Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunologic studies were performed on 16 patients with thyroid cancer. Circulating leukocyte counts increased, parallel to development of the terminal stage of disease, but total lymphocytes decreased. Serum immunoglobulin and complement were high, even though almost all patients showed negative antithyroid antibodies. Delayed skin hypersensitivity to bacterial and viral antigens and lymphocyte responsivity to PHA were not impaired at the initial stage of disease, but were impaired in terminal illness. Cell-mediated immunity (CMI) to tumor antigens(s) was measured using the assays of lymphotoxin, migration inhibition factor, and peripheral leukocyte migration inhibition. A few patients showed significant response to tumor antigen, but not to homogenates of Graves' thyroid gland. Active immunotherapy was applied to three patients. Two patients, who were in the terminal stage of illness, could not develop generalized CMI; immunization did not alter the patients' rapid downhill course. One patient developed in vitro evidence of CMI against cancer tissue antigens, associated with decrease in tumor size. Four months after immunization, CMI was impaired in autologous plasma culture, but not in cultures in allogenic normal plasma.
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PMID:Immunologic aspects of human thyroid cancer. Humoral and cell-mediated immunity, and a trial of immunotherapy. 118 83

A number of immunological parameters have been monitored for up to 6 weeks following 131I treatment for hyperthyroidism in Graves' disease. The aim was to examine whether this isotope treatment normalizes or further accentuates some immunological abnormalities which may be a manifestation of autoimmune reactions in these patients. It was confirmed that both the cellular composition and immunological reactivities of the patients' blood lymphocytes were abnormal before treatment. After 131I administration a slight lymphopenia occurred and the ratio between CD4 and CD8 positive T lymphocytes (helper-inducer/suppressor-cytotoxic), which was increased before treatment, increased further. Moreover, PWM-triggered IgM secretion in vitro was reduced by 50%. No other immunological parameters studied, such as secretion of other Ig classes, mitogenic responses of lymphocytes, and distribution of other lymphocyte subsets, changed to any detectable extent. It remains speculative whether the 131I-induced changes of the immune system may further accelerate the underlying autoimmune disease processes.
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PMID:Blood lymphocyte population following 131I treatment for hyperthyroidism. 182 98

NOD-H2(h4) mice, which express I-A(k) on the NOD background, spontaneously develop autoimmune thyroiditis, a model of Hashimoto thyroiditis in humans, by adding iodide in the drinking water. Parental NOD mice have previously been shown to have intrinsic numerical abnormalities in peripheral lymphocytes and lymphocyte subpopulations such as CD4(+)CD25(+) naturally occurring regulatory T cells (Treg). Therefore we first investigated whether the similar abnormalities exist in NOD-H2(h4) mice. We observed that, compared with other non-autoimmune disease prone BALB/c and C57BL/6 mice, NOD-H2(h4) mice have lower numbers of splenocytes, CD3(+)T, CD4(+)T and CD8(+)T cells but the ratios of Treg to CD4(+)T cells were comparable. Increasing the numbers of peripheral lymphocytes by Complete Freund's Adjuvant immunization or splenocyte transfer did not affect development of thyroiditis, indicating that lymphopenia does not play a critical role in the pathogenesis of thyroiditis. We next examined the significance of Treg by depleting this lymphocyte subset with anti-CD25 antibody. Treg depletion, performed 4days before the administration of NaI water for 8 weeks, significantly exacerbated thyroiditis (p<0.01). Anti-thyroglobulin antibody titers also increased by Treg depletion (p<0.01) without changing the IgG2b to IgG1 ratios. In addition, expression levels of mRNA for IFN-gamma and IL-4 were enhanced in parallel. However, T(4) levels were similar between antibody-treated and untreated groups. Additional anti-CD25 administration at 3 weekly intervals did not influence these results. These data, together with previous studies on other mouse models of inducible thyroiditis and Graves' disease, indicate the role played by Treg in keeping anti-thyroid autoimmune reaction in check in experimental autoimmune thyroid diseases.
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PMID:CD4+CD25+ naturally occurring regulatory T cells and not lymphopenia play a role in the pathogenesis of iodide-induced autoimmune thyroiditis in NOD-H2h4 mice. 1782 32

Reconstitution Graves' disease occurs in three settings. First, bone marrow transplantation from a donor with Graves' disease may cause this disease to appear in the recipient, as a result of adoptive immunity, although disordered immunoregulation secondary to graft-versus-host disease may also play a role. Second, alemtuzumab treatment for multiple sclerosis leads to the development of Graves' disease in up to a third of patients during the phase of naive T-cell expansion, which follows therapeutic lymphocyte depletion. Other reconstitution autoimmune phenomena, including immune thrombocytopaenic purpura, are also recognised after alemtuzumab administration. Finally, reconstitution Graves' disease may occur during a similar phase of CD4(+) T-cell expansion, which follows highly active antiretroviral therapy for human immunodeficiency virus infection. Again, this complication is part of a broader spectrum of immunoregulatory disturbances, which can arise after immune reconstitution. The mechanisms responsible for reconstitution Graves' disease are at present unclear, but may include a relative bias towards a Th2-mediated immune response and reduced competition for autoreactive lymphocytes to expand during the time when recovery from lymphopenia commences.
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PMID:Immune reconstitution syndrome and the thyroid. 1994 46

Graves' disease and other disorders of thyroid function may occur following treatment with novel anticancer agents or during periods of lymphocyte recovery after lymphopenia. There are three main settings for such lymphocyte reconstitution: recovery after a bone marrow or haematopoietic stem cell transplant, alemtuzumab treatment and the use of highly active antiretroviral therapy (HAART) for human immunodeficiency virus infection. The available evidence suggests that Graves' disease behaves as normal in most of these cases and should be treated conventionally, but it may follow a more favourable course in those receiving alemtuzumab or HAART. As spontaneous or drug-induced remission may be more likely in these two settings, first-line treatment should usually consist of an antithyroid drug.
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PMID:Graves' disease following immune reconstitution or immunomodulatory treatment: should we manage it any differently? 2452 93

Alemtuzumab is a highly efficacious therapy used in the treatment of multiple sclerosis (MS), but uncoupling of T and B cell repopulation during immune reconstitution associates with an increasing range of secondary B cell-mediated autoimmune complications. A 34-year-old woman developed Graves' disease 11 months following an initial course of alemtuzumab treatment for MS. Nine months following the second treatment with alemtuzumab, the patient presented with spontaneous intramuscular and subcutaneous haemorrhage due to development of an inhibitory autoantibody to coagulation factor VIII. Acquired haemophilia A (AHA) is an extremely rare complication in patients treated with alemtuzumab. Treatment with rituximab may induce a rapid remission of AHA; however, the patient's high John Cunningham virus (JCV) antibody index and alemtuzumab-induced T cell lymphopenia may lead to an increased risk of progressive multifocal leucoencephalopathy, a potential complication which was unacceptable to the patient.
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PMID:Acquired haemophilia A complicating alemtuzumab therapy for multiple sclerosis. 2921 66