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Biomedical subjects

O FitzGerald

Publications and source records attributed to O FitzGerald.

At least 55 records · Page 3Linked to original sources
PubMed1996

A clinical and serological comparison of familial and non-familial systemic lupus erythematosus in Ireland.

Seventeen families, in which the diagnosis of SLE could be verified in two relatives, were included in the study. The diagnosis was made according to the revised 1982 ARA criteria. We compared the 34 cases of familial SLE in these 17 families with 34 non-familial SLE controls matched for age, sex, ethnicity and duration of disease. Comparisons were made for the presence of 26 clinical and 11 serological features. The frequency of clinical features was similar between the groups. The frequency of anti-Ro antibody was higher in the non-familial group (15 out of 34 compared to 6 out of 34, P = 0.036, McNemar's test), although this was not significant after application of Bonferoni's correction for the number of comparisons. No cases of familial IgA or familial complement deficiency were identified. It was noted that 10 of the 34 non-familial patients and only one of the familial patients had the combination of anti-Ro antibody and photosensitivity. The findings of this study support the hypothesis that familial SLE and non-familial SLE are the same clinical entity, although there are differences in the subtypes of disease.

Adult↗
PubMed1994

Alterations in human endothelial cell morphology, proliferation and function by a macrophage-derived factor.

Changes in endothelial cell (EC) morphology occur at sites of physiological lymphocyte traffic and in areas of chronic inflammation. Previous studies have shown that EC shape changes also occur in vitro following exposure of EC monolayers to peripheral blood mononuclear cell (PBMC)-derived conditioned media (CM). In the present study, quantitative image analysis is used to define the cell of origin of the elongating factor(s), to examine changes in EC proliferation and function accompanying PBMC-induced human EC elongation and to identify the active PBMC-derived products responsible for this elongation. By separating mononuclear cells into subpopulations (macrophages, B cells and T cells) and adding conditioned media derived from these subpopulations to cultured ECs, the macrophage (M phi) is shown to be the primary cell of origin of the elongating factor(s). Furthermore, EC elongation is accompanied by both a dose-dependent decrease in cellular proliferation and an increase in prostacyclin production. These findings suggest that PBMC-induced changes in EC morphology may be associated with a shift from a proliferative state to a more secretory phase of the EC cycle. Finally, using recombinant factors it is shown that TNF alpha acting in combination with IL-1 may be the active PBMC-derived products which contribute to EC elongation.

Cell Division↗
PubMed1994

Immunohistochemical markers for arthritis in psoriasis.

OBJECTIVES: To examine the immunohistological features in the involved skin of patients with psoriatic arthritis (PA) (n = 15), compared with those in involved skin from patients with psoriasis but no arthritis (n = 5), and with a group with normal skin (n = 4), to identify markers for arthritis in psoriasis. METHODS: Skin was obtained from patients by 6 mm punch biopsy and normal skin was provided by the department of plastic surgery. Samples were stained with monoclonal antibodies against T cells (CD3, CD8, CD4, CD45Ro), B cells (CD20), macrophages (mac387), vascular endothelium (FVIII-related antigen) and a Langerhan's cell marker (p155). The number of cells/vessels staining with each monoclonal antibody was calculated and serial sections of skin were examined to estimate the presence of DR+ keratinocytes. RESULTS: There were significantly more CD45Ro T-cells and blood vessels in patients with psoriatic arthritis compared with both psoriasis alone, and with normal controls (p < 0.02). While B-cells were not seen in psoriasis without arthritis or in normal skin, a small but significant number were observed in PA (p < 0.02). Furthermore, while DR+ keratinocytes were present in both psoriatic arthritis and psoriasis skin, there were significantly more DR+ cells in the psoriatic arthritis epidermis compared with psoriasis alone (p < 0.02). CONCLUSIONS: This study suggests that increased numbers of CD45Ro T-cells, greater vascularity, the presence of B-cells, and increased numbers of DR+ epidermal cells are markers for arthritis in patients with psoriasis.

Adult↗
PubMed1993

Doppler echocardiographic evidence of left ventricular diastolic dysfunction in ankylosing spondylitis.

Although cardiac involvement in the form of conduction abnormalities or aortic regurgitation occurs in 5 to 10% of patients with ankylosing spondylitis, few studies have assessed left ventricular (LV) function. This study assesses the prevalence of both systolic and diastolic LV dysfunction and other cardiac abnormalities in patients with ankylosing spondylitis who have no clinical cardiac manifestations. Fifty-nine patients (49 men and 10 women, mean age 42 +/- 10 years) underwent full clinical examination, electrocardiography, 24-hour Holter monitoring and 2-dimensional, M-mode and Doppler echocardiography. Mean disease duration was 17 +/- 9 years (range 1 to 42). Seventeen patients had evidence of noncardiac extraarticular manifestations. Precordial examination was normal in all. An age- and sex-matched control group of 44 healthy subjects was also studied. On echocardiography, abnormal LV diastolic function was detected in 12 patients (20%). Prolonged isovolumic relaxation time, prolonged deceleration time, reduced rate of descent of flow velocity in early diastole (EF slope) and reversal of the early and late peak transmitral diastolic flow velocities (E/A ratio) were noted in 9 patients. In 3 patients there was an increased E/A ratio, reduced deceleration time and increased EF slope. Mild aortic regurgitation and mitral regurgitation was seen in 1 and 3 patients, respectively. No abnormalities of left atrial size, LV systolic or diastolic dimensions or wall thicknesses were noted. There was no correlation between the presence of LV diastolic dysfunction and age, disease severity, disease duration, or the presence of extraarticular manifestations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Lymphedema of the upper limb in patients with psoriatic arthritis.

Upper limb lymphedema occurs rarely in rheumatoid arthritis (RA) but has been reported only once in psoriatic arthritis (PsA). The pathogenesis is unknown. This study describes four patients (three women) with upper limb lymphedema, chronic symmetrical polyarthritis, and psoriasis. Three were seronegative, diagnosed PsA; one was seropositive. Age ranged from 39 to 64 years, duration of psoriasis was 6 to 42 years, and duration of arthritis was 6 to 12 years. Onset of lymphedema was unrelated to the extent or severity of arthritis, and no other cause for this condition was identified. Radiological appearances ranged from mildly abnormal to advanced joint destruction, but carpal disease was prominent in all patients. Lymphoscintigraphy was abnormal in three subjects. Lymphedema became bilateral in two and was associated with radiological progression of arthritis. Disease-modifying therapy produced improvement of lymphedema in two patients and correction of the lymphoscintigraphic abnormality in one. This study describes upper limb lymphedema in patients with PsA and suggests that local synovitis may play a role in its pathogenesis.

Adult↗
PubMed1992

Production of angiotensin converting enzyme by rheumatoid synovial membrane.

Vascular proliferation and mononuclear cell infiltration are prominent changes observed in synovium from actively inflamed joints of patients with rheumatoid arthritis. Angiotensin converting enzyme (ACE) is a halide activated peptidase produced mainly by endothelial cells and by activated monocytes. It has been proposed that levels of ACE activity in synovial fluid might reflect changes in membrane vascularity, the degree of monocyte infiltration, or the thickness of the lining layer. In this study, ACE activity in serum and synovial fluid samples from 18 patients with inflammatory arthritis was measured and compared with levels in 12 control subjects with non-inflammatory arthritis. Although serum levels were similar in the two groups, ACE activity in synovial fluid was significantly increased in the group with inflammatory arthritis compared with controls (mean (SE) 37 (5) v 19 (3)). Staining of synovial membranes from patients with rheumatoid arthritis with a monoclonal antibody to ACE localised ACE to the endothelium and to mononuclear cells of macrophage origin. ACE activity was then measured in supernatants of synovial membrane from patients with rheumatoid arthritis after one and seven days of culture. A significant increase in ACE activity was observed after seven days of culture (mean (SE) day 1, 17 (5) v day 7, 25 (3)). Levels of ACE activity, however, did not correlate with the lining layer thickness, with the number of macrophages per square millimetre, nor with the number of blood vessels per square millimetre of synovial tissue. No correlation was observed either between levels of ACE in the supernatant of synovial membrane and levels of interleukin 1 or interleukin 6. In conclusion, ACE is produced by the synovial membrane of patients with rheumatoid arthritis and is localised to monocytes and endothelial cells. Levels of activity do not directly reflect membrane vascularity, monocyte or macrophage number, or the thickness of the lining layer.

Adolescent↗
PubMed1991

Morphometric analysis of blood vessels in synovial membranes obtained from clinically affected and unaffected knee joints of patients with rheumatoid arthritis.

Synovial tissues from inflamed and noninflamed knee joints of 13 patients with untreated rheumatoid arthritis were examined for vascular proliferation and morphological alteration of endothelial cells. Perivascular mononuclear cell infiltration and increased thickness of the synovial lining layer were noted in tissues from inflamed and noninflamed joints of patients with rheumatoid arthritis; vascular proliferation and morphological alteration of endothelial cells to resemble high endothelial venules were seen only in tissues from inflamed joints of patients with rheumatoid arthritis. These observations suggest that the migration of mononuclear cells from the peripheral blood to the perivascular areas and lining layer occurs before vascular proliferation and morphological alteration of endothelial cells.

Arthritis, Rheumatoid↗
PubMed1989

Severe disability in rheumatoid arthritis: assessment following comprehensive rehabilitation.

26 patients with rheumatoid arthritis (RA) who presented with severe disability to a rheumatology unit were reviewed following comprehensive rehabilitation. This comprised in-patient evaluation, alteration in drug therapy, physical and occupational therapy and in many cases, orthopaedic surgery. Sustained benefit is observed 4-6 years later in terms of disease activity and functional class. The greatest improvement in functional class was noted in those patients who underwent joint replacement.

Adrenal Cortex Hormones↗
PubMed1987

Hypothenar hammer syndrome: an occupational cause of Raynaud's phenomenon.

Hypothenar hammer syndrome is an uncommonly recognized, occupationally associated cause of Raynaud's phenomenon, induced by traumatic compromise of the vascular supply to the hand. Two patients are presented, one with preexisting Raynaud's phenomenon who sought attention after the development of cutaneous ulcers. The features of the syndrome are reviewed, and the importance of its recognition in the appropriate occupational setting as a potentially curable form of Raynaud's phenomenon is emphasized.

Adult↗