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We describe a case of a patient with a functional coma ,and give a systemic review of literature. Functional coma is an extremely rare disorder with only 21 described cases in the literature. The disease is linked to a conversion disorder or a dissociative disorder and is predominantly found in females. Predisposing factors are a history of sexual or physical abuse, psychiatric disorders, previous episodes of functional coma, and recent surgery with general anesthesia. Several clinical signs are suggestive for the diagnosis, however none of them is sufficiently sensitive or specific. Therefore, functional coma remains an exclusion diagnosis. Vital signs must be normal, just as a routine blood examination, an electroencephalogram and imaging of the central nervous system. The most important differential diagnosis are catatonia, factitious disorder, and malingering. Spontaneous recovery can be expected after a duration of about 45 minutes to 4 days.

ObjectivesCombining disease-modifying antirheumatic drugs (DMARDs) with glucocorticoids (GCs) is an effective treatment strategy for early rheumatoid arthritis (ERA), yet the ideal schedule and feasibility in daily practice are debated. We evaluated different DMARD combinations and GC remission induction schemes in poor prognosis patients; and methotrexate (MTX) with or without GC remission induction in good prognosis patients, during the first treatment year.MethodsThe Care in ERA (CareRA) trial is a 2-year investigator-initiated randomised pragmatic open-label superiority trial comparing remission induction regimens in a treat-to-target approach. DMARD-inexperienced patients with ERA were stratified into a high-risk or low-risk group based upon presence of erosions, disease activity, rheumatoid factor and anticitrullinated protein antibodies. High-risk patients were randomised to a COBRA Classic (MTX + sulfasalazine + prednisone step-down from 60 mg), COBRA Slim (MTX + prednisone step-down from 30 mg) or COBRA Avant Garde (MTX + leflunomide + prednisone step-down from 30 mg) scheme. Low-risk patients were randomised to MTX tight step-up (MTX-TSU) or COBRA Slim. Primary outcome was the proportion of patients in 28 joint disease activity score calculated with C-reactive protein remission at week 52 in an intention-to-treat analysis. Secondary outcomes were safety and effectiveness (ClinicalTrial.gov identifier NCT01172639).Results98 COBRA Classic, 98 COBRA Slim (high risk), 93 COBRA Avant Garde, 47 MTX-TSU and 43 COBRA Slim (low risk) patients were evaluated. Remission was achieved in 64.3% (63/98) COBRA Classic, 60.2% (59/98) COBRA Slim (high risk) and 62.4% (58/93) COBRA Avant Garde patients at W52 (p=0.840); and in 57.4% (27/47) MTX-TSU and 67.4% (29/43) COBRA Slim (low risk) patients (p=0.329). Less adverse events occurred per patient with COBRA Slim (high risk) compared with COBRA Classic or COBRA Avant Garde (p=0.038). Adverse events were similar in MTX-TSU and COBRA Slim (low risk) patients (p=0.871). At W52, 76.0% patients were on DMARD monotherapy, 5.2% used GCs and 7.5% biologicals.ConclusionsMTX with a moderate-dose GC remission induction scheme (COBRA Slim) seems an effective, safe, low-cost and feasible initial treatment strategy for patients with ERA regardless of their prognostic profile, provided a treat-to-target approach is followed.Trial registration numbersEudraCT-number 2008-007225-39 and NCT01172639; Results.

ObjectivesTo compare the efficacy and safety of intensive combination strategies with glucocorticoids (GCs) in the first 16 weeks (W) of early rheumatoid arthritis (eRA) treatment, focusing on high-risk patients, in the Care in early RA trial.Methods400 disease-modifying antirheumatic drugs (DMARD)-naive patients with eRA were recruited and stratified into high risk or low risk according to classical prognostic markers. High-risk patients (n=290) were randomised to 1/3 treatment strategies: combination therapy for early rheumatoid arthritis (COBRA) Classic (methotrexate (MTX)+ sulfasalazine+60 mg prednisone tapered to 7.5 mg daily from W7), COBRA Slim (MTX+30 mg prednisone tapered to 5 mg from W6) and COBRA Avant-Garde (MTX+leflunomide+30 mg prednisone tapered to 5 mg from W6). Treatment modifications to target low-disease activity were mandatory from W8, if desirable and feasible according to the rheumatologist. The primary outcome was remission (28 joint disease activity score calculated with C-reactive protein ResultsData from 98 Classic, 98 Slim and 94 Avant-Garde patients were analysed. At W16, remission was reached in 70.4% Classic, 73.6% Slim and 68.1% Avant-Garde patients (p=0.713). Likewise, no significant differences were shown in other secondary endpoints. However, therapy-related AEs were reported in 61.2% of Classic, in 46.9% of Slim and in 69.1% of Avant-Garde patients (p=0.006).ConclusionsFor high-risk eRA, MTX associated with a moderate step-down dose of GCs was as effective in inducing remission at W16 as DMARD combination therapies with moderate or high step-down GC doses and it showed a more favourable short-term safety profile.EudraCT number:2008-007225-39.

Objective Infliximab treatment results in a decrease in synovial cellularity as early as 48 hours after initiation of therapy in patients with rheumatoid arthritis (RA). This study was undertaken to investigate whether infliximab induces apoptosis within the first 24 hours after infusion. Methods The percentage of apoptotic cells was determined by flow cytometry in blood drawn from 21 patients directly before, 1 hour after, and 24 hours after infliximab infusion. Synovial tissue samples obtained before, 1 hour after (n = 5), or 24 hours after (n = 5) initiation of therapy were subjected to immunohistochemistry to detect active caspase 3 and to TUNEL assay and electron microscopy to detect apoptosis. In addition, plasma levels of nucleosomes (generated during apoptosis) and C4b/c (an indicator of complement activation) were measured. Results There were no signs of apoptosis induction in peripheral blood monocytes or lymphocytes after infliximab treatment. Circulating lymphocyte counts were increased within 1 hour after infusion (P < 0.05). There was no definite evidence of apoptosis induction in the synovium, except in 1 patient 24 hours after the infliximab infusion. Consistent with these results, there was no increase in nucleosome levels nor were there signs of complement activation. Conclusion Our findings indicate that the rapid decrease in synovial cellularity observed after initiation of anti–tumor necrosis factor antibody therapy cannot be explained by apoptosis induction at the site of inflammation. It is tempting to speculate that the striking effects on synovial inflammation may be explained by other mechanisms, such as decreased migration toward the synovial compartment and reduced retention in the inflamed synovium.

Transient production of reactive oxygen species (ROS) plays an important role in optimizing transcriptional and proliferative responses to TCR signaling in T lymphocytes. Conversely, chronic oxidative stress leads to decreased proliferative responses and enhanced transcription of inflammatory gene products, and is thought to underlie the altered pathogenic behavior of T lymphocytes in some human diseases, such as rheumatoid arthritis (RA). Although the signaling mechanisms regulating ROS production in T lymphocytes has not been identified, activation of the small GTPase Ras has been shown to couple agonist stimulation to ROS production in other cell types. We find that Ras signaling via Ral stimulates ROS production in human T lymphocytes, and is required for TCR and phorbol ester-induced ROS production. The related small GTPase Rap1 suppresses agonist, Ras and Ral–dependent ROS production through a PI3K–dependent pathway, identifying a novel mechanism by which Rap1 can distally antagonize Ras signaling pathways. In synovial fluid T lymphocytes from RA patients we observed a high rate of endogenous ROS production, correlating with constitutive Ras activation and inhibition of Rap1 activation. Introduction of dominant-negative Ras into synovial fluid T cells restored redox balance, providing evidence that deregulated Ras and Rap1 signaling underlies oxidative stress and consequent altered T cell function observed in RA.

The T lymphocytes that reside in the synovium of the inflamed joints in patients with rheumatoid arthritis display severe hyporesponsiveness upon antigenic stimulation, which is probably due to their constant subjection to high levels of oxidative stress. Here we report that the synovial fluid T lymphocytes exert severely impaired phosphorylation of the adaptor protein linker for activation of T cells (LAT), a crucial component of the TCR-mediated signaling pathways. In healthy T lymphocytes, LAT is a membrane-bound protein and becomes phosphorylated by ζ-associated protein of 70 kDa (ZAP-70) upon TCR engagement. The molecular basis underlying the deficient phosphorylation of LAT and consequently the hyporesponsiveness of the synovial fluid T lymphocytes lies in the membrane displacement of LAT. We demonstrate that the subcellular localization of LAT is sensitive to changes in the intracellular levels of the antioxidant glutathione. The membrane anchorage of LAT, and consequently the phosphorylation of LAT and the cellular activation of the synovial fluid T lymphocytes upon TCR engagement, is restored in synovial fluid T lymphocytes after supplementation of the intracellular glutathione levels with N-acetyl-l-cysteine. These data suggest a role for the membrane displacement of LAT in the hyporesponsiveness of the synovial fluid T lymphocytes as a consequence of oxidative stress.

Selective 1,4-addition of water to butadiene monoxide can be achieved in a liquid phase catalytic process using ultrastable Y zeolite as Bronsted acid, potassium iodide, and an ether solvent. The reaction mechanism could be elucidated based on the occurrence of intermediate reaction products. Iodide is added to the terminal unsaturated carbon atom of a protonated butadiene monoxide molecule. The strong solvent effect observed can be rationalised based on the nucleophilicity of the iodide depending on the basicity of the ether function. With USY zeolite, the 2-butene-1,4-diol selectivity reaches 73.9% at 100% conversion when using 1,2-dimethoxyethane solvent, 2,5-dihydrofuran being the main by-product. With this catalytic system followed by an additional hydrogenation step, butadiene monoxide can be selectively converted into 1,4-butanediol.

Cobalt on carbon nanofiber model catalysts with very small dispersed cobalt particles of 5 nm were subjected to H(2)O/H(2) treatments at 20 bar and 220 degrees C. Using in situ Mossbauer spectroscopy we could unambiguously prove that oxidation of the nanoparticles by water will not occur when hydrogen is present. Only in a water/argon atmosphere did oxidation take place. This rules out oxidation as the deactivation mechanism in Fischer-Tropsch synthesis. Even more important, we define the relative humidity (RH) as a key parameter to understanding deactivation by water. At a RH below 25% sintering was absent even when measuring for 4 weeks, whereas at a high RH of 62% as much as half of the small super paramagnetic cobalt particles (5 nm) sintered into larger particles in 1 week. Activity loss as measured at Fischer-Tropsch conditions amounted to 73%, which could be directly related to the metal dispersion loss 77% due to sintering as evidenced by detailed TEM analysis of the spent sample.

The sections in this article are Introduction to GTL Basic Steps in GTL Synthesis Gas Production and Purification Purification of Natural Gas Sulfur Removal Hydrocarbon Removal Trace Components Removal Present Syngas Generation Technologies Non-catalytic Partial Oxidation (POX) Autothermal Reforming (ATR) Developments Purification of Syngas Fischer–Tropsch Reaction Reactor Types Catalysts Active Metals Carriers Promoters Reaction Mechanisms and Kinetics Catalyst Poisons Sulfur Compounds Others Mild Hydrocracking Process Description Catalysts Composition Other Requirements Reaction Mechanism Reactor Products LPG Naphtha Kerosene Base Oils Gas Oil Challenges in GTL, CTL and BTL Keywords: gas-to-liquids; synthesis gas; syngas; natural gas; Fischer–Tropsch; hydrocarbons

Background To date, intensive DMARD combination therapy with glucocorticoids (GCs) is the most effective treatment approach for the management of early Rheumatoid Arthritis (eRA). The ideal content of the combination and the dose of GCs are however not yet known. Objectives To compare different intensive combination treatment strategies associated with GCs in eRA patients with a poor prognosis at week (W)52 in the CareRA trial. Methods CareRA is a two year prospective investigator-initiated multicenter RCT rooted in daily practice. DMARD naive eRA patients were stratified into a high or low-risk group based on classical prognostic markers (presence of erosions, rheumatoid factor, anti-cyclic citrullinated protein and DAS28(CRP). High-risk patients (n=290) were randomized to 1 of 3 treatment strategies. 1) Cobra Classic (n=98): Methotrexate (MTX)+Sulphasalazine+60mg prednisone tapered weekly to 7.5mg daily from W7 2) Cobra Slim (n=98): MTX+30mg prednisone tapered to 5 mg daily from W6 3) Cobra Avant-Garde (n=94):MTX+Leflunomide +30mg prednisone tapered to 5 mg daily from W6 From W28, GCs were tapered in all patients and stopped at W34. A predefined treat to target approach was applied. From W40, we aimed for DMARD monotherapy. Efficacy measures were proportions of DAS28(CRP) remission, good EULAR response, clinically meaningful HAQ response, HAQ=0 (ITT analysis). Radiographic progression was measured via the Sharp Van der Heijde score. Adverse events related to therapy (AEs) were registered. Missing data were imputed by last observation carried forward. Results Remission rates were 64.3%, 60.2% and 62.8% in the Classic, Slim and Avant-Garde group respectively (p=0.837). Also no other efficacy outcomes did not differ between groups. 82% of X-ray images were available at baseline. Radiographic progression was minimal. SvH scores were 1.3±2.1, 1.3±2.5 and 1.0±1.4 at baseline and changed over 52 weeks 0.3±0.5, 0.4±1.1 and 0.3±0.6 in the Classic, Slim and Avant-Garde group respectively (p=0.581). The total numbers of AEs were 182 in 65 Classic patients, 125 in 64 Slim patients and 174 in 72 Avant-Garde patients (p=0.026). Serious AEs were reported in 3 Classic, 2 Slim and 3 Avant-Garde patients. Conclusions High rates of remission were achieved at week 52 with csDMARDs and GCs in all remission induction schemes. Cobra Slim showed comparable efficacy with less adverse events compared to DMARD combinations with moderate or high GC dosages. Disclosure of Interest None declared

Background Early intensive treatment to target is recommended in severe early Rheumatoid Arthritis (eRA). However, data are lacking in patients presenting without markers of poor prognosis. Objectives To compare Methotrexate (MTX) with or without Glucocorticoid (GC) remission induction in a tight control setting over 52 weeks in low-risk patients with eRA. Methods CareRA is a two year prospective investigator-initiated multicenter RCT rooted in daily practice. DMARD naive eRA patients were stratified into a high or low-risk group according to classical prognostic markers (presence of erosions, rheumatoid factor, anti-cyclic citrullinated protein and disease activity). In the low-risk arm, 43 patients were randomized to 15mg MTX monotherapy following a Tight Step Up (MTX-TSU) approach and 47 patients to a Cobra Slim schedule (MTX+30mg prednisone tapered to 5mg daily from W6). GCs were tapered from W28 and stopped at W34. A predefined treat to target approach was applied. Efficacy measures were proportions of DAS28(CRP) remission, good EULAR response, clinically meaningful HAQ response, HAQ=0 and Area Under the Curve (AUC) for DAS28(CRP) (ITT analysis). Radiographic progression was measured via the Sharp Van der Heijde (SvH) method. Adverse events related to therapy (AEs) were registered. No power was calculated in this explorative study. Missing data were imputed via last observation carried forward. Results Remission rates at week 52 were 57.4% and 67.4% in the MTX-TSU and Cobra Slim group respectively (p=0.329). MTX-TSU patients had a higher AUC for DAS28(CRP) than Cobra Slim patients over 52 weeks of treatment (p=0.017). No other efficacy scores differed between groups. 76% of X-ray images were available at baseline. Radiographic progression was minimal. SvH scores were 0.7±1.1 and 0.9±1.5 at baseline and changed over 52 weeks 0.2±0.3 and 0.3±0.4 in the MTX-TSU and Cobra Slim group respectively (p=0.184). The numbers of AEs were 48 in 27 MTX-TSU patients and 49 in 20 Cobra Slim patients (p=0.871). Two serious AEs (pulmonary infection and anemia) were registered in the Cobra Slim group. We observed numerically more treatment adaptations and IM/IA GC injections in MTX-TSU patients. Conclusions Both RA therapies achieved high remission rates in a tight control setting at week 52. However, remission induction with Cobra Slim resulted in a more rapid and sustained disease control. MTX with or without GC remission induction showed a comparable safety profile. Disclosure of Interest None declared

Objective Oxidative stress contributes to the inflammatory properties of rheumatoid arthritis (RA) synovial T lymphocytes. This study was undertaken to investigate the mechanisms leading to production of reactive oxygen species (ROS) and oxidative stress in RA synovial T lymphocytes. Methods ROS production in T lymphocytes from the peripheral blood (PB) of healthy donors and from the PB and synovial fluid (SF) of RA patients was measured by ROS-dependent fluorescence of 6-carboxy-2′,7′-dichlorofluorescein. Rap1 GTPase activation was assessed by activation-specific probe precipitation. Proliferation of RA PB and SF T lymphocytes was assayed by 3H-thymidine incorporation. In some experiments, RA PB T cells were preincubated with autologous SF or with PB or SF adherent cells. Experiments were performed in the absence or presence of transwell membranes or CTLA-4Ig fusion proteins. Short- and long-term stimulations of healthy donor PB T lymphocytes were performed with inflammatory cytokines, in the absence or presence of activating anti-CD28 antibodies. Results T lymphocyte ROS production and Rap1 inactivation were mediated by cell–cell contact with RA synovial adherent cells, and this correlated with T cell mitogenic hyporesponsiveness. CTLA4-Ig blockade of synovial adherent cell signaling to CD28 T cells reversed the inhibition of Rap1 activity and prevented induction of ROS. Introduction of active RapV12 into T cells also prevented induction of ROS production. Coincubation of T cells with stimulating anti-CD28 antibodies and inflammatory cytokines synergistically increased T cell ROS production. Conclusion Cell–cell contact between T cells and RA synovial adherent cells mediates Rap1 inactivation and subsequent ROS production in T lymphocytes following exposure to inflammatory cytokines. This process can be blocked by CTLA4-Ig fusion protein.

Objective To investigate the cellular and molecular sources of oxidative stress in patients with rheumatoid arthritis (RA) through analysis of the production of reactive oxygen species (ROS) in synovium. Methods Cytochemical procedures based on the 3,3′-diaminobenzidine (DAB)–Mn2+ deposition technique were used on unfixed cryostat sections of synovium from RA patients and rheumatic disease controls. For immunophenotyping, sections were incubated, fixed, and stained with fluorescein isothiocyanate–labeled antibodies. Fluorescence-activated cell sorter analysis of the ROS-reactive dye 6-carboxy-2′,7′-dichlorodihydrofluorescein diacetate-di(acetoxymethyl ester) was used to measure intracellular ROS in T lymphocytes from peripheral blood and synovial fluid. To determine which enzymes produced ROS, different inhibitors were tested. Results Large quantities of DAB precipitated in the majority of RA synovial T lymphocytes, indicative of intracellular ROS production. These ROS-producing T lymphocytes were observed throughout the synovium. Polymerization of DAB was observed to a lesser extent in other forms of chronic arthritis, but was absent in osteoarthritis. DAB staining of cytospin preparations of purified RA synovial fluid T cells confirmed the presence of ROS-producing cells. One of the ROS involved appeared to be H2O2, since catalase suppressed intracellular ROS production. Superoxide dismutase, which uses superoxide as a substrate to form H2O2, diphenyleneiodonium (an inhibitor of NADPH oxidase), NG-monomethyl-L-arginine (an inhibitor of nitric oxide synthesis), nordihydroguaiaretic acid (an inhibitor of lipoxygenase), and rotenone (an inhibitor of mitochondrial ROS production) failed to suppress ROS production. Conclusion Our findings show that chronic oxidative stress observed in synovial T lymphocytes is not secondary to exposure to environmental free radicals, but originates from intracellularly produced ROS. Additionally, our data suggest that one of the intracellularly generated ROS is H2O2, although the oxidase(s) involved in its generation remains to be determined.

Many chronic inflammatory diseases are associated with deregulated intracellular signal transduction pathways. Resultant pathogenic interactions between immune and stromal cells lead to changes in cell activation, proliferation, migratory capacity, and cell survival that all contribute to inflammation. Increasing efforts are now being made in the design of novel therapeutic compounds to interfere with signaling pathways in inflammatory diseases like rheumatoid arthritis (RA). In this review we will outline the major signal transduction pathways involved in the pathogenesis of RA. We will assess advances in targeting a number of key intracellular pathways, including nuclear factor-(kappa)B (NF-(kappa)B), mitogen-associated protein kinases (MAPKs), phosphoinositide 3-kinase (PI3K)/Akt, signal transducers and activators of transcription (STATs), and reactive oxygen species (ROS) production. Finally, we will discuss recently identified lead molecules and the progress of selected compounds towards becoming new drugs for the treatment of inflammatory diseases.

Background Whereas early intensive treatment to target is recommended in severe early Rheumatoid Arthritis (eRA), few data are available in patients presenting without bad prognostic markers. Objectives To evaluate the efficacy and safety of methotrexate (MTX) monotherapy compared to MTX combined with a glucocorticoid (GC) bridging scheme during the first 16 weeks of treatment in “low risk” eRA patients. Methods CareRA is a prospective two year investigator-initiated multicenter RCT rooted in daily practice. 400 eRA patients were stratified into a high or a low risk group. Low risk was defined as: - No erosions and ACPA and RF negative - Erosions, ACPA and RF negative and low disease activity (DAS28(CRP)≤3.2 - No erosions, ACPA and/or RF positive and low disease activity (DAS28(CRP) ≤3.2 Patients were randomized to 15 mg MTX, either with a bridging scheme of initially 30mg GCs tapered to 5 mg from week (W) 6 (Cobra Slim) or without GCs (MTX Tight Step Up (MTX-TSU)). Treatment modifications to target low disease activity were mandatory from W8 onwards. The primary outcome was remission (DAS28(CRP) Results We included 90 low risk patients: 24.4% were RF positive, 25.6% ACPA positive and 1.1% erosive, with a mean ± SD DAS28(CRP) of 4.53±1.62; 43 patients were randomized in the Cobra Slim and 47 in the MTX-TSU arm. At W16, 65.1% of the Cobra Slim and 46.8% of the MTX-TSU patients were in remission (p=0.081). A good EULAR response was achieved in 44.7% of MTX-TSU and 58.1% COBRA SLIM patients (p=0.202). A clinically meaningful HAQ response was reached in 53.2% of the MTX-TSU and 62.8% of the COBRA SLIM group (p=0.357). More patients had a HAQ=0 at W16 with the Cobra Slim (51.2%) compared to the MTX-TSU (23.4%) schedule (p=0.006). The mean± SD AUC of DAS28(CRP) was 11.18±4.25 and 13.84±4.58 for the Slim and MTX-TSU arm respectively (p=0.006). Treatment adjustments were performed in 27.9% of Slim and 40.4% of MTX-TSU patients (p=0.212). Until W16, therapy related AEs were reported in 39.5% of Slim and in 44.7% of MTX-TSU patients (p=0.622). Conclusions Although the primary outcome, remission, was only numerically different after 16 weeks of treatment, cumulative disease activity over time and proportion with normalized HAQ were in favor of the Cobra Slim group, while related AEs didn9t differ. Disclosure of Interest : None declared DOI 10.1136/annrheumdis-2014-eular.2144

In this report we describe the association of progressive anterior vertebral body fusion, generalized over-growth especially with large hands and feet and unusual thick skin and subcutaneous tissue of upper and lower limbs, and peculiar craniofacial appearance.

Thirty-three out-patients with rheumatoid arthritis completed the study intended to compare under double-blind conditions, 50 mg levamisole tablets with placebo. Patients were given the double-blind medication at a dosage of one tablet t.i.d. for 3 months, and at a dosage of one tablet t.i.d., on 2 consecutive days every week for the next 3 months. Pain score, duration of morning stiffness, articular index and E. S. R. were recorded at the start of treatment, after 3 months of treatment and at the end of treatment. The levamisole patients made significantly better progress than did the placebo patients: for E.S.R. after 3 months of treatment, and for E.S.R., pain and morning stiffness by the end of treatment. Ten levamisole patients and 5 placebo patients reported adverse reactions. These were mainly gastrointestinal symptoms in the levamisole-treated patients.

Using a quantitative method, scintigraphy of SI joints was performed by means of 99m technetium pyrophosphate in 21 patients with definite ankylosing spondylitis, in 17 control patients, and in 26 patients 'at risk', i.e. patients with complaints of back pain of the inflammatory type where on clinical grounds there was a possibility of sacroiliitis developing but with normal x-ray findings of the SI joints. Radioisotope uptake was higher in the ankylosing spondylitis group than in the other two groups, although the difference was not statistically significant with regard to the group 'at risk'. The high variance in the three groups considerably reduces the diagnostic value of the examination. In the ankylosing spondylitis group no correlation was found between radioisotope uptake and age, duration of disease, erythrocyte sedimentation rate, or radiological stage of scaroiliitis. Since the specificity and sensitivity of scintiscanning are lower than that of clinical and radiological diagnosis of the disease, we conclude that scintigraphy is not very helpful in the early diagnosis of sacroiliitis, at least by the techniques used here.

Thirty-three out-patients with rheumatoid arthritis completed the study intended to compare under double-blind conditions, 50 mg levamisole tablets with placebo. Patients were given the double-blind medication at a dosage of one tablet t.i.d. for 3 months, and at a dosage of one tablet t.i.d., on 2 consecutive days every week for the next 3 months. Pain score, duration of morning stiffness, articular index and E. S. R. were recorded at the start of treatment, after 3 months of treatment and at the end of treatment. The levamisole patients made significantly better progress than did the placebo patients: for E.S.R. after 3 months of treatment, and for E.S.R., pain and morning stiffness by the end of treatment. Ten levamisole patients and 5 placebo patients reported adverse reactions. These were mainly gastrointestinal symptoms in the levamisole-treated patients.

Trabecular bone mass was measured in the iliac crest of 129 cadavera of both sexes with a physical method based on the principle of Archimedes. Cortical bone mass was measured at the second metacarpal of the right hand with a graphimetric X-ray method in 77 cases. Trabecular and cortical bone mass decreased significantly with age in women but not in men. A significant correlation between cortical and trabecular bone mass was established in women.