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Biomedical subjects

G Spickett

Publications and source records attributed to G Spickett.

16 recordsLinked to original sources
PubMed2001

Pneumocystis carinii pneumonia after thoracic duct ligation and leakage.

A case of Pneumocystis carinii pneumonia was induced through immunosuppression following thoracic duct ligation. The patient initially presented with an esophageal adenocarcinoma, which was totally resected. She is human immunodeficiency virus-negative and not undergoing immunosuppressive treatment.

CD4 Lymphocyte Count↗
PubMed1999

Desensitization to co-trimoxazole (trimethoprim-sulphamethoxazole) in HIV-infected patients: is patch testing a useful predictor of reaction?

OBJECTIVE: To establish the safety and efficacy of desensitization to co-trimoxazole in hypersensitive HIV-infected subjects. To assess if delayed hypersensitivity (type IV) to co-trimoxazole predicts those unable to be desensitized. METHOD: desensitization to co-trimoxazole, comprising trimethoprim (T) 0.4 mg and sulphamethoxazole (S) 2 mg initially with doubling dose daily, full strength co-trimoxazole (T/S 160 mg/800 mg) at 10 days. Patch testing with 4.5% and 9% co-trimoxazole in yellow soft paraffin, CMI Multitest. RESULTS: nineteen patients, 18 male and one female, were recruited and completed the desensitization regime. Of these 80%(15) achieved successful desensitization. Three of those who reacted did so within 18 days. All patients were successfully managed in an outpatient setting. There were no major adverse reactions. Of those reacting none gave a positive patch test to co-trimoxazole and all showed absent delayed type hypersensitivity reactions to recall antigens. CONCLUSIONS: co-trimoxazole desensitization is a safe and efficacious procedure, with a success rate of 80% using the above regime. Patch testing with co-trimoxazole gives no useful information about those that reacted.

Adult↗
PubMed1995

CD4+ T cell subsets defined by isoforms of CD45 in primary biliary cirrhosis.

Primary biliary cirrhosis (PBC) is an autoimmune condition characterized by destruction of the intrahepatic bile ducts. Autoreactive CD4+ T cells have been reported both in the peripheral circulation and in the mononuclear cell infiltrate in the affected portal tracts. In this large study we have used two- and three-colour flow cytometry to determine the phenotypes of the CD4+ T cell subsets in the peripheral blood and liver-infiltrating lymphocytes of PBC patients (n = 43), normal controls (n = 19) and patients with alcoholic cirrhosis (n = 15), according to a novel classification based on the simultaneous expression of different isoforms of CD45. In PBC patients the proportion of peripheral blood CD4+ cells possessing the CD45ROhighRA- 'memory' phenotype was significantly increased, and the CD45RO-RAhigh 'naive' population was significantly decreased, compared with the two control groups. No significant differences in peripheral blood CD4+ T cell subsets were seen between patients with pre-cirrhotic and cirrhotic PBC. A similar, but more marked, shift towards the CD45ROhighRA- 'memory' phenotype was seen in the liver-infiltrating CD4+ T cells in PBC patients compared with alcoholic cirrhotics. Cells within the CD4+ memory subpopulation were further subgrouped according to expression of CD45RB, the level of expression of which has been associated with functional differences in the memory subset. In peripheral blood no differences were seen between PBC patients and controls with respect to the proportion of CD45ROhighRBhigh and CD45ROhighRBdim memory subsets. A statistically significant difference in the distribution of these memory subsets, with an increased memory-2/memory-1 ratio was observed in the liver-infiltrating CD4+ T cells of PBC patients compared with those from alcoholic cirrhotic patients. The potential implications of this observation are discussed.

Adult↗
PubMed1994

Study of B and T cell phenotypes in blood from patients with common variable immunodeficiency (CVID).

B and T cell phenotypes in peripheral blood from 71 CVID patients have been measured in a study using directly conjugated monoclonal antibodies and two colour flow cytometry. Data was compared between different patient groups (based on whether their B cells could secrete IgM or IgG in vitro) and normal donors. There was a clear correlation between abnormalities of both B and T cells and the different patient groups. There were reduced absolute numbers of circulating CD4+ T cells, particularly those of the CD4+.CD45RA+ subset, and of CD19+ B cells in those patients whose B cells failed to secrete IgM or IgG in vitro. This demonstrates an association between B cell lymphopenia, failure of B cell immunoglobulin production in vitro and T cell subset lymphopenia in CVID. It supports the view that this group of CVID patients has a disease involving T cell regulation of B cells of varying severity.

Antibodies, Monoclonal↗
PubMed1991

Alopecia totalis and vitiligo in common variable immunodeficiency.

Three cases of severe and irreversible alopecia occurring in patients with common variable immunodeficiency are described. In all three cases, hair loss developed after the diagnosis of immune deficiency; one of the patients also had extensive vitiligo. A fourth patient had vitiligo in the absence of alopecia. No change in the alopecia or vitiligo was noted in any patient as a result of immunoglobulin replacement therapy.

Adult↗
PubMed1989

B cell function in acquired "common-variable" hypogammaglobulinemia: proliferative responses to lymphokines.

We have compared the proliferative responses of an enriched population of B lymphocytes from patients with acquired (common variable) hypogammaglobulinemia (CVH) with the responses of cells from normal individuals. The uptake of [3H]thymidine into DNA was measured on stimulation with a range of interleukins (IL-2, IL-4, and IL-6) and solid-phase anti-IgM. Flow cytometry using CD19 and surface IgM showed that the "non-T" preparations from the peripheral blood of CVH patients either contained B cells within the normal range (30-40% of the cells) or in a minority group no B cells (less than 3% of the cells). Overall, there were no significant differences between the proliferative responses of patients' cells (in the group where normal numbers of B cells were present) and normal cells with any combination of stimulus used. No IgG was produced by cells from any patient and in only one patient was IgM production observed. This suggests that the primary B lymphocyte defect in CVH is in the differentiation phase in B cell function rather than in the growth phase. However, the presence or absence of B cells suggests that different defects exist in subgroups of patients with this disease.

Agammaglobulinemia↗
PubMed1989

Assessment of responses of normal human B lymphocytes to different isolates of human immunodeficiency virus: role of normal donor and of cell line used to prepare viral isolate.

The effect of different HIV-1 isolates on normal human B lymphocyte function has been studied in vitro. Production of IgM and IgG was measured by ELISA using a "standard" non-T preparation of B cells depleted of macrophages and T cells (but not of low-density accessory cells, LDC). Only one (H9/CBL-4) of five different isolates induced polyclonal production of immunoglobulin. Apart from intrinsic differences between isolates, important inherent variables were shown to affect the response. One was the mix of cell types in the responding preparation of B cells. This was tested by examining the effects of HIV-1 isolates independently on the accessory function of LDC and on B cell function when the LDC were removed. Isolate H9/HTLV-IIIRf was nonstimulatory on a B cell preparation containing LDC and suppressive on LDC accessory function yet could enhance function of B cells when the LDC were depleted. Another variable was the donor of the normal B cells. The B cell response was consistent with each donor but varied greatly with different donors. Thus, no single explanation emerges for the hypergammaglobulinemia in some adult AIDS patients and for the hypogammaglobulinemia in some pediatric cases. Additionally, the cell lines used to propagate the virus particularly affected the assay of B cells depleted of LDC. Uninfected supernatants had different effects on the B cell function, and these host cell effects (perhaps by release of cytokines or other mediators) may be exacerbated in infected cell lines. Our data show the complexity of the abnormal B cell function in AIDS.

Acquired Immunodeficiency Syndrome↗