CAMPATH-1H Therapy in Autoimmune Diseases
Vibeke Strand in Novel Therapeutic Agents for the Treatment of Autoimmune Diseases, 1997
Autoimmune diseases such as rheumatoid arthritis (RA) are considered to be T-cell-mediated and might therefore be expected to respond to therapies directed against the T lymphocyte. Previous therapies with lymphapheresis, total nodal irradiation, and thoracic duct drainage all showed clinical benefit, but responses were not maintained and the therapies were too toxic for routine use. More recently, cyclosporine (a fungal metabolite with a specific action against T cells) has been shown to be an effective therapy in autoimmune disease.
Historical Perspective and Rationale of HSCT for Autoimmune Diseases
Richard K. Burt, Alberto M. Marmont in Stem Cell Therapy for Autoimmune Disease, 2019
Autoimmune diseases have been defined as a fascinating but still poorly understood group of diseases, 1 which pose “some of the most baffling scientific questions and daunting clinical challenges in internal medicine.” 2 This intricated and still imperfectly elucidated background must be considered before reviewing the history and, even more so, the rationale of hematopoietic stem cell (HSC) therapy for severe autoimmune diseases (SADs). Their etiology is clearly multifactorial, as reflected in the concept of an integrated fabric of components known as the “mosaic of autoimmunity.” 3 There are, however, some distinctions which bear directly on the rationale of HSC transplantation for SADs.
Major Histocompatibility Complex and Autoimmune Disease
Richard K. Burt, Alberto M. Marmont in Stem Cell Therapy for Autoimmune Disease, 2019
The major histocompatibility complex (MHC) encodes a large number of molecules which are key participants in the function of the immune system. Included in the human MHC, known as human leukocyte antigen (HLA), are two classes of HLA molecules which are highly polymorphic, and which provide genetic restriction for T lymphocyte responses: HLA class I and HLA class II. Several of the HLA class II molecules are highly associated with, and likely to have a major role in, susceptibility to autoimmune diseases. However, the molecular mechanisms involved are still unclear. In this chapter we address the structure of the HLA molecules and the mechanisms for presenting antigens to the immune system, as well as the correlation of specific HLA alleles with autoimmune diseases.
Newly diagnosed iron deficiency anemia and subsequent autoimmune disease: a matched cohort study in Taiwan
Published in Current Medical Research and Opinion, 2020
Renin Chang, Kuo-An Chu, Mei-Chen Lin, Yi-Hsin Chu, Yao-Min Hung, James Cheng-Chung Wei
Objective: To explore whether newly diagnosed iron deficiency anemia (IDA) is associated with subsequent systemic autoimmune disease onset. Methods: The study identified 22,440 patients who received a diagnosis of IDA between 2000 and 2012 from a random sample of 1 million people from Taiwan’s National Health Insurance Research Database. The patients with IDA were randomly matched with 89,528 patients with no IDA by age, gender, and index year. We followed the 2 groups until systemic autoimmune disease onset. Cox proportional hazards analysis was used to determine autoimmune disease risk by age, gender, and comorbidities, in terms of hazard ratios (HRs) and 95% confidence intervals (CIs). Results: Adjusted HR (95% CI) of autoimmune disease in the IDA group was 2.37 (1.92–2.92) compared with the non-IDA group. The subgroup analysis indicated that a patient with IDA had a significantly greater risk of autoimmune disease if they were female or had the comorbidities of hypertension, hyperlipidemia, cancer, allergic rhinitis, urticaria, chronic obstructive pulmonary disease, or chronic liver disease. The autoimmune disease was significantly more likely to occur within 2 years after a new diagnosis of IDA. Conclusions: IDA significantly increases autoimmune disease risk, particularly in female patients and patients with certain comorbidities. Clinicians should conduct further clinical evaluations and laboratory tests of autoimmune disease in patients with IDA.
Analyses of hair and salivary cortisol for evaluating hypothalamic–pituitary–adrenal axis activation in patients with autoimmune disease
Published in Stress, 2017
Eva Montero-López, Ana Santos-Ruiz, Raquel González, Nuria Navarrete-Navarrete, Norberto Ortego-Centeno, Olga Martínez-Augustín, Manuel Rodríguez-Blázquez, María Isabel Peralta-Ramírez
Although many studies have shown that patients with autoimmune disease present a hypoactive hypothalamic–pituitary–adrenal axis (HPA), controversial results have been described. Our objective was to study HPA axis activity in women with autoimmune disease compared to healthy women. Therefore, we analyzed salivary cortisol over the course of a day, and hair cortisol concentrations from the three preceding months, from 65 women divided into two groups: healthy women (n = 30), with a mean age of 44.70 ± 11.65 years; and women with autoimmune disease (n = 35), with a mean age of 48.26 ± 9.04 years. The latter group comprises women with systemic lupus erythematosus (SLE), Sjögren’s syndrome (SS), and systemic sclerosis (SSc). Perceived stress and psychopathological symptomatology were also evaluated. Autoimmune disease group scored higher on the somatization subscale SCL-90-R and lower on the anxiety subscale than the control group. Regarding HPA axis activation, the area under curve for cortisol levels during the day was higher for the autoimmune disease group. In addition, higher cortisol levels in hair were found in the group with autoimmune disease. Our findings show greater short and long-term HPA axis activity in women with autoimmune disease than in healthy women.
Autoimmunity in dermatitis herpetiformis: Effect of a gluten-free diet
Published in Journal of Dermatological Treatment, 1991
Jp McFadden, Jn Leonard, Av Powles, L. Fry
Of 165 patients with dermatitis herpetiformis OH) assessed for autoimmune status, autoantibodies were present in 101 (61.2%) and autoimmune disease in 20 (12%) on prekntation; a further nine patients (5.5%) had developed autoimmune disease at follow up (mean 8.1 years). Autoimmune status did not correlate with severity of small-bowel enteropathy as assessed by microscopy or by intraepithelial lymphocyte count. There was also no correlation with age, sex, duration of rash before presentation or age at onset of rash. Of 162 patients followed up (mean 8.1 yrs), 156 were on definitive treatment. In all treatment groups there was an overall trend to development of autoimmune disease/autoantibodies in a minority of patients. Autoantibodies/ autoimmune disease developed in subjects initially autoantibody-negative in 5/26 (19%) on a strict gluten-free diet, 5/16 (31%) on drug therapy plus gluten avoidance and 2/19 (11%) on drug therapy alone. Treatment with a gluten-free diet did not result in resolution of autoimmune disease or disappearance of organ-specific antibodies in DH. These results indicate that development of autoimmune disease is independent of both gluten intake and severity of bowel disease, but is more likely to be due to an underlying immunological mechanism which is probably genetically determined.
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