Scandinavian journal of rheumatology. Supplement最新文献

The symptomatology of the fibromyalgia syndrome (FMS) often resembles an alteration in central nervous set points at least in three systems. The patients suffer under chronic pain in the region of the locomotor system, presumably reflecting a disturbed central processing of pain. Anxiety and depression often characterizes the clinical picture. Almost all of the hormonal feedback mechanisms controlled by the hypothalamus are altered. Characteristic for FMS patients are the elevated basal values of ACTH, follicle-stimulating hormone (FSH), and cortisol as well as lowered basal values of insulin-like growth factor 1 (IGF-1, somatomedin C), free triiodothyronine (FT3), and oestrogen. In FMS patients, the systemic administration of the relevant releasing hormones of corticotropin-releasing hormone (CRH), growth hormone-releasing hormone (GHRH), thyreotropin-releasing hormone (TRH), and luteinizing hormone-releasing hormone (LHRH) leads to increased secretion of ACTH and prolactin, whereas the degree to which TSH can be stimulated is reduced. The stimulation of the hypophysis with LHRH in female FMS patients during their follicular phase results in a significantly reduced LH response. All in all, the typical alterations in set points of hormonal regulation that are typical for FMS patients can be explained as a primary stress activation of hypothalamic CRH neurons caused by the chronic pain. In addition to the stimulation of pituitary ACTH secretion, CRH activates somatostatin on the hypothalamic level, which in turn inhibits the release of GH and TSH on the hypophyseal level. The lowered oestrogen levels could be accounted for both via an inhibitory effect of the CRH on the hypothalamic release of LHRH or via a direct CRH-mediated inhibition of the FSH-stimulated oestrogen production in the ovary. Serotonin (5HT), precursors like tryptophan (5HTP), drugs which release 5HT or act directly on 5HT receptors stimulate HPA axis, indicating a stimulatory serotonergic influence on HPA axis function. Therefore activation of the HPA axis may reflect an elevated serotonergic tonus in the central nervous system of FMS patients.

New developments in brain imaging lead to a better understanding of cortical and subcortical processes involved in pain perception and the establishment of chronic pain. For different forms of chronic pain long-term changes in cortical structures have been described. In patients with phantom limb pain and back pain alterations in the somatotopic organization of the primary somatosensory (SI) could be observed. The amount of this reorganization is correlated with the subjective pain rating. These changes, which are based on processes of neuronal plasticity, can partially be reversed by analgesic interventions. For the investigation of cortical processes concerning reorganization, EEG and MEG methods are most suitable because of their high temporal and spatial resolution. In conclusion, these findings open a new way for therapeutic interventions to prevent the development of chronic pain.

In the spinal cord, long descending pathways are known to exist which modulate pain sensations by either inhibiting or facilitating the discharges of spinal nociceptive neurones. In this article, the hypothesis is discussed that the pain of fibromyalgia may be due to a dysfunction of these pain-modulating pathways. Theoretically, two kinds of disturbance could lead to pain, namely reduced activity in the pain-inhibiting (antinociceptive) system or increased activity in the pain-facilitating (pronociceptive) pathways. Data from animal experiments show that interruption of the dorsal descending systems leads to hyperactivity of spinal nociceptive neurones, namely increase in background activity, lowering in stimulation threshold, and increase in response magnitude to noxious stimuli. The responses of the neurones to input from nociceptors in deep tissues were more strongly inhibited by the descending pathways than were responses to input from cutaneous nociceptors. Collectively, the findings indicate that the dorsal descending systems are tonicly active and have a particularly strong inhibitory action on neurones that mediate pain from deep tissues. If these systems operate in a similar way also in patients, an impairment of their function is likely to lead to 1. spontaneous deep pain (because of an increased background activity in nociceptive neurones supplying deep tissues), 2. tenderness of deep tissues (because of a lowered mechanical threshold of the same neurones), and 3. hyperalgesia of deep tissues (because of increased neuronal responses to noxious stimuli). These changes will affect large areas of the body because the descending inhibitory systems have widespread terminations in the spinal cord. Thus, a dysfunction of the descending inhibitory pathways could mimick to a large extent the pain of fibromyalgia.

Nonsurgical treatment methods involve pharmaceutical treatment, physical therapy, and occupational therapy The most common pharmaceutical treatment for pain is NSAID (nonsteroid antiinflammatory drugs) The risk for side effects of NSAID is greatest among the elderly and in patients with multiple diseases Cortisone has rapid and favorable effects, but the side effects decrease its usability Disease modifying drugs have good effects, but act slowly Immune system modifying treatments are being studied in early polyarthritis It is beneficial to individualize physical therapy Scientific documentation on unconventional treatment methods is insufficient Nonsurgical treatment of polyarthritis in adults is insufficient to avoid functional impairment, dependence on others, or pain in all patients. This field of treatment is advancing rapidly regarding both pharmacological and nonpharmacological therapies. Nevertheless, even in the future, many of these patients will still require rheumatic surgery.

Demographic changes during the next 10-20 years will significantly affect the future of arthritis care. Not only will the prevalence of chronic diseases increase among an increasingly aging population, but so will their incidence. The management of chronic diseases will become the primary clinical challenge for many physicians, especially rheumatologists. Patients will present to their rheumatologists expecting an accurate diagnosis to be made at the onset of their symptoms. To do so, clinicians will have to establish the pathophysiologic bases of the different types of arthritis, most likely through the use of sophisticated imaging techniques, such as high-resolution ultrasound. Treatment approaches will become more targeted. Agents that specifically inhibit the cyclooxygenase-2 (COX-2) isozyme will likely be used for symptomatic relief in arthritis patients. Other therapies will be targeted toward cartilage regeneration. suppression of the inflammatory process, and inhibition of metalloproteinases.

Functional disability in rheumatoid arthritis (RA) interferes with activities of daily living and severely affects patient quality of life. It results in increased levels of work disability and high medical costs. A new goal of RA therapy is to reduce or prevent functional disability. Patients' perception of overall health status in RA was assessed using several instruments (HAQ, MHAQ, SF-36, and PET) in Phase III double-blind, placebo-controlled, randomized trials comparing the new DMARD, leflunomide to sulfasalazine and methotrexate. Leflunomide significantly improved patient quality of life compared to placebo in both the European (P = 0.0001) and North American (P = 0.0001) studies. Reduction in HAQ scores with leflunomide (-0.50 vs -0.29; P = 0.0086) was significantly greater than sulfasalazine. Leflunomide also significantly reduced MHAQ scores versus methotrexate (-0.29 vs -0.15; P < or = 0.05). These changes were seen as early as Week 4. These results highlight the efficacy of leflunomide in RA therapy.

This article examines the most recently published scientific literature on arthritis therapy options and available mucosal-protective agents. Emphasis is placed on the risks of current nonsteroidal anti-inflammatory drug (NSAID) therapy, the options for reducing such risks, and the published information that either supports or refutes current thinking in these areas. A comprehensive evaluation is made of clinical data related to the use of Arthrotec (diclofenac/misoprostol) in the treatment of arthritis. A recent meta-analysis of the prophylaxis of NSAID-associated upper gastrointestinal complications is reviewed. The results of this meta-analysis should help to consolidate much of the current scientific literature on the safe and effective treatment of arthritis.

The aim of the study was to investigate the reliability and the validity of the Swedish version of the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). A total of 113 patients with ankylosing spondylitis were assessed with the BASDAI, the Swedish version of the Bath Ankylosing Spondylitis Functional Index (BASFI), the Bath Ankylosing Spondylitis Metrology Index (BASMI), the Bath Ankylosing Spondylitis Patient Global Score (BAS-G), and a questionnaire on their opinions of the relevance of the BASDAI. The test-retest stability investigation of the BASDAI over 24 hours did not show any difference between the two occasions (md 4.4, range 0.80-8.43 vs md 4.0, range 0-7.80, p > 0.05). The correlation coefficient between the BASDAI and the BASMI was r(s) = 0.07, between the BASDAI and the BASFI r(s) = 0.64, and between the BASDAI and the BAS-G r(s) = 0.80. Eighty percent of the patients considered the contents of the BASDAI to be relevant. The BASDAI, the BAS-G and the BASMI showed significant improvements after an intensive rehabilitation period. In conclusion the results of the present study indicate that the Swedish BASDAI is reliable and valid.