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Biomedical subjects

C Feighery

Publications and source records attributed to C Feighery.

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

Gliadin antibodies identify gluten-sensitive oral ulceration in the absence of villous atrophy.

This study demonstrates gluten-sensitive recurrent oral ulceration (ROU) in the absence of gastrointestinal abnormalities which is associated with a humoral response to wheat protein. Ten patients with severe ROU were investigated; all had normal small intestinal biopsies. Four patients had raised levels of antibodies to alpha gliadin, a wheat protein fraction; in three of these four, the ulceration remitted on treatment with a gluten-free diet (G.F.D.) and relapsed on gluten challenge. None of the remaining six patients had raised alpha gliadin antibody (AGA) levels and none responded to G.F.D. Thus raised AGA levels can be used to identify patients with ROU who are likely to respond to a GFD.

Adult↗
PubMed1991

Immunohistological analysis of the synovial membrane: search for predictors of the clinical course in rheumatoid arthritis.

Immunohistological features which might predict the clinical course and outcome of rheumatoid arthritis were sought by examining multiple synovial membrane samples obtained by needle biopsy from the knee joints of 57 patients who had not received disease modifying antirheumatic drugs. Clinical measurements, but not biopsies, were repeated one year and three years after starting treatment. A correlation between both the intensity of synovial lining layer thickening and mononuclear cell infiltration and the clinical status at the time of biopsy was seen. After three years of treatment the correlations were maintained in patients who had presented and persisted with milder disease but not in patients who had presented with more active disease.

Adolescent↗
PubMed1991

IgG subclasses in foetal cord and maternal serum: associations with infections in infancy and smoking in pregnancy.

We have investigated the associations between levels of umbilical cord and maternal IgG subclasses with maternal smoking habits in pregnancy and infection rate during the first year of life following the birth of 93 normal infants. There was a wide degree of normal biological variation of subclass levels between infants and also within mother/infant pairs. There were higher serum levels of IgG-1 in smoking mothers (P less than 0.001) compared to non-smokers. One year follow-up of the infants' infection rate was evaluated by postal questionnaire (n = 72; 77% response rate). There was a weak but significant inverse correlation between foetal cord levels of IgG-2 and infection rate (r = -0.38). There was however no observable increase in infection in the infants of smoking mothers despite reduced birth weight, increased IgG-1 levels and the continued exposure to passive smoking during the first year. The possible mechanisms of a longterm protective effect against infection of maternally derived IgG-2 and the effects of maternal smoking are discussed.

Female↗
PubMed1990

Recurrent disseminated intravascular coagulation and fulminant intra hepatic thrombosis in a patient with the anti-phospholipid syndrome.

We describe a patient with the lupus anti-coagulant who had recurrent episodes, over a 2 year period, of a severe and disseminated intravascular coagulopathy. This patient also had positive serological assays for syphilis and anti-cardiolipin antibodies. Associated with the coagulopathy were co-expressed episodes of liver disease, ultimately terminating in fulminant liver failure. At autopsy the features were characteristic of the Budd-Chiari syndrome. This is the first report to document how consumptive coagulopathy may present as a dominant feature of the anti-phospholipid syndrome. It also clearly describes an immune mediated thrombotic mechanism as a cause of hepatic veno-occlusive disorders. Furthermore, this case highlights the varied clinical spectrum of the anti-phospholipid syndrome and suggests that a high index of suspicion is required to ensure its diagnosis.

Adult↗
PubMed1990

Lymphocyte infiltration and the synthesis of IgM and IgA rheumatoid factors by rheumatoid synovial membrane.

IgM and IgA rheumatoid factor (RF) synthesis by synovial membrane mononuclear cells was measured in 14 patients with rheumatoid arthritis (RA). The results were compared with blood mononuclear cell cultures and correlated with the intensity of lymphocyte infiltration of the synovium. IgM RF was produced by all synovial cultures compared with 56% of blood cultures; IgA RF was produced by 86% of synovial cultures and by 21% of blood cultures. A correlation was observed between synovial IgM RF synthesis, but not IgA RF synthesis, and the intensity of T cell and B cell infiltration of the synovial membrane.

Adult↗
PubMed1990

Fluctuations in T helper subpopulations in relapsing-remitting multiple sclerosis.

Patients with active multiple sclerosis (MS) have been reported to have a depletion of CD4+ CD45R+ cells, the immature resting CD4+ subpopulation. Using Leu 3a(anti-CD4) and Leu 18(anti-CD45R), the frequencies and absolute numbers of CD4+ CD45R+ and CD4+ CD45R- subsets were measured in 30 patients with MS and 17 healthy controls. These subsets were monitored every 6 weeks over a 6 month period. CD4+ CD45R- cells were found to be increased in relapse compared to remission (p less than 0.005) while CD4+ CD45R+ levels were not significantly altered in relapse. However, the CD4+ subset ratio (CD4+ CD45R-/CD4+ CD45R+) was significantly higher in relapse compared with remission (p less than 0.002). Furthermore, these findings were upheld when data from the same 6 patients in relapse and remission was compared. Increased disease activity was not associated with changes in any of the other parameters measured (total T cells, total CD4+ cells, suppressor cells or activated T cells). These results suggest that relapse in MS is accompanied by the conversion of CD4+ CD45R+ resting cells to CD4+ CD45R- primed cells.

Adult↗
PubMed1990

HLA-DP and coeliac disease: family and population studies.

We investigated polymorphism of HLA-DP genes in three DR3 related diseases, confirming an association of coeliac disease with a Bgl II DP alpha polymorphism (a restriction fragment sized 3.5 kb present in 75% of patients compared to 34% of control subjects, p less than 0.001), and finding a weaker association with dermatitis herpetiformis (57% v 34%, p = 0.01) and no association with insulin dependent diabetes mellitus. The association with coeliac disease was further investigated. Msp I DP beta polymorphism was studied in 52 healthy subjects and 59 patients: a 4.9 kb fragment was present in 51% of patients with coeliac disease compared to 11.5% of control subjects (p less than 0.001). Furthermore, nearly all subjects with the DP alpha 3.5 kb fragment also had the DP beta 4.9 kb fragment. However, disease frequency was still increased in the DP alpha 3.5 positive/DP beta 4.9 negative group. In seven families, each with at least two affected members, while the DP alpha 3.5 fragment was frequently present in patients it did not preferentially segregate with any particular HLA haplotype--for example, those associated with DR3 or DR7--and therefore is not part of an extended haplotype associated with coeliac disease. We therefore conclude that a gene(s) in the HLA-DP region predisposes to coeliac disease independently of the HLA-DR/DQ regions.

Celiac Disease↗
PubMed1990

Chemiluminescence by polymorphonuclear leucocyte subpopulations in chronic inflammatory bowel disease. Influence of the cell separation procedure.

Chemiluminescence (CL) is a simple quantitative assay of polymorphonuclear leucocyte (PMNL) oxidative metabolism. PMNL CL was found to be significantly higher in patients with chronic inflammatory bowel disease than in normal controls (167 +/- 60 vs. 139 +/- 50 mV/10(5) cells, p less than 0.05). There were no significant differences between patients with ulcerative colitis and Crohn's disease. Disease controls with rheumatoid arthritis and with bronchiectasis also demonstrated elevated CL. These results were obtained using a two-step gelatin/Ficoll-Hypaque procedure for PMNL separation. However when PMNLs were prepared using a one-step Ficoll-Hypaque procedure PMNL CL was found to be depressed in chronic inflammatory bowel disease (CIBD). It was demonstrated that this disparity was caused by the elimination of low-density neutrophils with high CL production by the one-step procedure. These data indicate that reports of abnormal in vitro neutrophil function in CIBD should be interpreted with caution since separation techniques which are satisfactory in normal individuals may significantly influence results in patients with inflammatory diseases. Furthermore these data indicate the presence of a subpopulation of activated low-density PMNL in patients with CIBD.

Cell Separation↗
PubMed1990

Autoimmune angioedema: a new role for autoantibody in disease pathogenesis.

Angioedema may be due to hereditary forms of Cl-Inh deficiency, but recently an autoimmune form of angioedema has been described in which the mechanism is novel. While the peripheral blood monocytes of patients with autoimmune angioedema produce a normal, functionally active, 105 KD Cl-Inh in normal quantities, the Cl-Inh isolated from the patient's plasma exists in a dysfunctional lower molecular weight (96 KD) performance. Rather than bind and biologically inactivate the enzyme, a relatively common phenomenon in autoimmune disease, the autoimmune angioedema cleave the Cl-Inh molecule. The following sequence of events is proposed: structural and functionally normal Cl-Inh is synthesised and secreted, this secreted inhibitor is complexed by autoantibody and following enzyme interaction, denatured 96 KD Cl-Inh is proposed. This process depletes the pool of normal, functional Cl-Inh to critical levels and predisposes patients to episodes of oedema.

Angioedema↗
PubMed1990

Raised PPD antibodies in active pulmonary tuberculosis.

Antibodies to purified protein derivative of tuberculin (PPD) were measured in 47 patients with active pulmonary tuberculosis and in various control subjects using an enzyme linked immunosorbent assay. Raised IgG anti PPD antibodies were found in 30 patients with active tuberculosis, in one of 28 patients with miscellaneous non tuberculous diseases and in one of 49 healthy control subjects. This gave the assay a sensitivity of 65% and a specificity of 98%. Antibodies were also measured in a further 20 patients with suspected tuberculosis but in whom microbiological evidence was absent. In eight of these patients active tuberculous disease was subsequently validated on the basis of clinical response to chemotherapy: raised PPD antibodies were found in six of this group but in none of the remaining 12 patients in whom the diagnosis of tuberculosis was considered doubtful. Further studies showed that patients' PPD antibody level fell over a one year period of successful therapy and that tuberculin skin testing and BCG vaccination did not cause a rise in antibodies in healthy subjects. These results suggest that the measurement of PPD antibodies is a useful adjunctive test in the diagnosis of tuberculosis.

Antibodies, Bacterial↗
PubMed1990

Mixed connective tissue disease with arterial thrombosis, antiphospholipid antibodies and heparin induced thrombocytopenia.

We report a patient with mixed connective tissue disease (MCTD) who presented with thrombosis of the right femoral artery in association with antiphospholipid antibodies (aPL). When treated surgically and with heparin prophylaxis, she developed heparin induced thrombocytopenia and thrombosis which necessitated amputation of a lower limb. Thus our patient developed 2 separate groups of autoantibodies associated with thrombotic events. Our case highlights an association between thrombosis, aPL and MCTD. Furthermore, it emphasizes a need for intensive monitoring when hypercoaguable individuals with connective tissue disorders are treated with heparin.

Adult↗
PubMed1989

Changes in lymphocyte infiltration of the synovial membrane and the clinical course of rheumatoid arthritis.

Multiple samples of synovial membrane were obtained by needle biopsy from 24 patients with rheumatoid arthritis (RA) before, and 1 year after, standard antirheumatic drug therapy was given. Changes in the immunohistologic features of the synovial membrane (read blindly) were compared with the clinical course of RA in each patient. A composite clinical index of disease activity (IDA) and spontaneous in vitro synthesis of IgM rheumatoid factor (IgM-RF) by blood mononuclear cells were also measured before and after treatment. In 16 patients (group A), the IDA indicated 26-69% improvement, and the values for spontaneous IgM-RF decreased substantially. In 8 patients (group B), the IDA indicated deterioration or no improvement, and the values for spontaneous IgM-RF were unchanged. In group A patients, the intensity of the T cell infiltrate decreased from a mean score of 1.3 to a mean score of 0.8 (P = 0.025). The ratio of T helper cells to T suppressor/cytotoxic cells was greater than or equal to 2:1 in 90% of group A patients before treatment, compared with 20% of these patients after treatment (P = 0.016), and the number of biopsy samples that contained identifiable B cells decreased from 36% before treatment to 7% after treatment. In group B patients, there were no changes in the intensity of T cell infiltration, the ratio of T helper cells to T suppressor/cytotoxic cells, or the number of biopsy samples with identifiable B cells.

Antibodies, Monoclonal↗
PubMed1989

Lymphoid irradiation in intractable rheumatoid arthritis. Long-term followup of patients treated with 750 rads or 2,000 rads.

Twenty patients with intractable rheumatoid arthritis were randomized to receive 750 or 2,000 rads of lymphoid irradiation (LI) in a double-blind comparative study, and were followed for a maximum of 48 months (mean 40 months) after treatment. During followup, sustained immunomodulation (including lymphopenia, particularly of the T helper cell subset; reduced ratio of helper cells to suppressor cells; and impaired in vitro lymphocyte proliferation in response to phytohemagglutinin and pokeweed mitogen) was observed. Significant improvements in early morning stiffness, Ritchie articular index, pain score, grip strength, and 15-meter walk time were observed in both treatment groups, but these were not sustained through the followup period. Progressive joint damage was observed radiologically in both groups during followup. Thus, LI induced sustained immunosuppression, but resulted in only short-lived clinical improvement and was associated with progressive joint erosion in these patients.

Arthritis, Rheumatoid↗
PubMed1989

Expression and regulation of the HLA-DR antigen on circulating monocytes isolated from patients with rheumatoid arthritis.

Using a modified radioimmunoassay, surface labeling of HLA-DR antigens on monocytes revealed reduced densities in patients with active rheumatoid arthritis (RA) (P less than 0.001) and in gold-treated patients (P less than 0.01) versus normal controls. Significant enhancement of DR antigen expression (P = 0.01), with values similar to those of normal monocytes, occurred in patient monocytes preincubated at 37 degrees C overnight, but not in monocytes preincubated at 4 degrees C. This suggested that a temperature-dependent metabolic process is required to enhance antigen expression. The addition of cycloheximide totally inhibited the enhancement of DR antigen density. Incubation of monocytes with exogenous prostaglandin E2 (10(-5)M final concentration) caused a reduction of DR densities on control and on RA monocytes, although this decrease was more marked in the controls. Addition of indomethacin did not affect DR antigen levels on control monocytes, but greatly enhanced the expression of DR antigens on RA monocytes. When HLA-DR antigen levels were estimated in detergent-solubilized membrane preparations, monocytes from patients with active RA demonstrated normal-to-increased densities compared with control monocytes. Thus, although RA monocytes possess a normal ability to synthesize DR molecules, surface expression of these molecules is inhibited; this inhibition may be mediated by prostaglandin E2 acting as a negative suppressive signal.

Arthritis, Rheumatoid↗
PubMed1989

A strategy for the investigation of immunodeficiency.

In any patient who suffers from frequent infections or from a clinical disorder caused by opportunistic organisms, the possibility of an underlying defect in immune defense should be considered. The purpose of this review is to outline a strategic approach towards screening for immunodeficiency in such patients. It should be apparent that the majority of serious immune deficiency states can be detected using a series of relatively simple and readily available investigations. The detection and further definition of other immunodeficiencies may require more sophisticated tests to be performed. The development of new biological tools now permits many of these disorders to be defined at the genetic and molecular level. Finally, early diagnosis of immunodeficiency is important, since it may permit the introduction of corrective measures which can reduce the morbidity and mortality of these disorders.

Humans↗
PubMed1989

Immunohistological features in the synovium obtained from clinically uninvolved knee joints of patients with rheumatoid arthritis.

The spectrum of immunohistological change in the affected joints of patients with rheumatoid arthritis has been well described. In this study, the immunohistological features in synovial membrane obtained from apparently uninvolved knee joints of 16 patients with active untreated rheumatoid arthritis were examined and compared to tissue from control subjects. Synovial tissue was obtained by needle biopsy. Hyperplasia of the synovial lining layer, present in 69%, was the most frequently observed abnormality in synovium obtained from uninvolved joints. Perivascular mononuclear cell infiltration was present in 31% and consisted predominantly of helper T-cells. Increased vascularity and fibrin deposition were not notable features. Clinically overt synovitis emerged in only two patients during a follow-up period of up to 36 months. In conclusion, a considerable degree of histological change was observed in the apparently uninvolved knee joints of patients with active rheumatoid arthritis. The presence of subclinical synovitis challenges current concepts of disease activity and clinical remission. Further study is required to determine whether the features described may be associated with progressive joint erosion.

Arthritis, Rheumatoid↗