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Background: The presence of dyspeptic symptoms is a common finding in patients treated with non-steroidal anti-inflammatory drugs (NSAIDs). Some studies seem to support the involvement of Helicobacter pylori infection in [...]

Purpose: To evaluate the efficacy of methotrexate (MTX) in low (10 mg) weekly doses to decrease steroid requirements in steroid-dependent asthma. Population: 46 caucasian patients (P) were included from 1992 [...]

Up to 30% of patients with psoriasis develop joint disease, the course of which can be improved by early diagnosis and treatment. The aim of this study was to describe our experience with a new multidisciplinary psoriasis and psoriatic arthritis unit over a period of 4 years (2009-2012).

ABSTRACTThree Klebsiella oxytocaisolates and one Klebsiella pneumoniaeisolate from three children admitted to the Hematology Unit of Hospital Vall d'Hebron (Barcelona, Spain) exhibited a susceptibility pattern suggesting OXY β-lactamase hyperproduction. All the isolates contained a 95-kb plasmid that harbored blaOXY-1, which was transferred by electrotransformation but could not be self-transferred by conjugation. A qnrS1gene was also harbored in the blaOXY-1-carrying plasmid. This is the first report of a plasmid-encoded OXY β-lactamase.

ABSTRACTResistance to β-lactams and quinolones in two isogenic Enterobacter cloacaeisolates was studied. One was susceptible to cefoxitin and amoxicillin-clavulanate. The other one showed its natural β-lactam resistance pattern. Both isolates had a nonfunctional AmpR regulator. However, within the second one, the presence of a plasmid carrying ampRand qnrA1allowed reversion to the wild-type β-lactam resistance phenotype and decreased susceptibility to fluoroquinolones.

Objective. To analyse the frequency and prognostic factors of radiographic progression in a series of Spanish patients with early rheumatoid arthritis (RA) after 1 yr of treatment with disease-modifying anti-rheumatic drugs (DMARDs).
Methods. Sixty patients (47 females, 13 males) with RA with a disease duration shorter than 2 yr [mean (s.d.) duration 9.5±6.6 months] were treated with the same therapeutic protocol using gold salts as the first DMARD and methotrexate as a second option, and were followed up for 1 yr. Radiographic progression in the hands and feet (total radiographic Larsen score and the erosion joint count) was used as the outcome variable. Clinical, laboratory, immunogenetic and radiographic data were obtained at study entry. Disease activity and response to therapy were measured at 6 and 12 months.
Results. Erosive disease was found in 21.7% of patients at baseline and in 38.3% after 1 yr. Although a substantial reduction in disease activity was observed during the 1 yr follow-up [disease activity score (DAS28) 5.8±0.8 at entry and 3.9±1.3 at 12 months, P < 0.001], the Larsen score rose from 1.9±3.3 to 5.6±9.8 after 1 yr. In 26.6% of patients, a raised erosion joint count was observed after 1 yr. Radiographic progression in the total joint radiographic damage (increase in Larsen score of ≥2) was observed in 36.6%. In the multivariate analysis, baseline pain [visual analogue scale (VAS)] and the presence of two copies of the shared epitope were associated with radiographic progression in the erosion joint count. Disease duration before study entry, VAS pain and Larsen score at baseline were significant predictors of radiographic progression in total damage (Larsen score). Baseline radiographic damage had the highest positive predictive value for progression.
Conclusions. Radiographic progression was observed in up to 36.6% of patients with early RA after 1 yr of DMARD therapy in spite of a significant reduction in disease activity. Baseline factors, such as VAS pain, disease duration until DMARD therapy, damage score at baseline and the presence of two copies of the shared epitope, were associated with radiographic progression.

To analyze whether inflammatory disease activity plays a substantial role in the loss of bone mass observed in ankylosing spondylitis (AS) patients who have not yet developed ankylosis. A longitudinal cohort study of 34 patients with early AS (duration <10 years) without ankylosis was conducted. The mean followup was 19 months. Loss of bone mass in defined regions of the lumbar spine and femoral neck was analyzed by dual x-ray absorptiometry. Patients were grouped according to biologic parameters of disease activity (erythrocyte sedimentation rate or C-reactive protein level). Group 1 consisted of 14 patients with active disease; group 2 comprised 20 patients with inactive disease. Serum levels of interleukin-6 (IL-6) and of hormones (sex, thyroid, and calciotropic), vertebral mobility (Schober test), daily physical activity, and treatment administered were recorded every 6 months for all patients. At the end of the followup period, patients with active AS showed a significant reduction in bone mass in the lumbar spine (mean 1.01 gm/cm² at study entry versus 0.961 gm/cm² at followup [P = 0.005]) and femoral neck (0.849 gm/cm² versus 0.821 gm/cm² [P = 0.015]), which represented losses of 5% and 3%, respectively. In contrast, no significant reduction in bone mass was observed in patients with inactive AS. As expected, serum IL-6 levels were significantly higher in patients with active AS than in those with inactive disease (mean ± SD 8.3 ± 9 pg/ml versus 2.8 ± 5 pg/ml [P = 0.008]). No significant differences were observed between the 2 groups in any of the other variables analyzed. The observation that loss of bone mass in AS occurred only in patients with persistent active disease strongly suggests that inflammatory activity of the disease itself plays a major role in the pathophysiology of the early bone mineral disorders observed in these patients.