Thirty-five patients with Early Psoriatic Arthritis (EPA) (17 female and 18 male; mean age 25.6 years) entered this randomised 6-month study. At the enrolment, all patients were on non-steroidal anti-inflammatory drug (NSAID) therapy on demand and were divided in two matched groups (A and B). Group A continued NSAID therapy at full dosage in the following 3 months and then added methotrexate (MTX) for another 3 months. Group B was under the combination of NSAID and MTX for the entire 6-month period. Clinical and laboratory assessment included the count of tender joints and/or entheses (TJC), the count of swollen joints and/or entheses (SJC), patient's global assessment (PGA), physician's global assessment (PhGA), patient's assessment of pain (VAS), erythrocyte sedimentation rate (ESR) and serum concentration of C-reactive protein (CRP). All variables were done at baseline (T0), at 3 (T3) and at 6 months (T6). In both group A and in group B, there was a significant improvement of all variables at T3 and T6. However, in comparison to the patients of group A, patients included in group B showed a more rapid and marked improvement of TJC and SJC, which was statistically significant at T3 (p < 0.05). In contrast, the improvement of PGA, PhGA, VAS, ESR and CRP was not significantly different between groups. The early use of MTX in EPA patients markedly improves TJC and SJC. In fact, at T3, other markers used to quantify EPA disease activity, in particular PGA, PhGA, VAS, ESR and CRP, did not show significant differences in EPA patients treated with either NSAIDs or MTX. This finding suggests an incomplete control under MTX of the pathogenetic process and stimulates further interest on early use of other therapeutical approaches capable of modifying the course of disease.

Clostridium sordellii is an infrequent human pathogen. It has been demonstrated to be occasionally responsible for myonecrosis or gas gangrene. Interestingly, in the obstetric literature, some cases of postpartum maternal deaths have been associated with C sordellii infection causing a rapidly lethal toxin mediated syndrome. This is the first reported case of postpartum death in a 29 year old woman, in which a toxigenic C sordellii was isolated from the patient's blood antemortem during the fatal toxic shock, strongly indicating its role in this rare syndrome. (7 Clin Pathol 1997;50:259-260) Keywords: Clostridium sordellii; shock; toxin; postpartum. Case report A caesarean section was performed in a 29 year old woman, gravida 1, for cervical dystocia in the 41st week. The postoperative course was normal. Two days after delivery the patient was afebrile but complained of generalised weakness, dizziness in an orthostatic position, and pain in the epigastric region followed by hypotension (80/50 mm Hg), sinus tachycardia (1IO beats/minute), and low urinary output. The patient was given fluids and steroids but hypotension proved refractory. The abdomen was painful and tender. Ultrasonogram showed hyperperistalsis and anechoic areas scattered in the abdominal cavity; blood analysis showed noticeable haemoconcentration and hyperproteinemia. Laparotomy revealed a substantial amount of serosanguineous fluid, the peritoneum was lifted by a jelly-like retroperitoneal tissue, the appendiceal apex was hyperaemic and adhered to the rear parietal peritoneum, and the right adnexa appeared oedematous and thickened. Gall bladder, duodenum, stomach, ileum, ascendens, and transverse colon appeared thickened and ischaemic. Pancreas, spleen, and liver were normal. The patient underwent appendectomy and removal of the right adnexa, and was treated with antibiotics (intravenous cefotaxime 1 g three times a day.). Peritoneal exudate and blood were collected and cultured. Although clinical conditions partially improved, after a few hours the hypotension became refractory, her skin was pale and cool with cyanotic extremities, her temperature was normal, haematocrit was 57.6%, haemoglobin was 246 g/l, white cell count was 115 x 109/1; a decrease in total protein concentration (26 g/l), and calcium concentration (64 mg/l) was also observed. Because of serious cardiac conditions the patient was moved to an intensive care unit where she died six hours later. Clinical Pathology Microbiological studiesBlood was collected during laparotomy while the patient was on antibiotic therapy. Bactec 26A and Bactec 27A broths (Becton Dickinson Italia, Milan) were used to grow aerobes and anaerobes, respectively, in an automatic Bactec NR 730. Subcultures were performed using Schaedler agar (Difco Laboratories, Detroit, Michigan) supplemented with vitamin K for anaerobes, and mannitol salt agar, desoxycholate agar, Colombia blood agar and Sabouraud agar (Difco) for aerobes and yeasts. The peritoneal fluid was inoculated into thioglycollate and ...

Patients with arthritis who need treatment with biologics are carefully screened for possible previous exposure to tuberculosis to detect any latent tubercular infection (LTBI). The traditional method of screening for LTBI is not specific, because positivity could also depend on infection by atypical mycobacteria and bacillus Calmette-Guerin vaccination. In addition, the screening does not show high sensitivity, frequently presenting a false negativity because of immunosuppression caused by drugs used for arthritis. Recently, interferon-γ release assays (IGRA) have been used to screen LTBI with more sensitivity and specificity before treatment with anti-tumor necrosis factor-α drugs. Moreover, in our experience, IGRA are potentially useful in monitoring LTBI during biologic therapy.

Biological therapies and new imaging techniques have changed the therapeutic and diagnostic approach to spondyloarthritis. In patients with axial spondyloarthritis, tumor necrosis factor α (TNFα) inhibitor treatment is currently the only effective therapy in patients for whom conventional therapy with nonsteroidal anti-inflammatory drugs (NSAIDs) has failed. TNFα inhibitor treatment is more effective in preventing articular damage in peripheral joints than in axial ones. It is important to treat patients at an early stage of disease to reduce disease progression; moreover it is necessary to identify causes of therapy inefficacy in preventing joint damage in the axial subset.

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