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Systemic lupus erythematosus evaluation

Naked pDNA delivery of cytokines has also been evaluated in a number of mouse models of autoimmune disease. Naked pDNA delivery of TGF/3 to a murine model of systemic lupus erythematosus (SLE) led to lower serum IgG levels, decreased glomerulonephritis and increased survival (Raz et al., 1995). The pDNA (100 gg) was injected i.m. at 6, 10, 14, 18 and 22 weeks. Administration of IL-2 encoding pDNA had the opposite effect, resulting in increased semm IgG, increased glomerulonephritis, and decreased survival, demonstrating that a disease course could be significantly modulated by naked pDNA therapy. The pDNA (100 gg) was injected once in every two weeks for a total of five injections. Circulating semm levels of either IL-2 or TGF 0 w ere detected up to two weeks after the final pDNA injection into the muscle. [Pg.262]

In patients with a history of peptic ulcer or systemic lupus erythematosus the benefit-to-harm balance must be evaluated before prescribing ibuprofen. The first group is in danger of ulcer exacerbation and the second of a severe generalized hjrpersensitivity reaction. [Pg.1711]

Clearly, a complete evaluation for the presence of lung disease and pulmonary hypertension should be done so that appropriate therapy can be initiated early in the course of disease. Other rheumatologic conditions that may predispose to development of PAH are rheumatoid arthritis and systemic lupus erythematosus, especially in patients with Raynauds phenomenon. For patients in whom there is a reason to suspect acute inflammation or vasculitis, response to immunomodu-lation therapy may at least partially treat pulmonary hypertension (62). This may be particularly relevant in the lupus or mixed-connective tissue patient population. In particular, pulmonary hypertension also markedly improved in a series of patients who were responders to cyclophosphamide therapy. In the appropriate lupus patient who does not have fulminant systemic disease, one may have to consider lung biopsy to assess for inflammation and vasculitis. [Pg.151]

Warm autoimmune haemolytic anaemia may be either idiopathic or secondary to chronic lymphocytic leukaemia, lymphomas, systemic lupus erythematosus, or other autoimmune disorders or infections. Warm autoantibodies are responsible for 48-70% of autoimmune haemolytic anaemia cases and may occur at any age due to the secondary causes, however, the incidence increases starting around 40 years of age. There is an approximate 2 1 female predilection, possibly due to the association with other autoimmune diseases. Warm autoimmune haemolytic anaemia presents as a haemolytic anaemia of varying severity. The symptoms are those of anaemia (i.e. weakness, dizziness, fatigue, pallor, oedema, and dyspnoea on exertion) and haemolysis (i.e. jaundice, dark urine, and splenomegaly). The laboratory evaluation shows a reduced... [Pg.57]

A few examples of animal models used in immunotoxicologic testing of drugs include Brown Norway rat and Lewis rat models, which are described in detail below. Other established mouse models of autoimmune diseases, e.g.,systemic lupus erythematosus, collagen-induced arthritis,pristane-induced arthritis and systemic scleroderma, may be considered for potential application in immunotoxicology evaluation. [Pg.184]

Keegan S, Nadwodny K, Speal B, Herzyk D, Soos J. Adaptation of the systemic lupus erythematosus prone (NZB X NZW)F1 mouse strain for autoimmune toxicology evaluation. The Toxicologist CD 84 S-1, Abstract 910,2005. [Pg.187]

The role of both T and B lymphocytes in a variety of disease states beyond transplantation has become increasingly important in the past decade. This is especially true of those diseases frequently referred to as autoimmune in their etiology, such as rheumatoid arthritis, nephrotic syndrome, systemic lupus erythematosus, inflammatory bowel disease, and so on. In addition, several other major diseases are also known to have a component of T- or B-cell-mediated pathogenesis, for example, atopic dermatitis, psoriasis, and asthma. Until very recently, the mainstay of therapy for these diseases was the corticosteroids, which were often less than satisfactory in efficacy and often associated with undesirable side effects, especially in growing children and the elderly. Thus, the search for new agents with different mechanisms of action and which did not have the same adverse event profile as conventional corticosteroids led to the subsequent evaluation of drugs such as tacrolimus and sirolimus to treat several of these diseases. [Pg.425]

In June of 1994, a population-based retrospective cohort study was published which examined the risk of a variety of connective tissue diseases and other disorders after breast implantation [65]. In this study, all women in Olmsted County, Minnesota who received a breast implant between 1 January 1964 and 31 December 1991 (the case subjects) were studied. For each case subject, two women of the same age (within three years) from the same population who had not received a breast implant and who underwent a medical evaluation within two years of the date of the implantation in the case subject were selected as control subjects. Each woman s complete inpatient and outpatient medical records were interviewed for the occurrence of various connective tissue diseases (i.e., rheumatoid arthritis, systemic lupus erythematosus, Sjogren s syndrome, dermatomyositis, polymyositis, systemic sclerosis, ankylosing spondylitis. [Pg.563]

Concerns regarding potential HPV vaccine safety in systemic lupus erythematosus (SLE) patients were addressed by a prospective case-control study which evaluated the quadrivalent HPV vaccine. Fifty SLE patients were compared to 50 healthy controls. Importantly, no increase in SLE disease activity was observed in the 12-month follow-up period. However, seroconversion rates of antibodies to HPV serotypes (6,11,16 and 18) for the SLE group were lower than the control group, and the role of immunosuppressive therapy in SLE needs furtiier investigation [11 ]. [Pg.467]


See other pages where Systemic lupus erythematosus evaluation is mentioned: [Pg.135]    [Pg.689]    [Pg.1576]    [Pg.45]    [Pg.205]    [Pg.185]    [Pg.323]    [Pg.1003]    [Pg.561]    [Pg.510]    [Pg.546]   
See also in sourсe #XX -- [ Pg.1594 , Pg.1594 ]




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