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Biomedical subjects

G Loewi

Publications and source records attributed to G Loewi.

12 recordsLinked to original sources
PubMed1977

Levamisole in the treatment of Crohn's disease.

In 8 patients with active uncomplicated Crohn's disease who were not receiving any specific therapy, a clinical remission was induced with an elemental diet, and then an attempt was made to maintain this remission with levamisole. This regimen resulted in excellent control of the disease. A drug-induced arthritis developed in two patients and resolved spontaneously. There were no other significant side-effects.

Adolescent↗
PubMed1977

Nodular lymphoid hyperplasia of the bowel in primary hypogammaglobulinaemia: study of in vivo and in vitro lymphocyte function.

In vitro and in vivo lymphocyte function was studied in six patients with primary hypogammaglobulinaemia and nodular lymphoid hyperplasia (NLH) of the bowel. Lymphocyte transformation, numbers of circulating T and B lymphocytes, and delayed hypersensitivity skin tests did not significantly differ when compared with hypogammaglobulinaemic patients without NLH. However, patients with NLH had higher jejunal juice IgM concentrations and a tendency to higher serum IgM concentrations than those without NLH. The morphological features of NLH are similar to the germinal centres of lymph nodes but more closely resemble the follicle zone of Peyer's patches. These findings suggest that NLH represents a local immune response to antigens originating in the gut lumen.

Adolescent↗
PubMed1977

The effect of sera from patients with connective tissue diseases on red cell binding and phagocytosis by monocytes.

The uptake by human blood monocytes of sheep erythrocytes treated with rabbit anti-sheep antibody with or without mouse complement was assessed by a radioactive method to discover whether immune complexes would inhibit this reaction. It was found that sera from SLE patients inhibited uptake whereas normal sera enhanced. Some rheumatoid sera and rheumatoid joint fluids inhibited uptake whereas sera from juvenile rheumatoid patients did not.

Antigen-Antibody Complex↗
PubMed1976

Neutrophil dysfunction in Crohn's disease.

The migration of neutrophils into skin windows has been examined in patients with Crohn's disease and rheumatoid arthritis and compared with normal. Leucocyte migration was significantly lower in patients with Crohn's disease than in others. This abnormality of neutrophil function in Crohn's disease appears to be secondary to a defective acute inflammatory response as the neutrophils themselves were found to behave normally on in-vitro testing. A weak acute inflammatory response to particulate or antigenic material in the bowel wall could result in the chronic inflammation observed in this condition.

Blood Sedimentation↗
PubMed1976

Polyarthritis in adults with hypogammaglobulinaemia and its rapid response to immunoglobulin treatment.

Five patients with primary hypogammaglobulinaemia developed a severe polyarthritis that had some features in common with rheumatoid arthritis. Their joint disease could be distinguished from rheumatoid arthritis, however, by the dramatic improvement after gammaglobulin treatment. The arthritis of hypogammaglobulinaemia can, therefore, be included among the few potentially curable polyarthritides.

Adolescent↗
PubMed1976

Some cellular aspects of chronic inflammation in joint disease.

We have examined the nature of some mononuclear cells from inflamed synovial membranes of patients with rheumatoid arthritis. It was found that cells which remained in the supernatant medium after overnight culture of trypsinized tissue contained a variable number of lymphocytes which were shown to be T cells by rosetting and mitogen response. This suggests a source of T cell lymphokines with an effect on macrophages and thus a role in the maintenance of inflammation. Another role for mononuclear cells is suggest by the cytotoxicity of blood mononuclear cells directed against cultured synovial cells. This was found to occur in an autologous system using fibroblasts from rheumatoid synovium, but was not specific for rheumatoid arthritis. Stimulatory factors from rheumatoid joint effusion macrophages for blood lymphocytes were sought, but although blast transformation occurred, the results were equivocal. In this communication we set out to examine the nature of lymphoid cells in the synovial membrane and the role which they may play in the pathogenesis of chronic inflammation. We also briefly consider cell-mediated mechanisms of tissue injury. Since an active role of lymphoid cells pre-supposes the presence of an agent or agents which serve to stimulate them, we also report some recent attempts to find evidence for this. One of the striking histological features of the inflamed synovial tissue in rheumatoid arthritis, but also in some other forms of chronic arthritis, is the presence of lymphocytes and plasma cells. Immunofluorescent studies and organ culture studies have shown the presence and synthesis of immunoglobulins, predominantly the domain of plasma cells. The production of immunoglobulins, formation of complexes and activation of complement is a major factor in pathogenesis, but lymphocytes may also have a direct role through the production of lymphokines. Until recently these substances have been attributed to T lymphocytes, but Rocklin et al. (1) have recently shown that B cells may also be involved in certain experimental circumstances. The availability of synovectomy specimens from patients with rheumatoid arthritis has enabled us to examine the nature of lymphoid cells from synovial membranes. (This part of the work is reported fully elsewhere.

Arthritis, Rheumatoid↗
PubMed1975

[HL-A B27 associated rheumatic disease].

Report on a HL-A B27 positive female patient with the typical cardiac lesion occasionally found inankylosing spondylitis, peripheral arthritis, and acute anterior uveitis but without clinical or radiological evidence of spine or sacroiliac joint involvement. The concept of "HL-A B27 associated disease", including ankylosing spondylitis as well as Reiter's disease or other forms of seronegative rheumatic diseases, is suggested.

Aortic Valve↗
PubMed1975

Dichotomy between immunoglobulin synthesis by cells in gut and blood of patients with hypogammaglobulinaemia.

Eleven of fifteen patients with late-onset hypogammaglobulinaemia were found to have significant numbers of immunoglobulin-containing cells in the lamina propria of the gut. In six of them typical plasma cells were detected. In contrast the blood lymphocytes of only two of these patients could be induced to synthesise immunoglobulin by stimulation with pokeweed mitogen in vitro. Moreover, one patient in whom immunoglobulin-containing cells and plasma cells were detected in the rectum and jejunum failed to show similar cells in a peripheral lymph-node even after immunisation with pneumococcal polysaccharide type-III antigen in the drainage area of the node. It is possible, therefore, that the gut is a privileged site for the differentiation of B cells in these patients.

Adult↗
PubMed1975

Study of lymphoid cells from inflamed synovial membranes.

Synovectomy specimens from patients with rheumatoid arthritis were cultured and after 24 hours the nonadherent cells were removed. These were found to include cells with the morphological characteristics of lymphocytes. Using the sheep-cell rosetting test, up to 94% of these cells were found to be T cells, and while T cells could be found in all the supernatant cell populations studied, not all made a mitogen response. None or only a very small number of B cells were found by staining for surface immunoglobulin. The possible roles which T lymphocytes might play in chronic inflammation in the rheumatoid synovium are discussed in relation to experimental work, and factors which attract T cells into areas of nonspecific inflammation are similarly considered in the light of animal experiments.

Arthritis, Rheumatoid↗