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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of morphine (10 mg/kg/s.c.) on tryptophan (TRP), 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) levels were studied in normal and arthritic rats. (1) In normal rats morphine induced a discrete but significant increase of 5-HIAA levels in the forebrain and the spinal cord. (2) By contrast, in rats suffering from experimentally induced arthritis large modifications were apparent. The basal levels of TRP, 5-HT and 5-HIAA were significantly higher than in normal rats. Morphine induced clear increases of 5-HIAA and TRP in the forebrain, the brain stem and the spinal cord, without any modification of 5-HT. The effects were dose-dependent and suppressed by naloxone (1 mg/kg/i.m.). Statistical analysis clearly revealed that arthritic rats were much more sensitive to morphine. The results support the hypothesis of an activation of a 5-HT descending pathway by morphine which parallels the activation of the ascending pathway previously demonstrated by several authors and confirmed here.
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PMID:Changes in brain and spinal tryptophan and 5-hydroxyindoleacetic acid levels following acute morphine administration in normal and arthritic rats. 48 58

Prolactin secreted by rat anterior pituitary explants into organ culture medium was purified by salt fractionation and gel filtration. A yield of 22 mg/g was obtained, which clearly represented de novo synthesis and secretion of the hormone. Comparative characterization studies were performed on the secreted prolactin and pituitary extracted rat prolactin obtained from the National Institute of Arthritis, Metabolism and Digestive Disease. The biological and immunological activity estimates of both forms were comparable, although the specific activities of the secreted prolactin were somewhat lower than those of the pituitary prolactin. The secreted and extracted forms of prolactin appeared to be identical in primary structure as evidenced by similar amino acid compositions and identical NH2-terminal sequences. Circular dichroism spectra suggested that there may be differences in tertiary structure, since the positive tryptophan band at 292 nm, which eas observed with extracted hormone, was absent in the secreted prolactin.
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PMID:Comparison of secreted and extracted forms of rat pituitary prolactin. 95 31

The eosinophilia-myalgia syndrome (EMS) is a unique entity associated with products that contain L-tryptophan (L-trp). Studies of the underlying etiopathogenic processes are underway. EMS is a distinct syndrome, but shares features with eosinophilic fasciitis and other variants of systemic sclerosis. A wide spectrum of clinical manifestations has been described, but there is no consensus regarding treatment. We report the clinical and laboratory features of 12 patients. All were treated with nonsteroidal antiinflammatory drugs (NSAIDs) and analgesics with transient or minimal effect. Two received D-penicillamine (DP) and colchicine, with minimal improvement; one had no response to azathioprine (AZA). Eleven received corticosteroids and had improvement of general symptoms, arthralgias, arthritis, myalgias, skin changes, eosinophilia, and leukocytosis. Nevertheless, all but the latter two findings recurred when corticosteroids were tapered. Seven patients who were unresponsive to the former treatments received low-dose pulse oral methotrexate. Six exhibited continued improvement after a mean follow-up of 4.5 months, with good drug tolerance. Corticosteroids were tapered and, in some instances, discontinued without relapse or complications. One patient improved but later died of aspiration pneumonia. We conclude that methotrexate (MTX) is a therapeutic alternative for patients with severe or refractory EMS.
Semin Arthritis Rheum 1991 Oct
PMID:Treatment of the eosinophilia-myalgia syndrome. 174 39

The Centers for Disease Control has recently reported an association between the use of oral L-tryptophan preparations and a disease marked by severe myalgia, peripheral eosinophilia, and neuromuscular and cutaneous abnormalities. They have labeled the condition eosinophilia-myalgia syndrome. We report here the clinical and histopathologic findings in 4 patients who developed an illness resembling eosinophilic fasciitis following the initiation of oral L-tryptophan supplementation.
Arthritis Rheum 1990 Jul
PMID:Association of L-tryptophan and an illness resembling eosinophilic fasciitis. Clinical and histopathologic findings in four patients with eosinophilia-myalgia syndrome. 236 28

Eosinophilia-myalgia syndrome (EMS) is a recently described clinical entity that has been ascribed to taking over-the-counter preparations of the amino acid L-tryptophan. We describe 4 patients with EMS, 3 of whom presented with eosinophilic fasciitis, and we review the epidemiology of EMS reported in Maryland and discuss the possible pathophysiology of the disease. EMS should be considered in the differential diagnosis of severe myalgia, eosinophilia, and eosinophilic fasciitis.
Arthritis Rheum 1990 Jul
PMID:Eosinophilia-myalgia syndrome due to L-tryptophan ingestion. Report of four cases and review of the Maryland experience. 236 29

Anthranilic acid (ANA), a metabolite of tryptophan, was examined for its immunopotentiating properties. Administration of ANA (12 mg/kg/day, p.o.) significantly enhanced the development of adjuvant arthritis in rats, although not in a dose-related manner. ANA tended to enhance adjuvant disease moderately suppressed by pretreatment with cyclophosphamide (CY), an immunosuppressive agent. ANA (3-30 mg/kg/day, p.o.) also caused a dose-related enhancement in the antibody formation to sheep erythrocytes (SRBC) in mice.
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PMID:Enhancing activity of anthranilic acid on adjuvant arthritis in rats and antibody formation in mice. 277 15

In rats suffering from experimentally induced arthritis produced by Freund's adjuvant, there is a marked decrease in total serum tryptophan levels and a marked increase in plasma-free tryptophan levels at both 15 and 21 days after the administration of the adjuvant. Tryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels are increased in the brain and the spinal cord at 15 days. However, 21 days after administration of the adjuvant these levels returned to normal values in the brain, but remained increased in the spinal cord. These results are in agreement with investigations suggesting the possible involvement of the raphe-spinal system in response to pain stimuli but are contrary to the observation that there is a large decrease in plasma-free tryptophan levels in arthritic human patients. These opposite results still question the hypothesis of a relationship between changes in plasma-free tryptophan levels and the severity of pain.
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PMID:Total and free serum tryptophan levels and brain 5-hydroxytryptamine metabolism in arthritic rats. 616 24

Patients with systemic lupus erythematosis (SLE) often manifest features of other autoimmune diseases. In this review, we provide a detailed compendium of features of SLE that overlap with other conditions. This compendium is important because a critical feature in our understanding of autoimmunity has been the clustering of coexisting/different autoimmune diseases both within an affected patient and within a pedigree. Indeed, autoimmune disorders share a variety of similar clinical and serological defects. For example, all autoimmune disorders are associated with the elaboration of autoantibodies and/or the production of self-reactive mononuclear cell populations; many have high levels of immune complexes and defects in cell-mediated immunity. Several diseases share similar genetic backgrounds, as reflected by study of loci within the major histocompatibility complex. In part the coassociation is due to common genetic tendencies with different environmental precipitating agents (trigger mechanisms). It is likely that many factors can modulate the immune system to autoimmunity in the presence of an appropriate genetic background, eg, drugs, viral infections, UV irradiation, and toxins, ie, toxic oil syndrome and L-tryptophan-induced eosinophilic myalgia. The coexistence of SLE with other autoimmune diseases is an excellent venue to understand these events, and we believe that the presence of other autoimmune diseases in patients with SLE can be called the kaleidoscope of autoimmunity.
Semin Arthritis Rheum 1994 Oct
PMID:The coexistence of systemic lupus erythematosus with other autoimmune diseases: the kaleidoscope of autoimmunity. 783 52

Autoimmune diseases may be induced by physical and/or chemical environmental factors. A review of the available literature on mercuric chloride, iodine, silicone, anilides, L-tryptophan, vinyl chloride, and canavanine suggests three general mechanisms by which they may induce disease. First, oxidative damage probably is a frequent process involved in disease induction and pathogenesis. Second, certain compounds also may generate antigen-specific immune responses that could then cross-react with self-tissues. Other xenobiotics might bind to self-tissues and increase self-tissue immunogenicity. Third, physical and chemical agents may also modulate the immune system. Finally, in response to controversies surrounding the influence of human activities on global climate changes, the immunosuppressive effects of ozone and ultraviolet radiation are discussed.
Semin Arthritis Rheum 1993 Jun
PMID:Autoimmunity and selected environmental factors of disease induction. 834 47

The term eosinophilia myalgia syndrome (EMS) was coined in 1989 after a cluster of cases with symptoms of incapacitating myalgias and eosinophilia were reported. This syndrome has been only defined as varying degrees of myalgias and peripheral eosinophilia. Case reports of EMS are protean and do not show a consistent clinical picture, raising the question of whether this reflects a single disorder or is a conflation of various disorders. There have been only two studies evaluating the association of EMS with 1-tryptophan. These two included only 23 patients with EMS. Apart from the obvious statistical fragility inherent in such small studies, each is further weakened by differences in the mechanisms by which patients and controls were selected. Furthermore, the continued reports of EMS after 1-tryptophan was removed from the market raise additional questions about the association. Nonetheless, there has been an inordinate reliance on a history of 1-tryptophan ingestion in making the diagnosis of EMS. When presented case studies, clinicians were much more likely to make the diagnosis of EMS when a history of 1-tryptophan ingestion was included. These observations underscore the need for careful application of well-considered diagnostic criteria to the study of new syndromes and their potential associations.
Semin Arthritis Rheum 1997 Jun
PMID:Eosinophilia myalgia syndrome. 921 75


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