Nodular lymphoid hyperplasia with hypogammaglobulinaemia.
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Biomedical subjects
Publications and source records attributed to A D Webster.
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The defibrinating agent ancrod (Arvin) was used instead of heparin for intermittent haemodialysis. It was an effective, and apparently safe, anticoagulant and reduced the deposition of fibrin and leucocytes on the Cellophane membrane. Administration was more complicated and urea dialysance was less with ancrod than with heparin.
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Using parasite agglutination, indirect immunofluorescence, enzyme-linked immunosorbent assay, and immunoblotting, Giardia lamblia specific antibody was detected in 5 commercially available immunoglobulin (IgG) preparations. IgG antibodies to Entamoeba histolytica were either present in very low titre or were absent. Immunoblotting showed that anti-G. lamblia antibodies were detected towards a range of Giardia proteins, 25-200 kDa. These findings raise the possibility that pooled human IgG preparations could be evaluated in the treatment of chronic giardiasis which is refractory to conventional therapy.
We have compared the infectivity titres, reverse transcriptase levels and antigen titres in the supernatants from persistently infected cell lines that produce a variety of HIV-1 isolates. We found a poor correlation between the different assays, and a variability in viral activity dependent on culture medium.
The lack of antibody in hypogammaglobulinemic patients probably results in failure of mycoplasmas to be "neutralized" and accounts for the diminished ability of the patients to cope with these organisms escaping hematogenously from the respiratory and urogenital tracts. Furthermore Ureaplasma urealyticum and other mycoplasmas are ingested by neutrophils in the absence of opsonins, indicated by the fact that they are able to trigger the release of chemiluminescence from these cells; ureaplasmas are not killed during this process and it is possible that carriage occurs within phagocytes to various sites. Several mycoplasmal species have localized in joints and U. urealyticum organisms are no exception. They have been isolated from the purulent synovial fluids of at least three hypogammaglobulinemic patients in Canada, England and the United States, respectively, the arthritides responding to appropriate antibiotic therapy. In one male patient, however, repeated and prolonged episodes of arthritis over several years, associated with antibiotic-resistant ureaplasmas, responded only to the administration of specific hyperimmune serum. Apart from joint involvement subcutaneous abscesses have been seen, and in the latter patient persistent urethritis was caused by ureaplasmas, these being the only organisms recovered from the urethra. Chronic urethrocystitis/cystitis in hypogammaglobulinemic patients has been associated also with ureaplasmal infection. In addition polyarthritis with recovery of both ureaplasmas and Mycoplasma hominis from the joints has been seen in a kidney allograft patient on an immunosuppressive regimen. However, further evidence that ureaplasmas cause a problem in immunosuppressed patients or in those with the acquired immunodeficiency syndrome is lacking.
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In vivo and in vitro T lymphocyte function was studied in 64 patients with X-linked and common "variable" primary hypogammaglobulinaemia. Lymphopenia, splenomegaly, depressed in vitro lymphocyte transformation to mitogens and failure to manifest delayed hypersensitivity skin reactions occurred frequently in the common "variable" group, particularly those with adult onset disease. However, relative circulating T lymphocyte numbers and in vitro lymphocyte transformation in a mixed lymphocyte reaction with the CLA4 lymphoid cell line were normal. Antibody mediated and PHA induced lymphocytotoxicity were also normal. These findings indicate the presence of a generalised lymphocyte defect which is selective for certain T lymphocyte functions. Despite these apparent T lymphocyte defect, none of the patients suffered from the unusual opportunistic parasitic, viral or fungal infections which tend to occur in infants with severe primary defects of both T and B lymphocytes.