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  • 1
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective— To observe if a combination of a depot GnRH agonist and cyclical hormone replacement therapy decreases menstrual b od loss.Design— open, observational study comparing the objective assessment of menstrual blood loss before, during and after 3 months treatment.Subjects— 20 women with a subjective complaint of heavy menstrual loss in whom no cause could be discovered.Interventions— Each woman received 3 months of depot goserelin (Zoladex) combined with cyclical hormone replacement therapy (Cyclo-Progynova, 1 mg). Menstrual loss and symptoms were assessed before, throughout and after the study.Main outcome measures— Changes in objective and subjective assessments of menstrual blood loss and the acceptability of the treatment.Results— The median pretreatment menstrual loss was 68 ml (range 23–397). Only 8 (40%) of the patients had a loss exceeding 80 ml per period. The median blood loss was 30 ml, 16 ml, and 17 ml in the three treatment cycles (P 〈 0.001 Wilcoxon rank sum for the third cycle). There was a significant decrease in the median length of menstruation (P 〈 0.001) and the number of towels or tampons (P 〈 0.01) used per period in the third treatment cycle. There was a significant decrease (P 〈 0.005) in the number of women complaining of dysmenorrhoea, premenstrual symptoms, flooding and the passage of clots. Seventeen patients experienced hot flushes. Eighteen of the 20 patients were completely satisfied with the treatment and would have been happy to continue with it for longer than 12 months.Conclusions— The combination of a depot gonadotrophin releasing hormone agonist and cyclical hormone replacement therapy is a successful and acceptable treatment of dysfunctional uterine bleeding.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Insulin-dependent diabetes ; cellular immunity ; mouse ; streptozotocin ; auto-immunity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Anti-B cell auto-immunity may play a role in the pathogenesis of diabetes in mice resulting from multiple subdiabetogenic doses of the pancreatic B cell toxin, streptozotocin. In the present study we have investigated the cytotoxic anti-B cell response in these mice. A major role for B lymphocytes, macrophages, or their products in the cytotoxic response originally detected in vitro was eliminated by passing splenocytes from the mice treated with multiple subdiabetogenic doses of streptozotocin over a nylon wool column. The removal of the adherent cells enhanced the cytotoxicity against a rat insulinoma cell line in vitro by that expected due to enrichment of T-lymphocytes by approximately twofold. The induction of diabetes after multiple subdiabetogenic doses of streptozotocin is strain dependent. Mice of five strains were immunized with rat insulinoma cells, but only splenocytes from the two strains susceptible to multiple subdiabetogenic doses of streptozotocin demonstrated a significant cytotoxic response against the rat insulinoma cells in vitro. Mice pre-immunized with either the rat insulinoma cells or with syngeneic islets labelled in vitro with the hapten trinitrophenol developed hyperglycaemia more rapidly than control mice after multiple subdiabetogenic doses of streptozotocin. In the latter experiment the control mice immunized with complete Freund's adjuvant alone also became hyperglycaemic after a modified multiple subdiabetogenic dose of streptozotocin that did not cause diabetes in non-immunized mice. In mice pre-treated with either adjuvant or cyclophosphamide and then given a modified multiple subdiabetogenic dose of streptozotocin (35 mg/kg × 5 rather than 40 mg/ kg) the degree of hyperglycaemia was reduced and there was no protective effect of cyclophosphamide. However, the mice pre-treated with adjuvant again developed hyperglycaemia more rapidly and to a much higher level than did the mice given multiple subdiabetogenic doses of streptozotocin only. These additional data further support the hypothesis that B-cell destruction after multiple subdiabetogenic doses of streptozotocin results from triggering of an immune response against these insulin-producing cells.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Keywords Islet cell ; antigen ; autoimmunity ; autoantibody.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin-dependent diabetes mellitus (IDDM) is associated with autoantibodies to several pancreatic islet antigens. We have described an assay in which autoantibodies displace a radiolabelled monoclonal anti-islet antibody. Sera from 87 % of 429 children at time of diagnosis of IDDM were positive, while sera from control groups had much lower prevalences (1.3–19 %). Sera from 41.9 % of diabetic subjects remained positive after 20 years duration of IDDM. Sera from 23.6 % of parents and 37.9 % of non-diabetic siblings were positive. Twenty relatives who subsequently developed IDDM had the same prevalence of the antibodies (85 %) as did the patients at time of diagnosis. These findings confirm that the autoantibodies detected by monoclonal antibody (mAb) 1A2 are common at the onset of IDDM and their presence prior to the onset of hyperglycaemia suggests that this method may be useful in screening non-diabetic populations. The high prevalence of antibodies in relatives reduces the efficacy for diabetes prediction, but suggests either that generation of these antibodies is an autosomal dominant trait, or that the antigen detected by these antibodies is cross-reactive with a common environmental antigen. Differentiation between these hypotheses will await the identification of the specific islet-cell antigen detected by mAb 1A2. [Diabetologia (1996) 39: 1365–1371]
    Type of Medium: Electronic Resource
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