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Biomedical subjects

R Hällgren

Publications and source records attributed to R Hällgren.

At least 91 records · Page 5Linked to original sources
PubMed1991

Enumeration of IgA producing cells by the enzyme linked immunospot (ELISPOT) technique to evaluate sulphasalazine effects in inflammatory arthritides.

Numbers of IgA producing cells in peripheral blood were determined by the enzyme linked immunospot (ELISPOT) technique in 15 patients with inflammatory arthritides receiving sulphasalazine treatment. The numbers of IgA producing cells decreased significantly after the first three weeks of treatment. In 11 of the patients this decrease persisted, whereas a subsequent increase was seen in the four others; in two of these latter patients this increase coincided with a temporary withdrawal of the sulphasalazine treatment. A reduction of serum concentrations of IgA and haptoglobin was seen after three months' treatment. Eleven of the patients had a subjective improvement in their joint disease during the first three months of treatment. Analysis of circulating cells committed for IgA secretion may constitute one way of assessing gut associated immunity indirectly, and the present data suggest that sulphasalazine has a rapid effect on lymphocytes possibly originating from the gut and that such an effect precedes improvement in laboratory parameters and clinical symptoms in arthritic diseases.

Antibody-Producing Cells↗
PubMed1991

Cell recovery during segmental intestinal perfusion in healthy subjects and patients with Crohn's disease.

The recovery of cells arising from small intestinal mucosa alone was studied during continuous perfusion of a closed segment of jejunum. The perfusion technique minimised the contamination of the perfused segment with, for example, proteolytic enzymes from pancreas, allowing recovery of viable cells. The use of hyaluronidase in the perfusion fluid increased the recovery of cells fivefold, the median recovery being 8 x 10(6) cells. The cells were analysed with monoclonal antibodies and flow cytometry. Nearly all cells (98-99%) recovered during perfusion of healthy control subjects and patients with Crohn's disease were epithelial cells. The jejunal cells expressed HLA-DR in similar proportions--around 30%--in patients and control subjects. The ratio between CD4+ and CD8+ lymphocytes was similar (0.2) in control subjects and patients with inactive Crohn's disease but decreased (0.03) in patients with active Crohn's disease in the ileum.

Adult↗
PubMed1991

Localisation of hyaluronan in the human intestinal wall.

By using biotin labelled proteoglycan core protein and an avidin enzyme system, hyaluronan (hyaluronic acid) was visualised in specimens of human jejunum. Intense staining for hyaluronan was seen in the loose connective tissue of the villi and of lamina propria while the epithelial layer was unstained. The muscularis mucosae showed only faint staining. The accumulation of hyaluronan in the subepithelial layer of the jejunal mucosa indicates that the previously reported high jejunal secretion of hyaluronan is due to passive diffusion from the subepithelial interstitium. The physicochemical characteristics conferred by hyaluronan may be important for the villi function.

Biotin↗
PubMed1991

Activated eosinophil infiltration and deposits of eosinophil cationic protein in renal allograft rejection.

Eosinophil involvement in renal allograft rejection was elucidated with immunocytochemical techniques. Sections of renal biopsies were stained for immunoreactive eosinophils and extracellular deposits of eosinophil cationic protein (ECP). Activated eosinophils were identified by means of alkaline-phosphatase-linked monoclonal antibodies. In biopsies from patients with acute rejection of the interstitial type, a varying degree of eosinophil infiltration in the interstitium was seen. Minor extracellular deposits of ECP were present in areas with activated eosinophils. In acute vascular rejection, dense infiltration of activated eosinophils and secreted ECP were found in infarcted areas and in arterial walls with necrotic lesions. Dense accumulation of activated eosinophils and extracellular deposits of ECP were also seen in biopsies from non-transplanted patients with necrotizing renal vasculitides. These findings suggest that cytotoxic eosinophil granule proteins are involved in vascular injury in renal graft rejection and in necrotizing renal vasculitides. Eosinophil activation may also have a pathophysiological role in the interstitial lesions in renal graft rejection.

Antibodies, Monoclonal↗
PubMed1991

Accumulation of hyaluronan and tissue edema in experimental myocardial infarction.

Experimental myocardial infarction was induced in rats. The myocardial accumulation of hyaluronan (HA) and water during the development of infarction was measured. The extractable HA content of the infarcted area increased progressively from day 1 and on day 3 reached a threefold increase compared with the HA amounts in myocardium of sham operated controls. The relative water content of infarcted areas also increased progressively reaching a maximum value by day 3 and was strongly correlated with the HA accumulation. Affinity histochemistry visualized a thin rim of HA in the endoperimysium in healthy myocardium. By day 2 an interstitial edema with inflammatory cells was apparent. The widened endoperimysium stained extensively for HA. By its water-binding ability, interstitial accumulation of HA will contribute to the interstitial edema in infarcted myocardial tissue. An interstitial edema is likely to influence the electromechanical characteristics of the myocardium and facilitate reentry phenomena due to a loss of contact between muscle cells. The edema also induces an increased extracellular pressure and an altered myocardial wall compliance that might impair myocardial microcirculation. The findings are relevant to an understanding of the beneficial effect of hyaluronidase treatment in limiting cellular damage during myocardial ischemia.

Animals↗
PubMed1991

Alveolar accumulation of hyaluronan and alveolar cellular response in bleomycin-induced alveolitis.

Hyaluronan (HA) accumulating in the alveolar interstitial tissue of rats injured by a single intratracheal instillation of bleomycin has been visualized histologically and assayed. HA was present already by Day 1 after bleomycin treatment, increased to a maximum value on Days 3 and 7 and then declined. A time-dependent relationship between this early connective tissue response and the invasion of inflammatory cells in the alveolar tissue was apparent. The dominating invading cells by Day 1 were granulocytes showing positive staining for the monoclonal antibody OX-42 reflecting the C3b receptor. The numbers of macrophages expressing class II antigens started to increase on Day 1, reaching a maximum on Days 3-7 and then declined. Macrophages were the dominating OX-42+ cells by Day 7. The appearance of W3/13+ cells ("pan-T-lymphocytes") showed a similar pattern to that for the class II expressing macrophages. The number of cells expressing CD4 antigen increased until Day 3 and levelled off on Day 30 whilst the largest number of cells expressing CD8 antigen was seen on Day 30. Few cells expressing B-cell phenotype outside lymph nodules were identified. Alveolar lining epithelial cells, probably epithelial type II cells, expressed class II antigens by Days 3-14. The time-related accumulation of HA and the appearance of T-cells, macrophages and granulocytes expressing signs of activation suggests that these cells may be involved in the early connective tissue response of the lung injured by bleomycin.

Animals↗
PubMed1990

Hyaluronic acid accumulation and redistribution in rejecting rat kidney graft. Relationship to the transplantation edema.

By using biotin-labeled proteoglycan core protein and an avidin-enzyme system, hyaluronic acid (HA) was visualized in rat kidney. In the normal kidney, HA was localized in the extracellular space of the inner medulla and increased markedly towards the papillary tip. No staining for HA was seen in the interstitial tissue of the cortex or the outer medulla. During the development of rejection of allogeneic renal grafts, a progressive increase in accumulated HA was seen in the interstitial tissue of the cortex and outer medulla. The extractable amounts of HA increased, on average, 40 times in the cortex and outer medulla; no increase was measured in the inner medulla and papilla. The relative water content of the cortex and outer medulla also increased progressively and correlated with the HA accumulation. The extractable amounts of HA in syngeneic grafts increased by day 2 and then leveled off, indicating that surgical trauma may induce some transient HA accumulation after transplantation. Interstitial accumulation of HA, a glycosaminoglycan with unique water-binding qualities, would presumably influence water transport and osmotic activity and should thereby be implicated in the normal papillary function, but also in the development of the interstitial edema of the cortex and outer medulla during rejection of renal grafts.

Animals↗
PubMed1990

Enhanced local production of complement components in the small intestines of patients with Crohn's disease.

There is evidence that complement components may be formed locally in inflammatory lesions containing monocytes and macrophages. To investigate the role of complement in Crohn's disease we measured jejunal-fluid concentrations of the complement components C4, C3, and factor B by perfusion of a closed segment of the jejunum in 22 patients with Crohn's disease thought to be limited to the terminal ileum. The mean (+/- SEM) jejunal-fluid C4 concentration was 2.0 +/- 0.3 mg per liter, significantly higher than the mean level in 35 healthy controls (0.7 +/- 0.1 mg per liter; P less than 0.001). The mean C3 concentration was 1.0 +/- 0.1 mg per liter in the patients and 0.7 +/- 0.1 mg per liter in the controls (P less than 0.05). The factor B levels were similar in the two groups. Calculated rates of intestinal secretion of these components showed differences of the same magnitude. Leakage of protein from plasma was not increased. The jejunal-fluid:serum ratios of these complement proteins indicated that their appearance in the lumen of the jejunum was due to at least in part to local mucosal synthesis. The increased jejunal secretion of C4, but not C3 or factor B, paralleled the clinical activity of Crohn's disease. Values were normal in first-degree relatives of the patients (n = 13), patients with celiac disease (n = 8), and patients with ulcerative colitis (n = 4). We conclude that increased secretion of complement by clinically unaffected jejunal tissue in patients with Crohn's disease reflects the systemic nature of this disorder and may be due to the stimulated synthesis of complement by activated intestinal monocytes and macrophages.

Adolescent↗
PubMed1990

Increased expression of platelet-derived growth factor type B receptors in the skin of patients with systemic sclerosis.

The expression of B-type receptors for platelet-derived growth factor (PDGF) was investigated in skin biopsy samples from patients with systemic sclerosis (SSc), by immunohistochemical staining using monoclonal antibodies specific for the receptor. Whereas skin from healthy individuals lacked expression of PDGF-B receptors, receptor expression was seen in sclerodermatous skin lesions from 13 of 14 patients. Increased receptor expression was observed in dermal vessels, as well as on many stromal fibroblast-like cells close to these vessels. PDGF-B receptor expression was most pronounced within and around dermal vessels in which perivascular infiltrates of Leu-4-positive T lymphocytes and HLA-DR-positive, RFD7-positive activated macrophages were present. Both perivascular inflammatory cell infiltrates and PDGF-B receptor expression were generally also seen in macroscopically normal areas of the skin of the SSc patients, indicating that the observed phenotypic alterations may precede the macroscopically observable features of scleroderma in the skin. The observed induction of PDGF-B receptors, together with indirect indications of increased synthesis and release of PDGF, would be compatible with altered PDGF-mediated control of connective tissue cell growth as part of the molecular basis for development of the skin lesions in SSc.

Adult↗
PubMed1990

Magnetic resonance imaging of sacroiliac joint inflammation.

A consecutive series of 27 patients with symptoms compatible with sacroiliitis underwent magnetic resonance imaging (MRI) of the sacroiliac joints. The diagnostic sensitivity of MRI was similar to that of computed tomography or conventional radiography. However, MRI seems to have the potential of providing unique information about the disease process in sacroiliitis by demonstrating abnormalities in subchondral bone and periarticular bone marrow. The results of this study suggest that early inflammatory changes in sacroiliitis occur in the subchondral structures of the sacroiliac joints.

Adolescent↗
PubMed1990

The jejunal secretion of histamine is increased in active Crohn's disease.

Previous studies of mast-cell density and histamine content in biopsy specimens in patients with Crohn's disease have yielded conflicting results. In this in vivo study we have measured the jejunal secretion rate of histamine in patients with Crohn's disease (n = 15) of the terminal small bowel and in healthy controls (n = 24). The secretion studies were performed using a recently developed segmental jejunal perfusion system with a two-balloon, six-channel small tube. The histamine secretion rate was 152 +/- 29 (SEM) ng/cm small intestine per h in patients with Crohn's disease, which meant a significant increase (p less than 0.01) compared with the secretion rate in controls (71 +/- 11 ng/cm per h). Moreover, the secretion of histamine was related to the disease activity. Patients with active disease (n = 8) (i.e., Crohn's disease activity index greater than 150) had a mean histamine secretion rate of 193 +/- 47 ng/cm per h, while patients with inactive disease (Crohn's disease activity index less than 150) had a secretion rate not significantly increased compared with controls (105 +/- 24 ng/cm per h). The present data indicate increased mast-cell involvement of the small intestine in active Crohn's disease of the distal ileum. This finding might reflect the systemic nature of the disease process.

Adult↗
PubMed1990

Gliadin challenge-induced jejunal prostaglandin E2 secretion in celiac disease.

Jejunal prostaglandin E2 secretion in patients with adult celiac disease was studied under basal conditions and after local gliadin challenge. A newly developed tube system with occluding balloons was used to perfuse a jejunal segment. After an initial basal perfusion period of 40 minutes, an average of 12 mg +/- 3 (SEM) of crude gliadin was administered into the perfused segment. Perfusion continued for an additional 100 minutes and prostaglandin E2 was determined in the effluent with a radiometric method. Patients with histologically active celiac disease (n = 7) had higher basal jejunal secretion of prostaglandin E2, 523 +/- 229 pg.cm-1.h-1 (mean +/- SEM), than both celiac patients with normalized small bowel mucosa (n = 6), 160 +/- 44 pg.cm-1.h-1, and healthy controls (n = 18), 184 +/- 38 pg.cm-1.h-1, (P less than 0.05). After gliadin challenge of the jejunal segment, a significant increase (P less than 0.05) in prostaglandin E2 secretion was noted in patients with celiac disease (n = 10). The individual maximum increase was on average fivefold and occurred 60-100 minutes after gliadin administration. In healthy controls (n = 5), no alteration in prostaglandin E2 secretion was detected after gliadin challenge. Enhanced jejunal prostaglandin 2 synthesis may be involved in the pathophysiological processes initiated by gliadin in patients with celiac disease.

Adult↗
PubMed1990

Mitral regurgitation and diastolic flow profile in systemic sclerosis.

To evaluate the left ventricular filling characteristics in systemic sclerosis, we examined 30 consecutive patients, 15 men and 15 women, and related the findings to those from 48 age- and sex-matched controls. All patients were investigated by pulsed and continuous wave mitral Doppler, and M mode echocardiography. We found the A wave of the mitral flow velocity as recorded by pulsed wave Doppler to be higher in patients (0.74 +/- 0.07 vs 0.54 +/- 0.02 m/sec, P less than 0.002), while the E wave did not differ. The high A/E ratio indicating reduced distensibility, correlated to interventricular septal thickness (r = 0.53, P less than 0.001), and atrial emptying index (r = -0.55, P less than 0.001). Early filling was impaired, with a prolonged pressure half time (99 +/- 6 vs 84 +/- 4 msec, P less than 0.05), and a reduced first third filling fraction (0.41 +/- 0.02 vs 0.48 +/- 0.01, P less than 0.001). Mitral regurgitation was found in 67% of systemic sclerosis patients and in 15% of controls (P less than 0.001). Doppler measures of left ventricular filling properties were not related to the presence of mitral regurgitation or systolic blood pressure. We conclude that left ventricular distensibility and early filling properties are impaired in systemic sclerosis and not related to blood pressure, but rather to left ventricular wall thickness and therefore probably secondary to myocardial fibrosis. Mitral regurgitation is a common finding in systemic sclerosis.

Adult↗
PubMed1990

Impaired secretion of parathyroid hormone in patients with rheumatoid arthritis: relationship to inflammatory activity.

Hypocalcaemic tests, employing infusion of EDTA over 1 h, were performed in 22 patients with rheumatoid arthritis (RA) and 14 healthy controls. The basal levels of calcium and parathyroid hormone (PTH) were not significantly different in the two groups. The RA patients displayed a markedly impaired PTH response during infusion of EDTA compared with the controls although the reduction of plasma ionized calcium was similar. The PTH response was furthermore significantly, inversely, related to the inflammatory activity measured as sedimentation rate (r = 0.65; P less than 0.01), i.e. the more pronounced the inflammation, the less the capacity to secrete PTH. Since secretion of PTH is related to the intracellular calcium concentration of the parathyroid cells, these findings are in line with previous observations of a higher intracellular calcium content in inflammatory disease. They also support the earlier indications of reduced bone turnover in inflammatory arthritides. An insufficient parathyroid function could be one factor contributing to bone disease in these conditions.

Acute-Phase Reaction↗
PubMed1990

Non-invasive assessment of left ventricular diastolic function in patients with systemic sclerosis.

To evaluate the extent of left ventricular (LV) diastolic impairment in systemic sclerosis, we examined 30 consecutive patients (15 men and 15 women) with this condition, and compared the findings with the data for 48 age- and sex-matched randomly sampled controls. All patients were investigated by phonocardiography, pulse curve recording, and M-mode echocardiography. Twenty-three of 30 (77%) patients had LV hypertrophy and/or diastolic impairment. Interventricular septum (P = 0.0001), LV posterior wall (P less than 0.05), and the wall thickness to cavity dimension ratio (P less than 0.001) were increased in patients compared to controls, as was LV mass index (P less than 0.002). Five patients had asymmetric septal hypertrophy. LV end-diastolic dimension did not differ between groups. LV distensibility was impaired, as judged from apexcardiographic a/H ratio (P less than 0.05) and from an increased left atrial index (P less than 0.005). LV early filling was impaired, with a reduced left atrial emptying index (P = 0.0001), and a reduced rate of dimension increase in digitized M-mode (P less than 0.02). We found no evidence of impaired LV relaxation. Blood pressure did not differ between patients and controls. With longer duration of the disease, left atrial dimension appeared to increase (r = 0.42, P less than 0.05), while other variables were not related to disease duration. The impaired LV filling was not secondary to systolic dysfunction. We conclude that systemic sclerosis patients have an increased LV wall thickness, with impaired early filling properties and LV distensibility.

Body Composition↗
PubMed1990

Increase in activated T cells and reduction in suppressor inducer T cells in systemic sclerosis.

Blood lymphocytes from 37 patients with systemic sclerosis were characterised using monoclonal antibodies in a two colour flow cytometric (fluorescence activated cell sorter (FACS)) analysis. The ratio of helper CD4+ to suppressor/cytotoxic CD8+ T cells was raised in patients compared with that in 30 healthy controls owing to decreased CD8+ cells. In the patients CD4+ and CD8+ cells displayed an increased expression of the activation marker HLA-DR. The relative number of CD11b+ CD8+ lymphocytes (suppressor T cells) was normal, but the calculated absolute counts of this cell type were slightly reduced. The proportions and absolute numbers of suppressor inducer T cells, defined as CD45R+ CD4+ cells, were on average only half the levels observed in controls. These findings were not related to the inflammatory activity as measured by acute phase plasma proteins or serum immunoglobulins. Activated T cells were seen at all stages of the sclerotic process and especially during the early stages of the disease and in patients who had suffered occupational exposure to silica dust. A high proportion of activated T cells was also linked with impaired small intestine function but not with the degree of skin or lung involvement. A loss of suppressor inducer T cells was more pronounced later in the disease and in patients with the CREST (calcinosis, Raynaud's phenomenon, oesophageal dysmotility, sclerodactyly, telangiectasia) syndrome. These data provide further evidence for an involvement of T cell mediated immunity in the perpetuation of systemic sclerosis.

Adult↗