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Publikacja powstała na podstawie materiałów przygotowanych na konferencję "Choroby reumatyczne w nauce, publikacjach naukowych i w systemie ochrony zdrowia", dzięki wsparciu programu "Doskonała nauka" Ministra Nauki i Szkolnictwa Wyższego, Narodowego Instytutu Geriatrii, Reumatologii i Rehabilitacji oraz czasopisma "Reumatologia". Książka zawiera zbiór prezentacji i wykładów wybitnych specjalistów z dziedziny nauki medycznych oraz nauk o zdrowiu, ogłoszonych w dniach 18-21.11.2020 r. w Warszawie, które zostały ujęte w cykle tematyczne: Choroby reumatyczne w systemie ochrony zdrowia Leczenie chorób reumatycznych w Polsce Tworzenie ośrodków badań naukowych i europejskie sieci referencyjne Postęp i innowacyjność w leczeniu chorób reumatycznych i diagnostyce obrazowej prezentacja osiągnięć naukowych i prac badawczo-rozwojowych wybranych polskich ośrodków reumatologicznych wiedza oz zdrowiu w społeczeństwie, osiągnięcia czasopisma "Reumatologia"

Management of patients with rheumatoid arthritis according to the “treat-to-target” strategy requires achievement of remission or low disease activity when remission cannot be achieved (mostly in patients with advanced disease). The assessment of remission and low disease activity is based on a number of definitions depending on the applied instruments which do not always correspond to one another. The role of biomarkers and imaging techniques (ultrasound and magnetic resonance imaging) in predicting the risk for disease relapse after achieving remission and tapering disease-modifying antirheumatic drugs treatment are presented. The concept of achieving the full control of inflammation including residua synovial inflammation and drug free-remission is discussed.

Cardiovascular events are the main cause of the increased risk of death in patients with rheumatoid arthritis (RA). Death rates associated with cardiovascular diseases in RA are 50% higher in comparison with the general population. In the last decade several new technologies and new strategy in the treatment of RA were introduced but the risk of cardiovascular incidents remained unchanged. Various alterations of the lipid profile, observed in RA patients during the treatment with disease modifying antirheumatic drugs (DMARDs) are the subject of several and often contraversal studies. In this review we present and analyzed the results of current research on the lipid profile in RA patients treated with the synthetic and biologic DMARDs. The role of the lipid profile alterations in the pathogenesis of accelerated atherosclerosis in RA has been discussed.

Objectives: Rituximab is an effective treatment in patients with established rheumatoid arthritis (RA). The objective of the IMAGE study was to determine the efficacy of rituximab in the prevention of joint damage and its safety in combination with methotrexate (MTX) in patients initiating treatment with MTX. Methods: In this double-blind randomised controlled phase III study, 755 MTX-naïve patients with active RA were randomly assigned to MTX alone, rituximab 2×500 mg + MTX or rituximab 2×1000 mg + MTX. The primary end point at week 52 was the change in joint damage measured using a Genant-modified Sharp score. Results: 249, 249 and 250 patients were randomly assigned to MTX alone, rituximab 2×500 mg + MTX or rituximab 2×1000 mg + MTX, respectively. At week 52, treatment with rituximab 2×1000 mg + MTX compared with MTX alone was associated with a reduction in progression of joint damage (mean change in total modified Sharp score 0.359 vs 1.079; p=0.0004) and an improvement in clinical outcomes (ACR50 65% vs 42%; p

Elderly-onset rheumatoid arthritis (EORA), defined as rheumatoid arthritis (RA) with the onset at the age > or =60 differs sligthy at presentation from younger-onset RA (YORA) by a more equal sex distribution, a higher frequency of an acute onset, more frequent involvement of large joints, especially of the shoulder, and higher disease activity. Longitudinal studies have shown greater disease activity, more severe radiographic damage and functional decline in patients with EORA than in those with YORA. These differences were only found in seropositive patients. In seronegative EORA patients a less severe course of the disease and a better outcome have been observed, with the clinical manifestations of polymyalgia rheumatica or remitting seronegative symmetrical synovitis with pitting edema. This article is a review of available data concerning differences between EORA and YORA.

Objective. Amyloid A protein quantification in fat tissue is a new immunochemical method for detecting AA amyloidosis, a rare but serious disease. The objective was to assess diagnostic performance in clinical AA amyloidosis.Methods. Abdominal subcutaneous fat tissue of patients with AA amyloidosis was studied at the start of an international clinical trial with eprodisate (NC-503; 1,3-propanedisulfonate; Kiacta (TM)), an antiamyloid compound. All patients had renal findings, i.e. proteinuria (>= 1 g/day) or reduced creatinine clearance (20-60 ml/min). Controls were patients with other types of amyloidosis and arthritic patients without amyloidosis. Amyloid A protein was quantified by ELISA using monoclonal antihuman serum amyloid A antibodies. Congo red stained slides were scored by light microscopy in a semiquantitative way (0 to 4+).Results. Ample fat tissue (>50 mg) was available for analysis in 154 of 183 patients with AA amyloidosis and in 354 controls. The sensitivity of amyloid A protein quantification for detection of AA amyloidosis (>11.6 ng/mg fat tissue) was 84% (95% CI: 77-89%) and specificity 99% (95% CI: 98-100%). Amyloid A protein quantification and semiquantitative Congo red scoring were concordant. Men had lower amyloid A protein values than women (p Conclusions. Amyloid A protein quantification in fat tissue is a sensitive and specific method for detection of clinical AA amyloidosis. Advantages are independence from staining quality and observer experience, direct confirmation of amyloid AA type, and potential for quantitative monitoring of tissue amyloid over time.

Objective To examine the efficacy and safety of different rituximab doses plus methotrexate (MTX), with or without glucocorticoids, in patients with active rheumatoid arthritis (RA) resistant to disease-modifying antirheumatic drugs (DMARDs), including biologic agents. Methods A total of 465 patients were randomized into 9 treatment groups: 3 rituximab groups (placebo [n = 149], 500 mg [n = 124], or 1,000 mg [n = 192] on days 1 and 15) each also taking either placebo glucocorticoids, intravenous methylprednisolone premedication, or intravenous methylprednisolone premedication plus oral prednisone for 2 weeks. All patients received MTX (10–25 mg/week); no other DMARDs were permitted. Results Significantly more patients who received 2 500-mg or 2 1,000-mg infusions of rituximab met the American College of Rheumatology 20% improvement criteria (achieved an ACR20 response) at week 24 (55% and 54%, respectively) compared with placebo (28%; P < 0.0001). ACR50 responses were achieved by 33%, 34%, and 13% of patients, respectively (P < 0.001), and ACR70 responses were achieved by 13%, 20%, and 5% of patients (P < 0.05). Changes in the Disease Activity Score in 28 joints (−1.79, −2.05, −0.67; P < 0.0001) and moderate to good responses on the European League Against Rheumatism criteria (P < 0.0001) reflected the ACR criteria responses. Glucocorticoids did not contribute significantly to the primary efficacy end point, ACR20 response at 24 weeks. Intravenous glucocorticoid premedication reduced the frequency and intensity of first infusion–associated events; oral glucocorticoids conferred no additional safety benefit. Rituximab was well tolerated; the type and severity of infections was similar to those for placebo. Conclusion Both rituximab doses were effective and well tolerated when added to MTX therapy in patients with active RA. The primary end point (ACR20 response) was independent of glucocorticoids, although intravenous glucocorticoid premedication improved tolerability during the first rituximab infusion.

An open-label study indicated that selective depletion of B cells with the use of rituximab led to sustained clinical improvements for patients with rheumatoid arthritis. To confirm these observations, we conducted a randomized, double-blind, controlled study.We randomly assigned 161 patients who had active rheumatoid arthritis despite treatment with methotrexate to receive one of four treatments: oral methotrexate (or =10 mg per week) (control); rituximab (1000 mg on days 1 and 15); rituximab plus cyclophosphamide (750 mg on days 3 and 17); or rituximab plus methotrexate. Responses defined according to the criteria of the American College of Rheumatology (ACR) and the European League against Rheumatism (EULAR) were assessed at week 24 (primary analyses) and week 48 (exploratory analyses).At week 24, the proportion of patients with 50 percent improvement in disease symptoms according to the ACR criteria, the primary end point, was significantly greater with the rituximab-methotrexate combination (43 percent, P=0.005) and the rituximab-cyclophosphamide combination (41 percent, P=0.005) than with methotrexate alone (13 percent). In all groups treated with rituximab, a significantly higher proportion of patients had a 20 percent improvement in disease symptoms according to the ACR criteria (65 to 76 percent vs. 38 percent, Por =0.025) or had EULAR responses (83 to 85 percent vs. 50 percent, Por =0.004). All ACR responses were maintained at week 48 in the rituximab-methotrexate group. The majority of adverse events occurred with the first rituximab infusion: at 24 weeks, serious infections occurred in one patient (2.5 percent) in the control group and in four patients (3.3 percent) in the rituximab groups. Peripheral-blood immunoglobulin concentrations remained within normal ranges.In patients with active rheumatoid arthritis despite methotrexate treatment, a single course of two infusions of rituximab, alone or in combination with either cyclophosphamide or continued methotrexate, provided significant improvement in disease symptoms at both weeks 24 and 48.

Polymyalgia rheumatica is a rheumatic disease which mainly affects the elderly, and is seldom diagnosed in patients 50 years of age. Patients may present with spiking fever, malaise, fatigue, weight loss and other features suggesting inflammation, which in each case requires differential diagnosis from malignancies. Neoplastic disease in turn can manifest itself in symptoms resembling those of polymyalgia, which are named "polymyalgia-like syndrome" and are in fact paraneoplastic syndromes presenting as polymyalgia rheumatica. These observations suggest that a careful clinical evaluation and a long term follow-up are necessary for a correct diagnosis of polymyalgia rheumatica.

Summary Background The effect of Helicobacter pylori in patients receiving non-steroidal anti-inflammatory drugs (NSAIDs) is unclear. We investigated the effects of H pylori eradication in patients with current or previous peptic ulceration, dyspepsia, or both who continued to use NSAIDs. Methods 285 patients were randomly assigned omeprazole 20 mg, amoxycillin 1000 mg, and clarithromycin 500 mg, twice daily (n=142, H pylori eradication treatment), or omeprazole with placebo antibiotics (n=143, controls) for 1 week. All patients received omeprazole 20 mg once daily for 3 weeks until endoscopy, and, if the ulcer was not healed, 40 mg once daily until repeat endoscopy at 8 weeks. Ulcer-free patients with mild dyspepsia continued NSAIDs but not antiulcer treatment. We investigated ulcers with endoscopy at 1, 3, and 6 months and with carbon-13-labelled urea breath test at 3 months. Findings The estimated probability of being ulcer-free at 6 months was 0.56 (95% CI 0.47–0.65) on eradication treatment and 0·53 (0·44–0·62) on on control treatment (p=0·80). Time to treatment failure did not differ between groups for ulcers or dyspepsia alone, per-protocol analysis, or final H pylori status. 66% (58–74) of the eradication group compared with 14% (8–20) of the control group had a final negative H pylori result (p vs 100% at 8 weeks, p=0·006). Interpretation H pylori eradication in long-term users of NSAIDs with past or current peptic ulcer or troublesome dyspepsia led to impaired healing of gastric ulcers and did not affect the rate of peptic ulcers or dyspepsia over 6 months.

To examine the clinical significance of neutrophil gelatinase in rheumatic diseases, plasma and synovial fluid (SF) gelatinase levels were determined in 62 patients with rheumatoid arthritis (RA), 12 patients with ankylosing spondylitis (AS), 18 patients with osteoarthritis (OA) and 17 healthy controls. The gelatinase level was measured by enzyme-linked immunoassay (ELISA). The assay had a sensitivity of 1 ng/ml and a working range of 5-25 ng/ml. Gelatinase levels were significantly higher in the plasma of patients with RA and of patients with RA complicated by amyloidosis or vasculitis as compared to those of healthy controls. Moreover, the mean value of gelatinase in the plasma of patients with RA complicated by vasculitis was found to be significantly higher than that of RA patients without vasculitis. A significant increase in gelatinase concentration was also observed in the plasma of AS patients but not in the plasma of patients with OA. The concentration of gelatinase in the RA SF samples was much higher (18-fold) than the level of the enzyme in the plasma of RA patients. There was also a higher concentration of gelatinase (four-fold) in OA SF compared with OA plasma. The results suggested that circulating gelatinase may reflect some degree of neutrophil activation in patients with inflammatory arthritis, especially in those with RA complicated by vasculitis. However, the results did not allow a differentiation between chronic and acute inflammation.

We determined HLA-A, -B, -C and -DR antigens in 83 patients with rheumatoid arthritis (RA) and reactive secondary amyloidosis (RSA), 60 in Finland and 23 in Poland, and compared the results with control RA patients and blood donors. There were no significant differences in the frequencies of HLA between the RA patients with and those without RSA in either Finland or Poland, and no significant differences between the Finnish and Polish patients with RSA. All the RSA patients from Finland and 70% of the RSA patients from Poland were seropositive. In the development of RSA, the prolonged period of inflammatory stimuli may play a more important role than genetic factors.

Polymyalgia rheumatica is a rheumatic disease which mainly affects the elderly, and is seldom diagnosed in patients50 years of age. The prevalence of polymyalgia rheumatica is approximately 16.8 to 53.7 per 100,000 of the population50 years of age. Patients may present with spiking fever, malaise, fatigue, weight loss and other features suggesting inflammation, which in each case requires differential diagnosis from malignancies. Neoplastic disease in turn can manifest itself in symptoms resembling those of polymyalgia, which are named "polymyalgia-like syndrome" and are in fact paraneoplastic syndromes presenting as polymyalgia rheumatica. These observations suggest that a careful clinical evaluation and a long term follow-up are necessary for a correct diagnosis of polymyalgia rheumatica.

INTRODUCTION Thyroid abnormal function and and/or autoimmune thyroid disease (ATD) are observed in 6% to 33.8% patients with rheumatoid arthritis (RA). OBJECTIVES The aim of the study was to determine whether ATD is more prevalent in patients with RA compared to the control group involving age and sex-matched subjects without RA and whether these patients should be screened for thyroid disease. PATIENTS AND METHODS In 100 patients with RA and 55 patients without RA (control group) hormonal thyroid function and antithyroid antibodies were assessed. RESULTS ATD was more prevalent (16%) in patients with RA than in the control group (9%). The difference was no statistically significant. The RA patients with concomitant ATD had lower RA activity than non-ATD RA patients. Antithyreoglobulin (anti-TG) and antithyroid peroxidase (anti-TPO) antibodies were present in similar percentage of patients with RA (12% and 15%, respectively) and in the control group (9% and 18%, respectively). The most common thyroid dysfunction observed in both groups was subclinical hypothyroidism. An association between thyroid dysfunction and clinical symptoms suggestive of thyroid disease in RA patients was not demonstrated. In patients with RA low free triiodothyronine concentrations were significantly more common. CONCLUSIONS A higher prevalence of ATD in female RA patients compared with controls indicates the need for screening not only of thyroid function, but also of the presence of anti-TPO antibodies as the ATD marker in RA patients. Their presence does not correlate with the occurrence of thyroid disorders in RA patients. Monitoring of thyroid function is of particular importance since as already shown the course of thyroid disease in RA patients is often asymptomatic.

Reactive arthritis (ReA) is a non-purulent joint inflammation that usually follows bacterial gastrointenstinal or urogenital infections. The classic presentation of ReA is characterized by an asymmetric arthritis usually in the lower limbs associated with urethritis, conjunctivitis and occurrence of other articular or extra-articular manifestations. ReA is classified as a type of seronegative spondyloarthopathy. Approximately 65-85% of patients with ReA are HLA-B27 positive. Regardless of the preceding infection, the clinical picture is similar, but management can differ according to the triggering infection. Treatment of Chlamydia-induced ReA should be started with antibiotics because of several mechanisms by which Chlamydia can cause persistent infection. The disease may have an acute or self-limited course, however some patients develop chronic arthritis.

Published data were reviewed to evaluate the occurrence of antiphospholipid antibodies (aPL) in rheumatoid arthritis (RA) patients and to investigate their clinical relevance in this population. The mean prevalence of aPL in RA patients was calculated at 28%. Few studies have found a relationship between aPL and thrombosis, particularly in combination with other risk factors. Conflicting results have been reported on the association of anticardiolipin antibodies (aCL) positivity and neurologic symptoms, Reynaoud's phenomenon, radiologic erosions, extra-articular RA manifestations, rheumatoid factor, and atherosclerosis. Some studies, however, suggest that there is a correlation present between those antibodies and C-reactive protein levels, rheumatoid factor (RF) and antinuclear antibodies. Tumor necrosis factor blocking agents may cause an induction of aCL, but it seems like they do not cause any clinical features related to the antiphospholipid syndrome.

Rozpoznanie zesztywniającego zapalenia stawów kręgosłupa (ZZSK) ustala się średnio po 5–7 latach od wystąpienia pierwszych objawów. Proponowany algorytm diagnostyczny u chorych z podejrzeniem wczesnego ZZSK może pomóc lekarzom w ustaleniu właściwego rozpoznania, zanim pojawią się ewidentne zmiany radiologiczne Rezonans magnetyczny jest bardzo użytecznym badaniem w diagnostyce wczesnej postaci ZZSK. Jest bardzo ważne, aby ustalić rozpoznanie ZZSK jak najwcześniej i w aktywnej postaci choroby rozpocząć intensywne leczenie, w tym również inhibitorami TNF-α, zanim wystąpią nieodwracalne zmiany strukturalne. Diagnosis of ankylosing spondylitis (AS) is still delayed by 5-7 years. The proposed diagnostic algorithm in patients with suspected early AS may help physicians confidently diagnose patients before definite radiographic changes are detectable. Magnetic resonance imaging is a useful imaging modality for detecting early changes of AS. It is critical to make an early diagnosis of AS and in active cases start intensive therapy including anti-TNF-α agents before irreversible damage takes place.

Osteoarthritis is the most common joint disease in the general population. In recent years there has been a significant expansion of knowledge pertaining to the complex parthogenesis of this degenerative disease and the roles played in its course by the inflammatory process, the various components of cartilage, and cytokines. Improved research methods and the introduction of new medications (including selective COX-2 inhibitors) for the treatment of osteoarthritis have made it possible to develop new treatment protocols. This article discusses contemporary views on the pharmacological treatment of osteoarthritis and the possibility of influencing the symptomatology of the disease and the structure of cartilage. Promising methods of treating osteoarthritis are presented.

IgA, IgG and IgM antibodies against Yersinia Yop proteins, Yersinia LPS and Salmonella LPS from different serogroups were determined by enzyme-linked immunosorbent assay (ELISA) in a 885 serum samples and 92 synovial fluids. The control group consisted of 200 healthy blood donors. Compared with control subjects, patients with arthritis showed significantly increased titres of antibodies against Yersinia Yop, Yersinia LPS and Salmonella LPS appropriately in 21.7%, 44.0% and 56.0% serum samples. The prevalence of positive antibody levels was highest in Yersinia serogroup O3 and Salmonella serogroup B and D antibodies. The IgA titres were found to be much higher in adults than in children and youngsters but IgM titres consequently decreased with age. Investigation of synovial fluids obtained from patients with arthritis showed that Yersinia and Salmonella antibodies in synovial fluid mirror those in serum by concentration, by specificity and by distribution in classes.

Objective To test the hypotheses that 1) proinflammatory cytokines affect osteoprotegerin (OPG) and soluble receptor activator of nuclear factor κB ligand (sRANKL) production and therefore the OPG and sRANKL levels differ in rheumatoid arthritis (RA) patients in comparison with healthy individuals; and 2) anti–tumor necrosis factor α (anti–TNFα) therapy influences OPG and sRANKL levels. Methods Sera were obtained from healthy individuals or RA patients receiving the combination of infliximab and methotrexate. Peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) were isolated from RA patients. Fibroblast-like synoviocytes (FLS) were isolated from synovial tissue obtained at total knee replacement in RA patients. Supernatants from cells stimulated with cytokines were collected after culture in vitro. Concentrations of OPG and sRANKL were determined by enzyme-linked immunosorbent assays. Results A strong positive correlation between OPG concentration and age was observed in healthy individuals but not in RA patients. The OPG and sRANKL levels were higher in RA patients than in healthy controls. Cultured FLS spontaneously secreted much higher amounts of OPG than PBMCs or SFMCs. Proinflammatory cytokines enhanced OPG production. Anti-TNFα treatment resulted in the normalization of serum OPG and sRANKL levels in RA patients without influencing the OPG:sRANKL ratio. Conclusion Although higher serum levels of OPG and sRANKL are present in RA patients than in healthy individuals, the ratio of OPG:sRANKL is similar. There is an age-dependent increase of OPG but not sRANKL levels in healthy subjects. Anti-TNFα treatment results in the normalization of elevated levels of OPG and sRANKL in RA patients.

Background Secondary amyloidosis is a serious complication of rheumatoid arthritis and may result in significant morbidity and early death. The knowledge on standard and effective management of patients with secondary amyloidosis is limited. Objectives The objective of the study is follow up observation of RA patients with established reactive amyloidosis concerning the clinical aspects of the disease, acute phase reactants and the response to cytostatic treatment. Methods 43 patients with rheumatoid arthritis and histologically confirmed secondary amyloidosis were followed for 3 to 6 (mean 4,6) years. The patients were treated with cyclophosphamide or methotrexate combined with small doses of prednizone. Clinical symptoms, laboratory tests and general outcome were analysed after 3 to 6 years of development of amyloidosis. Results The time from the diagnosis of RA to the development of amyloidosis was 4 to 16 years, mean 8,7 years. In all patients advanced radiological changes were observed (radiological Steinbrocker stage III or IV). The most common symptoms of amyloidosis were: proteinuria-27(62,8%), nephrotic syndrom -12(27,9%), diarrhoea-4(9,3%). In most of the patients the course of RA was very severe since the onset and high activity parameters were observed despite treatment. Amyloidosis was histologically confirmed by subcutaneous fat tissue biopsy in 38(88,4%) cases. In 8 patients amyloid deposits were found in other organs (kidney, stomach, salivary gland). After the treatment with cyclophosphamide or methotrexate we observed decrease of some activity parameters (ESR, CRP) and decrease of proteinuria level. The treatment was well tolerated and we didn?t observe serious side effects. In the observed group 7(16,3%) patients died after 3 to 6 years of the diagnosis of amyloidosis. The most common cause of death were uremia (4/7) and infections (2/7). Conclusion Aggressive treatment with cytostatics influences the survival of patients with reactive amyloidosis in RA. The time of survival in 83,7% of the observed patients was longer than 4,6 years. The outcome of patients with RA and reactive amyloidosis is better when the diagnosis of amyloidosis is confirmed in the early stage of the disease.

Background Difficulty in the diagnosis of early rheumatoid arthritis (ERA) in the aspect of differential diagnosis. Objectives The diagnosis of rheumatoid arthritis (RA) is based on ACR criteria, which are clinical, radiological and immunological. During the first month after onset the diagnosis is often difficult because of a frequently ?atypical? presentation and a lack of radiological changes. Rheumatoid factor has low specify and is often negative in ERA. The other non-rheumatological disorders (viral infection, neoplastic and endocrine diseases) may also in the early stage present like RA symptoms. The objective of this study was to revised the preliminary diagnosis of ERA in hospitalised patient. Methods Clinical examination (including laboratory tests and X ray), immunological tests: RF, antikeratin antibodies (AKA). Results During the last 26 month 510 RA patients (according ACR criteria) were hospitalised in Rheumatology Department. Among this group of patients 94 (18%) were admitted with the preliminary diagnosis ERA. All of this patients group fulfilled the first four clinical ACR criteria The duration of the disease was varied 3 to 9 months. All patients were carefully examined according number of painful and swollen joints, their symmetry and localisation, presence of RF, AKA antibodies and radiological erosions. In cases were RA diagnosis was doubtful other needful examination were done. The diagnosis of ERA was established in 48 (52%), but in 46 (48%) was excluded. ERA patients were predominately women, symmetrical polyarthris of the hands was present in 45 (52%). RF in 28 (58%), radiological erosions were found in 5 (10%). In group of patients with excluded ERA the following diagnosis was established: osteoarthritis 14 (31%), RA ? like (nonclassified) 13 (28%), reactive arthritis 3(7%), hepatitis viral infection 2 (4%), neo 2 (4%), Hashimoto syndrome 5 (11%), Sjogren syndrome 2 (4%), Polymialgia 2 (4%), Fibromialgia 3 (7%). AKA were present in 30 (62%) patients in group with established diagnosis of RA and RF was present in 28 (58%) patients in this group. AKA was present in 10 (21%) patients with different diagnosis and RF was observed in 8 (17%) patients in this group. Conclusion 1) ACR criteria are insufficient in aspect of differential diagnosis of ERA and non ERA. 2) Present RF and AKA are more specific in ERA than in non ERA patients.3) The diagnosis of ERA should be established by specialists. References Hassfeld W, Steiner G, Graninger W, Witzmann G, Schweitzer H, Smolen JS. Autoantibody to the nuclear antigen RA 33: a marker for early RA. Br J Rheumatol. 1993;32:199–203 Paimela L, Gripenberg M, Kuski P, Leirisalo ? Repo M. Antikeratin antibodies: diagnostic and progostic markers for early rheumatoid arthritis. Ann Rheum Dis. 1992;51:743–6

The aim of the study was to compare the efficacy and the effects on the mucosa of the gastrointestinal tract (GIT) of nabumetone and diclofenac retard in patients with osteoarthritis (OA). An open, multicentre, randomised, comparative, endoscopy-blind parallel group study included 201 patients with nabumetone and 193 patients with diclofenac retard suffering from moderate to severe OA of the knee or hip joint. Twelve clinical efficacy variables were assessed and a portion of the population underwent gastroduodenoscopy. All patients exhibited significant improvement in pain severity and pain relief (p50.001 and p50.0001, respectively) but there were no differences between the groups for all the efficacy variables. Eleven per cent of patients on nabumetone and 19% on diclofenac experienced GIT side-effects. Sixty-nine patients with nabumetone and 61 with diclofenac underwent gastroduodenoscopy. The differences in the mucosal grade for the oesophagus, stomach and duodenum at baseline were not significant. In the oesophagus there were significantly less changes after treatment with nabumetone (p = 0.007) than with diclofenac; there were similar findings in the stomach (p50.001) but the difference in the duodenum was not significant. This study indicates that nabumetone and diclofenac retard have similar efficacy in the treatment of OA, but nabumetone has significantly fewer GIT side-effects.

The effect of Helicobacter pylori in patients receiving non-steroidal anti-inflammatory drugs (NSAIDs) is unclear. We investigated the effects of H. pylori eradication in patients with current or previous peptic ulceration, dyspepsia, or both who continued to use NSAIDs.285 patients were randomly assigned omeprazole 20 mg, amoxycillin 1000 mg, and clarithromycin 500 mg, twice daily (n=142, H. pylori eradication treatment), or omeprazole with placebo antibiotics (n=143, controls) for 1 week. All patients received omeprazole 20 mg once daily for 3 weeks until endoscopy, and, if the ulcer was not healed, 40 mg once daily until repeat endoscopy at 8 weeks. Ulcer-free patients with mild dyspepsia continued NSAIDs but not antiulcer treatment. We investigated ulcers with endoscopy at 1, 3, and 6 months and with carbon-13-labelled urea breath test at 3 months.The estimated probability of being ulcer-free at 6 months was 0.56 (95% CI 0.47-0.65) on eradication treatment and 0.53 (0.44-0.62) on on control treatment (p=0.80). Time to treatment failure did not differ between groups for ulcers or dyspepsia alone, per-protocol analysis, or final H. pylori status. 66% (58-74) of the eradication group compared with 14% (8-20) of the control group had a final negative H. pylori result (p0.001). Fewer baseline gastric ulcers healed among eradication-treatment patients than among controls (72 vs 100% at 8 weeks, p=0.006).H. pylori eradication in long-term users of NSAIDs with past or current peptic ulcer or troublesome dyspepsia led to impaired healing of gastric ulcers and did not affect the rate of peptic ulcers or dyspepsia over 6 months.