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ID PMID Title PublicationDate abstract
8835255 Validation of the Italian version of the Stanford Childhood Health Assessment Questionnair 1995 Nov The Stanford Health Assessment Questionnaire developed by Singh et al. to measure functional status in children with chronic arthritis (CHAQ) was translated into Italian (I-CHAQ), with minor modifications to obtain cross-cultural equivalence. This version was evaluated in a series of 96 patients with juvenile rheumatoid arthritis (JRA), both males and females ranging in age from 3 to 19 years (mean age 9.9 years). All three onset subtypes and all four classes of disability were represented in the sample. The questionnaire was filled in by the parents if the children were less than 8 years of age (23 cases), and by the children themselves in all other cases; a health professional was always present to provide assistance. As expected, JRA patients with a systemic or polyarticular disease onset had higher scores than those with a pauciarticular onset, and there were statistically significant differences in disability index values between patients from different Steinbrocker functional classes. The instrument showed good reproducibility in a test-retest over a two-week period, a high correlation between the child and parent scores, excellent internal reliability, and good convergent and discriminant validity.
8604722 Selection and use of laboratory tests in the rheumatic diseases. 1996 Feb 26 Current clinical practice relies heavily on serologic testing for the prompt and accurate diagnosis of rheumatic diseases. Serologic testing should be used to support the findings of the history and physical examination, and, in some cases, to monitor disease activity. The inflammation of the rheumatoid arthritis (RA), polymyalgia rheumatica, and temporal arteritis can be assessed by the erythrocyte sedimentation rate (ESR). The C-reactive protein (CRP, an acute-phase protein) test, which is newer, correlates more closely than ESR with clinical and radiographic parameters of RA inflammation. The rheumatoid factor test is nonspecific as a screen for RA, and some argue that it is also insensitive (accounting for the existence of "seronegative" RA). High titers of rheumatoid factor are associated with progressive joint inflammation, erosions, and disability. Antinuclear antibody (ANA) tests are likewise nonspecific, but ANA subtypes have proved to be very specific for subtypes of connective tissue diseases. Examples are the presence of anti-DNA antibody in systemic lupus erythematosus; anti-centromere antibody in the CREST syndrome of scleroderma; anti-histone antibody in drug-induced lupus; and anti-Ro antibody in neonatal lupus. Anti-neutrophil cytoplasmic antibodies (ANCA) are a new group of auto-antibodies seen in Wegener's granulomatosis. Brief case descriptions are presented to illustrate appropriate selection of these antibody tests as well as tests for antiphospholipid antibodies and cryoglobulins.
8252806 Adjuvant arthritis is associated with changes in the glycosylation of serum IgG1 and IgG2b 1993 Dec The increased amounts of agalactosyl IgG (N-linked oligosaccharides terminating with N-acetylglucosamine (GlcNAc) in the serum of patients with rheumatoid arthritis (RA) and other chronic inflammatory diseases have suggested that agalactosyl IgG may be involved in the pathogenesis of RA. We have now evaluated the incidence of agalactosyl IgG in the Lewis rat during the course of adjuvant arthritis (AA). The modification in glycosylation of IgG was measured by means of polyclonal and monoclonal anti GlcNAc antibodies as well as by the lectin concanavalin A (Con A). The results show that Lewis rats undergo a change in serum IgG glycosylation during the course of AA. As in human RA patients, rats with AA lack terminal galactose on IgG heavy chain oligosaccharides, and the terminal GlcNAc or mannose residues are thus exposed. The degree of agalactosyl IgG was positively correlated with the incidence of disease, peaked 20 days after disease induction, and the IgG gradually reverted to the fully glycosylated form thereafter. The post-arthritic glycosylation profile was very similar to that characteristic of the naive animal. Purified IgG was shown to contain two IgG subclasses, IgG1 and IgG2b, which underwent changes in glycosylation. Western blot analysis revealed that IgG1 expressed a higher degree of terminal mannose, whereas IgG2b expressed a higher degree of terminal GlcNAc. These findings raise the question of the possible involvement of agalactosyl IgG in immune complex-mediated inflammation.
8881769 Crystallization of a complex between the Fab fragment of a human immunoglobulin M (IgM) rh 1996 Aug Rheumatoid factors (RF) are the characteristic autoantibodies found in patients with rheumatoid arthritis. They recognize epitopes in the Fc region of immunoglobulin G (IgG) and are often of the IgM isotype. In order to analyse the nature of RF-Fc interactions, we have crystallized a complex between the Fab fragment of a human monoclonal IgM rheumatoid factor (RF-AN) and the Fc fragment of human IgG4. The stoichiometry of the complex within the crystals was found to be 2:1 Fab:Fc. The crystals diffracted X-rays to 0.3 nm resolution, and the space group was C2, with cell dimensions a = 16.03 nm, b = 8.19 nm, c = 6.42 nm, beta = 98.3 degrees. We have also determined the sequence of the variable region of the RF-AN light chain, not hitherto reported. This belongs to the V lambda III-a subgroup and is closely related to the germline gene Humlv318, from which it differs in three amino acid residues. This is the first reported crystallized complex between a human autoantibody and its autoantigen.
8796980 Molecular and cellular interactions in rheumatoid synovium. 1996 May There is growing evidence that distinct molecular and cellular interactions in the rheumatoid synovium result in a complex cascade of pathophysiologic events. These interactions finally lead to progressive joint destruction, in a way that is different from all other joint diseases. Keystones are inflammation, proliferation of synovial cells, and attachment and invasion of synovial fibroblasts (in)to adjacent cartilage and bone, mediated by continuous release of matrix-degrading enzymes. Advances in molecular biology have provided numerous new data on the rheumatoid arthritis interaction cascade. Major research topics involve the balance of proinflammatory and inhibitory cytokines, the role of adhesion molecules in attachment of synovial fibroblasts to cartilage, and the localization of various matrix-degrading enzymes in the synovial lining. The results of the research reviewed here also provide a basis for future therapies including gene therapy.
8061689 [Quantification of serum interference in immune complex phagocytosis in seronegative spond 1994 Jan Pathological samples (55) of serum selected from patients with Seronegative Spondylarthropathies, Systemic Lupus Erythematosus and Rheumatoid Disease were studied. The serum of all these patients showed negative rheumatoid factor by latex fixation reaction. The determination of the interference on the phagocytosis of gamma globulin aggregated by guinea pig's macrophages was obtained by one formula. The serum characterization was determined by selecting the ones that presented the most expressive results in the phagocytosis interference, by facilitation or inhibition. The results, in absolute and percentage values, showed the predominance of the interference phenomenon in phagocytosis, with significant statistical values (p < 0.05), when compared with normal serum. The comparative analysis among the diseases studied in the quantification of the serum interference in the phagocytosis of the immunocomplexes has not showed any significant difference. The phagocytosis inhibition occurred with more preponderance in the serum of patients with Reiter's Syndrome and Psoriatic Arthritis; in serum patients with Reiter's Syndrome there was a statistically significant difference in the inhibition of the phagocytosis (p = 0.0247). The serum characterization did not show that the serum fraction was responsible for the phagocytosis interference. In this stage it has been verified that there has not been an uniformity in the graphic curve of dilutions studied. The possibility of the existence of more than one element with interference in the phagocytosis of the studied immunocomplexes was mentioned.
7519484 Clinical and immunological analysis of annular erythema associated with Sjögren syndrome. 1994 Clinical and immunopathological analysis was performed on 24 cases of Sjögren syndrome with annular erythema (AESjS). AESjS predominantly appears on the cheek of the face where skin temperature is relatively low in comparison with other sites. VCAM-1 and ICAM-1 were strongly expressed on endothelial cells of AESjS, while epidermal expression of ICAM-1 was focal and weak. VCAM-1 mRNA expression was also much more intense compared to systemic lupus erythematosus. The lymphocyte response to staphylococcal enterotoxin B was higher in AESjS than that of controls, and cells positive for T cell receptor V beta 6,9,12 were expanded after the culture. Superantigen-driven endothelial-cell-dependent T cell infiltration to the skin plays a crucial role in AESjS.
1567491 Arthritis and hypertension in patients with systemic lupus erythematosus. 1992 Apr OBJECTIVE: The purpose of this study was to test the hypothesis that patients with systemic lupus erythematosus (SLE) who have, as part of their disease, persistent rheumatoid-like arthritis are less likely to be hypertensive than are other patients with SLE. METHODS: A retrospective chart analysis of 662 patients with SLE seen in a university clinic was performed. RESULTS: Data analysis revealed that hypertension and persistent arthritis were inversely correlated, particularly in those patients without nephritis and particularly in black patients. CONCLUSION: We conclude that rheumatoid-like arthritis in patients with SLE is protective against hypertension, and speculate that this protection is conferred by a higher frequency of the DR4 allele.
8412435 [Comparative experimental studies of mechanical and holmium laser synovectomy]. 1993 The goal of this study was to evaluate tissue reactions in rabbit knees following laser synovectomy using a holmium:YAG laser (wavelength: 2.1 microns) and to compare these results with those found after conventional mechanical abrasion treatment. Chronic arthritis was immunologically induced in one knee joint each of 48 rabbits. Twelve served as controls, 12 were sham-operated, 12 were exposed to laser radiation, and 12 others were treated according to conventional methods. In the laser group, a pulse length of 1 ms at a repetition rate of 3 Hz resulted in a pulse energy of 600 mJ. After periods of 1 day, 1 week and 1 and 3 months, respectively, three animals from each group were sacrificed and the synovialis was examined macroscopically and histologically using light and electron microscopy. Edema, acute inflammation, and coagulation necrosis occurred immediately following laser therapy. After 1 week, the synovial layer showed slight fibrosis, which was comparable to that found in the controls. One month later the surface appeared to be smooth. The mechanical abrasion caused hemorrhage and necrosis. Fibrosis was pronounced in all capsular layers, and after 3 months the surface appeared coarse and villous in this group. Based on these preliminary findings, holmium-laser synovectomy may offer an alternative to existing therapeutic techniques in the treatment of rheumatoid arthritis. The arthroscopic approach could prevent additional capsular fibrosis associated with mechanical irritation.
8435176 Autoimmune exocrinopathy presenting as recurrent parotitis of childhood. 1993 Mar OBJECTIVE: To describe a case of autoimmune exocrinopathy in a child at the age of 3 months who presented with the original diagnosis of recurrent parotitis. DESIGN: This a case report of a 9-year-old girl with recurrent parotitis who was later found to have Sjögren's syndrome. The literature relating to primary Sjögren's syndrome in the pediatric population is reviewed. SETTING: The patient was seen in the rheumatology and otolaryngology clinics at a university medical center. INTERVENTIONS: This study did not address therapy. MAIN OUTCOME MEASURE: Diagnosis of Sjögren's syndrome. RESULTS: The patient had xerostomia, an abnormal result of a salivary gland biopsy, SSA and SSB antibodies, and the histocompatibility antigens HLA-B8 and HLA-DR3 that are associated with Sjögren's syndrome. CONCLUSION: Primary Sjögren's syndrome should be considered in cases of recurrent parotitis of childhood. More studies are needed to assess the natural history of autoimmune exocrinopathy in children.
7997855 Role of the bowel flora for development of immunity to hsp 65 and arthritis in three exper 1994 Dec An infectious aetiology in rheumatoid arthritis (RA) has for long been suggested, although no conclusive evidence for this is at present available. Lately a large interest has been devoted to the involvement of heat shock proteins (hsps) in autoimmune disorders due to their conserved structure and immunogenic properties. Immunity to hsps has been observed both in human autoimmune conditions and in experimental models of autoimmune disease. We have studied the role of the bacterial flora and hsp immunity in the arthritic response in three experimental models of arthritis; type II collagen arthritis (CIA), adjuvant arthritis (AA) and oil induced arthritis (OIA); by using germ free and conventional DA rats. A high incidence of severe arthritis developed in all the models evaluated irrespectively of whether the animals were in the conventional or germ free state. This confirms earlier results which show a minor effect of the bacterial flora in CIA and AA in high responder strains. These results also show that a severe OIA can develop in germ free animals. Despite the severe arthritic response induced, no serum antibody levels to hsp 65 could be detected in the germ free animals, which was in contrast to the conventional animals where a positive anti-hsp 65 serum response was seen in 35-80% of the animals with CIA, AA or OIA. These results show that development of a humoral response to hsp 65 in these models of arthritis is dependent on the presence of a bacterial flora. Further, the lack of humoral immunity in germ free animals despite a severe arthritic response indicates that humoral immunity to hsp 65 is not involved in development of disease in these three models of experimental arthritis.
8018333 Characterization of phospholipase A2 from human nasal lavage. 1994 Jul A secreted form of phospholipase A2 (PLA2) has been implicated in inflammatory disorders such as rheumatoid arthritis and sepsis. To determine if PLA2 may also play a role in allergic rhinitis, we have measured enzymic activity in nasal lavage from allergic subjects. Enhanced activity of PLA2 in the lavage was observed following nasal challenge with antigen or histamine. The PLA2 in the nasal lavage was partially purified by acid extraction, size exclusion chromatography, and ion exchange chromatography. The partially purified enzyme from nasal lavage was subsequently compared to a recombinant form of human PLA2 identified in synovial fluid from arthritic patients. The two enzymes showed similar molecular weights (15 to 16 kD) on SDS-PAGE, and both reacted with a rabbit polyclonal antiserum raised to a galactokinase-PLA2 fusion protein. The enzymatic activities of the two PLA2s were indistinguishable when compared for ionic dependence, substrate selectivity, and sensitivity to inhibitors. These results suggest that the PLA2 induced in nasal lavage in response to challenge by antigen is very similar to the extracellular PLA2 found in synovial fluid from subjects with rheumatoid arthritis and may play a role in the inflammatory processes associated with allergic rhinitis.
8129779 Cysteine proteinase inhibitors decrease articular cartilage and bone destruction in chroni 1994 Feb OBJECTIVE: To determine the effects of peptidyl fluoromethyl ketones on the in vitro activity of purified cathepsins B and L, on tissue cysteine proteinase activity, and on cartilage and bone destruction in experimental arthritis. METHODS: The effects of the fluoroketones on cathepsins B and L in vitro and the effects of oral administration of fluoroketones on ex vivo cysteine proteinase activity in tissue homogenates were determined by measuring the inhibition of fluorogenic substrate cleavage. To determine the effects on arthritis, animals were injected with adjuvant or type II collagen, treated orally with the fluoroketones, and the severity of arthritis was assessed by clinical, histologic, and radiologic methods. RESULTS: All of the fluoroketones tested were potent inhibitors of purified cathepsins B and L activity. Oral administration of the fluoroketones reduced tissue cysteine proteinase activity by up to 77%. In addition, fluoroketone treatment significantly reduced the severity of clinical joint disease and decreased the destruction of articular cartilage and bone. Quantitative analysis of radiographic images indicated that treatment significantly reduced soft tissue changes, periosteal proliferation, and bone erosion, but only partially reduced juxtaarticular osteoporosis. CONCLUSION: These studies suggest that cysteine proteinase inhibitors may limit tissue destruction in diseases such as rheumatoid arthritis.
8428243 Differentiating persistent from self-limiting symmetrical synovitis in an early arthritis 1993 Feb Early rheumatoid arthritis (RA) must be differentiated from benign self-limiting polyarthritis because of the risks associated with treatment of RA. Conventional, widely available clinical and laboratory variables, measured at first clinic visit, were studied for their ability to predict persistence in 112 patients with up to 6 months of joint symptoms. Those 65 patients with symmetrical peripheral polyarthritis were followed for 1 year: 36 who underwent spontaneous remission were classified self-limiting synovitis (SLS); the remaining 29 were termed persistent synovitis (PS). Univariate analysis suggested more severe disease in PS at presentation but showing considerable overlap with SLS, making clinical discrimination difficult. Multivariate analysis confirmed this overlap but identified a subset of most helpful variables. The RA latex was the most powerful variable, yet accounted for only 45% of the variability in outcome. Combining a positive RA latex with an ESR > 30 mm/h carried a relative risk for PS of 4.33, with specificity 94% but sensitivity only 69%. Self-limiting synovitis initially could not be distinguished from early RA: hence RA may exist in two forms, the traditional persistent form and a less well recognized abortive form.
8929773 Cathepsin G and elastase in synovial fluid and peripheral blood in reactive and rheumatoid 1996 Jan The purpose of the study was to evaluate the involvement of serine proteinases cathepsin G and elastase on pathomechanisms in synovial fluid (SF) of patients with reactive (ReA) and rheumatoid, (RA) arthritis. Cathepsin G, elastase, and their endogenous inhibitors alpha1-antichymotrypsin (alpha1-ACT) and alpha1-proteinase inhibitor (alpha1-PI) were identified immunohistochemically from SF and peripheral blood (PB) of patients with ReA and RA. Cathepsin G and elastase activities in SF and PB were measured spectrophotometrically. Dot-immunostaining was used to identify cathepsin G, elastase, but also alpha1-ACT and alpha1-PI from SF and PB. Cathepsin G and elastase-like activities (IU/I) were slightly elevated in ReA SF compared to the corresponding peripheral blood values (11.4 +/- 9.2 vs 4.8 +/- 1.7, NS, and 5.1 +/- 2.8 vs 2.3 +/- 2.2, NS), which was similar to what was seen in RA (16.4 +/- 6.2 vs 0.53 +/- 0.4, p < 0.05, and 6.51 +/- 1.8 vs 1.22 +/- 0.58, p < 0.05). Although some samples did not contain cathepsin G and/or elastase-like activities, all samples contained immunoreactive enzyme, but also alpha1-ACT and alpha1-PI. In ReA SF, in contrast to monocytes, all polymorphonuclear (PMN) cells contained cathepsin G and elastase. Cathepsin G and elastase activities correlated with each other (r = 0.78, p < 0.05) suggesting PMN / primary granules as their likely source. There was a closer association between the cathepsin G or elastase and SF leukocyte count in ReA than in RA. In ReA and RA SF elevated cathepsin G and elastase activities are detected compared to activity levels in PB suggesting local production mainly from PMNs. The co-existence of highly cellular SF and cathepsin G and elastase activity in the documented presence of endogenous inhibitors in ReA SF together with the, known, usually self-remitting clinical course of ReA, suggest a brisk and even exaggerated local PMN serine proteinase release; sparing of joints does not seem to be due to lack or inhibition of PMN responses but rather to a successful down-regulation or cessation of the responses initially elicited.
8793411 Altered body water distribution in subjects with juvenile rheumatoid arthritis and its eff 1996 Jun OBJECTIVE: To assess the reliability of bioelectric impedance analysis (BIA) for predicting total body water (TBW) and extracellular water (ECW) in children affected by juvenile rheumatoid arthritis (JRA). SUBJECTS: Thirty-nine children affected by JRA and 23 healthy children of similar age (11.0 +/- 3.6, range 3.0-19.0 y) were recruited for the study. METHODS: TBW and ECW were measured by deuterium oxide and bromide dilution, respectively. Bioelectric impedance (Z) was measured at frequencies of 5, 50 and 100 kHz. The prediction of TBW and ECW from BIA was based on the impedance index (ZI = height2/Z, cm2/omega). RESULTS: TBW standardized per kg of body weight and ECW standardized per litre of TBW were significantly higher in JRA as compared to control patients (59.7 +/- 2.4 vs 57.7 +/- 2.7% and 44.5 +/- 4.6 vs 38.1 +/- 7.9%, with P < 0.005 and P < 0.0001, respectively). Moreover, intracellular water standardized per litre of TBW was significantly lower in JRA than in control subjects (55.5 +/- 4.6 vs 62.5 +/- 8.1, with P < 0.0001). In both controls and patients, the use of ZI at 5kHz offered the more accurate prediction of ECW. However, the use of ZI at 100 kHz did not offer a better prediction of TBW as compared to its value of 50 kHz. Control-generated formulae for predicting water compartments from BIA [TBW = 0.716 x ZI at 100 kHz-1.504, r = 0.934, s.e.e. = 2.2 l;:ECW = 0.430 x ZI5-3.652, r = 0.869(7) s.e.e. = 1.7 l] underestimated TBW and ECW in JRA patients. However, population-specific formulae [TBW (1) = 0.766 x ZI at 100 kHz-0.053, r = 0.939, s.e.e. = 2.8 l; ECW (l) = 0.399 x ZI at 5 kHz-0.283, r = 0.886, s.e.e. = 1.7 l] allowed an accurate prediction of TBW and ECW in JRA patients, taking into account their altered body water distribution. CONCLUSIONS: Altered water distribution impedes the use of formulae developed on healthy children to predict TBW and ECW from BIA and JRA patients. It is hypothesized that chronic inflammation and subclinical malnutrition may be responsible for the altered body water distribution of JRA patients. Traditional body composition models may require adjustments for use in JRA children due to their altered body hydration and water distribution.
8524878 Structural basis for major histocompatibility complex (MHC)-linked susceptibility to autoi 1995 Dec 5 Human T-cell-mediated autoimmune diseases are genetically linked to particular alleles of MHC class II genes. Susceptibility to pemphigus vulgaris (PV), an autoimmune disease of the skin, is linked to a rare subtype of HLA-DR4 (DRB1*0402, 1 of 22 known DR4 subtypes). The PV-linked DR4 subtype differs from a rheumatoid arthritis-associated DR4 subtype (DRB1*0404) only at three residues (DR beta 67, 70, and 71). The disease is caused by autoantibodies against desmoglein 3 (DG), and T cells are thought to trigger the autoantibody production against this keratinocyte adhesion molecule. Based on the DRB1*0402 binding motif, seven candidate peptides of the DG autoantigen were identified. T cells from four PV patients with active disease responded to one of these DG peptides (residues 190-204); two patients also responded to DG-(206-220). T-cell clones specific for DG-(190-204) secreted high levels of interleukins 4 and 10, indicating that they may be important in triggering the production of DG-specific autoantibodies. The DG-(190-204) peptide was presented by the disease-linked DRB1*0402 molecule but not by other DR4 subtypes. Site-directed mutagenesis of DRB1*0402 demonstrated that selective presentation of DG-(190-204), which carries a positive charge at the P4 position, was due to the negatively charged residues of the P4 pocket (DR beta 70 and 71). DR beta 71 has a negative charge in DRB1*0402 but a positive charge in other DR4 subtypes, including the DR4 subtypes linked to rheumatoid arthritis. The charge of the P4 pocket in the DR4 peptide binding site therefore appears to be a critical determinant of MHC-linked susceptibility to PV and rheumatoid arthritis.
1643449 Kinins--key mediators in inflammatory arthritis? 1992 Aug Recent evidence suggests an important role for kinins in the generation of pain, swelling and the cellular damage associated with inflammatory joint disease. Kinins are considered to be pro-inflammatory peptides for a variety of reasons. They stimulate c fibres in the synovium to cause pain and increase extravasation of fluid to produce swelling. Kinins possess the capacity to release neurotransmitters (substance P, acetylcholine) and a second wave of mediators (interleukin-1, tumour necrosis factor, interleukin-8, prostaglandins, leukotrienes). The steady levels and turnover of kinins is regulated by formation (enzymic action of kininogenases on endogenous substrates called kininogens) and by metabolism (kininases, peptidases that hydrolyse kinins). These components of the kinin system can enter the synovial joint space either by transudation from the plasma or from degranulating neutrophils chemotactically attracted into the synovium from which they migrate into the synovial fluid. If kinins are involved, one would expect neutrophil derived mediators of the system to dominate in rheumatoid arthritis and psoriatic arthritis and plasma derived products to be more important in osteoarthritis and gout. But, the question whether any of the functions attributed to each component of the system can be considered to be a primary factor in the cellular pathology of inflamed joints remains to be established. Future investigations, including therapeutic trials with kinin antagonists and kallikrein inhibitors, will need to address the differential role of the kallikreins and kinins in the different types of synovitis, on symptoms of inflammation and on any remedial effects on the progression of tissue damage within the joint.
8846105 Biphasic changes in behavioral, endocrine, and sympathetic systems in adjuvant arthritis i 1996 Adjuvant arthritis (AA) is an experimental model for rheumatoid arthritis, and is induced most easily in inbred Lewis rats by an intradermal injection of heat-killed Mycobacterium tuberculosis (MT) in incomplete Freund's adjuvant. Susceptivity to the arthritis in Lewis rats is thought to be related to a defect in their responses of the hypothalamo-pituitary-adrenal (HPA) axis to the disease. Because the use of an inbred strain is necessary for our immunological studies, we examined in Lewis rats changes in behavior, the HPA axis, and sympathetic nerve activities during development of the adjuvant arthritis. Following intradermal injections of heat-killed MT in adjuvant, the arthritis began to develop on day 12, reaching its maximum severity on day 21, and remained at the level for over a month. The body temperature rose from day 0 to 5 (the primary phase--before the onset of the arthritis). It then fell to normal temperature, and again rose from day 10 to 21 (the secondary phase--with fully developed arthritis). The behavioral (physical activity, food, and water intake) and hormonal parameters [plasma adrenocorticotropic hormone (ACTH) and corticosterone levels] also changed in two phases, similar to those observed in the temperature responses. No change in plasma vasopressin level was observed. Sympathetic nerve activities, assessed by changes in plasma noradrenalin levels, increased more in the primary than in the secondary phase. The possible causes for the biphasic changes associated with development of arthritis are discussed.
8728887 [Post-traumatic psoriatic arthritis. 2 cases]. 1996 Jan 6 Physical trauma is generally accepted as a possible factor in the pathogenesis of rheumatoid arthritis. In the last ten years, there have been a few rare case reports of physical trauma precipitating psoriasic arthritis. We observed two such cases following an occupational accident discovered one and a half year and two and a half year after onset of the first clinical manifestations. In the first case, a 43-year-old man had a fracture of the right calcaneus in March 1991. He was treated with nailing and also required emergency surgery of the posterior tibial artery. The tibiotarsal joint was normal radiologically. Pain persisted after treatment and in 1993 he presented with psoriasis of the scalp and several other localizations together with Hallopeau's acrodermatitis continua of the ankle, pathognomonic for psoriasic arthritis. Salazosufapyridin was given. The second case was a 50-year-old man who had major pain in both wrists immediately after falling on the palm of his hands in 1992. Bilateral carpal tunnel syndrome developed which did not respond well to surgery. In 1993, he developed inflammatory synovitis and also had psoriasis mainly located at the elbows. Immunological tests were negative. Cortisone and salazosulfapyridin were not particularly effective and the patient later developed arthritis of the hip and ankle joints. Physicians should be aware of physical trauma as a causative factor in psoriasic arthritis due to the potential legal implications. Criteria for imputability are: single major physical trauma, absence of clinical signs prior to the trauma, continuous clinical course, first signs occurring then predominating at the joint exposed to trauma. The pathophysiology of this type of arthritis is not well understood. Deep Koebner's phenomena could be involved. Activation of substance P has also been hypothesized.