than with antiplatelet drugs or controls untreated with rHuEpo (128.5 +/- 28 versus 100.6 +/- 13.5 versus 98.7 +/- 14 mmHg respectively, P = 0.0047), TPR was also higher in patients without antiplatelet drugs than in the 2 other groups (1919 +/- 433 versus 1576 +/- 359 versus 1418 +/- 324 din.seg.cm-5m2 respectively, P = 0.0231), but CI did not differ among the three groups. At 20 weeks, MAP was still higher in patients without antiplatelet drugs than in patients with antiplatelet drugs or controls not on rHuEpo therapy respectively (112.9 +/- 24.6 versus 91.0 +/- 9.0 versus 101.7 +/- 14.1 mmHg respectively, P = 0.075), but at this stage TPR and Cl did not differ among the three groups. CONCLUSIONS: These data reinforce the previous observation that antiplatelet therapy may prevent the development of rHuEpo-induced hypertension.

Adult↗
PubMed1994

Immunohistochemical characterization of inflammatory cells and immunologic activation markers in muscle and nerve biopsy specimens from patients with systemic polyarteritis nodosa.

OBJECTIVE: To investigate the phenotype of infiltrating cells in classic lesions of polyarteritis nodosa (PAN). METHODS: Twenty-one muscle and 10 sural nerve biopsy samples from 24 patients with systemic PAN were studied using avidin-biotin-peroxidase and alkaline phosphatase-anti-alkaline phosphatase immunohistochemical techniques. RESULTS: The inflammatory infiltrates consisted mainly of macrophages (41%) and T lymphocytes (41%), particularly of the CD4+ subset. Granulocytes were present in varying quantities (0-45%) and were more abundant in heavily infiltrated vessels and in those with fibrinoid necrosis. Dendritic cells could be identified in 4 samples. Proliferating and interleukin-2 receptor-expressing cells, present in 71% and 79% of the patients, respectively, were more frequent in untreated patients. CONCLUSION: T cell-mediated immune mechanisms may play a role in the development and perpetuation of PAN lesions.

Adult↗
PubMed1994

Signaling through CD50 (ICAM-3) stimulates T lymphocyte binding to human umbilical vein endothelial cells and extracellular matrix proteins via an increase in beta 1 and beta 2 integrin function.

Regulated adhesion of T lymphocytes to antigen-presenting cells, endothelial cells and extracellular matrix proteins is crucial in T lymphocyte activation and migration to the sites of injury. In this study, we show that three monoclonal antibodies (mAb) recognizing different epitopes on the CD50 (ICAM-3) molecule increase T lymphocyte adhesion to tumor necrosis factor (TNF)-stimulated human umbilical vein endothelial cells and extracellular matrix proteins. These phenomena are mediated by an increase in beta 1 and beta 2 integrin avidity since (a) CD50-induced adhesion to endothelial cells was abrogated by simultaneous blocking of beta 1- and beta 2-mediated adhesion pathways but not by interfering with either one individually, (b) CD50 mAb increased beta 1 integrin-mediated adhesion to extracellular matrix proteins and to fibronectin-derived synthetic peptides, (c) CD50 mAb enhanced T lymphocyte binding to ICAM-1 transfectants, and (d) CD50 mAb did not modify surface expression patterns of beta 1 or beta 2 integrins on T lymphocytes. Our data suggest that constitutively expressed CD50 (ICAM-3) can play a pivotal role in initiating a cascade of adhesion events which may be crucial in immune activation and in the development of inflammatory lesions.

Antigens, CD↗