Reactive arthritis following Yersinia pseudotuberculosis infection.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A L Bell.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
During a five month period in the summer of 1987, seven cases of reactive arthritis were seen at Musgrave Park Hospital, Belfast. Of the seven patients, five were male and two female. Their ages ranged from 13 to 44 (mean: 26 +/- 4) years. Five patients gave a preceding short history of diarrhoea which was usually mild. All patients presented with acute inflammatory oligoarthritis which predominantly affected the lower limbs. The knees were involved in 100%, the ankles in 70% with enthesopathy in 30% of cases. The diagnosis was confirmed in all cases by positive serology for Salmonella enteritidis. In three patients, stool cultures grew a particular strain of Salmonella enteritidis (phage type 4). Six patients were HLA-B27 positive. It is not possible to estimate the prevalence of reactive arthritis in this outbreak because there were different sources of infection and the total number of gastroenteritis cases was unknown. However, gut infections with Salmonella enteritidis are becoming increasingly common in this community and throughout the Western world. Over the past two years, in our area, there has been an almost thirty-fold increase in the number of recorded cases of infections due to this organism. By far the commonest source of infection appears to be poultry and egg products.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Three human adult femurs were examined using anteroposterior (AP) roentgenograms in anatomical position and in 15 degrees, 30 degrees, and 45 degrees of internal and external rotation. Relatively small (15 degrees or less) amounts of femoral rotation can cause significant changes in proximal femoral dimensions on supine AP hip roentgenograms, and the magnitude of these changes increases with rotation. Fifteen degrees of rotation can change it by almost 3 mm. These changes are comparable to the medullary canal expansion of a normal adult femur over a five- to ten-year period. These changes in measured proximal femoral dimensions with rotation necessitate either an improved roentgenographic technique or precise rotational matching of standard supine roentgenograms to obtain accurate measurements of their changes over time.
Ecto-5'nucleotidase (5'NT) activity in the plasma membrane of peripheral blood monocytes from patients with multiple sclerosis (MS), rheumatoid arthritis (RA), myasthenia gravis (MG), motor neuron disease (MND), and from normal control subjects of similar age was determined by radioisotopic assay. The activity in unstimulated monocytes cultured for 24 and 48 hours was found to be higher than normal in 56% of patients with active relapsing MS, 29% of patients with RA, and 7% of patients in the MG/MND group. While the enzyme activity was reduced after cultivation of the cells with recombinant interferon-gamma (gamma-IFN) in all of the groups studied, the percentage reduction was significantly greater in monocytes from patients with active relapsing MS who were in relapse at the time of sampling (p = 0.03). HLA-DR expression was monitored using immunofluorescence staining with monoclonal antibody and showed that similar numbers of monocytes in all patient and control groups expressed this antigen. Thus, while high monocyte 5'NT activity was found principally in patients with active relapsing MS and in some patients with RA, the monocytes from patients with MS were, in addition, exquisitely sensitive to stimulation with gamma-IFN.
We compared the mechanical performance of the Orthofix pelvic external fixator with that of the Pittsburgh triangular frame (PTF) on eight fresh-frozen cadaver pelves with experimentally created Malgaigne (double-vertical) fracture/dislocations. The pelves were quasi-statically loaded in longitudinal compression and loss of reduction (i.e., failure) was defined as 1.5 cm of diastasis at either of the fracture/dislocation sites. The Orthofix frame-pelvis complex (four 6-mm half-pins) was comparable to the PTF-pelvis complex (eight 5-mm half-pins) in terms of load to failure and overall stiffness, but was 4-7 times stiffer at lower load levels. Both frame-and-pin complexes deformed moderately at the pin-bone interface, but, while the PTF also showed moderate displacement between frame components, the Orthofix had almost no frame intercomponent motion.
A 46-year-old man with AIDS, receiving inhaled pentamidine for Pneumocystis carinii pneumonia (PCP) prophylaxis, developed bilateral upper lobe infiltrates. Bronchoalveolar lavage confirmed the diagnosis of PCP. Therapy with intravenous trimethoprim-sulfamethoxazole (TMP-SMX) was begun, with gradual resolution of these infiltrates noted. An explanation for the development of upper lobe PCP, despite aerosol chemoprophylaxis, is presented and emphasizes the importance of aerosol particle size (and therefore of nebulizer type) on the distribution of inhaled pentamidine.
Explore the source record for details and available documents.
Acute alveolar injury (AAI) was induced in dogs by injection of N-nitroso-N-methylurethane. Two to 20 days after injection, alveolar lavage phospholipids were quantified. Lavage surfactant was partially purified by centrifugation (27,000 g for 2 h), and further purified by centrifugation in NaBr density gradient (100,000 g for 4 h). Phospholipids, neutral lipids, surfactant-associated proteins, and surface properties of partially purified and purified surfactants were analyzed. Lavage disaturated phosphatidylcholine (DSPC) decreased to 37% of control at peak injury (Days 6 to 8) and increased to near normal during recovery (Days 10 to 20). Lavage phosphatidylglycerol (PG) decreased to 22% of control at peak injury and remained in that range through recovery. In both partially purified and purified surfactants, percentages of phosphatidylcholine (PC), DSPC, phosphatidylethanolamine, and cholesterol in all phases of injury and recovery were not different from those in control animals. However, percentage of PG decreased markedly during injury and remained low through recovery, whereas those of phosphatidylinositol and lysoPC increased with injury and remained elevated through recovery. The PC-to-sphingomyelin ratio (L/S ratio) and percentage of triglyceride decreased during injury and returned to control values during recovery. Surfactant apoprotein of molecular weight 38,000 from partially purified and purified surfactant decreased markedly at peak injury and recovered to normal during recovery. During early and peak injury, both preparations failed to reduce surface tension below 19 dyne/cm and their isopycnic densities were altered. These studies indicate that, in addition to decreased quantity, qualitative changes in lipids and apoproteins and reduced surface activity of the surfactant occur during nitrosourethane-induced AAI.(ABSTRACT TRUNCATED AT 250 WORDS)
The 4-aminoquinolines chloroquine (CQ) and hydroxychloroquine (HCQ), and previously the 9-aminoacridine mepacrine (quinacrine) (MP), have been widely used in the treatment of inflammatory disorders such as rheumatoid arthritis and systemic lupus erythematosus. Their effects are believed to be mediated through phagocytic cells but the precise biochemical basis remains uncertain. We have investigated the effects of these drugs on monocyte superoxide anion (SO) generation elicited by 5 different stimuli-opsonised zymosan (STZ), FMLP, A23187, TPA and fluoride--and sought correlations with effects on two processes which have been linked with monocyte activation, namely arachidonate (AA) release and transmethylation of phosphatidyl ethanolamine (PE) to phosphatidylcholine (PC). In all experiments conditions were adjusted to achieve leucocyte concentrations of drug comparable to those found during in vivo therapy. Neither CQ nor HCQ had any marked effect on SO release induced by TPA, A23187 or fluoride ion, excluding a significant effect on protein kinase C (PKC), calmodulin-dependent kinase(s) or the membrane-bound, superoxide generating NADP(H) oxidase. In contrast MP inhibited the response to TPA and A23187. Each drug also had different effects on surface receptor-dependent responses; thus HCQ inhibited FMLP- but not STZ-induced SO release, whereas CQ and MP inhibited the response to both stimuli. Each drug also displayed different effects on AA release and phospholipid (PL)-methylation; MP and HCQ, but not CQ, inhibited STZ-stimulated AA release while MP and CQ but not HCQ inhibited basal rates of PL-methylation in mononuclear cells (MNC). However, only MP inhibited PL-methylation in an enriched monocyte population. We conclude that despite their close structural similarity, MP, CQ and HCQ each have different metabolic effects and their actions cannot simply be attributed to inhibition of lysosomal functions. Other possible mechanisms of action are discussed. The selective effects of each drug also provide further evidence for multiple pathways of monocyte activation.
Rates of superoxide (SA) generation by blood monocytes stimulated ex vivo were studied before and during corticosteroid treatment of rheumatoid arthritis (RA) patients, in control patients and in healthy controls. The direct effect on stimulated SA production of pre-incubating cells with prednisolone in vitro was also studied. Significant inhibition of monocyte SA output stimulated with IgG-treated zymosan (ITZ) and fluoride ion (F), but not serum-treated zymosan (STZ) was demonstrated following steroid therapy in RA. No inhibitory effect of prednisolone could be demonstrated in vitro, using ITZ, STZ and F as stimuli. Our data on blood monocyte yields, size and cytochemistry suggest that the in vivo effect is due to a shift in blood monocyte traffic.
The capacity of monocytes from patients with rheumatoid arthritis to generate superoxide anion in vitro after stimulation with serum treated zymosan (STZ) or IgG treated zymosan (IgTZ) was studied before and during therapy with penicillamine (n = 9) or sodium aurothiomalate (AuTM) (n = 12). Significant increases in rates of STZ (p less than 0.01) and IgTZ (p less than 0.02) stimulated superoxide anion production were seen after successful therapy (14 patients), which were paralleled by a significant increase in serum thiol levels. Patients who did not respond clinically to therapy (n = 4) showed a smaller mean increase in serum thiol levels and had high mean rates of in vitro superoxide production before and after second-line therapy. Three patients were withdrawn from the study. The data suggest that successful therapy with penicillamine or AuTM may be associated with monocyte activation, and possible mechanisms are discussed.
Ophthalmoscopy and three tests of visual function were undertaken in 39 patients with rheumatoid arthritis receiving treatment with antimalarial drugs and in a control group of 16 patients with rheumatoid arthritis who were not receiving such treatment. Visual contrast sensitivity, macular threshold to red light, and central visual fields to red targets were not significantly different in treated patients and controls. There were no abnormalities in visual acuity, but 11 of 76 eyes of treated patients showed minor macular abnormalities on ophthalmoscopy that were not seen in control patients, suggesting that ophthalmoscopy may be the most sensitive measure of early drug toxicity. Five rheumatologists were able to identify 52 of 65 minor changes detected by an ophthalmologist. These studies, and a critical review of published reports, suggest that in clinical practice antimalarial drugs can be administered safely to patients with rheumatoid arthritis without the need for repetitive routine examination by an ophthalmologist or the use of complicated physiological tests. Recording of visual acuity in each eye and ophthalmoscopy by the prescribing doctor may be all that are required to detect early antimalarial maculopathy.
Lung surfactant was isolated from bronchoalveolar lavage of dogs during the late phase of recovery (15 days) from acute alveolar injury induced by subcutaneous injection of N-nitroso-N-methylurethane. This surfactant was compared with surfactant from control dogs in terms of in vitro surface properties, phospholipid composition and protein content, and those of its subfractions. Phospholipid composition and protein content were similar in the two groups, except that phosphatidylglycerol (PG) was markedly reduced and phosphatidylinositol (PI) was increased in the experimental group. In both, isopycnic densities of their subfractions in continuous sucrose density gradient were identical. The time course of surfactant adsorption was similar in both groups. Minimum surface tension (gamma min) was 4.1 +/- 1.5 dynes/cm in the experimental dogs and 3.8 +/- 1.3 dynes/cm in the controls. Surface compressibility (SC), stability index (SI), and dynamic respreadability (DR) of the surfactants from the two groups were nearly identical. When compared to an artificial surfactant composed of dipalmitoyl phosphatidylcholine (DPPC) and PG in 9:1 molar ratio a mixture of DPPC-PI 9:1 prepared identically showed similar gamma min, SC, SI, and DR, and a much higher surface adsorption rate. These results suggest that PG is not essential for normal in vitro surfactant function and that its role may be assumed by PI.
Acute alveolar injury closely resembling that seen in humans was induced in dogs by subcutaneous injection of N-nitroso-N-methylurethane. Necrosis of alveolar epithelial cells was observed during early injury. Proliferation of immature epithelial cells which began during early injury and became massive after peak injury was followed by their differentiation to mature type II cells during recovery. Quantities of diphosphatidylglycerol (DPG) and of phosphatidylglycerol (PG) in alveolar lavage and in post-lavage lung tissue were measured. An increase in tissue DPG coincided with a sharp decrease in tissue and lavage PG during early injury. DPG was not detectable in the lavage. During late recovery, tissue DPG increased threefold over controls. This increase was accompanied by persistence of a 50% decrease in tissue PG and 83% decrease in lavage PG. Biosynthesis of DPG and PG in isolated lung mitochondria demonstrated that DPG was formed from PG in the presence of CDP-diglyceride. These findings suggest that the low level of PG in the surfactant complex during acute alveolar injury is due to increased turnover of PG to DPG in the lung.
Lysolecithin acyltransferase (EC 2.3.1.23) activities in lung homogenates and in subcellular fractions, and fatty acid composition of phosphatidylcholine (PC) in lung lavage were studied in dogs with acute alveolar injury induced by N-nitroso-N-methylurethane. The specific activity in the microsomal fraction was 10 and 3 times higher than those of homogenate and mitochondrial fractions, respectively. Both the lysolecithin acyltransferase activities and the proportions of palmitate in alveolar lavage PC increased during the early phase of injury (days 2-4), and decreased during peak injury (days 6-8). Such correlation was not found during the recovery period (day 15). During recovery, specific and total activities of the enzyme were nearly 2- and 3-fold, respectively, those of controls. Nevertheless, the palmitate proportions in PC were normal, indicating that the increased enzyme activity in vitro was not reflected in increased PC palmitate during recovery. This finding indicates that the enzyme activity per cell was normal during recovery and suggests that the increase in specific and total activities is due to massive regeneration of type II cells and that the enzyme is localized mainly in these cells. The decrease in the proportion of palmitate in lavage PC during peak injury may lead to abnormality of surfactant function.