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UPDATE: 26 January, 2009. Related article.
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Rituximab is a (monoclonal antibody genetically engineered) drug mainly used as a treatment for Non-Hodgkin's Lymphoma. It may also be used for the treatment of Rheumatoid Arthritis. Now you may receive it if you have fatigue from a thyroid related (generally thought of as auto-immune) dis-order called Sjogren's.
Make sure if this is proposed to you that you get this information that the drug may cause
severe and sometimes fatal infusion reactions. Tell your doctor right away if you develop blurred vision, cough, dizziness, drowsiness, headache, hives, itching, swelling, trouble breathing, or wheezing, while you receive or after you receive Rituximab .
Severe and sometimes fatal kidney problems and skin reactions may also occur during treatment with Rituximab . Tell your doctor right away if you experience decreased urination; red, swollen, peeling, or blistered skin; or skin or mouth sores or ulcers.
Rarely, a severe and sometimes fatal viral infection of the brain has been reported with the use of Rituximab in certain patients. Tell your doctor right away if you notice new or worsening medical problems such as changes in thinking (eg, confusion, disorientation), loss of balance or coordination, muscle weakness, trouble walking or talking, or unusual eye movements or vision changes.
You might also pursue proper thyroid testing, as thyroid dysfunction often is associated with fatigue.
And it now might be related to low levels of vitamin D-
Researchers at UCLA tried to show that low vitamin D would make an autoimmune thyroid problem worse. Their experiment was based on the idea that vitamin D has a dampening effect on an excessive and inappropriate immune response in many areas of your body, so they figured this was likely to apply to the thyroid as well. This turned out not to be the case, but what they did find was rather surprising.
First they created two groups of mice, one with vitamin D in their diet and the other with none. Even before they started their experiment they found that the vitamin D deficient mice had low levels of thyroxine (t4), meaning they were actually hypothyroid prone when the experiment was conducted. When the experiment was performed, vitamin D lacking mice did not have an excessive immune response as expected. Rather, they developed persistent hyperthyroidism because their thyroid glands were less able to withstand the stress of the experiment and were more sensitive to the autoimmune antibodies that both sets of mice were being exposed to. Simply put, a lack of vitamin D makes your thyroid more susceptible to injury that could result in hyperthyroidism.
While this is an animal study, the findings are important. First, it means that a lack of vitamin D contributes to the possibility of low thyroid. Second, it means that many irritants are likely to aggravate your thyroid to a greater extent if you lack vitamin D. For example, there are many chemical irritants in the environment that irritate your thyroid gland, such as perchlorate and fluoride. If you lack vitamin D you are more likely to be adversely affected by them.
This may be part of the reason that so many people feel metabolically worse and gain weight as the winter months move along. It is simple to make sure you take some extra D in the winter and doing so may help you keep your metabolism and thyroid from suffering the winter blues. Courtesy Wellness Resources.
Rituximab May Ease Fatigue in Sjogren's Syndrome By David Douglas
NEW YORK (Reuters Health) Nov 06 - Results of a pilot study suggest that rituximab may reduce fatigue in patients with Sjogren's syndrome and thus may improve quality of life, UK researchers report in the November issue of the Annals of the Rheumatic Diseases.
Dr. Paul Emery of Allerton Hospital, Leeds, and colleagues studied 17 patients with a fatigue score of more than 50 on a 100-mm visual analogue scale. They were randomized in a double-blind fashion to receive 2 infusions of rituximab 1 g or placebo. All patients also received oral and intravenous steroids.
At 6 months, 7 of the 8 patients receiving rituximab showed a greater than 20% improvement in the VAS for fatigue. This was true of only 5 of the 9 patients who had placebo.
Overall, there was a significant 36.8% improvement in fatigue VAS in the rituximab group compared to a non-significant 17.9% improvement in the placebo group. General health was also significantly improved in the active treatment group, but not in the placebo group.
There was also a significant difference in measures of social functioning and a trend towards improved mental health scoring in the rituximab group.
Commenting on the findings, Dr. Emery told Reuters Health that "this was the first randomized controlled trial in Sjogren's syndrome to show benefit, in particular a significant improvement in fatigue, a major issue for patients. This pilot study will now be followed by a more definitive study."
Ann Rheum Dis 2008;67:1541-1544.
IODINE AND SJOGREN'S SYNDROMEWe encourage - especially in darker and colder seasons - the use of iodine supplementation. This need is increased with fluoridated municipal water supplies and use of fluoride based drugs in the antibiotic, antidepressant, anticholesterol and antiosteoporosis drugs et al. We also encourage the proper use of selenomethionine in the support of proper thyroid function.
Thyroid dysfunction in primary Sjogren's syndrome: a long-term followup study.
D'Arbonneau F, Ansart S, Le Berre R, Dueymes M, Youinou P, Pennec YL.
Arthritis Rheum. 2003 Dec 15;49(6):804-9.
"OBJECTIVE: To evaluate the prevalence of thyroid dysfunction and related autoantibodies in patients with primary Sjogren's syndrome (pSS), and to determine whether these abnormalities develop over time. METHODS: pSS patients (n = 137) and controls (n = 120) were investigated for thyroid dysfunction and for the presence of anti-thyroid peroxidase antibody (anti-TPO) and antithyroglobulin antibody (ATG). Followup time for patients was 1-16 years, and 72 of the 120 controls were reevaluated 3 years after initial evaluation. RESULTS: Thyroid disease was more frequent in the pSS patients than in the controls (30% versus 4%; P < 10(-4)), as were anti-TPO and ATG (11% versus 3%; P < 0.02, and 3% versus 1%, not significant). Ten of 107 euthyroid pSS patients dropped out of the study, and thyroid dysfunction became apparent at followup in 12 of the remaining 97. Most of the patients with thyroid-related autoantibodies at entry developed autoimmune thyroid disease thereafter. CONCLUSION: Thyroid dysfunction is frequent in pSS patients, and those prone to develop thyroid disorders are identified by thyroid-related autoantibodies, or by rheumatoid factor and anti-Ro/SSA activity."
Thyroid disease in primary Sjogren syndrome. Study in a series of 160 patients.
Ramos-Casals M, Garcia-Carrasco M, Cervera R, Gaya J, Halperin I, Ubieto I, Aymami A, Morla RM, Font J, Ingelmo M.
Medicine (Baltimore). 2000 Mar;79(2):103-8.
"We studied 160 consecutive patients (147 female and 13 male) with primary Sjogren syndrome (SS) to determine the prevalence and clinical significance of thyroid disease in a large series of patients with primary SS from our unit and to compare the prevalence and significance with those in 75 individuals without SS from a primary care center. Serum levels of thyroid hormones (free thyroxine, triiodothyronine, and thyroid-stimulating hormone) and autoantibodies against thyroglobulin (TgAb) and thyroid peroxidase (TPOAb) were measured in all SS patients and in 75 control patients. Fifty-eight (36%) of the 160 patients with primary SS had evidence of thyroid disease. Autoimmune thyroid disease (ATD) was diagnosed in 32 (20%) patients and nonautoimmune thyroid disease (NATD) in 26 (16%). No significant differences were found when these prevalences were compared with those in control patients. On the other hand, comparing those patients with altered hormonal profiles, patients with NATD showed mainly hyperthyroidism (10/17, 59% versus 2/20, 10% in patients with ATD, p = 0.001). Finally, when clinical and immunologic manifestations of SS were analyzed in patients with and without thyroid disease, respectively, we found that patients with thyroid disease had a higher prevalence of female gender (98% versus 88%, p = 0.03), antiparietal cell autoantibodies (33% versus 12%, p = 0.002), TgAb (30% versus 5%, p < 0.001), and TPOAb (40% versus 5%, p < 0.001). In conclusion, thyroid disease occurred in more than one-third of patients with primary SS; the main cause was ATD, which was present in 20% of the patients studied. We note that no significant differences were observed when the prevalence of thyroid disease (either ATD or NATD) was compared with that in a control group of similar age and gender. Our results indicate that middle-aged women (with or without SS) should be screened periodically for thyroid function."
Autoimmune thyroid disease in primary Sjogren's syndrome.
Perez B, Kraus A, Lopez G, Cifuentes M, Alarcon-Segovia D.
Am J Med. 1995 Nov;99(5):480-4.
"PURPOSE: To evaluate the prevalence of autoimmune thyroid disease and thyroid dysfunction in patients with primary Sjogren's syndrome. PATIENTS AND METHODS: Thyroid function of 33 patients with primary Sjogren's syndrome was clinically and biochemically evaluated. Thyroid hormones and autoantibodies against thyroid peroxidase, thyroglobulin, and thyroid hormones were measured. RESULTS: Autoimmune thyroid disease and thyroid dysfunction were found in 15 cases (45%): autoimmune thyroiditis in 8 (24%); autoimmune hyperthyroidism in 2 (6%); and reversible iodine-induced hypothyroidism in the remaining 5 (15%). One or more of the evaluated autoantibodies were detected in 8 euthyroid patients (24%). Overall, the prevalence of autoantibodies against thyroid peroxidase, thyroglobulin, thyroxine, and triiodothyronine was 45%, 18%, 42%, and 36%, respectively. CONCLUSIONS: The high prevalence of autoimmune thyroid disease and thyroid dysfunction found in primary Sjogren's syndrome, using sensitive immunologic and thyroid function tests, suggest that both diseases are more frequently associated than it was previously thought, and should be sought clinically and by laboratory tests in all patients with primary Sjogren's syndrome."
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